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Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions
Abstract
The purpose of the study was to examine the effect of exercise timing on postprandial lipemia responses. Subjects were 21 recreationally trained men (ages 27 +/- 1.7 yr). Each subject performed four trials: 1) Control (fat meal only), 2) Post (exercise 1 h after a fat meal), 3) 1 h-Pre (exercise 1 h before a fat meal), and 4) 12 h-Pre (exercise 12 h before a fat meal). In each trial, subjects had a standard fat meal to induce postprandial hypertriglyceridemia. Blood samples were taken at 0 h (immediately before the fat meal) and at 2, 4, 6, 8, and 24 h after the meal. In the exercise trials, each subject exercised at 60% of maximal O2 consumption for 1 h. The results indicated that triglyceride area under the curve scores in premeal-exercise trials were lower (P < 0. 05) than those in Post and Control. At 24 h, total high-density lipoprotein (HDL)-cholesterol in the premeal-exercise trials was higher (P < 0.05) than that at 0 h, whereas total HDL-cholesterol was not changed in Control and Post. At 24 h, HDL subtype 2-cholesterol was higher (P < 0.05) in the premeal-exercise trials than in Control, which did not differ from Post. These results suggest that exercising before a fat meal may have a beneficial effect on the triglyceride response and HDL metabolism, which may blunt atherosclerotic process induced by the fat meal.
... The power calculation and sample size determination were based on the comparison of TG area scores in our previous study. 26 The calculated effective sample size was 1.88. The sample size necessary to make this kind of study significant at p < 0.05 was about 10 subjects. ...
... Twelve hours after each exercise session, participants ingested a high-fat meal (100 g fat). Choosing a protocol that included exercise 12 h prior to fat loading was based on previous findings, 26,32 which documented that exercising 12 h prior to fat loading more effectively attenuated postprandial lipemia than 24 h prior to or 1 h after a fat-meal intake. The exercise regiments were well tolerated by all participants. ...
... Thereafter, the speed remained constant, and the treadmill grade was raised by 2 % every minute until exhaustion. 26 The following criteria were used to determine VO 2max , oxygen uptake plateau, heart rate exceeding age-predicted maximal heart rate (220-age), or respiratory exchange ratio (RER) exceeding 1.10. ...
Objective
The purpose of this study was to investigate the effects of different exercise intensities on postprandial lipemia (PHTG) and insulin resistance in healthy individuals.
Methods
Participants were 10 adult males with normal fasting triglyceride (TG) concentrations (age = 34 ± 2.8 y, body mass = 72.9 ± 2.4 kg, fasting plasma TG = 1.36 ± 0.18 mmol/l, VO2max = 43.7 ± 3.0 ml/kg/min, fasting glucose = 5.2 ± 0.2 mmol/l and fasting Homeostatic Model Assessment for Insulin Resistance (HOMA2-IR) = 1.7 ± 0.3). In this study, each participant performed a control trial (Ctr, no exercise), and 3 exercise trials at 40 % (40%T), 60 % (60%T), and 70 % (70%T) of their VO2max. In the exercise trials, participant jogged on a treadmill for 1 h at a designated intensity. A fat-rich meal was consumed by each participant 12 h after exercise. Blood samples were taken at 0 h (before the meal), and 2 h, 4 h, 6 h, 8 h, and 24 h after the meal. The plasma TG, area score under TG concentration curve over an 8 h-period (TG tAUC) after the meal, and HOMA2-IR were analyzed.
Results
Our results showed that at 2 h, 4 h, and 6 h after the meal, TG in all exercise trials were lower than Ctr (p < 0.05) but did not differ from each other. All the exercise trials were lower in TG tAUC scores than Ctr (p < 0.02), but differences were not observed among the exercise trials. In comparison to Ctr, a significant difference in HOMA2-IR in both 60 % T and 70 % T (p < 0.05 and p < 0.01, respectively) was observed, but not in 40 % T.
Conclusion
The results suggest that exercising at low to moderate exercise intensity for 1 h sufficiently attenuates a fat meal induced PHTG. Moderate exercise intensity also effectively mitigates insulin resistance.
... High-intensity interval training (HIIT), and moderate-intensity interval training (MICT) are known to be among common non-pharmacological protocols for metabolism controlling and associated condition such as obesity by regulating hunger, satiety, and appetite perception [8].Several studies have reported the importance of MICT in improving body composition, cardiovascular tness, insulin resistance (IR), and lipid pro le [8][9][10]. While other investigations show similar physiological adaptation after either HIIT or MICT [11]. ...
... Increased hormone-sensitive lipase (HSL) activity induced by exercise through AMP kinase activation, increased epinephrine and glucagon activity, and downstream events cause lipolysis and free fatty acids released from adipose tissue and intracellular TG concentration [9]. Lipid oxidation provides strong evidence for the role of exercise adaptation in improving blood lipid pro les through [35] increased lipoprotein lipase (LPL) activity and hydrolyzing TG and LDL [9]. ...
... Increased hormone-sensitive lipase (HSL) activity induced by exercise through AMP kinase activation, increased epinephrine and glucagon activity, and downstream events cause lipolysis and free fatty acids released from adipose tissue and intracellular TG concentration [9]. Lipid oxidation provides strong evidence for the role of exercise adaptation in improving blood lipid pro les through [35] increased lipoprotein lipase (LPL) activity and hydrolyzing TG and LDL [9]. Compared to other groups, HIIT + S decreased FBS more signi cantly in this study. ...
Background: Abdominal obesity is a common phenomenon in metabolic syndrome (MetS). Inducing satiety by weight management plays an important role in reducing the risk of obesity and consequently MetS. This study was investigated effect of sodium alginate supplementation plus HIIT and MICT on CCK and PYY increment in MetS men.
Methods: For this purpose, 40 men with MetS volunteered and were randomly divided into five groups as follow: HIIT groups with supplement (n=8, 4*4 min bouts at 85-95% of HRpeak, with 3 min of active recovery at 50-70% HRpeak, 3 ses/week), HIIT (n=8, 4*4 min bouts at 85-95% of HRpeak, with 3 min of active recovery at 50-70% HRpeak, 3 ses/week), MICT with supplement (n=8, 30 min at 60-70% HRpeak, 3 ses/week), MICT (n=8, 30 min at 60-70% HRpeak, 3 ses/week) and control group (n = 8, no exercise). The HITT+S and MICT+S groups consumed 1.5 g of Sigma sodium alginate (made in the USA) solution in 100 mg of sweet water (7 g of fructose), 30 minutes before 3 main meals three days per week during 8 weeks.
Results: After 8 weeks of interventions, CCK and PYY were markedly increased in the studied groups, this increase was significantly greater in the HIIT+S than other groups. Also, the MetS Z score was significantly decreased in all studied groups and this decrease was significantly higher in the HIIT+S than other groups (P <0.05).
Conclusion: The results showed that HIIT and MICT led to an overall improvement in men with MetS. However, combining sodium alginate supplementation triggers these improvements.
Trial registration: IRCT20190916044788N1. Registered 12 march 2020, https://www.irct.ir/
... Le timing de l'exercice a aussi montré avoir un effet sur la lipidémie. En effet, un exercice effectué avant le repas permettrait une meilleure régulation des triglycérides (Haxhi et al., 2013;Zhang et al., 1998) Ces résultats concernant la sensation de satiété sont en contradiction avec ceux apportés par ...
... Recent studies effectively show that the beneficial effects of exercise might also depend on its timing during the day or its delay/position regarding a meal (Reid, Thivel, et Mathieu., 2019b). Some studies for instance showed that performing acute exercise one to three hours after a meal could enhance the glycemic response in patients with type II diabetes (Borror et al., 2018;Chacko, 2016;Haxhi et al., 2013;Teo et al., 2018) while others showed a better postprandial lipemia response when exercise was performed immediately before the meal (Petitt & Cureton, 2003;Zhang et al., 1998Zhang et al., , 2004. ...
... et du HDL cholestérol(Zhang et al., 1998) comparativement à un exercice effectué après le repas chez des adultes sains. Ces résultats restent néanmoins à confirmer puisqueKatsanos et al. (2004) observent un effet bénéfique que l'exercice soit réalisé avant ou après le repas(Katsanos & Moffatt, 2004). ...
L'augmentation de la surcharge pondérale, de l'obésité et de leurs complications métaboliques chez les enfants nécessite le développement de stratégies de gestion du poids innovantes, efficaces et intégratives. L'exercice physique est une composante essentielle des interventions multidisciplinaires de perte de poids, et il n'est plus considéré comme une simple source de dépense énergétique supplémentaire mais reconnu pour ses effets potentiels sur le contrôle alimentaire. Le but du présent travail a été d'évaluer l'effet du Timing Exercise-Repas (programme TIMEX, pour TIming Meal - EXercice) sur l'apport énergétique, les sensations d'appétit et la récompense alimentaire chez des adolescents en situation d'obésité. Si d’après nos résultats, il semblerait bénéfique de favoriser des exercices plutôt à proximité du repas, il apparaît nécessaire de considérer également le délai entre l’exercice et le repas qui le précède. Nos résultats suggèrent que ces adaptations nutritionnelles à l’exercice puissent, de surcroît, être optimisées à travers une interaction timing – intensité, avec un effet potentialisé via un exercice de haute intensité. Nos études expérimentales étant les premières au niveau mondial chez l’adolescent en situation d’obésité, elles appellent à la réalisation de travaux supplémentaires pour en confirmer les résultats. Il semble cependant primordial aujourd’hui de considérer le timing de l’exercice comme un élément essentiel de nos prescriptions en activité physique pour optimiser la prise en charge des adolescents en situation d’obésité.
... When developing a program in which higher intensity exercise is established, a shorter duration may be utilized. Exercising at 60-70% of VO2MAX for a duration of 0.5-1 hour also decreases PPT in males ages 21-39; it is currently unknown if postmenopausal women will elicit the same response [6]. ...
... An acute bout of 30 minutes of moderateintensity exercise did not attenuate PPT levels within four hours following a high fat meal in postmenopausal women. The change in PPT overtime is consistent with the normal curve experienced by researchers (Figure 1) [4][5][6][7][8]. No changes in LDL, HDL, or TC were observed. ...
... The fat content which was ingested by the participants in this study totaled 57g. This fat content is similar to that of previous studies which have shown a successful decrease in PPT with exercise by having their participants ingest 40g, 56.8 ± 6.1g, and 100g [1,6,13]. There has also been success using a ratio of fat-ingested to body mass to determine how much fat should be ingested by each individual [5,7,8]. ...
There is an increased instance of circulating triglycerides among older adults which could lead to atherosclerosis; therefore, we sought to determine if 30 minutes of moderate-intensity exercise, prior to a high fat meal, attenuates postprandial triglycerides (PPT) in postmenopausal women. Five postmenopausal women (59.8 years), participated in an exercise trial consisting of 30 minutes of moderate-intensity exercise 60% heart rate reserve (HRR), heart rate, blood pressure, and blood lipids collected. Following exercise participants ingested a high-fat meal (62 grams CHO, and 57 grams fat) and rested for four hours. Lipid levels were collected at 1, 2, 3, and 4 hours post-feeding. The control trial did not exercise and were given the high fat meal followed by rest. A randomized cross-over design was utilized, in which all subjects participated in the control and exercise trial. There was no difference in PPT between the control and exercise trials. PPT increased from pre-exercise in both trials (p<0.05) (pre-feeding 88.4±26.7 con. 93.6±36.8 ex., 1hr 141±51.7 con. 139±65.4 ex., 2hrs 195±32.7 con. 166±82.4 ex., 3hrs 203±52.2 con. 185±78.1 ex., 4hrs 179±22.4 con. 193±50.5 ex). Glucose values were similar between trials; peaking post-feeding followed by a gradual return to baseline in both trials (p<0.05) (pre-feeding 86±5.5 con. 84.6±5.8 ex., 1hr 117±11.3 con. 125±23.5 ex., 2hrs 104±4.1 con., 113±16.7 ex., 3hrs 97.4±6.3 con., 88.6±11.6 ex., 4hrs 87.6±6.7 con., 81.2±9 ex). 30 minutes of moderate-intensity exercise does not attenuate PPT in postmenopausal women.
... However, Johnson et al. (2015) found that exercise 12 h prior to a HFM was ineffective for attenuating PPL even though Johnson et al. and Zhang et al. both had participants exercise at 60% VO 2 max for 60 min [46]. Additionally, exercise performed immediately before ingestion of a HFM has also been shown to be effective for attenuating PPL [90,91]. Collectively, this evidence reinforces the idea that pre-meal exercise benefits for PPL are relatively acute and are highly dependent on energy expenditure and participant characteristics. ...
... Moderate-intensity exercise, however, has been shown to attenuate PPL with a duration more representative of typical exercise habits. Zhang et al. (1998) showed that 60 min of moderateintensity exercise (60% VO 2 max) was effective for attenuating PPL when performed one hour or 12 h prior to a HFM [91]. To further support the benefits of moderate-intensity exercise, two previous studies have indicated that as little as 30 min of brisk walking at a moderate-intensity can be effective for attenuating PPL [102,107]. ...
... Moderate-intensity exercise, however, has been shown to attenuate PPL with a duration more representative of typical exercise habits. Zhang et al. (1998) showed that 60 min of moderateintensity exercise (60% VO 2 max) was effective for attenuating PPL when performed one hour or 12 h prior to a HFM [91]. To further support the benefits of moderate-intensity exercise, two previous studies have indicated that as little as 30 min of brisk walking at a moderate-intensity can be effective for attenuating PPL [102,107]. ...
Postprandial lipemia is an independent risk factor for development of cardiovascular disease. Postprandial inflammation following the prolonged elevation of triglycerides occurring subsequent to ingestion of high-fat meals, provides a likely explanation for increased disease risk. Substantial evidence has shown that acute exercise is an effective modality for attenuation of postprandial lipemia following a high-fat meal. However, much of the evidence pertaining to exercise intensity, duration, and overall energy expenditure for reducing postprandial lipemia is inconsistent. The effects of these different exercise variables on postprandial inflammation is largely unknown. Long-term, frequent exercise, however, appears to effectively reduce systemic inflammation, especially in at-risk or diseased individuals. With regard to an acute postprandial response, without a recent bout of exercise, high levels of chronic exercise do not appear to reduce postprandial lipemia. This review summarizes the current literature on postprandial and inflammatory responses to high-fat meals, and the roles that both acute and chronic exercise play. This review may be valuable for health professionals who wish to provide evidence-based, pragmatic advice for reducing postprandial lipemia and cardiovascular disease risk for their patients. A brief review of proposed mechanisms explaining how high-fat meals may result in pro-inflammatory and pro-atherosclerotic environments is also included.
... This attenuation is generally thought to be an acute response, dependent on both the timing of the exercise bout and the energy expended during the bout. Exercise performed ϳ12-16 h before consumption of an HFM has been shown to be effective in reducing PPL (Zhang et al. 1998). Additionally, an acute bout of exercise stimulates a unique anti-inflammatory cascade of cytokines, beginning with an increase in IL-6 from the contracting muscle (Petersen and Pedersen 2005). ...
... A single bout of moderate exercise performed 12 h before an HFM has been shown to be effective for attenuating postprandial lipemia (Zhang et al. 1998). Several studies have reported that sedentary men who perform exercise for 30 min prior to the HFM show an attenuated PPL response (Murphy et al. 2000). ...
... The 60-min moderate-intensity exercise protocol in the current study did not reduce PPL. Although this duration of exercise has previously been reported to be effective for reducing PPL (Zhang et al. 1998), it is possible the energy expenditure was not high enough given the physical activity habits of our subjects. The review by Katsanos (2004) suggests that an energy expenditure between 600 and 700 kcal may be necessary to see a reduction in PPL for recreationally active individuals. ...
A high-fat meal (HFM) induces an increase in blood lipids (postprandial lipemia; PPL), systemic inflammation, and acute airway inflammation. While acute exercise has been shown to have anti-inflammatory and lipid-lowering effects, it is unknown whether exercise prior to an HFM will translate to reduced airway inflammation post-HFM. Our purpose was to determine the effects of an acute bout of exercise on airway inflammation post-HFM and to identify whether any protective effect of exercise on airway inflammation was associated with a reduction in PPL or systemic inflammation. In a randomized cross-over study, 12 healthy, 18- to 29-year-old men (age, 23.0 ± 3.2 years; height, 178.9 ± 5.5 cm; weight, 78.5 ± 11.7 kg) consumed an HFM (1 g fat/1 kg body weight) 12 h following exercise (EX; 60 min at 60% maximal oxygen uptake) or without exercise (CON). Fractional exhaled nitric oxide (FENO; measure of airway inflammation), triglycerides (TG), and inflammatory markers (high-sensitivity C-reactive protein, tumor-necrosis factor-alpha, and interleukin-6) were measured while fasted at 2 h and 4 h post-HFM. FENO increased over time (2 h: CON, p = 0.001; EX, p = 0.002, but not by condition (p = 0.991). TG significantly increased 2 and 4 h post-HFM (p < 0.001), but was not significant between conditions (p = 0.256). Inflammatory markers did not significantly increase by time or condition (p > 0.05). There were no relationships between FENO and TG or systemic inflammatory markers for any time point or condition (p > 0.05). In summary, an acute bout of moderate-intensity exercise performed 12 h prior to an HFM did not change postprandial airway inflammation or lipemia in healthy, 18- to 29-year-old men.
... Most studies evaluate the late acute effect 12 h post-exercise, and the influence of this time on the lipid curve. Studies that have evaluated the immediate acute response diverge with respect to the exercise protocol used, present reduced sample size, and included nonobese individuals [7][8][9][10][11][12][13]. Furthermore, these studies have also presented contradictory results about the lipid curve: in some studies [3][4][5][6][7][8] the exercise it was shown to have a reducing effect and on others [9][10][11][12] no effect was evidenced. ...
... Most studies evaluate the late acute effect 12 h post-exercise, and the influence of this time on the lipid curve. Studies that have evaluated the immediate acute response diverge with respect to the exercise protocol used, present reduced sample size, and included nonobese individuals [7][8][9][10][11][12][13]. Furthermore, these studies have also presented contradictory results about the lipid curve: in some studies [3][4][5][6][7][8] the exercise it was shown to have a reducing effect and on others [9][10][11][12] no effect was evidenced. Therefore, the aim of this study was to evaluate the effect of acute moderate intensity physical exercise on the lipid response in patients with central obesity by means of a self controlled intervention study. ...
... All the individuals registered in the service, who presented central type obesity were invited to participate in the study. Forty volunteers met the following inclusion criteria of the study: age between 18 to 30 years, waist circumference >80 cm for women and >94 cm for men [12] and sedentarism, the latter determined by the International Physical Activity Questionnaire Short version (IPAQ) [14]. This questionare consists of eight discursive questions that provide information about the duration (minutes/day) and frequency (days/week) of trekking and every day activities performed in sitting position or that require moderate and vigorous physical effort, classifying the level of physical activity into 4 categories (sedentary, insufficiently active, active and very active [15]. ...
... Kadar trigliserida postprandial dipengaruhi oleh berbagai faktor antara lain olahraga dan asupan makanan. Penurunan kadar trigliserida postprandial saat berolahraga dipengaruhi oleh peningkatan aktivitas enzim Lipoprotein Lipase (LPL) yang dirangsang saat berolahraga (Zhang, Thomas, Ball, 1998). Enzim LPL merupakan enzim yang menghidrolisis trigliserida dalam plasma. ...
... Penelitian yang dilakukan Ziogas (1997) menyatakan bahwa olahraga senamaerobik mengurangi peningkatan kadar trigliserida plasma setelah makan makanan tinggi lemak (Zhang, Thomas, Ball, 1998 ...
The majority of studies have found that aerobic exercise can reduce the increment of triglyceride postprandial in plasma. Therefore, the author is doing this research to know the difference of triglyceride concentration in plasma between-group who joint high impact exercise and group who joint body language exercise after given the same amount and dietary composition which had done high impact and body language exercise before. Twenty men (19-39 years old) did high impact or body language exercises for 1 hour. Two hours later, they were given dietary composition with carbohydrates 60% and fat 25%. Then the triglyceride postprandial concentrations were measured 3, 5, and 6 hours after the given dietary food. The result showed that the triglyceride concentration of high impact group was higher than body language group 3 hours after given dietary food (122.167 ± 17.11627 vs 111.67± 7.86554 mg/dL) and there was no difference between the high impact and body language group 5 hours (96.167 ± 7.25029 vs 94.0 ± 16.66133mg/dL) and 6 hours after given dietary food (77.5 ± 8.8261 vs 78.167 ± 14.27469 mg/dL).In conclusion, the triglyceride concentration of the high impact group was higher than the body language group 3 hours after given the same amount and dietary composition. But, there was no difference between triglycerides concentration of body language group and high impact group 5 and 6 hours after given the same amount and dietary composition which had done high impact and body language exercise before.
... Exercise has been a well-documented method to attenuate the rise in postprandial lipemia (23)(24)(25)(26)(27) and prevent long-term impairment to cardiovascular health and function (28)(29)(30). However, recent epidemiological evidence suggests that exercise training may not reduce the incidence of disease and other morbidities, and even death, in people who spend a large amount of time sitting (31,32). ...
... In both of these studies, a 1-h bout of exercise at~65% V O 2peak failed to improve postprandial metabolic responses when activity and steps per day were low. The lowering of postprandial triglycerides the day after exercise is a typical response, at least in subjects not limiting steps per day (23,(25)(26)(27). The present design emphasizes the consequences of daily physical inactivity beyond responses to a single bout of acute exercise and into a paradigm of short-term aerobic training. ...
Purpose:
This study determined if the level of background physical inactivity (steps per day) influences the acute and short-term adaptations to intense aerobic training.
Methods:
Sixteen untrained participants (23.6 ± 1.7 yr) completed intense (80%-90% V˙O2peak) short-term training (5 bouts of exercise over 9 d) while taking either 4767 ± 377 steps per day (n = 8; low step) or 16,048 ± 725 steps per day (n = 8; high step). At baseline and after 1 d of acute exercise and then after the short-term training (posttraining), resting metabolic responses to a high-fat meal (i.e., plasma triglyceride concentration and fat oxidation) were assessed during a 6-h high-fat tolerance test. In addition, responses during submaximal exercise were recorded both before and after training during 15 min of cycling (~79% of pretraining V˙O2peak).
Results:
High step displayed a reduced incremental area under the curve for postprandial plasma triglyceride concentrations by 31% after acute exercise and by 27% after short-term training compared with baseline (P < 0.05). This was accompanied by increased whole-body fat oxidation (24% and 19%; P < 0.05). Furthermore, stress during submaximal exercise as reflected by heart rate, blood lactate, and deoxygenated hemoglobin were all reduced in high step (P < 0.05), indicating classic training responses. Despite completing the same training regimen, low step showed no significant improvements in postprandial fat metabolism or any markers of stress during submaximal exercise after training (P > 0.05). However, the two groups showed a similar 7% increase in V˙O2peak (P < 0.05).
Conclusion:
When completing an intense short-term exercise training program, decreasing daily background steps from 16,000 to approximately 5000 steps per day blunts some of the classic cardiometabolic adaptations to training. The blunting might be more pronounced regarding metabolic factors (i.e., fat oxidation and blood lactate concentration) compared with cardiovascular factors (i.e., V˙O2peak).
... Kadar trigliserida postprandial dipengaruhi oleh berbagai faktor antara lain olahraga dan asupan makanan. Penurunan kadar trigliserida postprandial saat berolahraga dipengaruhi oleh peningkatan aktivitas enzim Lipoprotein Lipase (LPL) yang dirangsang saat berolahraga (Zhang, Thomas, Ball, 1998). Enzim LPL merupakan enzim yang menghidrolisis trigliserida dalam plasma. ...
... Penelitian yang dilakukan Ziogas (1997) menyatakan bahwa olahraga senamaerobik mengurangi peningkatan kadar trigliserida plasma setelah makan makanan tinggi lemak (Zhang, Thomas, Ball, 1998 ...
The majority of studies has found that aerobic exercise can reduce the increment oftriglyceride postprandial in plasma. Therefore, the author is doing this research to know thedifference of triglyceride concentration in plasma between group who joint high impact exerciseand group who joint body language exercise after given the same amount and dietary compositionwhich had done high impact and body language exercise before. Twenty men (19-39 years old) didhigh impact or body language exercise for 1 hour. Two hours later, they were given dietarycomposition with carbohydrate 60% and fat 25%. Then the triglyceride postprandial concentrations were measured 3, 5, and 6 hours after the given dietary food. The result showedthat the trygliceride concentration of high impact group was higher than body language group 3hours after given dietary food (122.167 17.11627 vs 111.67 7.86554 mg/dL) and there were nodifference between high impact and body language group 5 hours (96.167 7.25029 vs 94.0 16.66133mg/dL) and 6 hours after given dietary food (77.5 8.8261 vs 78.167 14.27469mg/dL).In conclusion, the trygliceride concentration of high impact group was higher than body language group 3 hours after given the same amount and dietary composition. But, there were nodifference between trygliceride concentration of body language group and high impact group 5and 6 hours after given the same amount and dietary composition which had done high impact andbody language exercise before.
... Next, the speed was increased by 0.8 km/h every 1 minute until 10.5 km/h. The speed then remained constant, and the treadmill slope was raised by 2% every 1 minute until exhaustion [33]. ...
... In the second, third, and fourth trials, the participants visited the laboratory in an overnight fasted state and were supplemented with taurine or a placebo 90 minutes before the effort. The exercise protocol was composed of a single bout of running at 60% of their VO2 max (controlled by heart rate through the frequency meter) for one hour on a treadmill (the same running speed in all tests) [33]. Heart rate was collected by a heart rate monitor at four moments (in all experiments): preexercise, after 30 minutes of exercise, after 60 minutes of exercise, and 15 minutes post-exercise. ...
Based on the fact that taurine can increase lipid metabolism, the objective of the present study was to evaluate the effects of different doses of acute taurine supplementation on lipid oxidation levels in healthy young men after a single bout of fasting aerobic exercise. A double-blind, acute, and crossover study design was conducted. Seventeen men (age 24.8 ± 4.07y; BMI: 23.9 ± 2.57 kg/m²) participated in the present study. Different doses of taurine (TAU) (3 g or 6 g) or placebo were supplemented 90 minutes before a single bout of fasting aerobic exercise (on a treadmill at 60% of VO2 max). The subjects performed three trials, and each one was separated by seven days. Blood samples were collected at baseline and after the exercise protocol of each test to analyze plasma levels of glycerol and taurine. Lipid and carbohydrate oxidation were determined immediately after exercise for 15 minutes by indirect calorimetry. We observed that TAU supplementation (6 g) increased lipid oxidation (38%) and reduced the respiratory coefficient (4%) when compared to the placebo (p < 0.05). However, no differences in lipid oxidation were observed between the different doses of taurine (3 g and 6 g). For glycerol concentrations, there were no differences between trials. Six grams of TAU supplementation 90 minutes before a single bout of aerobic exercise in a fasted state was sufficient to increase the lipid oxidation post-exercise in healthy young men.
... With an ever-increasing fat content per meal in a Western diet, individuals perpetually have an increased level of triglyceride-rich lipoproteins in circulation throughout the day. Increased triglyceride-rich lipoproteins after consumption of a meal have been associated with impaired endothelial function (Vogel et al. 1997) and increased atherosclerotic plaque formation (Zhang et al. 1998), leading to cardiometabolic disease (Hyson et al. 2003;Parnell et al. 2018;Teeman et al. 2016). Thus, a decrease in triglyceride-rich lipoproteins after meal ingestion has been suggested to attenuate the risk of many cardiometabolic diseases (Lee et al. 2018;Teeman et al. 2016). ...
... These data suggest that exercise elicits a greater effect on postprandial fat oxidation when the test meal is consumed on the same day as the exercise. The greatest effect of exercise on the attenuation of postprandial lipemia is observed when exercise is performed 8-24 h prior to the test meal (Freese et al. 2014;Zhang et al. 1998). This immediate effect of exercise on fat oxidation is an integral part of the multifaceted process of how acute exercise attenuates postprandial triglyceride concentrations, particularly the day after exercise. ...
The purpose of this systematic review was to synthesize and evaluate current literature examining the effects of exercise on postprandial fat oxidation, as well as to provide future direction. A quantitative review was performed using meta-analytic methods. A moderator analysis was performed to investigate potential variables that could influence the effect of exercise on postprandial fat oxidation. Fifty-six effects from 26 studies were retrieved. There was a moderate effect of exercise on postprandial fat oxidation (Cohen’s d = 0.58 (95% CI, 0.39 to 0.78)). Moderator analysis revealed that sex, age, weight status, training status, exercise type, exercise intensity, timing of exercise, and composition of the meal challenge significantly affected the impact of prior exercise on postprandial fat oxidation. The moderator analysis also indicated that most previous studies have investigated the impact of prior moderate-intensity endurance exercise on postprandial fat oxidation in young, healthy, lean men. Suggested priorities for future research in this area include (i) an examination of sex differences in and/or female-specific aspects of postprandial metabolism; (ii) a comprehensive evaluation of exercise modalities, intensities, and durations; and (iii) a wider variety of test meal compositions, especially those with higher fat content.
NoveltyA systematic review of the impact of exercise on postprandial fat oxidation was performed using meta-analytic methods.
Analysis revealed a moderate effect of exercise on postprandial fat oxidation.
The presented data support a need for future studies to investigate sex differences and to include comprehensive evaluations of exercise modalities, intensities, and duration.
... Lipoprotein Lipase activity has been shown to increase in the thigh approximately 4 hours following exercise by (Zhang, Thomas & Ball 1998) Freese and colleagues (2011) noted that their conclusions could have been due to of the effect of energy replacement immediately following the exercise bout, which has been noted in several other research studies (Burton et al.,2008;Harrison et al., 2009). In addition, energy replacement has been shown to attenuate the effects of exercise on PPL when compared to the effects of exercise on PPL during an exercise-induced energy deficit (Freese et al., 2011). ...
... The effects of high-intensity exercise may not have been seen in this study due to the brief duration of time reserved to acquire postprandial blood samples. This observation is supported by previous studies that have indicated that the increase in LPL activity is not seen until approximately four hours post-exercise (Zhang, Thomas & Ball, 1998), and would therefore be absent in the current study which examined postprandial blood concentration for up to three hours post-exercise. Other research has noted similar conclusions, as well as the observation that LPL activity is not influenced by the increase in insulin (Kiens et al., 1989), indicating that insulin produced from a high-carbohydrate meal would not attenuate LPL activity following exercise. ...
Introduction: Moderate-intensity aerobic exercise has been shown to attenuate the
rise in triglycerides in during the postprandial period, however the effects of acute
bouts of high-intensity exercise on postprandial lipemia and glycemia have not
been explored. The purpose of this study was to examine the effects of acute highintensity
interval training on postprandial lipemia and postprandial glycemia.
Methods: Ten healthy males participated in a randomized crossover design
consisting of one high-intensity exercise session and one sedentary control
session, followed by consumption of a mixed meal. Blood triglyceride and glucose
concentrations were monitored following the consumption of the meal.
Results: High-intensity interval exercise produced a lowering effect (p<.05) on
postprandial glucose incremental area under the curve. No significant results were
observed in triglyceride concentration.
Conclusion: Postprandial glycemia, but not lipemia, was effected by acute highintensity
interval exercise. Future studies should explore any prolonged effects of
high-intensity exercise on postprandial lipemia and glycemia.
... 16 Compared to the study involving Rajasthanis in India the mean value in the present study appeared to be high10 which is probably consistent with those involving Chinese. 17 It may be mentioned that among the Saudis mean hsCRP level was found to be 2.7, which substantiate the view that race and geographic distribution influence the level. ...
... It resembles other studies in several populations. 10,17 The relationship between TG and hsCRP is consistent with other studies. 7,10,17 Binary logistic regression analysis revealed the relationship when adjusted with gender, BMI and cholesterol level. ...
Background: Metabolic diseases are affecting human health all over the world. These chronic disease states are associated with high sensitive CRP. The present study aims to measure hsCRP and lipid levels in a group of healthy adults to work out the normal hsCRP levels and explore its relationship to lipidemic and anthropometric variables.Materials and Methods: A total of 149 adults, age 30-60 yrs, healthy subjects were recruited in this study. Vital statistics were taken along with measurement of blood glucose, triglyceride, total cholesterol, high density lipoprotein, low density lipoprotein and hsCRP levels. Data were analyzed using statistical Package for Social Program (SPSS) for Windows version 10.Results: Mean (±SD) hsCRP was 2.46±1.89 (mg/l) with a cut off value of 3mg/l. Of the total 149 subjects 102 (66.4%) and 47 (31.5%) subjects had hsCRP level below and above the cutoff respectively. Triglyceride was significantly higher (p=0.033) and HDL was lower in subjects with high hsCRP. Total cholesterol and LDL was almost similar in both groups. Binary logistic regression showed significant negative association between hsCRP and HDLc (p=0.029) and but the model excluding HDL-c showed significant positive association (p=0.03) with triglyceride.Conclusion: About one-third of healthy Bangladeshi adults may have chronic subclinical inflammation and thus may have a risk of cardiovascular disorders. More than one-third healthy Bangladeshi adults have one or more type of dyslipidemia and the subclinical chronic inflammation in healthy Bangladeshi adults has a positive association with their serum triglyceride and negative association with their HDL-cholesterol levels.DOI: http://dx.doi.org/10.3126/jpn.v4i8.11591 Journal of Pathology of Nepal; Vol.4,No. 8 (2014) 644-648
... Accumulating moderate-intensity exercise (MIE) the day before a high fat meal has been shown to lower postprandial plasma glucose and TAG concentrations, and improve endothelial function in adolescent boys [13]. However, the timing of the exercise stimulus in relation to a high fat meal is known to effect the subsequent lipaemia [14], and no study with adolescents has addressed the impact of exercise accumulated on the same day as the test meal, or if the intensity of accumulated exercise influences the postprandial response. The latter point is important to consider as there is evidence showing that performing high-intensity exercise is superior than MIE at modifying cardiometabolic risk factors in youth [15,16], even when the total amount of high-intensity exercise performed is small (~4 min) [17]. ...
... In agreement with our data, a recent study has shown that performing 135 min of walking during the postprandial period did not reduce plasma TAG concentrations in adolescent boys and girls [31]. Furthermore, Zhang et al. have previously demonstrated in adults that PPL was only attenuated when exercise was performed 1 hour before a HFM, compared to when identical exercise was performed during the postprandial period [14]. Therefore, accumulating exercise during the postprandial period may only have a limited effect on PPL. ...
To examine the influence of exercise intensity on postprandial health outcomes in adolescents when exercise is accumulated throughout the day.
19 adolescents (9 male, 13.7±0.4 years old) completed three 1-day trials in a randomised order: (1) rest (CON); or four bouts of (2) 2×1min cycling at 90% peak power with 75s recovery (high-intensity interval exercise; HIIE); or (3) cycling at 90% of the gas exchange threshold (moderate-intensity exercise; MIE), which was work-matched to HIIE. Each bout was separated by 2hours. Participants consumed a high fat milkshake for breakfast and lunch. Postprandial triacylglycerol (TAG), glucose, systolic blood pressure (SBP) and fat oxidation were assessed throughout the day.
There was no effect of trial on total area under the curve (TAUC) for TAG (P=0.87). TAUC-glucose was lower in HIIE compared to CON (P=0.03, ES=0.42) and MIE (P=0.04, ES=0.41), with no difference between MIE and CON (P=0.89, ES=0.04). Postprandial SBP was lower in HIIE compared to CON (P=0.04, ES=0.50) and MIE (P=0.04, ES=0.40), but not different between MIE and CON (P=0.52, ES=0.11). Resting fat oxidation was increased in HIIE compared to CON (P=0.01, ES=0.74) and MIE (P=0.05, ES=0.51), with no difference between MIE and CON (P=0.37, ES=0.24).
Neither exercise trial attenuated postprandial lipaemia. However, accumulating brief bouts of HIIE, but not MIE, reduced postprandial plasma glucose and SBP, and increased resting fat oxidation in adolescent boys and girls. The intensity of accumulated exercise may therefore have important implications for health outcomes in youth.
Copyright © 2015. Published by Elsevier Inc.
... For instance, these brief exercises included (a) 3 sets of 1-min light intensity jogging + 30 s of rest; total duration of 4 min for each exercise bout, every 30 min throughout the day, 20 times in total; (b) 3 sets of 15 min bouts at 3 METs after a meal 84 ; (c) resistance exercise (up to 40% of their bodyweight) 85 (d) 10 × 1 min HIIT (10 × 1 min work-bouts at 95-120% of individual peak power output, separated by 1 min low-intensity cycling) 72 ; and (e) 4 bouts including 3 min at 56.5 ± 3.9 % VO 2 max after breakfast. 86 Interestingly, postprandial exercise also reduced acute elevations in serum triglyceride levels after high-fat meals and reduced functional derangements from lipid-induced oxidative stress [87][88][89] , suggesting post-meal exercise may benefit both glucose and lipids to support cardiovascular health. Collectively, these findings suggest "exercise desserts " immediately post-meal may yield optimal benefit for attenuating postprandial spikes. ...
Exercise is a first-line therapy recommended for patients with type 2 diabetes (T2D). Although moderate to vigorous exercise (e.g. 150 min/wk) is often advised alongside diet and/or behavior modification, exercise is an independent treatment that can prevent, delay or reverse T2D. Habitual exercise, consisting of aerobic, resistance or their combination, fosters improved short- and long-term glycemic control. Recent work also shows high-intensity interval training is successful at lowering blood glucose, as is breaking up sedentary behavior with short-bouts of light to vigorous movement (e.g. up to 3min). Interestingly, performing afternoon compared with morning as well as post-meal versus pre-meal exercise may yield slightly better glycemic benefit. Despite these efficacious benefits of exercise for T2D care, optimal exercise recommendations remain unclear when considering, dietary, medication, and/or other behaviors.
... Studies investigating the impacts of high-fat meal feeding in healthy participants have reported increased total monocyte intracellular pro-inflammatory cytokine concentrations as well as alterations in total and subset-specific monocyte concentrations (Deopurkar et al. 2010;Hyson et al. 2002;McFarlin et al. 2017;Strohacker et al. 2012). An abundance of studies have demonstrated that acute aerobic exercise performed 1-24 h before highfat meal consumption can attenuate postprandial lipemia in healthy individuals, albeit with dependence on exercise intensity (Chu et al. 2016;Katsanos et al. 2004;Teeman et al. 2016;Zhang et al. 1998). Variable evidence exists as the effects of preprandial aerobic exercise on high-fat mealinduced inflammation. ...
Background:
Elevated low-density lipoprotein (LDL) and triglyceride concentrations are associated with future cardiovascular risk in young adults. Conversely, chronic physical activity is generally accepted to reduce CVD risk. Atherosclerosis is a major underlying cause of CVD, and atherogenesis is mediated by peripheral monocytes and monocyte-derived macrophages. The study aimed to determine if an individual's physical activity level impacts the phenotype of monocytes and monocyte-derived macrophages when stimulated with LDL and fatty acid ex vivo.
Methods:
Peripheral blood mononuclear cells (PBMCs) were obtained from healthy, young adults of differing physical activity levels before and after a single bout of moderate intensity exercise (25 min at 60% of VO2peak). PBMCs were stimulated with LDL and palmitate ex vivo prior to differentiation into macrophages. Monocyte subset percentages and monocyte-derived macrophage expression of phenotypic (CD86, CD206) and functional (CCR2, ERK 1/2) markers were evaluated by flow cytometry.
Results:
Compared to baseline, ex vivo LDL and palmitate stimulation decreased (p = 0.038) non-classical monocyte percentage from 24.7 ± 3.2 to 21.5 ± 2.6% in all participants. When ex vivo lipid stimulation was preceded by acute exercise, non-classical monocyte percentage was similar to baseline levels (p = 0.670, 25.8 ± 2.15%). Macrophage CD86/CD206 was increased from 1.30 ± 0.14 to 1.68 ± 0.19 when preceded by acute exercise in all participants. No differences were observed between participants of differing physical activity levels.
Conclusions:
Findings suggest that acute exercise modulates monocyte phenotype after LDL and palmitate stimulation in a protective manner, however, chronic physical activity does not alter monocyte/macrophage responses to any experimental condition in this population.
... Pappas et al., 2021 Share the effects of Spirulina supplementation on redox status and performance following a muscle damaging protocol. Essa redução do TAG pode estar relacionada a realização da atividade física, já que estudos mostram que o exercício realizado 1 dia ou 1h, antes da refeição gordurosa diminui efetivamente a lipemia pós-prandial (ZHANG et al., 1998;COHEN;GOLDBERG, 1960;ALDRED, 1995;MURPHY et al.,2000). Porém, no Chaouachi et al. ...
O exercício ou treino de resistência extenuante podem gerar estresse e danos musculares. E nutrição adequada pode favorecer para recuperação, tratamento e melhora desempenho. Nesse sentido, tem-se a prescrição dos suplementos alimentares, dentre eles, tem-se a Spirulina, por seus compostos e potencial antioxidante e anti-inflamatório. O objetivo do estudo foi avaliar os benefícios, riscos e dosagem da Spirulina na nutrição esportiva. Para alcançar o proposto, foi realizada revisão sistemática da literatura nas bases de dados da PUBMED, BVS Saúde e Portal Capes, no período dos últimos 10 anos, incluindo artigos em inglês e português, utilizando o cruzamento dos descritores em saúde (DesCS): Spirulina and Nutrição esportiva, Cianobactérias and Nutrição esportiva, Spirulina and atletas, Spirulina and desempenho atlético. Finalizando a pesquisa, foram encontrados um total de 9 artigos elegíveis. Observou-se que os indivíduos, dependendo do tipo de exercício e com uso da suplementação da Spirulina (≥4,5g por dia), apresentaram efeito benéfico no perfil lipídico, tempo à fadiga, na imunidade, melhora nos parâmetros cardiorrespiratórios, no índice de massa corporal e estresse oxidativo. Entretanto, não houve alteração nos parâmetros de jogadores de rugby. Além disso, de modo geral, as vias de atuação não estão claras, pois a Spirulina apresenta diversidades de compostos. Conclui-se que o uso de Spirulina pode atuar sinergicamente dependendo do tipo de exercício físico promovendo melhora a danos ocasionados pelo estresse oxidativo, à fadiga e melhora dos parâmetros da composição corporal e perfil lipídico e cadiorrespiratório. Porém, mais estudos são incentivados para verificar se o uso prolongado pode apresentar toxicidade. Também, incluir nos estudos a população feminina para verificar se o comportamento é semelhante aos achados com o sexo masculino.
... However, to date, there are no studies that have assessed the effect of upper-body exercise performed 12-18 h prior to a test meal. Seminal work by Zhang et al. (1998) on the role of exercise timing revealed that exercising 12 h before PPL assessment may have a better overall effect on triglyceride concentrations compared with exercise performed 1 h before. Furthermore, the expression of LPL, believed to be a primary mechanism for PPL reductions, peaks >8 h following exercise completion (Seip et al. 1997). ...
A single bout of cycling or running performed in the evening can reduce postprandial lipaemia (PPL) the following morning, although this is currently unknown for upper-body exercise. The aim of this study was to determine if a bout of arm-crank exercise (high-intensity interval [HIIE] or moderate-intensity continuous [MICE]), can attenuate PPL in noninjured individuals. Eleven healthy and recreationally active participants (eight males, three females; age: 27 ± 7 years; body mass index: 23.5 ± 2.5 kg·m–2) volunteered to participate in three trials: HIIE (10 × 60 s at 80% peak power output), MICE (50% peak power output of isocaloric duration), and a no-exercise control condition. Each exercise bout was performed at 18:00, and participants consumed a standardised evening meal at 20:00. Following an overnight fast, a 5-h mixed-macronutrient tolerance test was performed at 08:00. There were no significant differences in triglyceride incremental area under the curve between HIIE (192 ± 94 mmol·L–1 per 300 min), MICE (184 ± 111 mmol·L–1 per 300 min), and the no-exercise condition (175 ± 90 mmol·L–1 per 300 min) (P = 0.46). There were no significant differences in incremental area under the curve for glucose (P = 0.91) or insulin (P = 0.59) between conditions. Upper-body MICE and HIIE performed in the evening do not influence PPL the following morning, in normotriglyceridemic individuals. Clinical Trials Registration: NCT04277091.
Novelty: Arm-crank exercise has no effect on PPL when performed the evening prior to a mixed-macronutrient meal test.
Upper-body sprint interval exercise should be investigated as a potential solution to reduce PPL.
... Although most exercise studies report reductions in PPTG levels after a high-fat test meal, the variability in the results is large. Factors such as exercise mode (i.e., resistance vs. endurance), exercise dose (i.e., duration and intensity), 19,20 the induced caloric deficit, 21 and the timing between exercise and the high-fat meal 22 can affect the PPTG response to exercise. 15 Although, most exercise studies have been conducted in healthy individuals, a few reports suggest that individuals with MetS and CVD could also benefit from exercise that lowers PPTG levels. ...
Background
Individuals at risk of suffering cardiovascular disease (CVD) present larger increases in blood triglyceride (TG) concentration after a high-fat meal than healthy individuals. This postprandial hypertriglyceridemia (PPTG) is an independent risk factor for CVD. Prescription of statins and a bout of prolonged exercise are both effective in lowering PPTG. We aimed to evaluate the comparative effectiveness of statins versus a bout of aerobic exercise in reducing fasting and postprandial blood TG in individuals at high risk of developing CVD.
Methods
Thirty-seven studies from a systematic literature search of the PubMed, EMBASE, and Cochrane databases were included in this review. The selected studies conducted trials involving statin therapy (n = 20) or a bout of aerobic exercise (n = 19) and measured their impact on PPTG as an outcome. Two studies analyzed both treatments and were included in duplicate. The meta-analysis was constructed using a random-effects model to calculate the mean difference (MD). Student's t test was used to compare the data sets for statins vs. exercise.
Results
Overall, statin and exercise interventions showed a similar reduction in PPTG levels, with an MD of –0.65 mmol/L for statins (95% Confident Interval (95%CI): –0.54 to –0.77; p < 0.001) and -0.46 mmol/L for exercise (95%CI: –0.21 to –0.71; p < 0.01). However, statins lowered fasting TG more than exercise (MD = –1.54 mmol/L, 95%CI: –2.25 to –0.83; p = 0.009).
Conclusion
Although aerobic exercise is effective in lowering blood TG, statins seem to be more efficient, especially in the fasted state. A combination of exercise and statins might reveal a valuable approach to the treatment and prevention of CVD. More studies are required to determine the underlying mechanisms and the possible additive effects of these interventions.
... Previous studies showed that both an acute bout of RT (Ormsbee et al., 2007), and a 26-week RT program (Hunter et al., 2000), increased fat oxidation and energy expenditure. Some studies have shown that RT reduces both abdominal subcutaneous (Ibañez et al., 2005) and visceral adiposity (Treuth et al., 1995;Zhang et al., 1998), in the absence of body weight changes. In the present study, VAI, BAI, TyG, TyG-BMI and TyG-WC indices were reduced following the consumption of GC and RT. ...
Background
Green coffee supplementation has demonstrated beneficial anti-inflammatory and anti-obesity effects. Accordingly, we examined the effects of a green coffee (GC) extract concurrent to elastic band resistance training (EBRT) on insulin resistance, adiposity indices [Visceral (VAI), Body (BAI)] TyG-related indicators (TyG-BMI and TyG-WC) in obese women.
Methods
Obese participants (N=60, 30-50y, BMI >30 kg/m²) were randomized equally into a randomized, double-blind, placebo-controlled trial: (1) Placebo (PLA), (2) PLA+ Resistance training, (3) PLA+R, (4) GC, GC+Resistance training (GC+R). Treatment capsules contained 500 mg of GC and 50% chlorogenic acid (250 mg) for 8-wks. Resistance training consisted of 3 sessions per/wk/60-min. Paired-sample t-test and two-factor ANOVA were used for within and between-group comparisons.
Results
We observed a significant pre/post reduction for HOMA-IR (Primary Outcome; mean (SD) for the PLA+R (3.67±0.70 vs. 3.22±0.74 mg/dL) and GC+R (3.88±0.54 vs. 3.21±0.61, both p<0.001), but not GC 3.79±0.77 vs. 3.54±0.71, P=0.058) and PLA 3.41±0.76 vs. 3.69±0.95, P=0.21). Both GC+R (P=0.005) and PLA+R were significant vs. PLA (P=0.011). Secondary outcomes included a significant reduction in glucose for PLA+R (94.61±8.12 vs. 89.08±9.70 mg/dL) and GC+R (94.36±10.67 vs. 84.5±11.02 mg/dL, both P<0.001), but not GC (94.07±7.39 vs. 91.79±8.50 mg/dL, P=0.07) and PLA (91.46±10.28 vs. 99.92±20.12 mg/dL, P=0.053). Both GC+R (P=0.002) and PLA+R were significantly different (P=0.019) vs. PLA. Finally, Apo A-I significantly improved for GC+R compared vs. PLA, P=0.033) and BAI significantly improved for. PLA+R (P=0.021), GC+R (P=0.006) and GC vs. PLA.
Conclusion
Despite no synergistic exercise and green coffee treatment effects, exercise improved most TyG parameters and lipid profiles in obese women.
... This contrasts findings from noninjured populations that a single acute bout of MICE or HIIE performed 12-18 h before a standardized meal attenuates the postprandial triglyceride response (11,36). Although studied less extensively, prior research indicates that this effect appears to still hold true when exercise is performed immediately (≤1 h) before the tolerance test (37,38). However, it appears that the magnitude of this effect is partially dependent on the energy expended during exercise, and there may be an exercise energy expenditure threshold needed to elicit changes in postprandial triglycerides (20,39). ...
Purpose:
The acute effects of a single bout of upper-body exercise on postprandial metabolism in persons with spinal cord injury is currently not well understood. The primary aim of this study was to evaluate the effects of a single bout of upper-body high-intensity interval exercise (HIIE) and moderate-intensity continuous exercise (MICE), in comparison to a no-exercise control (REST) condition on postprandial metabolic responses in persons with chronic paraplegia.
Methods:
10 participants (eight males, two females, age: 49 ± 10 yrs, time since injury: 22 ± 13 yrs) with chronic paraplegia took part in a randomised cross-over study, consisting of three trials: HIIE (8 x 60 s at 70% peak power output (PPEAK)), MICE (25 min at 45% PPEAK), and REST, at least 3 days apart. Exercise was performed in the fasted state, and participants consumed a mixed-macronutrient liquid meal 1-h post-exercise. Venous blood and expired gas samples were collected at regular intervals for 6-h post-meal consumption.
Results:
There were no significant differences in postprandial iAUC for triglycerides (p=0.59) or glucose (p=0.56) between conditions. Insulin iAUC tended to be lower following MICE (135 ± 85 nmol/L· 360 min-1) compared to REST (162 ± 93 nmol/L · 360 min-1), but this did not reach statistical significance (P=0.06, d=0.30). Participants reported a greater fondness (P=0.04) and preference for HIIE over MICE.
Conclusions:
Following an overnight fast, a single bout of upper-body exercise before eating, has no effect on postprandial metabolism in persons with chronic paraplegia, irrespective of exercise intensity. This suggests that alternative exercise strategies may be required to stimulate postprandial substrate oxidation for this population.
... 1 Recent studies effectively show that the beneficial effects of exercise might also depend on its timing during the day or its delay/position regarding a meal. 1 Some studies for instance showed that performing acute exercise one to 3 hours after a meal could enhance the glycemic response in patients with type II diabetes 2-5 while others showed a better postprandial lipemia response when exercise was performed immediately before the meal. [6][7][8] Looking at the alarming progression of overweight and obesity among children and adolescents, it seems necessary to deepen our understanding on the effects of exercise on overall energy balance, in order to optimize our weight loss strategies. It is now clear that physical exercise does not only impact energy expenditure, it also affects ...
Background
While the beneficial effects of exercise on appetite might depend on its timing during the day or relative to a meal, this remains poorly explored in youth.
Objectives
To examine the importance of meal timing (+30 vs +90 minutes) after performing exercise on energy intake, appetite and food reward in adolescents with obesity.
Methods
Eighteen adolescents with obesity randomly completed three conditions: (a) lunch (12:00 pm) set 30 minutes after a rest session (11:00 am); (b) lunch (12:00 pm) set 30 minutes after an exercise session (11:00 am)(MEAL‐30); (c) lunch (01:00 pm) set 90 minutes after an exercise session (11:00 am)(MEAL‐90). Lunch and dinner ad libitum energy intake was assessed, food reward (LFPQ) assessed before and after lunch, and before dinner, appetite sensations were assessed at regular intervals.
Results
Energy intake was lower at MEAL‐90 than MEAL‐30 and CON at lunch (P < .05 and P < .01, respectively) and lunch + dinner combined (P < .001). A decrease in intake (g) of protein, fat and carbohydrate was observed. Post‐exercise hunger was lower on MEAL‐90 compared with CON. No condition effects were found at lunch for food reward.
Conclusions
Delaying the timing of the meal after exercise might help affect energy balance by decreasing ad libitum energy intake without increasing hunger and by improving satiety in adolescents with obesity.
... Some studies have for instance shown a better glycemic control when exercise is performed within one to three hours after food intake in patients with type II diabetes [2][3][4][5]. However, a better lipemia response to a meal has been shown when exercise is performed before the meal compared with after [6][7][8]. Other studies have questioned the interest of the timing of exercise on sleep [9][10][11], with an evening exercise allowing a better subjective feeling of sleep quality [11] , a decrease in daytime sleepiness [11], a relevant sleep phase progression [9] and a better sympathetic regulation (HR and body temperature) [10]. ...
The prevention and management of chronic diseases, particularly overweight and obesity, relies on multidisciplinary strategies mainly combining dietary approaches with physical activity. Recently, the timing of exercise (time of the day as well as delay/position relative to a meal) has been suggested as an important parameter to consider when prescribing physical activity. Some studies have for instance shown the interest of the timing of exercise on the glycemia, sleep and body composition regulation. However, the impact of exercise-timing on appetite control and energy intake remains unclear. This is why, the present paper questions whether physical exercise, depending on its timing during the day and related to a meal, can affect energy intake, appetite sensations and food reward. Although evidences remain actually limited, exercising during the morning; and particularly close to lunch, might have a better impact on overall energy balance through reduced subsequent energy intake, without leading to compensatory intakes at the following meals. Importantly, dealing with the timing of exercise to optimize energy balance (and affect energy intake and appetite) does not only require to consider its time during the day (morning vs. afternoon or evening), but also and maybe mainly its order/position (pre vs. post) and delay regarding meals. While the actual literature remains limited in this area, the present paper tends to highlight the importance of considering the timing of exercise to optimize our impact on the overall energy balance, and to encourage the elaboration of further studies to better understand and determine the potential effect of this timing of exercise, in order to find the best combination between the different exercise characteristics, intensity, duration, modality, to empower these effects.
... The problem with large high-fat test meals is that at very high doses of dietary lipids there is no clear dose dependence of postprandial hypertriglyceridemia on the fat load. However, a dose-dependent increase has been reported for mixed meals (650-950 kcal) with moderate intake of fat (30-60 g, 50%-65% of total energy content) and a significant proportion of carbohydrates (50-100 g, 25%-40% of total energy content) to ensure the effective release of insulin (Zhang et al. 1998). These parameters were used to design the test diet in the current study. ...
Today, awareness has been raised regarding high consumption of n-6 polyunsaturated fatty acids (PUFA) in western diets. A comprehensive analysis of total and individual postprandial fatty acids profiles would provide insights into metabolic turnover and related health effects. After an overnight fast, 9 healthy adults consumed a mixed meal comprising 97 g carbohydrate and 45 g fat, of which 26.4 g was linoleic acid (LA). Nonesterified fatty acids (NEFA), phospholipid fatty acids (PL-FA) and triacylglycerol fatty acids (TG-FA) were monitored in plasma samples, at baseline and hourly over a 7-h postprandial period. Total TG-FA concentration peaked at 2 h after the meal and steadily decreased thereafter. LA from TG18:2n-6 and behenic acid from TG22:0 showed the highest response among TG-FA, with a biphasic response detected for the former. PL-FA exhibited no change. Total NEFA initially decreased to nadir at 1 h, then increased to peak at 7 h. The individual NEFA showed the same response curve except LA and some very-long-chain saturated fatty acids (VLCSFA, ≥20 carbon chain length) that markedly increased shortly after the meal intake. The similarities and dissimilarities in lipid profiles between study subjects at different time points were visualized using nonmetric multi-dimensional scaling. Overall, the results indicate that postprandial levels of LA and VLCSFA, either as NEFA or TG, were most affected by the test meal, which might provide an explanation for the health effects of this dietary lifestyle characterized by high intake of mixed meals rich in n-6 PUFA.
... Although most do not suffer from the negative effects of these atherogenic changes until middle-age, the damage can begin as early as childhood, making reductions in postpran-dial hypertriglyceridemia an important factor in reducing cardiovascular disease risk later in life (Hong 2010). In adults, post-meal exercise can have beneficial effects on the lipemic response to a high-fat meal (Katsanos and Moffatt 2004); however, research also indicates that exercise after a high-fat meal has no (Zhang et al. 1998), or the equivalent to pre-meal exercise (Katsanos and Moffatt 2004) lipid-lowering effects. A review by Haxhi et al. concluded that in adults, pre-meal exercise is more effective for lowering triglycerides and increasing high-density lipoproteincholesterol in the subsequent postprandial state in individuals with hypertriglyceridemia (Haxhi et al. 2013), potentially because of higher adipose tissue lipolytic and total lipid oxidization compared with post-meal exercise (Enevoldsen et al. 2004;Bennard and Doucet 2006). ...
Currently, exercise prescription relies heavily on parameters included in the FITT principle: frequency, intensity, time (duration), and type of exercise. In this paper, the benefits of including timing (FITT+T), referring to when exercise is performed in relation to meal-time, is discussed. Current research indicates that timing is outcome-specific. Total energy and lipid intakes, and postprandial hypertriglyceridemia can be reduced when exercise is performed pre-meal, while glycemic control is improved with post-meal exercise. Although findings indicate that timing can aid in obesity management and cardiometabolic-risk reduction, most research involves adult subjects and acute investigations. Some research with children, concerning the effect of timing on appetite, indicates that pre-meal exercise helps regulate energy balance, but also identifies key differences in response compared with adults. Overall, current findings support the benefits of timing, but research is required to establish guidelines that are specific to the pediatric population and their health-related goals, while incorporating other FITT components.
... We hypothesized that allowing participants to leave the laboratory between the baseline and 4-h follow-up blood draw would not significantly alter TG results. This hypothesis was based in part on null findings from studies that investigated whether postprandial exercise of moderate energy expenditure modifies the TG response curve (e.g., [7]). ...
Background: A large post-meal triglyceride (TG) response is an independent risk factor for cardiovascular disease, but postprandial lipemia assessments are not clinically practical in their current form. Therefore, we assessed the validity of an abbreviated, clinically feasible protocol in measuring postprandial lipemia. Method: Eighteen healthy adults (8 male and 10 female) completed 3 high-fat meal trials in random order: (1) a Standard in Lab (SL) protocol wherein blood draws (to determine TG) were made from a catheter at baseline and hourly for 6 h; (2) an Abbreviated in Lab (AL) protocol in which participants remained in the laboratory but blood draws were only made at baseline and 4 h post-meal; and (3) an Abbreviated with Freedom (AF) protocol in which participants vacated the laboratory between the meal and the 4-h blood draw. Results: TG increase from baseline was very similar (p = 0.93) across the 3 trials (SL: 68.5 ± 62.7 mg/dL; AL: 71.1 ± 58.0 mg/dL; AF: 66.7 ± 46.4 mg/dL), as were 4-h TG levels (SL: 144.6 ± 84.2 mg/dL; AL: 171.4 ± 88.2 mg/dL; AF: 157.7 ± 76.7 mg/dL; p = 0.49). Similarly, total and incremental area under the curve (AUC) were not significantly different across the trials (p = 0.12 and 0.91, respectively). Conclusion: The TG results of the clinically feasible, abbreviated protocol were similar to those of the more exhaustive standard protocol. The AF protocol could be a valid and feasible clinical tool for measurement of postprandial lipemia and assessment of cardiovascular risk, although studies in larger and more diverse cohorts are needed.
... We hypothesized that allowing participants to leave the laboratory between the baseline and 4-h follow-up blood draw would not significantly alter TG results. This hypothesis was based in part on null findings from studies that investigated whether postprandial exercise of moderate energy expenditure modifies the TG response curve (e.g., [7]). ...
Background: A large post-meal triglyceride (TG) response is an independent risk factor for cardiovascular disease, but postprandial lipemia assessments are not clinically practical in their current form. Therefore, we assessed the validity of an abbreviated, clinically feasible protocol in measuring postprandial lipemia. Method: Eighteen healthy adults (8 male and 10 female) completed 3 high-fat meal trials in random order: (1) a Standard in Lab (SL) protocol wherein blood draws (to determine TG) were made from a catheter at baseline and hourly for 6 h; (2) an Abbreviated in Lab (AL) protocol in which participants remained in the laboratory but blood draws were only made at baseline and 4 h post-meal; and (3) an Abbreviated with Freedom (AF) protocol in which participants vacated the laboratory between the meal and the 4-h blood draw. Results: TG increase from baseline was very similar (p = 0.93) across the 3 trials (SL: 68.5 ± 62.7 mg/dL; AL: 71.1 ± 58.0 mg/dL; AF: 66.7 ± 46.4 mg/dL), as were 4-h TG levels (SL: 144.6 ± 84.2 mg/dL; AL: 171.4 ± 88.2 mg/dL; AF: 157.7 ± 76.7 mg/dL; p = 0.49). Similarly, total and incremental area under the curve (AUC) were not significantly different across the trials (p = 0.12 and 0.91, respectively). Conclusion: The TG results of the clinically feasible, abbreviated protocol were similar to those of the more exhaustive standard protocol. The AF protocol could be a valid and feasible clinical tool for measurement of postprandial lipemia and assessment of cardiovascular risk, although studies in larger and more diverse cohorts are needed.
... Il rischio ereditario di sviluppare DM2 viene ridotto con un aumento della quota settimanale di AF (9). Il potente effetto dell'AF sul metabolismo è stato più volte documentato: una seduta di AF moderata-vigorosa aumenta i livelli di HDL e riduce l'insensibilità all'insulina (10). Anche piccole dosi di AF lieve-moderata (es. ...
Objectives:
Physical activity is a key element in the prevention, treatment and rehabilitation of many diseases.
Methods:
In the context of an adequate lifestyle, its practice amplifies the health benefits and increases the fitness, and furthermore counteracts the development and progression of chronic non-communicable diseases, modulating many risk factors. Its function is important in all life cycles and helps to keep the functional capabilities and independence even with aging.
Results:
While inadequate physical activity (due to a sedentary lifestyle) is currently the fourth leading cause of mortality in developed countries, being one of the main public health issues, strong scientific evidences show that a regular and sufficient dose of physical activity reduces by about 30% the risk of premature death, cardiovascular disease and stroke, type II diabetes, colon and breast cancer, depression.
Conclusions:
Several guidelines and recommendations define the type, intensity, frequency and duration of physical activity, and many lifestyle preventative interventions prove its effectiveness and sustainability. Although so far a minority of the population actually adheres to the recommendations, the epidemiological strenght of lifestyle-oriented programs is considerable: quitting sedentariness, even low doses of physical activity are protective for health and reduce by about 22 % the risk of premature death. Physical activity is also an important therapeutic tool for patients with cardiovascular diseases, hypertension, diabetes II, cancer, chronic obstructive pulmonary diseases; an appropriate dosage reduces the risk of recurrence and disease progression, improves the control of clinical parameters and increases the patient's quality of life.
... The association between the timing of exercise and the timing of meals has long been acknowledged on blood lipid profiles (16), but only recently has this association been identified as playing a potentially important role in maintaining glycemic control (17)(18)(19)(20). For instance, Heden et al. (20) showed exercise conducted in the postprandial period significantly reduced the glucose area under the curve (AUC) in individuals with T2DM relative to preprandial exercise. ...
Purpose:
The timing of exercise relative to meal consumption has recently been identified as potentially moderating the effectiveness of exercise on glycemic responses in type 2 diabetes mellitus (T2DM). The aim of this study was to systematically review the literature related to exercise timing, relative to meal consumption, and glycemic control in individuals with T2DM.
Methods:
Systematic searches in PubMed, EMBASE, CINAHL, Cochrane Library and ClinicalTrials.gov Registry databases were performed to identify articles published in English from inception to October 2017. Two authors independently extracted data and evaluated the quality of studies using the Cochrane Collaboration Data Collection Form and Cochrane Collaboration Risk of Bias Assessment Tool respectively. A qualitative synthesis was performed on the included studies, and results summarized in tables.
Results:
19 randomized controlled trials (RCTs) with a total of 346 participants were included. Improvements in glycemia (glucose concentrations and glucose-AUC) and insulin-AUC appeared more consistent when exercise was performed during the post-meal period as compared to the pre-meal period, however, this observation was largely based on indirect comparisons between studies.
Conclusions:
There is some evidence from RCTs that exercise performed 30 min after meal consumption may convey greater improvements in glycemic control for individuals with T2DM. However, there are only two studies which have directly assessed the role of exercise timing on glycemic management and adopted methodologies are heterogeneous. Future low risk trials in this field are warranted.
... Exercise training prior to high-fat meal ingestion has been shown to have an attenuating effect on postprandial metabolism [5,6]. In the same line, studies have reported that energy expenditure through prior exercise is related to the magnitude of this effect [7,8]. ...
Background: There is evidence to suggest that postprandial lipemia are is linked to the impairment of endothelial function, which is characterized by an imbalance between the actions of vasodilators and vasoconstrictors. The aim of this study was to determine the effects of a 12-week high-intensity training (HIT) and moderate continuous training (MCT) protocol on postprandial lipemia, vascular function and arterial stiffness in inactive adults after high-fat meal (HFM) ingestion.
Methods: A randomized clinical trial was conducted in 20 healthy, inactive adults (31.6 ± 7.1 years). Participants followed the two exercise protocols for 12 weeks. To induce a state of postprandial lipemia (PPL), all subjects received a HFM. Endothelial function was measured using flow-mediated vasodilation (FMD), normalized brachial artery FMD (nFMD), aortic pulse wave velocity (PWV) and augmentation index (AIx). Plasma total cholesterol, high-density lipoprotein cholesterol (HDL-c), triglycerides and glucose were also measured.
Results: The effects of a HFM were evaluated in a fasted state and 60, 120, 180, and 240 minutes postprandially. A significant decrease in serum glucose between 0 min (fasted state) and 120 min postprandially was found in the HIT group (P=0.035). Likewise, FMD (%) was significantly different between the fasted state and 60 min after a HFM in the HIT group (P=0.042). The total cholesterol response expressed as area under curve (AUC)(0-240) was lower following HIT than following MCT, but no significant differences were observed (8%, P>0.05). Similarly, triglycerides AUC(0-240) was also lower after HIT compared with MCT, which trended towards significance (24%, P=0.076). The AUC (0-240) for the glucose response was significantly lower following HIT than MCT (10%, P=0.008). FMD and nFMD AUC(0-240) were significantly higher following HIT than following MCT (46.9%, P=0.021 and 67.3%, P=0.009, respectively). PWV AUC(0-240) did not differ following between the two exercise groups (2.3%, P>0.05).
Conclusions: Supervised exercise training mitigates endothelial dysfunction and glucose response induced by PPL. Exercise intensity plays an important role in these protective effects, and medium-term HIT may be more effective than MCT in reducing postprandial glucose levels and attenuating vascular impairment.
... However, a high CHO diet might cause a rise in very-low-density lipoprotein (VLDL) concentration [11][12][13] and a reduction in the level of high-density lipoprotein cholesterol (HDL-C) [14], which were considered to increase the risk of CVD. Previous study showed exercise intervention might elevate the level of HDL-C, increase lipoprotein lipase (LPL) activity [15], increase the transportation of blood lipids into the muscle cells for storage or use, and lower postprandial TG concentrations [11,16]. Katsanos and colleagues [17] showed that following moderate-intensity endurance exercise there was significantly lower insulin concentration and TG area under the curve (AUC) over 6 h after ingestion of a high-fat meal when compared to the no exercise trial. ...
Ingestion of low glycemic index (LGI) carbohydrate (CHO) before exercise induced less insulin response and higher fat oxidation than that of high GI (HGI) CHO during subsequent exercise. However, the effect on the subsequent postprandial lipid profile is still unclear. Therefore, the aim of this study was to investigate ingestion of CHO drinks with different GI using fructose and glucose before endurance exercise on the subsequent postprandial lipid profile. Eight healthy active males completed two experimental trials in randomized double-blind cross-over design. All participants ingested 500 mL CHO (75 g) solution either fructose (F) or glucose (G) before running on the treadmill at 60% VO2max for 1 h. Participants were asked to take an oral fat tolerance test (OFTT) immediately after the exercise. Blood samples were obtained for plasma and serum analysis. The F trial was significantly lower than the G trial in TG total area under the curve (AUC; 9.97 ± 3.64 vs. 10.91 ± 3.56 mmol × 6 h/L; p = 0.033) and incremental AUC (6.57 ± 2.46 vs. 7.14 ± 2.64 mmol/L × 6 h, p = 0.004). The current data suggested that a pre-exercise fructose drink showed a lower postprandial lipemia than a glucose drink after the subsequent high-fat meal.
... (21) A modified heparin-MnCl2 method was used to determine HDL-C concentrations. (22) A modified Friedewald equation was used to determine serum LDL-C concentrations as this equation was shown to be the most accurate for determining postprandial LDL-C concentrations. (23) 4-Challenge meal: After an overnight fast, all participants were invited to eat a well-balanced low cost big breakfast meal which essentially contains carbohydrates, fats, proteins, fibers, vitamins and minerals. ...
Background: A well balanced diet is important for normal function of endothelial cells. Diets high
in fat and/or calories can lead to hypertriglyceridemia and postprandial lipidemia and thus are
considered a risk factor for the development of atherosclerosis. Big meals may result in chronic
elevations in the level of atherogenic lipoproteins as well as evoking chronic inflammatory response.
Both may lead to pathological changes on the arterial vessel wall and myocardium.
Objective(s): To study the effect of the size of a well-balanced meal on the lipid profile in the post
prandial state and its effect on the endothelial function, ventricular filling and diastolic function.
Methods: one group pretest-posttest study was carried out on 40 young healthy lean volunteers aged
30 to 39 years who after overnight fast were invited to eat a big breakfast meal. Postprandial blood
samples were then drawn after 3-4 hours to determine changes induced by the big meal in the blood.
On the following day, the same procedure was adopted but with a breakfast meal which contains
only one third of the size of the big meal (small meal). The items of comparison between the two
meals included: The changes induced by both types of meals on the lipid profile of the blood by
assessing the postprandial levels of TG, TC, LDL-C, HDL-C and FFAs; assessment of the
inflammatory response by assessing postprandial levels of CRP; The changes induced on endothelial
cell functions by assessing the postprandial levels of ET1 and NO; and the changes induced by the
two types of meals on the left ventricular function as determined by echo Doppler as well as tissue
Doppler imaging (TDI).
Results: The big meal was associated with elevations in TG, TC, LDL-C, CRP, ET1 and NO
(P=0.001, 0.021, 0.057, 0.110, 0.002, 0.001respectively). The small meal showed significant
increase in levels of HDL-C (P=0.001) and FFAs (P=0.048). The diastolic function of the left
ventricle showed significant reduction after the ingestion of the big meal versus the small meal.
Conclusions: The study concluded that big meal size negatively impact lipid homeostasis and
endothelial function and the recognition of this possible danger of big meals can lead to the
possibility of prevention of atherosclerosis through controlling of the meal size.
... Participants consumed the test meal within 15 minutes of the pre-meal blood draw. The high-fat milk shake was composed of 255 mL of whipping cream and 74 g of ice cream (1,010 kcals, 100 g fat, 99 g saturated fat, 17 g carbohydrate and 3 g protein) , Zhang, et al., 1998. ...
Reductions in postprandial lipemia have been observed following aerobic exercise of sufficient energy expenditure. Increased excess postexercise oxygen consumption (EPOC) has been documented when comparing high- versus low-intensity exercise. The contribution of EPOC energy expenditure to alterations in postprandial lipemia has not been determined. The purpose of this study was to evaluate the effects of low- and high-intensity exercise on postprandial lipemia in healthy, sedentary, overweight and obese men (age, 43 ± 10 years; peak oxygen consumption, 31.1 ± 7.5 mL·kg⁻¹·min⁻¹; body mass index, 31.8 ± 4.5 kg/m²) and to determine the contribution of EPOC to reductions in postprandial lipemia. Participants completed 4 conditions: nonexercise control, low-intensity exercise at 40%–50% oxygen uptake reserve (LI), high-intensity exercise at 70%–80% oxygen uptake reserve (HI), and HI plus EPOC re-feeding (HI+EERM), where the difference in EPOC energy expenditure between LI and HI was re-fed in the form of a sports nutrition bar (Premier Nutrition Corp., Emeryville, Calif., USA). Two hours following exercise participants ingested a high-fat (1010 kcals, 99 g sat fat) test meal. Blood samples were obtained before exercise, before the test meal, and at 2, 4, and 6 h postprandially. Triglyceride incremental area under the curve was significantly reduced following LI, HI, and HI+EERM when compared with nonexercise control (p < 0.05) with no differences between the exercise conditions (p > 0.05). In conclusions, prior LI and HI exercise equally attenuated postprandial triglyceride responses to the test meal. The extra energy expended during EPOC does not contribute significantly to exercise energy expenditure or to reductions in postprandial lipemia in overweight men.
... Clearly, these different meal trials produced different effects on HDL cholesterol. Previous evidence has shown that the response of HDL cholesterol is inversely related to the magnitude of postprandial lipemia (13), and it has been speculated that the lowering of HDL cholesterol in response to HFM consumption can be an avenue by which HFMs induce deleterious cardiovascular effects (24). ...
Background: A substantial increase in triglycerides (TGs) after a meal is associated with an increased risk of cardiovascular disease. Most studies investigating the effects of a meal on TGs have not used meals that reflect typical consumption.
Objective: The objective of this study was to compare the TG and inflammatory responses of true-to-life meals, containing moderate fat and energy contents, with a high-fat, high-energy, low-carbohydrate meal (HFM) typically used to test TG responses.
Methods: Nine healthy, insufficiently active men [mean ± SD age: 25.1 ± 6.7 y; body mass index (in kg/m2): 25.8 ± 7.0; <150 min moderate- to vigorous-intensity physical activity/wk] completed 3 meal trials in random order: an HFM (17 kcal/kg, 60% fat), a moderate-fat meal (MFM; 8.5 kcal/kg, 30% fat), and a biphasic meal (BPM), in which participants consumed the full MFM at baseline and 3 h postmeal. Blood samples were collected via an indwelling catheter at baseline and hourly for 6 h.
Results: Peak blood TGs were significantly greater ( P = 0.003) after the HFM (285.2 ± 169.7 mg/dL) than after the MFM (156.0 ± 98.7 mg/dL), but the BPM (198.3 ± 182.8 mg/dL) was not significantly different from the HFM ( P = 0.06) or the MFM ( P = 0.99). Total area under the curve for TGs was greater after the HFM (1348.8 ± 783.7 mg/dL × 6 h) than after the MFM (765.8 ± 486.8 mg/dL × 6 h; P = 0.0005) and the BPM (951.8 ± 787.7 mg/dL × 6 h; P = 0.03), although the MFM and BPM were not significantly different ( P = 0.72). There was a significant time-by-meal interaction for interferon γ, but not for interleukins 6, 8, or 10.
Conclusion: These findings in insufficiently active, healthy young men suggest that the large TG response after HFMs in previous studies may not reflect the metabolic state of many individuals in daily life.
... Current research has determined the optimal time to measure PPT following an oral fat tolerance tests (OFTT) is 12-16 hours post-exercise (14,24,28). Exercise benefits measured directly prior to, or directly after, a high-fat meal show a decrease in effectively reducing PPT when compared to measured exercise benefits at 12 hours prior to the high-fat meal (30). Research concerning lipid metabolism commonly utilizes a younger population (20-50 years of age), creating a scarcity in data corresponding to older adults. ...
International Journal of Exercise Science 9(5): 677-684, 2016. To determine whether 90 minutes of moderate-intensity exercise, prior to a high fat meal, attenuates postprandial triglycerides (PPT) in older adults. Eight sedentary older adult volunteers (mean ± SD age = 58 ± 8 years, BMI 26.5 ± 4.2); completed two trials consisting of exercise and a no-exercise control. Exercise trials involved 90 minutes of moderate-intensity exercise 60% heart rate reserve (HRR). Following exercise, an overnight fast of 12-16 hours was performed. Participants were given a high fat meal that consisted of 146 grams of CHO, and 92 grams of fat and instructed to rest. Lipid levels were collected at pre-feeding, 1, 2, 3, and 4 hours post feeding. The control trial involved no exercise, performed an overnight fast of 12-16 hours, and was given the high fat meal followed by four hours of rest and data collection. There was no difference in PPT between the control and exercise trials (p < 0.05). Triglycerides (TG) increased in both trials over pre-feeding values (pre-feeding 123.
... It has been estimated that during exercises, intramuscular TG could provide as much as 20% -25% of the energy for muscles to work. Enhanced epinephrine and glucagon during exercise activate adenylate cycles, thereby increasing cyclic adenosine monophosphate (cAMP) (15). Increased cAMP phosphorylates activates hormone-sensitive LPL, which hydrolyzes intracellular TGs in skeletal muscle and the myocardium, as well as in adipose tissue, during exercise, to provide free fatty acids as an energy source. ...
Background: Metabolic syndrome is considered a risk factor for many chronic diseases, such as type II diabetes and cardiovascular diseases (CVD). The syndrome is the result of various factors, including poor nutritional diets, sedentary lifestyles, and genetic predisposition. Physical activity and good nutrition can prevent metabolic syndrome.
Objectives: The aim of the present study was to compare the effects of continuous and discontinuous training on metabolic syndrome components in non-athlete, middle-aged woman.
Patients and Methods: Forty-five non-athlete women who met the study criteria voluntarily participated in this study. The participants were divided randomly into three groups: continuous, discontinuous, and control (n = 15 in each group). Twenty-four hours before the beginning of the training program, a blood sample was obtained from each participant in the fasting state .The two training groups participated in sports activities designed to produce a heart rate of 50 - 70 beats/minute for 8 weeks, three times a week, for 60 - 90 minutes. The continuous training group performed the activities in one session, and the discontinuous training group performed them in two sessions, for the same time and intensity. Twenty-four hours after the completion of the 8-week program, all the measurements were performed similar to the pretest phase. The data were analyzed using a one-way analysis of variance (ANOVA).
Results: The discontinuous training significantly decreased each participant’s weight (P = 0.04) and systolic blood pressure (BP) (P < 0.01), whereas it significantly increased their triglyceride (TG) (P < 0.01) and high-density lipoprotein cholesterol (HDL-c) levels (P < 0.01). However, there was no significant change in diastolic BP, low-density lipoprotein cholesterol (LDL-c), or glucose. In the continuous training group, the TG level decreased significantly (P < 0.01).
Conclusions: This study demonstrated that a regular physical activity program in the form of discontinuous training improved metabolic syndrome indexes in non-athlete, middle-aged women. Discontinuous training seems to be an efficient, safe, and inexpensive way to reduce and prevent metabolic syndrome.
... 23 The authors linked this result to the higher rate of TG removal and the greater SOD activity provoked by exercise. 23,64 Working from the assumption that physical exercise sessions have the capacity to acutely stimulate antioxidant defense, 29,65 interventions have investigated whether the effect is sustained after an HFM. It was demonstrated that a single session of physical exercise the previous day is capable of increasing TAS hours after an HFM. ...
It is extremely important for public health to identify strategies that can prevent development of atherosclerosis. There are several modifiable metabolic risks that can induce onset of this disease, but the most investigated of these risk is increased postprandial lipemia after a high fat meal because this factor can increase oxidative damage and endothelial dysfunction. Physical exercise is indicated for prevention of development of these risk factors. The objective of this study was to search the literature for published studies investigating the acute and subacute effects on oxidative stress and endothelial function of physical exercise associated with postprandial lipemia and compare their results. Articles published up to February 2015 in Portuguese, Spanish or English were included. After an extensive review, it was concluded that the acute and subacute effects of physical could be capable of attenuating parameters of cardiovascular risk after consumption of a high fat meal.
... Asimismo Zang JQ. y cols. (1998) compararon el efecto de realizar 60 minutos de ejercicio, al 60% VO2max, en ayuna de 12 horas, con respecto a hacerlo en estado postprandial (ejercicio 1 hora post ingesta), concluyendo que realizar ejercicio en estado de ayuno provoca benefi cios metabólicos respecto a los triglicéridos y el metabolismo del HDL (high density lipoprotein), lo que disminuye la progresión de los procesos ateroscleróticos (54). ...
The high rate of obesity in sedentary population, coupled with the increase in diseases associated with this lifestyle, have led us to seek new strategies to enhance the physical training that will favor mobilization, uptake and utilization of fats and glucose. Doing exercise in the fasted state is one that has proved more promising. There is sufficient evidence on the benefits of physical activity during fasting producing a favorable hormonal environment, activation of mediators such as AMPKand LPL activation, among others. Performing aerobic exercise of moderate intensity in this environment favors fasting lipid oxidation, decreasing intramyo-cellular triglycerides, visceral fat and LDL cholesterol, compared with the benefits of exercise in the postprandial state. There is an important need for more studies of physical activity in the fasted state that include patients with chronic non-transmissible diseases and resistance training.
... However, studies are difficult to compare due to different measurement methods, meal composition and size, timing of exercise, exercise mode, intensity and duration. Inadequate energy expenditure [36] and/or inadequate exercise timing relative to the meal may explain the lack of exercise induced reduction in postprandial glucose [37] -and/or triglyceride excursion [38], etc. The acute effect of different exercise modes and timing of these on the postprandial response of the LV certainly needs to be further investigated in type 2 diabetes as the time course of adaptation may be different in the heart/endothelium than normal body weight persons. ...
Type 2 diabetes aggravates the postprandial metabolic effects of food, which increase cardiovascular risk. We investigated the acute effects of fast food on postprandial left ventricular (LV) function and the potential effects of pre-exercise in type 2 diabetes individuals.
We used a cross-over study including 10 type 2 diabetes individuals (7 male and 3 females; 53.4 ± 8.1 years; 28.3 ± 3.8 kg/m(2); type 2 diabetes duration 3.1 ± 1.8 years) and 10 controls (7 male and 3 females; 52.8 ± 10.1 years; 28.5 ± 4.2 kg/m(2)) performing high intensity interval exercise (HIIE; 40 min, 4 × 4min intervals, 90-95 % HRmax), moderate intensity exercise (MIE; 47 min, 70 % HRmax) and no exercise (NE) in a random order 16-18 hours prior to fast-food ingestion. Baseline echocardiography, blood pressure and biochemical measurements were recorded prior to and 16-18 hours after exercise, and 30 minutes, 2 hours and 4 hours after fast food ingestion.
LV diastolic (peak early diastolic tissue velocity, peak early diastolic filling velocity), and systolic workload (global strain rate, peak systolic tissue velocity, rate pressure product) increased after consumption of fast food in both groups. In contrast to controls, the type 2 diabetes group had prolonged elevations in resting heart rate and indications of prolonged elevations in diastolic workload (peak early diastolic tissue velocity) as well as reduced systolic blood pressure after fast food consumption. No significant modifications due to exercise in the postprandial phase were seen in any group.
Our findings indicate that fast-food induces greater and sustained overall cardiac workload in type 2 diabetes individuals versus body mass index and age matched controls; exercise 16-18 hours pre-meal has no acute effects to the postprandial phase.
ClinicalTrials.gov: NCT01991769 .
Context
Physical activity, exercise, or both are a staple of lifestyle management approaches both for type 1 diabetes mellitus (T1DM) and type 2 diabetes (T2DM). While the current literature supports both physical activity and exercise for improving glycemic control, reducing cardiovascular risk, maintaining proper weight, and enhancing overall well-being, the optimal prescription regimen remains debated.
Evidence Acquisition
We searched PubMed and Google Scholar databases for relevant studies on exercise, insulin sensitivity, and glycemic control in people with T1DM and T2DM.
Evidence Synthesis
In patients with T1DM, exercise generally improves cardiovascular fitness, muscle strength, and glucose levels. However, limited work has evaluated the effect of aerobic plus resistance exercise compared to either exercise type alone on glycemic outcomes. Moreover, less research has evaluated breaks in sedentary behavior with physical activity. When considering the factors that may cause hypoglycemic effects during exercise in T1DM, we found that insulin therapy, meal timing, and neuroendocrine regulation of glucose homeostasis are all important. In T2DM, physical activity is a recommended therapy independent of weight loss. Contemporary consideration of timing of exercise relative to meals and time of day, potential medication interactions, and breaks in sedentary behavior have gained recognition as potentially novel approaches that enhance glucose management.
Conclusion
Physical activity or exercise is, overall, an effective treatment for glycemia in people with diabetes independent of weight loss. However, additional research surrounding exercise is needed to maximize the health benefit, particularly in “free-living” settings.
The increasing prevalence of metabolic syndrome is associated with major health and socioeconomic consequences. Currently, physical exercise, together with dietary interventions, is the mainstay of the treatment of obesity and related metabolic complications. Although exercise training includes different modalities, with variable intensity, duration, volume, or frequency, which may have a distinct impact on several characteristics related to metabolic syndrome, the potential effects of exercise timing on metabolic health are yet to be fully elucidated. Remarkably, promising results with regard to this topic have been reported in the last few years. Similar to other time-based interventions, including nutritional therapy or drug administration, time-of-day-based exercise may become a useful approach for the management of metabolic disorders. In this article, we review the role of exercise timing in metabolic health and discuss the potential mechanisms that could drive the metabolic-related benefits of physical exercise performed in a time-dependent manner.
The purpose of this systematic review was to synthesize the results from current literature examining the effects of prior exercise on the postprandial triglyceride (TG) response to evaluate current literature and provide future direction. A quantitative review was performed using meta-analytic methods to quantify individual effect sizes. A moderator analysis was performed to investigate potential variables that could influence the effect of prior exercise on postprandial TG response. Two hundred and seventy-nine effects were retrieved from 165 studies for the total TG response and 142 effects from 87 studies for the incremental area under the curve TG response. There was a moderate effect of exercise on the total TG response (Cohen’s d = −0.47; p < .0001). Moderator analysis revealed exercise energy expenditure significantly moderated the effect of prior exercise on the total TG response ( p < .0001). Exercise modality (e.g., cardiovascular, resistance, combination of both cardiovascular and resistance, or standing), cardiovascular exercise type (e.g., continuous, interval, concurrent, or combined), and timing of exercise prior to meal administration significantly affected the total TG response ( p < .001). Additionally, exercise had a moderate effect on the incremental area under the curve TG response (Cohen’s d = −0.40; p < .0001). The current analysis reveals a more homogeneous data set than previously reported. The attenuation of postprandial TG appears largely dependent on exercise energy expenditure (∼2 MJ) and the timing of exercise. The effect of prior exercise on the postprandial TG response appears to be transient; therefore, exercise should be frequent to elicit an adaptation.
Inflammation is a protective response to infection or injury; however, persistent microtraumas at the tissue level may result in chronic low-grade inflammation that plays both direct and indirect roles in the development of many diseases and aging. The purpose of this review is to describe the underlying physiology of low-grade inflammation and highlight potential inflammation lowering effects of physical activity (PA). Unique contributions of this review are to introduce the concept of inflammation phenotype flexibility in contrast to the low-grade inflammation state and describe how PA influences inflammation phenotype by altering muscle, gut, adipose, and postprandial metabolism. Pro-inflammatory M1 macrophages and cytokines—such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6—contribute to low-grade inflammation. Among the mechanisms that commonly contribute to low-grade inflammation are dysfunctional adipose tissue, a leaky gut, gut microbiota that promotes inflammation, and large postprandial glycemic and lipidemic responses. Physical activity may lower inflammation by decreasing M1 macrophages in visceral adipose tissue, decreasing adipose tissue volume, production of anti-inflammatory myokines, promotion of butyrate-producing members of the gut microbiota, improved gut barrier function, and lowering of postprandial glycemic and lipidemic responses. While exercise has many anti-inflammatory mechanisms, phenotype conversion is complex, multifaceted, and difficult to achieve. Our understanding of how PA influences inflammation must include acute exercise-induced anti-inflammatory effects, contribution to the inflammation state from multiple sources in the body, and phenotypic shifts underpinning low-grade inflammation.
Acute exercise improves postprandial lipemia, glucose tolerance, and insulin sensitivity, all of which are risk factors for cardiovascular disease. However, recent research suggests that prolonged sedentary behavior might abolish these healthy metabolic benefits. Accordingly, this study aimed to elucidate the impact of an acute bout of exercise on postprandial plasma triglyceride, glucose, and insulin concentrations after 4 days of prolonged sitting (~13.5 h/day). Ten untrained to recreationally active men ( n = 5) and women ( n = 5) completed a counterbalanced, crossover study. Four days of prolonged sitting without exercise (SIT) were compared with 4 days of prolonged sitting with a 1-h bout of treadmill exercise (SIT + EX; 63.1 ± 5.2% V̇o 2max ) on the evening of the fourth day. The following morning, participants completed a high-fat/glucose tolerance test (HFGTT), during which plasma was collected over a 6-h period and analyzed for triglycerides, glucose, and insulin. No differences between trials ( P > 0.05) were found in the overall plasma triglyceride, glucose, or insulin responses during the HFGTT. This lack of difference between trials comes with similarly low physical activity (~3,500–4,000 steps/day) on each day except for the 1-h bout of exercise during SIT + EX the day before the HFGTT. These data indicate that physical inactivity (e.g., sitting ~13.5 h/day and <4,000 steps/day) creates a condition whereby people become “resistant” to the metabolic improvements that are typically derived from an acute bout of aerobic exercise (i.e., exercise resistance).
NEW & NOTEWORTHY In people who are physically inactive and sitting for a majority of the day, a 1-h bout of vigorous exercise failed to improve lipid, glucose, and insulin metabolism measured the next day. It seems that something inherent to inactivity and/or prolonged sitting makes the body resistant to the 1 h of exercise preventing the normally derived metabolic improvements following exercise.
Background:
Triglyceride (TG) concentration is used as a marker of cardio-metabolic risk. However, diurnal and possibly weekday variation exists in TG concentrations.
Objective:
To investigate weekday variation in TG concentrations among 1.8 million blood samples drawn between 2008 and 2015 from patients in the Capital region of Denmark.
Design:
Plasma TG was extracted from a central clinical laboratory information system. Weekday variation was investigated by means of linear mixed models.
Results:
In addition to the profound diurnal variation, the TG concentration was 4.5% lower on Fridays compared to Mondays (P<0.0001). The variation persisted after multiple adjustments for confounders and was consistent across all sensitivity analyses. Out-patients and in-patients, respectively, had 5.0% and 1.9% lower TG concentrations on Fridays compared to Mondays (both P<0.0001). Highest weekday variations in TG concentrations were recorded for out-patients between the age of 9 to 26 years, with up to 20% higher values on Mondays compared to Fridays (all P<0.05).
Conclusions:
Triglyceride concentrations were highest after the weekend and gradually declined during the week. We suggest that unhealthy food intake and reduced physical activity during the weekend increase TG concentrations which track into the week. This weekday variation may carry implications for public health and future research practice.
This study investigated the ability of healthy young adults to walk 30 minutes postprandially to attenuate the glycemic response to a candy bar. Seventeen volunteers had blood glucose measured at baseline, 30 minutes, and 60 minutes on 3 days. Participants walked lightly for 30 minutes postprandially on day 3. Without postprandial exercise, there was a blood glucose spike; the differences between baseline, 30-minute, and 60-minute values were significantly different (P < .01). With postprandial exercise, baseline and 30-minute values were not significantly different. In conclusion, light walking for 30 minutes postprandially can blunt the spike in blood glucose.
Acute exercise transiently improves endothelial function, and protects the vasculature from the deleterious effects of a high fat meal (HFM). We sought to identify whether this response is dependent on exercise intensity in adolescents.
Twenty adolescents (10 male, 14.3 ± 0.3 y) completed three 1-day trials: 1) rest (CON); 2) 8x1 min cycling at 90% peak power with 75s recovery (high-intensity interval exercise; HIIE); 3) cycling at 90% of the gas exchange threshold (moderate-intensity exercise; MIE) one hour before consuming a HFM (1.50 g∙kg(-1) fat). Macrovascular and microvascular endothelial function were assessed before and immediately after exercise, and three hours after the HFM by flow mediated dilation (FMD) and laser Doppler imaging (peak reactive hyperaemia; PRH).
FMD and PRH increased one hour after HIIE (P<0.001, ES=1.20 and P=0.048, ES=0.56) but were unchanged after MIE. FMD and PRH were attenuated three hours after the HFM in CON (P<0.001, ES=1.78 and P=0.02, ES=0.59). FMD remained greater three hours after the HFM in HIIE compared to MIE (P<0.001, ES=1.47) and CON (P<0.001, ES=2.54), and in MIE compared to CON (P<0.001, ES=1.40). Compared to CON, PRH was greater three hours after the HFM in HIIE (P=0.02, ES=0.71) and MIE (P=0.02, ES=0.84), with no differences between HIIE and MIE (P=0.72, ES=0.16). Plasma [triacylglycerol] and [total antioxidant status] were not different between trials.
Exercise intensity plays an important role in protecting the vasculature from the deleterious effects of a HFM. Performing HIIE may provide superior vascular benefits than MIE in adolescent groups.
Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.
1. Skinfold thickness, body circumferences and body density were measured in samples of 308 and ninety-five adult men ranging in age from 18 to 61 years.
2. Using the sample of 308 men, multiple regression equations were calculated to estimate body density using either the quadratic or log form of the sum of skinfolds, in combination with age, waist and forearm circumference.
3. The multiple correlations for the equations exceeded 0.90 with standard errors of approximately ±0.0073 g/ml.
4. The regression equations were cross validated on the second sample of ninety-five men. The correlations between predicted and laboratory-determined body density exceeded 0.90 with standard errors of approximately 0.0077 g/ml.
5. The regression equations were shown to be valid for adult men varying in age and fatness.
Increasing plasma free fatty acids decreased the degree of glycogen depletion, and increased the citrate concentration, in slow-red (soleus) and fast-red (deep portion of vastus lateralis) muscle during exercise (approx. 50% depletion of glycogen, as against 75% in control animals). There was no effect in fast-white muscle (superficial portion of vastus lateralis). Glycogen concentration in the liver decreased by 83% in controls, but only by 23% in animals with increased free fatty acids during exercise. The decreased glycogen depletion may be partly explained by the findings that (a) plasma-insulin concentration was two- to three-fold higher in animals with increased plasma free fatty acids and (b) the exercise-induced increase in plasma glucagon was lessened by increased free fatty acids. Blood glucose was higher in the animals with increased free fatty acids after the exercise. The rats with increased plasma free fatty acids utilized approx. 50% as much carbohydrate as did the controls during the exercise.
The effects of exercise and a physiological increase in plasma insulin concentration on muscle lipoprotein lipase activity (mLPLA), leg exchange of glucose, and serum lipoprotein levels were investigated in healthy young men. During euglycemic hyperinsulinemia (n = 7) at 44 mU.liter-1, m-LPLA in non-exercised muscle decreased from 30 +/- 7.4 mU.g-1 wet weight (w.w.) (mean +/- SE) to 19 +/- 3.3 (P less than 0.05). Furthermore, the decrease in m-LPLA correlated closely (r = 0.97, P less than 0.05) with the increase in leg glucose uptake. Moreover, basal m-LPLA correlated with the insulin-induced increase in leg glucose uptake (r = 0.93, P less than 0.05). In the control group (n = 6) in which saline was infused in place of insulin and glucose, m-LPLA in nonexercised muscle did not change with time. No change in m-LPLA was observed immediately after one-legged knee extension exercise, but 4 h after exercise m-LPLA was higher (P less than 0.05) in the exercised thigh (47 +/- 17.8 mU.g-1 w.w.) compared with the contralateral nonexercised thigh (29 +/- 6.3 mU.g-1 w.w.). This difference was not found 8 h after exercise. The triacylglycerol content of serum lipoproteins decreased during insulin infusion. It is concluded that in contrast to the effect on adipose tissue, physiological concentrations of insulin decrease m-LPLA in proportion to the effect of insulin on muscle glucose uptake, while muscle contractions cause a local, delayed, and transient increase in m-LPLA. Further-more, basal m-LPLA is an indicator of muscle insulin sensitivity.
Ten healthy young men exercised for 1.5 and 3 hours, respectively, 4 to 6 weeks apart at the same work intensity, corresponding to 77% of the individual maximal heart rate. In the fasting state 1 mL of 10% Intralipid/kg body weight was injected IV, the fractional removal rate was calculated (k2-value), and fasting lipid and apolipoprotein C-I, C-II, and CIII concentrations were determined one day before, immediately before, immediately after, and one day after the exercise: measurements were also made two and three days after the three-hour session. An increase of the k2-value was found only the day after the three-hour exercise (+66%, P less than .01), while after the 1.5-hour exercise the k2-value was not changed. One and two days after the three-hour exercise the fasting serum triglyceride concentration was significantly decreased by 33% and 16%, respectively. Serum triglyceride concentration was decreased also the day after the shorter session (-17%, P less than .05). Decreases in serum cholesterol concentrations were significant after both exercise bouts, but the significance disappeared if corrections for the changes in calculated plasma volume were made. Serum level of C apolipoproteins was decreased one day after the three-hour exercise, while it was not changed after the shorter exercise. This study shows that prolonged exercise produces an increase in the removal rate of Intralipid triglycerides from the bloodstream, that this change is related to the duration of exercise, and that some time is required following the exercise, before it is manifest.
Lipoprotein lipase (LPL) is regulated by exercise in humans, but the effects of exercise on LPL expression in different tissues and the molecular mechanisms involved are unclear. We assessed the effects of 5-13 consecutive days of supervised exercise on tissue LPL expression as well as fasting plasma lipids and lipoproteins in 32 sedentary, weight-stable adult men. In skeletal muscle, exercise training increased the mean LPL mRNA level by 117% (P = 0.037), LPL protein mass by 53% (P = 0.038), and total LPL enzyme activity by 35% (P = 0.025). In adipose tissue, mean LPL mRNA, protein mass, and activity did not change. Exercise decreased triglycerides [from 172 +/- 4.3 to 127 +/- 3.2 (SE) mg/dl, P = 0.002], total cholesterol (from 188 +/- 1.2 to 181 +/- 1.0 mg/dl, P = 0.011), and very low-density lipoprotein-cholesterol (from 30.1 +/- 0.9 to 22.0 +/- 0.8, P = 0.004) and increased high-density lipoprotein cholesterol (HDL-C; from 43.4 +/- 0.35 to 45.0 +/- 0.37, P = 0.030) and HDL2-C (from 6.6 +/- 0.21 to 7.7 +/- 0.19, P = 0.021). Changes in muscle but not adipose tissue heparin-releasable LPL activity were inversely correlated (r = -0.435, P < 0.034) with changes in triglycerides. These data suggest the existence of an exercise stimulus intrinsic to skeletal muscle, which raises LPL activity in part by pretranslational mechanisms, a process that contributes to the improvement in circulating lipids seen with physical activity.
The hypothesis that plasma chylomicrons in persons who ingest a cholesterol-rich diet are atherogenic is evaluated. Evidence is presented that in humans, and experimental animals, chylomicron remnants as well as low-density lipoproteins are taken up by arterial cells. In persons who do not have familial hyperlipoproteinemia, atherogenesis may occur during the postprandial period. Research directions that may contribute to the evaluation of chylomicron remnants as a risk factor for atherogenesis are discussed. Lipoprotein studies after administration of a test meal containing fat and cholesterol are urgently needed.
Seven young, healthy subjects performed bicycle exercise with a working load leading to exhaustion after one hour of work. The tests were done in the afternoon in the fed state. The serum insulin concentrations decreased from 22 to 4 mU/l and plasma glucagon increased from 241 to 340 pg/l already after 30 min of work. The level of adipose tissue lipoprotein lipase activity (LPLA) did not fall as had been expected, but increased. The skeletal muscle LPLA was unchanged. The results indicate that during the first hour of heavy exercise the heparin-releasable LPLA in tissues is not influenced by the work induced changes in serum hormone levels.
The status of fasting triglycerides as a risk factor for coronary artery disease (CAD) has been considered weak because in multivariate analyses, triglycerides tend to be eliminated by high density lipoprotein (HDL) cholesterol. To further evaluate the role of triglycerides in CAD, we employed postprandial lipemia as a more informative means of characterizing triglyceride metabolism. In 61 male subjects with severe CAD and 40 control subjects without CAD as verified by angiography, we measured cholesterol; triglycerides; HDL cholesterol; HDL2 cholesterol; and apolipoproteins A-I, A-II, and B in fasting plasma and triglycerides before and 2, 4, 6, and 8 hours after a standardized test meal. Both the maximal triglyceride increase and the magnitude of postprandial lipemia (area under the triglyceride curve over 8 hours after the meal) were higher in cases than in control subjects. Single postprandial triglyceride levels 6 and 8 hours after the meal were highly discriminatory (p < 0.001), and by logistic-regression analysis displayed an accuracy of 68% in predicting the presence or absence of CAD. In this respect, accuracy was higher than that of HDL2 cholesterol (64%) and equal to that of apolipoprotein B (68%), the most discriminatory fasting parameter. Multivariate logistic-regression analysis was performed to reduce the number of risk factors to those that were statistically independent. This statistical procedure selected postprandial but not fasting triglycerides into the most accurate multivariate model, which also contained the accepted risk factors HDL2 cholesterol, apolipoprotein B, and age. This model classified 82% of subjects correctly. We conclude that triglycerides are independent predictors of CAD in multivariate analyses including HDL cholesterol, provided that a challenge test of triglyceride metabolism such as postprandial lipemia is used. The study suggests that the metabolism of triglycerides is a critical determinant of cholesterol metabolic routing. The findings support the concept that the negative association between HDL cholesterol levels and CAD actually originates in part from a positive relation between CAD and plasma triglycerides, as ascertained in the postprandial state.
Lipoprotein lipase (LPL) is anchored with high affinity to heparan sulphate proteoglycans on the luminal surface of the capillary endothelium. The levels of pre-heparin perfusate LPL activity increased from 16 +/- 1 to 145 +/- 6 U/hindlimb (nine-fold increase) in hindlimb muscle of exercise-trained rats measured immediately after the last bout of work. At the same time, post-heparin perfusate LPL activity decreased from 63 +/- 2 to 13 +/- 1 U/hindlimb (p less than 0.001). These results provide evidence that exercise-training has a heparin-like effect on capillary-bound LPL. The total amount of LPL (i.e., pre-heparin perfusate plus post-heparin perfusate) was twofold greater in the hindlimb of the trained animals versus the controls. The effect of exercise on muscle LPL activity appears to last for as long as 5 days after cessation of exercise. Serum triglycerides were reduced 38% and plasma free fatty acids increased fourfold. These results provide evidence that training increases the capacity to remove triglycerides from circulation.
The evidence linking hypertriglyceridemia and coronary artery disease (CAD) is reviewed. A positive correlation between plasma triglyceride level and CAD incidence has been demonstrated in most prospective studies on univariate analysis. However, the significance is weakened on multivariate analysis, in particular when level of high-density lipoprotein (HDL) cholesterol is taken into account, perhaps because of the close metabolic interrelation between the triglyceride-rich lipoproteins and HDL particles. Recent analyses of clinical data have shown that the combination of elevations of low-density lipoprotein cholesterol and triglyceride and low levels of HDL cholesterol confers particularly high risk for CAD. The U.S. National Institutes of Health Consensus Development Conference on Triglyceride, High Density Lipoprotein, and Coronary Heart Disease in February 1992 made recommendations to integrate more fully HDL cholesterol and triglyceride levels into the assessment and treatment of dyslipidemia and CAD risk. Treatment of hypertriglyceridemia should focus on diet and weight control, exercise, and smoking cessation, as well as control of other major risk factors for CAD, notably hypercholesterolemia and hypertension.
It has been suggested that a postprandial accumulation of triglyceride-rich lipoproteins promotes the development of atherosclerosis. This study was designed to test the hypothesis that postprandial lipemia is independently associated with intima-media thickening of the extracranial carotid arteries.
Forty-seven middle-aged, moderately hypercholesterolemic individuals were recruited for a 1-day study of the lipemic response to a standard high-fat test meal. The formula was fed at a dose of 65 g fat/m2 body surface area, after a 14-hour fast, and blood was obtained for triglyceride analysis hourly for 8 hours. A baseline lipid profile was obtained. Each subject underwent a carotid ultrasound examination. The extent of alimentary lipemia (peak triglyceride response) was correlated with the carotid artery wall thickness as measured by B-mode ultrasound.
Univariate analyses indicated an inverse correlation between peak triglyceride response and high density lipoprotein cholesterol concentration and a direct correlation with male sex, baseline triglyceride concentration, background fat intake, and waist-to-hip ratio. Of these, the only variable that showed a univariate correlation with B-mode score was peak triglyceride response. Age and cigarette smoking were also correlated with B-mode score in univariate analyses. The correlation coefficient (r = 0.52) between peak triglyceride response to a fat-rich meal and B-mode score was significant (p less than 0.002) and remained so in multivariate analysis. Forward-selection stepwise regression resulted in the inclusion of only peak triglyceride response (p = 0.001) and smoking history (p = 0.005) as important predictors of carotid wall thickness in a linear model.
The association between lipemic response and carotid wall thickness suggests that prolonged exposure of arterial wall cells to triglyceride-rich chylomicron remnants enhances the atherogenic process.
To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin:cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C), n = 18, 28.6 years, SD 5.2, 50.1 ml.kg-1.min-1 maximal O2 uptake (VO2max), SD 5.3; endurance trained athletes (T), n = 18, 31.4 years, SD 8.8, 65.0 ml.kg-1.min-1 VO2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol.ml-1.h-1, SD 16.7 vs T 65.0 nmol.ml-1.h-1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol.ml-1.h-1, SD 23.5, +48.6%, P less than 0.001; (T) 83.5 nmol.ml-1.h-1, SD 24.3, +29.1%, P less than 0.01. Neither the pre nor the postexercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.
Triglycerides are transported by the largest and most lipid-rich of the lipoprotein particles, namely, chylomicrons and very low density lipoproteins (VLDL). These particles are buoyant because of the high triglyceride content, which makes up approximately 90% by weight of the chylomicron and 70% by weight of the VLDL. The chylomicron transports exogenous or dietary fat and cholesterol, whereas VLDL transports endogenous triglyceride and cholesterol in lipoproteins synthesized and secreted by the liver. Both chylomicrons and VLDL are hydrolyzed at the capillary surface by the enzyme lipoprotein lipase. Lipoprotein lipase catalyzes the hydrolysis of triglyceride in the lipid core of these particles, producing smaller particles known as remnants. We currently believe the remnants are atherogenic and that this is one reason why hypertriglyceridemia may predispose to coronary artery disease. Chylomicron remnants are recognized and removed by hepatic receptors that contain apolipoprotein (apo) E. The rate of clearance of remnant particles depends on which subfraction of apo E is present. Particles containing apo EII are removed more slowly than those with apo EIII and EIV. The dietary cholesterol from the chylomicron remnant particles is thought to down-regulate the hepatic low-density lipoprotein (LDL) receptors. VLDL remnants, also called intermediate-density lipoprotein (IDL), contain apo E and may be removed by the liver through the LDL or B/E receptor. The decrease in activity of these receptors results in apparent oversynthesis of LDL, the end-product of VLDL and IDL metabolism. LDL is the major cholesterol carrier, followed by high-density lipoprotein (HDL).(ABSTRACT TRUNCATED AT 250 WORDS)
The cellular control of intramuscular triglyceride (TG) metabolism involves two major identified lipases: hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL). Recently, the presence of HSL in muscle has been unequivocally demonstrated. However, although it is thought that HSL is responsible for intramuscular TG lipolysis, direct evidence for this is lacking. There is evidence to suggest that HSL and LPL are simultaneously activated under a variety of conditions. The two muscle lipases appear to be turned on by the same signal and function as a coordinated unit in meeting the energy demands of muscle. At a time when HSL is presumably hydrolyzing endogenous TG, LPL is sent to the capillary beds in search of substrate. TG uptake from circulation is highly related to muscle LPL activity. Exercise training increases LPL activity in plasma and in parenchymal cells in muscle. These results suggest that training may increase the capacity to clear TG from circulation and that LPL might have a role in replenishing muscle TG stores that have been decreased with exercise.
Alimentary lipemia was studied in 12 healthy young men with and without exercise. Three sets of experiments were performed. While continuous exercise of 90 min duration significantly reduced postprandial triglycerides by 26% (study I), this effect could not be observed when exercise was interrupted for 5 min after each 25 min (study II). Plasma free fatty acid concentrations, in the latter experiment, were significantly higher (by 311%) than during rest. When, in a third experiment continuous exercise was compared with intermittent physical activity, the latter condition significantly increased postprandial triglyceridemia, most probably due to precipitous rises of free fatty acids on each interruption of ergometry. It is concluded that in the third experiment the balance between triglyceride removal and triglyceride synthesis was shifted toward the latter. Whether exercise lowers, leaves unaltered, or raises plasma triglyceride levels may depend on subtle changes of experimental design.
Lipoprotein lipase (LPL) activity in postheparin plasma of 38 normolipidemic volunteers was related to the magnitude of postprandial lipemia after a fat meal, to triglyceride content of high density lipoprotein2 (HDL2), to hepatic lipase (HL) activity, and to HDL2 levels. LPL activity correlated indirectly with lipemia, triglyceride content of HDL2, HL activity, and levels of HDL2 but not of HDL3. HL activity correlated directly with lipemia and indirectly with HDL2 levels. Triglyceride content of HDL2 correlated directly with lipemia and indirectly with HDL2 levels. In HDL2, abundance of apolipoprotein (apo) A-II and the apoA-I/apoA-II ratio varied widely. The latter correlated positively with LPL activity and HDL2 levels, and, inversely, with HL activity, lipemia, and triglyceride content of HDL2. The study suggests that HDL-cholesterol is not an independent parameter of lipid transport, but is strongly affected by triglyceride metabolism through lipolytic enzymes, as exemplified by postprandial lipemia that affect both composition and plasma levels of HDL2.
In the foregoing discussion we have included precipitation methods for HDL analysis that we consider to be among the most accurate and extensively characterized compared to analyses performed with the ultracentrifuge. The emphasis has been on the precipitation steps rather than on the analysis of cholesterol in the lipoprotein fractions. It is evident, however, that the accuracy of the cholesterol method itself will influence the overall reliability of the measurements even when the lipoprotein fraction has been separated adequately. Ideally, the cholesterol measurements would be made with reference methods. Since this is usually not practical with large numbers of samples, the accuracy and precision of the method employed should be established with respect to a reference method, such as that of Abell et al., before being used for routine cholesterol measurements. Finally, it should be mentioned that the conditions used in the methods discussed here were developed for human plasma or serum, and in the authors' experience may have to be modified for the adequate separation of plasma lipoproteins in other species.
We studied the effects of a single exercise session on lipid and lipoprotein concentrations and on postheparin plasma lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase activities (HTGLA) in 11 trained (T) and ten untrained (UT) men. Subjects exercised on a bicycle ergometer at 80% of their maximal heart rate for one (UT) or two hours (T). Blood samples were drawn 24 hours before and at ten minutes and 24, 48, and 72 hours after exercise. Values were analyzed before and after adjustment for estimated changes in plasma volume (PV). High density lipoprotein cholesterol (HDL-C) increased 2 +/- 4 mg/dL in T (P less than 0.05) and 1 +/- 2 mg/dL in UT subjects beginning 48 hours after exercise. This increase was magnified by adjusting for the 5% to 8% postexercise expansion of PV. The increase in HDL in the T subjects was produced by increases in the HDL2-C subfraction (+3 +/- 4 mg/dL, P less than 0.05) whereas HDL3 increased in the UT men (+2 +/- 3 mg/dL, P less than 0.05). LPLA did not change in either subject group when estimated PV changes were ignored but increased 11% (P less than 0.05) at 24 hours after exercise when PV was considered. HTGLA was 11% below baseline in the UT men 24 to 72 hours after exercise (P less than 0.05) but showed no change in either subject group after adjustment for PV. These results demonstrate that exercise acutely increases HDL levels by raising the HDL2 subfraction in T and the HDL3 subfraction in UT men.(ABSTRACT TRUNCATED AT 250 WORDS)
A bout of swimming to exhaustion resulted in an approximately 70% depletion of triglyceride stores in the red portion of the quadriceps muscle in rats. In contrast intramuscular triglycerides were unchanged in the white portion of quadriceps, and decreased only 25% in soleus muscle which is made up predominantly of intermediate fibers. Cardiac triglycerides underwent a small (11%) and statistically not significant reduction. Glycogen stores were reduced approximately 70% in all 3 types of skeletal muscle, and 32% in the heart. Liver glycogen was almost completely depleted, resulting in hypoglycemia. Assuming complete oxidation of the glycogen and triglycerides that disappeared from red muscle, triglycerides supplied roughly two-thirds as much energy to the working red fibers as did glycogen.
The role of glucagon in regulating the lipoprotein lipase activities of rat heart and adipose tissue was examined. When starved rats were fed glucose, heart lipoprotein lipase activity decreased while that of adipose tissue increased. Glucagon administration to these animals at the time of glucose feeding prevented the decline in heart lipoprotein lipase activity, but had no effect on the adipose tissue enzyme. When glucagon was administered to fed rats, heart lipoprotein lipase activity increased to levels found in starved animals but there was no change in the adipose tissue enzyme. It is suggested that the reciprocal lipoprotein lipase activities in heart and adipose tissue of fed and starved animals may be regulated by the circulating plasma insulin and glucagon concentrations.
In this study, we have investigated the effects of alimentary lipemia in 15 normotriglyceridemic individuals on high density lipoproteins2 (HDL2) with respect to structure, composition, and substrate efficacy for hepatic lipase in vitro. In the study subjects, HDL2 levels ranged widely from 4.7 to 151.7 mg/dl plasma. HDL2 were isolated in the postabsorptive (pa) state and in the postprandial (pp) state, i.e., 7 h after ingestion of a standard fatty meal. In going from the pa state to the pp state, HDL2 exhibited higher flotation rates and lower densities due to a decreased proportion of protein (38.7----36.2%) and a higher abundance in phospholipid (32.5----34.9%). There was a variable increase in triglyceride at the expense of cholesteryl esters; this increase was correlated positively with the magnitude of pp lipemia (r = 0.69, P less than 0.01) and inversely with HDL2 levels (r = -0.72, P less than 0.01). Hdl2 fractions were incubated with human hepatic lipase in vitro. Product lipoproteins formed from lipolysis of pa-HDL2 and triglyceride-poorer pp-HDL2 were reduced in phospholipid content (by 25 and 50%, respectively) but remained in the size and density range of native HDL2. By contrast, a major fraction of triglyceride-richer pp-HDL2 was converted to particles with density, size, and apoprotein composition of native HDL3. Changes consistent with these findings in vitro were observed in vivo also, where 15 h postprandially, individuals with high-level lipemia showed a decrease in HDL2 and rise in HDL3, while those with lower-level lipemia did not. This study indicates that the magnitude of postprandial lipemia determines the proportion of triglyceride in pp-HDL2, which in turn determines whether or not HDL2 are converted to HDL3 by hepatic lipase action.
We investigated the acute effects of prolonged exercise on lipoprotein metabolism. Serum lipid and lipoprotein concentrations and plasma postheparin lipolytic activity were measured in ten well-trained men (ages 21 to 39) the day before and after a 42 km foot race. LDL cholesterol decreased by 10% (113 +/- 31 to 103 +/- 32 mg/dL, P less than 0.01) and total HDL-cholesterol levels increased by 9% (65 +/- 18 to 71 +/- 19 mg/dL, P less than 0.01) the day after the race. No changes in the concentration of apolipoprotein A-I or A-II occurred. Triglyceride levels decreased by 39% (95 +/- 38 to 58 +/- 23 mg/dL, P less than 0.001). Two days after the race, total HDL cholesterol (74 +/- 21 mg/dL, P less than 0.05) and the HDL2 subfraction (37 +/- 19 mg/dL, P less than 0.05) remained significantly elevated compared to pre-race values. Most dramatically, the level of lipoprotein lipase activity measured in postheparin plasma nearly doubled after the race, demonstrating that vigorous exercise acutely increases this enzyme activity. The increase in lipoprotein lipase activity probably mediated the fall in serum triglycerides after exercise and may also account for the increase in HDL cholesterol.
The magnitude and duration of the serum triacylglycerol response to a fatty meal may be predictive of coronary artery disease. Exercise can modify this aspect of cardiovascular risk but the effective intensity, duration and timing of exercise is uncertain.
The influence of a single period of walking on the lipaemic response to a high-fat meal (1.2g fat and 71 kj per kilogram body mass) was examined in 12 normolipidaemic young adults (aged 21-33 years, six men and six women). The meal was ingested on two different occasions in a balanced, crossover design. In the control phase, participants rested for 6 h after consuming the meal; in the exercise phase, they walked on a treadmill for 1.5 h at 40% of their maximal oxygen uptake, starting 1.5 h after the meal, and then rested for a further 3 h. Lipid and lipoprotein levels were measured in venous blood taken during the fasted state and at intervals for 6 h after the meal.
The area under the triacylglycerol-time curve was 24 +/- 11% lower during the exercise phase (P < 0.05) than during the control phase because serum triacylglycerol concentrations were lower during recovery from exercise, 3-6 h after the meal.
Prolonged walking starting 1.5 h after the consumption of a fatty meal attenuates postprandial lipaemia in normolipidaemic young adults.
In order to determine whether exercise mode affects recovery energy expenditure, 7 active men (average age 25 yrs) performed a control rest and three submaximal exercise bouts in counterbalanced order in separate weeks. The bouts, designed to involve three levels of eccentric muscular activity, included 60% VO2max jog (60 J), 60% downhill (-5%) jog (60 DH), 60% cycling (60 C), and a control session. Following a 24-hr period of regulated activity and diet, subjects exercised for 60 min. VO2 and RER were assessed during 48 hrs of regulated recovery. Total energy use was elevated following 60 C and 60 DH versus control, and fat energy use was elevated following 60 J, 60 DH, and 60 C versus control. For combined trials, the total energy use was higher at 1, 2, and 9 hrs postexercise. These results do not support the hypothesis that eccentric muscular activity affects the magnitude of recovery energy expenditure.
The purpose of this study was to examine the effect of one bout of low-intensity exercise on the lipemic response to a high-fat meal. Twelve (six women, six men) normolipidemic adults aged 25.8 +/- 1.2 years (mean +/- SEM) took part in two trials. In the exercise trial, subjects walked for 2 hours on a treadmill at 30.9% +/- 1.6% of maximal oxygen uptake (VO2 max) 15 hours before ingestion of the test meal. In the control trial, subjects rested the day before the test meal. After a 12-hour fast, blood samples were obtained by venous cannulation before ingestion and hourly after ingestion for 6 hours. Serum was analyzed for triacylglycerol (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and HDL2-C, apolipoproteins (apos) A-I and B, free fatty acids (FFA), free glycerol, glucose, and insulin. TG values were corrected for free glycerol. Fasting serum TG and peak TG concentrations were lower (Wilcoxon, P < .05) for the exercise trial than for the control trial (0.74 +/- 0.03 v 0.92 +/- 0.08 and 1.98 +/- 0.18 v 2.59 +/- 0.32 mmol.L-1, respectively). The total lipemic response (area under the TG/time curve, normalized to the 0-hour level) was 31% +/- 7% lower in the exercise trial (4.28 +/- 0.66 v 6.46 +/- 1.08 mmol.L-1.h, P < .01). No differences were found between trials in the other parameters. These results show that a single bout of low-intensity exercise reduces the extent of postprandial lipemia in normolipidemic young adults. One possible mechanism is enhanced lipoprotein lipase (LPL) activity in the exercised skeletal muscle.
Nineteen young male normolipidemic volunteers sequentially consumed three test meals consisting of cream only, sucrose only, or cream with sucrose. These oral fat-tolerance tests showed an amplification of the postprandial excursion of serum triglyceride and cholesterol concentrations when sucrose was included in a lipid-rich meal compared with both the cream-only meal and the sucrose-only meal. The triglyceride concentration increase occurred only in the late postprandial phase whereas the cholesterol concentration was increased for the entire 8 h studied. The increased triglyceride and cholesterol concentrations in the triglyceride-rich lipoprotein (TRL) fraction accounted for most of the increase. The clearance of an intravenous lipid emulsion was measured before and 2 and 4 h after a sucrose meal. The two postprandial clearance rates were 34% slower than the fasting value. These data indicate that sucrose-induced postprandial hypertriglyceridemia may be induced by an inhibition of the clearance of triglyceride. The slower rate of lipolysis may cause the accumulation of cholesterol in TRL.
We have previously shown that the lipaemic response to a fatty meal was reduced when prolonged (2 h) low intensity exercise was taken some hours before eating. The purpose of this study was to test the hypothesis that the effect is quantitatively greater after exercise of moderate intensity than after exercise at low intensity. Six men and six women, mean age 26.9 (SEM 1.5) years, took part in three trials, each conducted over 2 days; on the afternoon of day 1 of each of two exercise trials the subjects walked on a treadmill for 90 min at either 31 (SEM 1) % or 61 (SEM 1) % of maximal oxygen uptake, i.e. low and moderate intensity, respectively; on the control trial the subjects refrained from exercise on day 1. On the morning of day 2 of each trial they ingested a test meal (1.28 g fat, 1.44 g carbohydrate, 76 kJ energy.kg-1 body mass); blood samples were obtained in the fasted state and for 6 h after the meal. Fasting serum triacylglycerol concentration and the area under the postprandial triacylglycerol-time curve were lower than in the control trial (P < 0.05) after moderate intensity walking but not after low intensity walking. The results suggest that the mitigation of the lipaemic response to a meal high in fat and carbohydrate is related to the intensity and/or the energy expenditure of the preceding exercise.
This study compared the effects of low and moderate intensity walking on postprandial lipemia, holding energy expenditure constant. Nine healthy normolipidemic subjects (5 men, 4 women; age 27.7 +/- 0.9, fasting, plasma triacylglycerol 0.95 +/- 0.18 mmol.l-1, mean +/- SEM) who were physically active but not endurance-trained undertook three trials, each over 2 d, in a balanced design. On the afternoon of day 1 they either refrained from exercise (Control), walked for 3 h at low intensity (Walk low, 32 +/- 1% VO2max), or walked for 1.5 h at moderate intensity (Walk moderate, 63 +/- 1% VO2max). The following morning, after a 12-h fast, they consumed a high-fat meal (1.3 g fat, 1.2 g carbohydrate, 0.2 g protein, 76 kJ energy per kg body mass). Blood and expired air samples were obtained before the meal and for 6 h afterward. Postprandial lipemia (total area under triacylglycerol concentration vs time curve) was lower than control after low intensity walking as well as after moderate intensity walking (both P < 0.05) but did not differ between the two walking trials (Control, 8.09 +/- 1.09 mmol.l-1 h; Walk low, 5.46 +/- 0.63 mmol.l-1.h; Walk moderate, 5.53 +/- 0.58 mmol.l-1.h). The increase in energy production following the test meal did not differ between trials, but fat oxidation was increased in the fasting and postprandial states for both walking trials, compared with control (P < 0.05).
The purpose of this study was to examine differences in postprandial hypertriglyceridemia (PP-HTG) and low density lipoprotein (LDL) subfraction distribution among groups of men and women with different fitness levels. Fifty-four men and women (ages 30-53 yr) were recruited based on their previous two-year activity level: sedentary (S), recreational exercisers (R), and endurance trained (T). After a 24-h dietary preparation, blood was collected, and LDL subfractions were separated and analyzed for cholesterol (C) and apoprotein B100. Plasma triglyceride (TG) concentration was assessed before and at 2, 4, 6, and 8 h after fat meal. PP-HTG was significantly higher for the S group compared with the two activity groups. LDL3-C and LDL3-apoprotein B100 were significantly higher for the S group compared with the T group and for men compared with women. These findings suggest that both recreational and competitive aerobic training are associated with a lower TG response after a fatty meal. However, higher volume aerobic training may be necessary to reduce the number of dense LDL molecules and their cholesterol content.
Postprandial lipemia: a key for the conversion of high density lipoprotein 2 into high density lipoprotein 3 by hepatic lipase
- J R Patsch
- S Prasad
- A M Gotto
- G Bengtsson-Olivecrona
Patsch, J. R., S. Prasad, A. M. Gotto, Jr., and G. Bengtsson-Olivecrona. Postprandial lipemia: a key for the conversion of
high density lipoprotein 2 into high density lipoprotein 3 by hepatic lipase. J. Clin. Invest. 74: 2017-2023, 1984.
Lipase regulation of muscle triglyceride hydrolysis
- L B Oscai
- D A Essid
- W K Palmer
Oscai, L. B., D. A. Essid, and W. K. Palmer. Lipase regulation
of muscle triglyceride hydrolysis. J. Appl. Physiol. 69: 1571-1577, 1990.