No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Higher Insulin-sensitizing Response after Sprint Interval Compared to Continuous Exercise
Abstract
This study investigated which exercise mode (continuous or sprint interval) is more effective for improving insulin sensitivity. Ten young, healthy men underwent a non-exercise trial (CON) and 3 exercise trials in a cross-over, randomized design that included 1 sprint interval exercise trial (SIE; 4 all-out 30-s sprints) and 2 continuous exercise trials at 46% VO2peak (CELOW) and 77% VO2peak (CEHIGH). Insulin sensitivity was assessed using intravenous glucose tolerance test (IVGTT) 30 min, 24 h and 48 h post-exercise. Energy expenditure was measured during exercise. Glycogen in vastus lateralis was measured once in a resting condition (CON) and immediately post-exercise in all trials. Plasma lipids were measured before each IVGTT. Only after CEHIGH did muscle glycogen concentration fall below CON (P<0.01). All exercise treatments improved insulin sensitivity compared with CON, and this effect persisted for 48-h. However, 30-min post-exercise, insulin sensitivity was higher in SIE than in CELOW and CEHIGH (11.5±4.6, 8.6±5.4, and 8.1±2.9 respectively; P<0.05). Insulin sensitivity did not correlate with energy expenditure, glycogen content, or plasma fatty acids concentration (P>0.05). After a single exercise bout, SIE acutely improves insulin sensitivity above continuous exercise. The higher post-exercise hyperinsulinemia and the inhibition of lipolysis could be behind the marked insulin sensitivity improvement after SIE.
... Therefore, the purpose of this study was to examine the modifying effect of exercise on the acute hemodynamic response to a standardized oral glucose tolerance test (OGTT). Given the paucity of data to support modality-specific effects of exercise on the hemodynamic response to an OGTT, we aimed to investigate 3 broad types of conventional exercise that are known to enhance insulin sensitivity acutely after exercise: continuous leg cycling (Mikines et al. 1988;Ortega et al. 2015), interval leg cycling (Little et al. 2014;Ortega et al. 2015), and whole-body resistance exercise (Koopman et al. 2005). We hypothesized that exercise enhances the bulk flow response to a standard OGTT, and that this effect would primarily be observed in the exercised limbs (i.e., the legs in response to cycling, and arms and legs in response to resistance exercise), with similar responses between exercise conditions. ...
... Therefore, the purpose of this study was to examine the modifying effect of exercise on the acute hemodynamic response to a standardized oral glucose tolerance test (OGTT). Given the paucity of data to support modality-specific effects of exercise on the hemodynamic response to an OGTT, we aimed to investigate 3 broad types of conventional exercise that are known to enhance insulin sensitivity acutely after exercise: continuous leg cycling (Mikines et al. 1988;Ortega et al. 2015), interval leg cycling (Little et al. 2014;Ortega et al. 2015), and whole-body resistance exercise (Koopman et al. 2005). We hypothesized that exercise enhances the bulk flow response to a standard OGTT, and that this effect would primarily be observed in the exercised limbs (i.e., the legs in response to cycling, and arms and legs in response to resistance exercise), with similar responses between exercise conditions. ...
... It should be noted that because of measurement difficulties, shear profiles in exercising limbs are still unknown and may be exposed to a different shear stress pattern than previously reported for inactive limbs. Given the exercisemediated elevated anterograde shear exposure and the known prominent impact of different forms of exercise on postexercise insulin sensitivity (Koopman et al. 2005;Little et al. 2014;Ortega et al. 2015), we originally hypothesized that all exercise modes would have a similar, positive impact on the hyperglycemic hemodynamic response. However, we did not observe a clear preconditioning effect of any specific exercise protocol on the vascular response to an OGTT. ...
Exercise elicits direct benefits to insulin sensitivity but may also indirectly improve glucose uptake by hemodynamic conditioning of the vasculature. The purpose of this study was to examine the modifying effect of 3 different types of exercise on the vascular response to an oral glucose challenge. Twenty healthy adults (9 women, 11 men; aged 23 ± 3 years) completed a standard oral glucose tolerance test (OGTT) at rest, as well as 1.5 hours after moderate continuous cycling exercise (30 min; 65% peak oxygen consumption), high-intensity interval cycling exercise (10 × 1 min at 90% peak heart rate), and lower-load higher-repetition resistance exercise (25–35 repetitions/set, 3 sets). Brachial and superficial femoral artery blood flow, conductance, and oscillatory shear index were measured throughout the OGTT. Regardless of rested state or exercise preconditioning, the OGTT induced reductions in brachial artery blood flow and conductance (p < 0.001), and transient increases in brachial and superficial femoral artery oscillatory shear index and retrograde blood flow (p < 0.01). Continuous cycling and resistance exercise were followed with a small degree of protection against prolonged periods of oscillatory flow. Our findings imply transient peripheral vasoconstriction and decreased limb blood flow during a standard OGTT, for which prior exercise was unable to prevent in healthy adults.
Novelty:We investigated the impact of continuous, interval, and resistance exercise on the hemodynamic response to an OGTT.
Our findings suggest decreased upper-limb blood flow during an OGTT is not prevented by prior exercise in healthy adults.
... A single bout of exercise positively impacts glucose regulation for up to 24 hr (Koopman et al., 2005). This improvement in glucose regulation is apparent with various types of exercise (Breen et al., 2011;Gillen et al., 2012), although high-intensity exercise may to be superior to moderate-intensity exercise for improving insulin sensitivity (Ortega et al., 2015;Rynders et al., 2014). Sprint interval exercise has been shown to produce improvements in insulin area under the curve (AUC) and the insulin sensitivity index when measured 30-min postcessation of the exercise bout in healthy males (Ortega et al., 2015). ...
... This improvement in glucose regulation is apparent with various types of exercise (Breen et al., 2011;Gillen et al., 2012), although high-intensity exercise may to be superior to moderate-intensity exercise for improving insulin sensitivity (Ortega et al., 2015;Rynders et al., 2014). Sprint interval exercise has been shown to produce improvements in insulin area under the curve (AUC) and the insulin sensitivity index when measured 30-min postcessation of the exercise bout in healthy males (Ortega et al., 2015). Whether or not improvements such as these would occur in sleep-restricted individuals remains unknown. ...
... Exercise. The exercise protocol used in this study was based on previous research by Ortega et al. (2015), who demonstrated a 142% increase in intravenous glucose tolerance test (IVGTT)derived insulin sensitivity measured 30 min following sprint interval exercise in healthy males. All exercise was performed on a cycle ergometer (Monark Ergomedic 894E; Monark), preceded and proceeded with a 5-min warm-up and cooldown at 70 W. ...
Experimental sleep restriction (SR) has demonstrated reduced insulin sensitivity in healthy individuals. Exercise is well-known to be beneficial for metabolic health. A single bout of exercise has the capacity to increase insulin sensitivity for up to 2 days. Therefore, the current study aimed to determine if sprint interval exercise could attenuate the impairment in insulin sensitivity after one night of SR in healthy males. Nineteen males were recruited for this randomized crossover study which consisted of four conditions—control, SR, control plus exercise, and sleep restriction plus exercise. Time in bed was 8 hr (2300–0700) in the control conditions and 4 hr (0300–0700) in the SR conditions. Conditions were separated by a 1-week entraining period. Participants slept at home, and compliance was assessed using wrist actigraphy. Following the night of experimental sleep, participants either conducted sprint interval exercise or rested for the equivalent duration. An oral glucose tolerance test was then conducted. Blood samples were obtained at regular intervals for measurement of glucose and insulin. Insulin concentrations were higher in SR than control ( p = .022). Late-phase insulin area under the curve was significantly lower in sleep restriction plus exercise than SR (862 ± 589 and 1,267 ± 558; p = .004). Glucose area under the curve was not different between conditions ( p = .207). These findings suggest that exercise improves the late postprandial response following a single night of SR.
... It has been shown to be effective at decreasing blood glucose immediately post exercise (24), and after 12 (23,33), and 16 weeks (28), but has also been shown to have no effect (30). Physiological blood glucose adaptations to resistance training have been shown to be similar to aerobic training (3, 12,15,22,27,29,37), while reducing total workout time. A dilemma with resistance training for affecting blood glucose is that there is no standardized protocol to follow relative to intensity and duration, thus the mixed results. ...
... A dilemma with resistance training for affecting blood glucose is that there is no standardized protocol to follow relative to intensity and duration, thus the mixed results. High intensity, interval training structured in a short duration model have been shown to decrease blood glucose (3, 12,15,22,27,29,37). Jump plyometrics are a form of short duration, high intensity exercise that normally involve low repetitions, thereby reducing fatigue and maximizing the storage and release of kinetic energy (32). ...
... Exercise choice can be categorized by oxygen consumption, anaerobic, aerobic, force production, continuous or plyometric. Ortega et al. demonstrated increased acute blood glucose uptake at 30m, 24h, and 48h post-exercise with sprint and aerobic exercise compared to no exercise, and greater positive effects at 30 min' post with sprint training compared to aerobic training (22). Little et al. reported similar findings with blood glucose uptake being greater with sprint training compared to aerobic training (15). ...
Plyometric exercise is popular in commercial exercise programs aiming to maximize energy expenditure for weight loss. However, the effect of plyometric exercise on blood glucose is unknown. The purpose of this study was to investigate the effect of relatively high intensity plyometric exercise on blood glucose. Thirteen subjects (6 females age= 21.8 ± 1.0 yrs.; height= 163.7 ± 7.8 cm; mass= 60.8 ± 6.7 kg and 7 males age= 22.0 ± 2.6 yrs.; height= 182.3 ± 3.6 cm; mass= 87.4 ± 12.5 kg) volunteered to participate. Subjects completed two random conditions on two separate days, consisting of either five sets of 10 maximal effort countermovement squat jumps (SJ) with 50 seconds' rest between sets or quiet sitting (SIT) for the time equated to the SJ duration (~4min). Immediately after each condition, subjects drank 75g of anhydrous glucose (CHO) in 100ml of water. Blood glucose measurements were taken via finger prick pre and immediately post SJ or SIT, and 5, 15, 30, and 60 min post. A 2x6 (condition x time) ANOVA revealed a significant interaction where SJ blood glucose was lower at 15 (114.0 ± 14.6 mg/dl) and 30 (142.1 ± 22.5 mg/dl) min compared to SIT (15min 130.8 ± 14.0 mg/dl and 30min 159.3 ± 21.0 mg/dl). The current plyometric protocol attenuated CHO-induced blood glucose at 15 and 30 min. This may be due to increased physiological stress applied to the muscles, thus increasing muscular glucose uptake.
... The effect of a single bout of HIT on insulin sensitivity has also been explored and the majority of studies in healthy lean or overweight populations report that there is no effect when measure 14-72 hours post-exercise (Brestoff et al., 2009;Richards et al., 2010;Whyte et al., 2013). However, Ortega et al. (2014) recently reported a substantial increase in insulin sensitivity (measured via intravenous glucose tolerance testing (IVGTT)) which lasted for at least 48 hours post-exercise. Likewise, Little et al (2014) recently reported a reduction in mean 24 h glucose concentrations and 24 h postprandial glucose AUC following a single bout of maximal HIT (10 × 1 min >90% HRmax) in a small cohort of overweight men. ...
... Similarly, HIT did not appear to attenuate the systemic glucose or insulin response to a high-fat mixed meal challenge administered 14 hours post-exercise, although the overall lipemic response was reduced (Freese et al., 2011;Gabriel et al., 2012). However, a recent HIT study has demonstrated improvements in estimates of insulin sensitivity measured using an intravenous glucose tolerance test which remained for 48 hours into the recovery period (Ortega et al., 2014). In disparity to our hypothesis, we could detect no increase in insulin sensitivity measured 14-16 hours following an acute bout of vigorous intensity aerobic exercise (45 minutes at ~75% V O2peak). ...
... Thus, these results will require confirmation in a further much larger study, ideally using a randomised controlled * research design. In agreement with the majority of previous (Brestoff et al., 2009;Richards et al., 2010;Whyte et al., 2013) but not all (Ortega et al., 2014) Specifically, we used a 3 day post-training time point for our assessment and it is possible that insulin sensitivity may have been improved (either more consistently or to a greater extent) in the days prior to the assessment. Further studies will be required to appraise this caveat. ...
... Increased contraction-mediated muscle glucose uptake generally subsides within 3 h following exercise cessation. Subsequently, peripheral insulin sensitivity is enhanced via insulin-dependent mechanisms for up to 48 h following exercise in adults with and without insulin resistance (Devlin and Horton 1985;Mikines et al. 1988;Perseghin et al. 1996;Koopman et al. 2005;Ortega et al. 2015). The insulin-sensitizing effects of moderate-intensity continuous exercise are well-established (e.g., running or cycling for 60-90 min at 50%-75% V _ O 2max ) (Mikines et al. 1988;Perseghin et al. 1996), but other types of exercise are also effective. ...
... For example, low-intensity walking for 60 min in the afternoon improves insulin sensitivity the following morning in adults with obesity, measured with the hyperinsulinemic-euglycemic clamp (Newsom et al. 2013). On the other end of the intensity-duration spectrum, short, high-intensity efforts, involving 4-6 "all out" 30-S sprints interspersed with 4 min of recovery, has also been shown to improve insulin sensitivity for up to 48 h in healthy males, as assessed via an intravenous glucose tolerance test (Ortega et al. 2015). While less research has evaluated the effects of resistance exercise, a 40 min session that targeted the lower-body and performed at 75% of 1 repetition maximum (1-RM) improved insulin sensitivity by $13% in young males when measured 24 h post-exercise using an intravenous insulin tolerance test (Koopman et al. 2005). ...
Type 2 diabetes (T2D) is a rapidly growing yet largely preventable chronic disease. Exaggerated increases in blood glucose concentration following meals is a primary contributor to many long-term complications of the disease that decrease quality of life and reduce lifespan. Adverse health consequences also manifest years prior to the development of T2D due to underlying insulin resistance and exaggerated postprandial concentrations of the glucose-lowering hormone insulin. Postprandial hyperglycemic and hyperinsulinemic excursions can be improved by exercise, which contributes to the well-established benefits of physical activity for the prevention and treatment of T2D. The aim of this review is to describe the postprandial dysmetabolism that occurs in individuals at risk for and with T2D, and highlight how acute and chronic exercise can lower postprandial glucose and insulin excursions. In addition to describing the effects of traditional moderate-intensity continuous exercise on glycemic control, we highlight other forms of activity including low-intensity walking, high-intensity interval exercise, and resistance training. In an effort to improve knowledge translation and implementation of exercise for maximal glycemic benefits, we also describe how timing of exercise around meals and post-exercise nutrition can modify acute and chronic effects of exercise on glycemic control and insulin sensitivity.
Novelty:Exaggerated postprandial blood glucose and insulin excursions are associated with disease risk.
Both a single session and repeated sessions of exercise improve postprandial glycemic control in individuals with and without T2D.
The glycemic benefits of exercise can be enhanced by considering the timing and macronutrient composition of meals around exercise.
... Elevated cardiorespiratory fitness is a protective factor against obesity-related metabolic dysfunctions (Hamer and O'Donovan, 2010). Similar adaptations in VO 2max/peak have been consistently reported after HIIT and MICT programs in obese/overweight patients (Ortega et al., 2015;Mora-Rodriguez et al., 2016;Batacan et al., 2017;Guadalupe-Grau et al., 2018). To our knowledge, we are the first to apply a polarized volume training program to an untrained and overweight population, and to show that POL training-induced superior cardiorespiratory fitness adaptations compared to MICT and HIIT training. ...
... However, the optimal exercise-dose to reduce obesity-induced hyperglycemia and hyperinsulinemia have not been fully established. Previous studies have compared the effect of HIIT compared to MICT insulin sensitive surrogates with contradictory results (Mitranun et al., 2014;Fisher et al., 2015;Ortega et al., 2015;Cocks et al., 2016;De Lorenzo et al., 2018). We found that fasting glucose was reduced only in the POL group, without changes in fasting insulin, insulin sensitivity index or HOMA-IR. ...
Introduction: Volume and intensity are major variables governing exercise training–mediated beneficial effects in both athletes and patients. Although polarized endurance training optimizes and maximizes physiological gains in highly trained individuals, its cardiometabolic protective-effects have not been established. The purpose of the present single site, randomized-controlled trial was to compare the effects of 12-weeks of high-intensity interval training (HIIT), moderate-intensity continuous training (MICT), and polarized volume training (POL) programs on cardiometabolic risk factors in young overweight and obese women.
Materials and methods: A total of 64 overweight/obese young women (age 23.3 ± 3.8 y, body mass index 33.8 ± 3.8 kg/m2) were randomly assigned to four groups: control group (CTRL), polarized volume training group, moderate-intensity endurance training group, and high-intensity interval training group. The cardiorespiratory capacity, glycemic and lipid profiles, whole-body substrate utilization, and body composition were assessed before and after the intervention. Results: After the intervention, VO2peak and power output at VO2peak increased in all exercised-groups (time effect: p<0.0001). Power output at VT1 was increased only in the POL group compared to the CTRL group (p=0.019). Relative fold changes in fasting plasma glucose concentrations decreased only in POL group (p=0.002). Training induced a significant increase in relative fat oxidation in all the groups (time effect: p<0.001). Relative fat oxidation increased only in the POL group compared to the CTRL group (training effect: p=0.032).
Conclusion: Twelve-weeks of polarized volume training showed overall superior effects on cardiorespiratory fitness, basal glycemic control, and substrate oxidation in comparison to MICT and HIIT training modalities. These data suggest that polarized volume training is an effective non-pharmacological treatment strategy for reducing cardiovascular disease risk factors in young overweight and obese women.
... Bramwell [16] demonstrated persistent improved vascular function as measured by flow-mediated dilation even 2 hours after HIIT. Improved insulin sensitivity was still evident after a comparable single exercise session for as long as 48 hours after the exercise bout [18]. In a recently published study in adolescent schoolchildren, participants of the intervention group experienced after 7 weeks of HIIT a significant decrease in systolic BP of 5 mmHg, whereas diastolic BP remained unchanged [19]. ...
... High-intensity interval training (HIIT) has been proven beneficial for running performance [4, 5, 6] and research has documented beneficial effects of various types of HIIT on fitness and health. HIIT has been proven superior to moderate-intensity continuous aerobic exercise for improving insulin sensitivity [7] and cardiorespiratory fitness in healthy subjects [4] and shorter bouts of exercise in contrast to a common moderate exercise program can protect against development of arterial hypertension [8]. Emerging evidence now suggests that in contrast to pressure measured in the brachial artery central pressure is better related to future cardiovascular events. ...
Background:
Regular physical activity is known to reduce arterial pressure (BP). In a previous investigation, we could prove that even a single bout of moderate-intensity continuous exercise (MICE) causes a prolonged reduction in BP. Whether high-intensity interval training (HIIT) has a favourable influence on BP, and therefore may be followed subjects and methods by a prolonged BP reduction, should be examined on the basis of blood pressure response after exercise and during a subsequent stress test.
Patients and methods:
In 39 healthy men (aged 34 ± 8 years, BMI 24 ± 2), peripheral and central BP were measured noninvasively at rest and at the end of a 2-min cold pressor test (CPT) using a Mobil-O-Graph (24 PWA monitor, IEM). Following HIIT (6 x 1 min at 98% of the previously determined maximum wattage, 4-min rest between intervals) BP was measured again throughout 60 min of rest and thereafter during a CPT. The results were compared with those obtained before HIIT.
Results:
Similar to MICE, peripheral and central BPs were significantly (p < 0.05) lower 45 min after HIIT. When analysing peripheral BP during a CPT before and after exercise, significantly lower systolic (p < 0.001) and diastolic (p = 0.008) pressures were established after HIIT. This was true for systolic (p = 0.002) and diastolic (p = 0.006) central BP as well. Although there were no more significant differences between pressures at rest before and 60 min after exercise, the increase in peripheral systolic pressure due to CPT was significantly slower after HIIT (p = 0.019) when compared with BP during CPT before exercise. This was true for central systolic BP as well (p = 0.017).
Conclusion:
HIIT leads to a BP reduction, which can still be detected up to 45 min after completion of the training. Even 60 min after exercise, pressures during a CPT showed a reduced augmentation, indicating an attenuated hemodynamic response to stress testing after HIIT.
... ments of MetS, its concomitant application may be burdensome for many patients. The main reason is that AIT results in large muscle glycogen depletion [23], and its restoration requires abundant carbohydrate ingestion [6], which is not provided when following a calorie restriction diet. There is a compelling need for lifestyle interventions that treat obesity and metabolic syndrome and its associated health risks. ...
... e., E + D, • ▶ Fig. 3). AIT results in large muscle glycogen depletion [23] and its restoration requires abundant carbohydrate ingestion in diet [6]. The mild calorie restriction during the 16 weeks of training in the E + D group likely prevented full replenishment of muscle glycogen stores. ...
Our purpose in this study was to investigate efficient and sustainable combinations of exercise and diet-induced weight loss (DIET), in order to combat obesity in metabolic syndrome (MetS) patients. We examined the impact of aerobic interval training (AIT), followed by or concurrent to a DIET on MetS components. 36 MetS patients (54±9 years old; 33±4 BMI; 27 males and 9 females) underwent 16 weeks of AIT followed by another 16 weeks without exercise from the fall of 2013 to the spring of 2014. Participants were randomized to AIT without DIET (E CON, n=12), AIT followed by DIET (E-then-D, n=12) or AIT concurrent with DIET (E+D, n=12) groups. Body weight decreased below E CON similarly in the E-then-D and E+D groups (~5%). Training improved blood pressure and cardiorespiratory fitness (VO2peak) in all groups with no additional effect of concurrent weight loss. However, E+D improved insulin sensitivity (HOMA) and lowered plasma triglycerides and blood cholesterol below E CON and E-then-D (all P<0.05). Weight loss in E-then-D in the 16 weeks without exercise lowered HOMA to the E+D levels and maintained blood pressure at trained levels. Our data suggest that a new lifestyle combination consisting of aerobic interval training followed by weight loss diet is similar, or even more effective on improving metabolic syndrome factors than concurrent exercise plus diet.
© Georg Thieme Verlag KG Stuttgart · New York.
... One metaanalysis [14] found limited evidence that appropriate exercise regimens increase cardiovascular risk, highlighting the need of investigating the effects of aerobic exercise, strength training, or both on cardiovascular risk factors. It has been demonstrated that exercise affects metabolism, and several research studies have shown that endurance training sessions can enhance insulin sensitivity and glucose tolerance [15][16][17][18][19]. A modest quantity of fat consumption or infusion during exercise can improve insulin resistance [3,20,21]. ...
Surrogate markers of metabolic syndrome complications is high levels of glucose and/or cholesterol in the blood. The purpose of this research is to determine whether or not various intensity exercise has a beneficial impact on blood glucose and cholesterol levels in young adults. As a consequence, this study was investigated about how exercise's influence on lowering the risk of metabolic diseases may be moderated by other factors, including by milk intake. Studies were conducted using a quasi-experimental, single-blind research design. Thirty-five participants were randomly assigned to one of four groups: control (C), moderate intensity (M), high intensity (H), or intermittent (I). The Sysmex XN-1000 is used for checking blood content, while the Cobas Pro is used to analyze blood chemistry in the lab. Using tools like the analysis of variance (ANOVA), the Mann-Whitney test, and the Pearson correlation coefficient, researchers may gauge the importance of inherent correlations and examine how group-level phenomena and interactions affect those coefficients. To sum up, we found that there was a statistically significant difference in glucose levels between the control group and the experimental group (p = 0.012 < 0.05), yet this difference was accompanied by a negative trend showing a rise in content. Also, there was a favorable tendency toward lower glucose and cholesterol levels across all compositions, while it was not statistically significant (p value > 0.05). To sum up, practically all of the variables point to a favorable tendency that that does not statistically significant – in the effect of exercise intensity combined with milk consumption. Exercise and milk intervention have been shown to have positive impacts, but further investigation or longer training sessions are needed to determine their true magnitude.
... Acute exercise has the capacity to transiently increase antioxidant activity (11,29,65,70) and can improve insulin sensitivity and whole-body glucose uptake for up to 24-48 h postexercise (11,14,66,(84)(85)(86)(87)(88)(89). As such, exercise prior to meal ingestion may be a potential method to decrease postprandial oxidative distress and to mitigate the health complications associated with elevated blood glucose and lipid levels (9,14,70). ...
Background
Biomarkers of oxidation-reduction (redox) homeostasis are commonly measured in human blood to assess whether certain stimuli (e.g., high-glucose ingestion or acute exercise) lead to a state of oxidative distress (detrimental to health) or oxidative eustress (beneficial to health). Emerging research indicates that redox responses are likely to be highly individualized, yet few studies report individual responses. Furthermore, the effects of complex redox stimuli (e.g., high-glucose-ingestion after exercise) on redox homeostasis remains unclear. We investigated the effect of acute exercise (oxidative eustress), high-glucose ingestion (oxidative distress), and high-glucose ingestion after exercise (both oxidative eu/distress), on commonly measured redox biomarkers in serum/plasma.
Methods
In a randomized crossover fashion, eight healthy men (age: 28 ± 4 years; BMI: 24.5 ± 1.5 kg/m² [mean ± SD]) completed two separate testing conditions; 1) consumption of a high-glucose mixed-nutrient meal (45% carbohydrate [1.1 g glucose.kg⁻¹], 20% protein, and 35% fat) at rest (control trial), and 2) consumption of the same meal 3 h and 24 h after 1 h of moderate-intensity cycling exercise (exercise trial). Plasma and serum were analyzed for an array of commonly studied redox biomarkers.
Results
Oxidative stress and antioxidant defense markers (hydrogen peroxide, 8-isoprostanes, catalase, superoxide dismutase, and nitrate levels) increased immediately after exercise (p < 0.05), whereas nitric oxide activity and thiobarbituric acid reactive substances (TBARS) remained similar to baseline (p > 0.118). Nitric oxide activity and nitrate levels decreased at 3 h post-exercise compared to pre-exercise baseline levels. Depending on when the high-glucose mixed nutrient meal was ingested and the postprandial timepoint investigated, oxidative stress and antioxidant defense biomarkers either increased (hydrogen peroxide, TBARS, and superoxide dismutase), decreased (hydrogen peroxide, 8-isoprostanes, superoxide dismutase, nitric oxide activity, nitrate, and nitrite), or remained similar to pre-meal baseline levels (hydrogen peroxide, 8-isoprostanes, TBARS, catalase, superoxide dismutase and nitrite). Redox responses exhibited large inter-individual variability in the magnitude and/or direction of responses.
Conclusion
Findings highlight the necessity to interpret redox biomarkers in the context of the individual, biomarker measured, and stimuli observed. Individual redox responsiveness may be of physiological relevance and should be explored as a potential means to inform personalized redox intervention.
... The superior effects of SIT dissipated over the post-exercise period, however, with similar improvements in insulin sensitivity relative to baseline in both HIIT and MICT observed for up to 48 h. 30 In contrast, amongst mixed cohorts of males and females, neither 5 Â 30 s 31 nor 2 Â 20 s 32 "all out" cycling sprints elicited improvements in insulin sensitivity when measured the next day (~14-16 h post-exercise) using oral glucose tolerance tests (OGTT). Collectively, the few existing studies investigating the impact of acute SIT on insulin sensitivity have produced mixed results and the influence on glycemic control remains unclear. ...
High-intensity and sprint interval training (HIIT and SIT, respectively) enhance insulin sensitivity and glycemic control in both healthy adults and those with cardiometabolic diseases. The beneficial effects of intense interval training on glycemic control include both improvements seen in the hours to days following a single session of HIIT/SIT and those which accrue with chronic training. Skeletal muscle is the largest site of insulin-stimulated glucose uptake and plays an integral role in the beneficial effects of exercise on glycemic control. Here we summarize the skeletal muscle responses that contribute to improved glycemic control during and following a single session of interval exercise and evaluate the relationship between skeletal muscle remodelling and improved insulin sensitivity following HIIT/SIT training interventions. Recent evidence suggests that targeting skeletal muscle mechanisms via nutritional interventions around exercise, particularly with carbohydrate manipulation, can enhance the acute glycemic benefits of HIIT. There is also some evidence of sex-based differences in the glycemic benefits of intense interval exercise, with blunted responses observed after training in females relative to males. Differences in skeletal muscle metabolism between males and females may contribute to sex differences in insulin sensitivity following HIIT/SIT, but well-controlled studies evaluating purported muscle mechanisms alongside measurement of insulin sensitivity are needed. Given the greater representation of males in muscle physiology literature, there is also a need for more research involving female-only cohorts to enhance our basic understanding of how intense interval training influences muscle insulin sensitivity in females across the lifespan.
... However, during the last years, the application of training programmes that include high-intensity aerobic interval training has grown. Accordingly, high-intensity aerobic interval training programmes reduce blood pressure [7], improve cardiorespiratory fitness [8] and heart function [9], induce mitochondrial biogenesis [10] and improve insulin sensitivity [11]. Although the two training programmes (moderate training [MT] and high-intensity training [HIT]) are effective to reduce cardiovascular risk factors, previous studies have demonstrated that HIT is superior to MT in reversing risk factors [6]. ...
Background:
The aim of the present study was to analyse the effect of 12 weeks of training, 7 weeks of detraining and 16 weeks of retraining using a moderate or high intensity training programme on cardiovascular risk factors in hypertensive patients.
Method:
Thirty-four patients took part in the study. The intensity training was 80-90% of maximum heart rate for the high-intensity training (HIT) group (n = 15) and at 50-70% of maximum heart rate for the moderate training (MT) group (n = 19). Blood pressure, body composition, lipid profile, fasting glucose, strength and cardiovascular fitness were analysed.
Results:
The first training period did not decrease blood pressure, but the second training period saw significant decreases in blood pressures in HIT group. Moreover, 12 weeks of MT or HIT did not decrease body mass, body mass index or fat mass. However, after 7 weeks of detraining, the inclusion of a second training period using HIT saw decreases in these body composition variables. Both training periods and intensities improved high-density lipoprotein and low-density lipoprotein, but only HIT decreased total cholesterol. In addition, after 7 weeks of detraining, the lipid profile variables returned to baseline values. Additionally, 16 weeks of retraining with HIT or MT decreased blood glucose significantly. Moreover, MT and HIT training programmes in both periods improved cardiorespiratory fitness, but with 7 weeks of detraining, it returned to baseline values.
Conclusion:
Our data demonstrated the effectiveness of the inclusion of a MT or HIT programme as adjuvant therapy in hypertensive patients.
... Similarly, unchanged OGTT-derived insulin sensitivity was also observed in response to a very low-volume SIT protocol involving 2 × 20 s cycle sprints within a 10-min time commitment amongst a mixed-sex cohort of healthy young adults [84]. It is unclear if the lack of acute improvement in insulin sensitivity observed in mixed-sex cohorts is different from that which is observed in men alone, as there are reports of both improved intravenoustolerance test-derived insulin sensitivity in healthy men [85] and unchanged OGTT-derived insulin sensitivity in men with overweight [86], measured ~ 24 h after a single session of low-volume SIT. Thus, while it is possible that the low exercise volume of SIT is insufficient to acutely improve insulin sensitivity independent of sex, comparisons between men and women are warranted in this regard. ...
Interval training is a form of exercise that involves intermittent bouts of relatively intense effort interspersed with periods of rest or lower-intensity exercise for recovery. Low-volume high-intensity interval training (HIIT) and sprint interval training (SIT) induce physiological and health-related adaptations comparable to traditional moderate-intensity continuous training (MICT) in healthy adults and those with chronic disease despite a lower time commitment. However, most studies within the field have been conducted in men, with a relatively limited number of studies conducted in women cohorts across the lifespan. This review summarizes our understanding of physiological responses to low-volume interval training in women, including those with overweight/obesity or type 2 diabetes, with a focus on cardiorespiratory fitness, glycemic control, and skeletal muscle mitochondrial content. We also describe emerging evidence demonstrating similarities and differences in the adaptive response between women and men. Collectively, HIIT and SIT have consistently been demonstrated to improve cardiorespiratory fitness in women, and most sex-based comparisons demonstrate similar improvements in men and women. However, research examining insulin sensitivity and skeletal muscle mitochondrial responses to HIIT and SIT in women is limited and conflicting, with some evidence of blunted improvements in women relative to men. There is a need for additional research that examines physiological adaptations to low-volume interval training in women across the lifespan, including studies that directly compare responses to MICT, evaluate potential mechanisms, and/or assess the influence of sex on the adaptive response. Future work in this area will strengthen the evidence-base for physical activity recommendations in women.
... Besides the acute effects of exercise on glycemic control, after 16 weeks of HIIT, we found in patients with metabolic syndrome that insulin sensitivity assessed by HOMA-IR and C SI did not improve when bodyweight reductions were not significant [35]. In contrast, in young healthy volunteers we reported [36] that a bout of exercise increased insulin sensitivity assessed by IVGTT (CS I ). Therefore, the characteristics of the sample, the timing of exercise with respect to both, meals and measurements, and the absence of a negative energy balance may explain the lack of significant insulin-sensitizing effects of the exercise alone condition. ...
Purpose
To determine the separated and combined effects of metformin and exercise on insulin sensitivity and free-living glycemic control in overweight individuals with prediabetes/type 2 diabetes (T2DM).
Methods
We recruited 16 adults with BMI of 32.7 ± 4.3 kg m⁻² and insulin resistance (HOMA-IR 3.2 ± 0.4) under chronic metformin treatment (1234 ± 465 g day⁻¹) enrolled in a high-intensity interval training (HIIT) program. Participants underwent four 72-h experimental trials in a random-counterbalanced order: (1) maintaining their habitual metformin treatment (MET); (2) replacing metformin treatment by placebo (CON); (3) placebo plus two HIIT sessions (EX + CON), and (4) metformin plus two HIIT sessions (MET + EX). We used intermittently scanned continuous glucose monitoring (isCGM) during 72 h in every trial to obtain interstitial fluid glucose area under the curve (IFGAUC) and the percentage of measurements over 180 mg dL⁻¹ (% IFGPEAKS). Insulin sensitivity was assessed on the last day of each trial with HOMA-IR index and calculated insulin sensitivity (CSI) from intravenous glucose tolerance test.
Results
IFGAUC was lower in MET + EX and MET than in CON (P = 0.011 and P = 0.025, respectively). In addition, IFGAUC was lower in MET + EX than in EX + CON (P = 0.044). %IFGPEAKS were only lower in MET + EX in relation to CON (P = 0.028). HOMA-IR and CSI were higher in CON in comparison with MET + EX (P = 0.011 and P = 0.022, respectively) and MET (P = 0.006 and P < 0.001, respectively). IFGAUC showed a significant correlation with HOMA-IR.
Conclusion
Intense aerobic exercise in patients with diabetes and prediabetes under metformin treatment reduces free-living 72-h blood hyperglycemic peaks. This may help to prevent the development of cardiovascular complications associated with diabetes.
... Exercise has profound effects on metabolism and previous research has shown that an acute bout of endurance exercise results in a transient increase in insulin sensitivity and glucose tolerance (Mikines et al., 1988;Annuzzi et al., 1991;Brestoff et al., 2009;Jensen et al., 2011;Cartee, 2015b;Ortega et al., 2015;Jelstad et al., 2019). Exercise prior to lipid infusion alleviates insulin resistance (Schenk and Horowitz, 2007;Pehmoller et al., 2012;Phielix et al., 2012), but less is known about the effects of exercise on glucose tolerance during an LCHF diet. ...
Low-carbohydrate-high-fat (LCHF) diets are efficient for weight loss, and are also used by healthy people to maintain bodyweight. The main aim of this study was to investigate the effect of 3-week energy-balanced LCHF-diet, with >75 percentage energy (E%) from fat, on glucose tolerance and lipid profile in normal weight, young, healthy women. The second aim of the study was to investigate if a bout of exercise would prevent any negative effect of LCHF-diet on glucose tolerance. Seventeen females participated, age 23.5 ± 0.5 years; body mass index 21.0 ± 0.4 kg/m², with a mean dietary intake of 78 ± 1 E% fat, 19 ± 1 E% protein and 3 ± 0 E% carbohydrates. Measurements were performed at baseline and post-intervention. Fasting glucose decreased from 4.7 ± 0.1 to 4.4 mmol/L (p < 0.001) during the dietary intervention whereas fasting insulin was unaffected. Glucose area under the curve (AUC) and insulin AUC did not change during an OGTT after the intervention. Before the intervention, a bout of aerobic exercise reduced fasting glucose (4.4 ± 0.1 mmol/L, p < 0.001) and glucose AUC (739 ± 41 to 661 ± 25, p = 0.008) during OGTT the following morning. After the intervention, exercise did not reduce fasting glucose the following morning, and glucose AUC during an OGTT increased compared to the day before (789 ± 43 to 889 ± 40 mmol/L∙120min–1, p = 0.001). AUC for insulin was unaffected. The dietary intervention increased total cholesterol (p < 0.001), low-density lipoprotein (p ≤ 0.001), high-density lipoprotein (p = 0.011), triglycerides (p = 0.035), and free fatty acids (p = 0.021). In conclusion, 3-week LCHF-diet reduced fasting glucose, while glucose tolerance was unaffected. A bout of exercise post-intervention did not decrease AUC glucose as it did at baseline. Total cholesterol increased, mainly due to increments in low-density lipoprotein. LCHF-diets should be further evaluated and carefully considered for healthy individuals.
... On the other hand, exercise prevents the blunting of lipolysis during BWL [12] and may counteract this effect. Thus, exercise training that maintains lipolysis may reduce the full effect of BWL in restoring insulin actions although, again, exercise training may compensate for this reduction by improving muscle glucose transport and glucose disposal as stored glycogen [41]. This counteracting actions of exercise versus diet would explain the similar improvements in CS I in our EXER and CONT groups when they attained BWL ! ...
Aim
To determine whether exercise training improves insulin actions through concomitant body weight loss (BWL).
Methods
Subjects (aged 55 ± 8 years) with metabolic syndrome (MetS), prediabetes (fasting blood glucose: 111 ± 2 mg·dL⁻¹, HbA1c: 5.85 ± 0.05%) and abdominal obesity (waist circumference: 104 ± 7.9 cm) were randomly allocated to either a group performing aerobic interval training (EXER; n = 76) or a sedentary group receiving lifestyle counselling (CONT; n = 20) for 16 weeks.
Results
At baseline, insulin sensitivity (according to HOMA2 and intravenous glucose tolerance test; CSI), body composition and VO2max were similar between the groups. After the intervention, both groups had similar BWL (1–2%), but only the EXER group showed decreased [mean (95% CI)] trunk fat mass [from 18.2 (17.4–18.9) to 17.3 kg (16.6–17.9); P < 0.001] and HOMA2 scores [from 1.6 (1.5–1.7) to 1.4 (1.3–1.5); P = 0.001], and increased VO2max [from 2.07 (1.92–2.21) to 2.28 (2.11–2.45) LO2 ·min⁻¹; P < 0.001]. However, CSI did not improve in any group. Within-group subdivision by BWL (≤ 0%, 0–3%, ≥ 3%) revealed higher CSI in those with BWL ≥ 3% in both groups. Trunk fat mass reductions were closely associated with CSI and HOMA-IR improvement (r = − 0.452–0.349; P < 0.001).
Conclusion
In obese MetS subjects with prediabetes, 3% BWL is required for consistent improvement in insulin sensitivity. Thus, exercise-training programmes should be combined with calorie restriction to achieve BWL levels that prevent the development of diabetes.
... More tryptophan entering the brain will lead to greater production of 5-HTP and serotonin, and finally secretion of melatonin, resulting in sleepiness [29,30]. Notably, as a single bout of SIT training increases insulin sensitivity [31], it may implied that exercise influences the extension of these physiological responses to HGI meals and the beneficial effect on sleep-related parameters. ...
The aim of the current study was to investigate the effect of the glycemic index of post-exercise meals on sleep quality and quantity, and assess whether those changes could affect the next day’s exercise performance. Following a baseline/familiarization phase, 10 recreationally trained male volunteers (23.2 ± 1.8 years) underwent two double-blinded, randomized, counterbalanced crossover trials. In both trials, participants performed sprint interval training (SIT) in the evening. Post-exercise, participants consumed a meal with a high (HGI) or low (LGI) glycemic index. Sleep parameters were assessed by a full night polysomnography (PSG). The following morning, exercise performance was evaluated by the countermovement jump (CMJ) test, a visual reaction time (VRT) test and a 5-km cycling time trial (TT). Total sleep time (TST) and sleep efficiency were greater in the HGI trial compared to the LGI trial (p < 0.05), while sleep onset latency was shortened by four-fold (p < 0.05) and VRT decreased by 8.9% (p < 0.05) in the HGI trial compared to the LGI trial. The performance in both 5-km TT and CMJ did not differ between trials. A moderate to strong correlation was found between the difference in TST and the VRT between the two trials (p < 0.05). In conclusion, this is the first study to show that a high glycemic index meal, following a single spring interval training session, can improve both sleep duration and sleep efficiency, while reducing in parallel sleep onset latency. Those improvements in sleep did not affect jumping ability and aerobic endurance performance. In contrast, the visual reaction time performance increased proportionally to sleep improvements.
... The majority of studies in this area have investigated the association between habitual PA levels and insulin sensitivity/metabolic disease risk or the influence of acute or chronic exercise on indices of insulin sensitivity and glucose control. The beneficial associations reported between habitual PA and insulin sensitivity/metabolic disease risk [1,5,29] are supported by studies showing that both acute exercise [24,30] and exercise training [26,27] improve insulin sensitivity and glucose control. Few studies have examined the impact of short-term alterations in habitual PA on these measures. ...
This study determined if varying physical activity (PA) the day prior to an oral glucose tolerance test (OGTT) differentially influenced postprandial glucose and insulin kinetics. Fifteen healthy, young adults participated in three OGTT trials the morning after performing 50% (LOW), 100% (HABITUAL), or 150% (HIGH) of their habitual PA (determined by 7-day pedometry). Trials were randomized and separated by at least 1-wk. For each OGTT trial, blood glucose and insulin were measured after an overnight fast and at 30-min intervals for 2 h following ingestion of the glucose beverage. Between-trial differences were analyzed using a general linear model with repeated measures. Subjects successfully achieved the desired percentage of habitual steps prior to each trial: LOW: 51±5%, HABITUAL: 99±6%, and HIGH: 149±9%. Fasting blood glucose and glucose total area under the curve (AUC) did not differ between trials. Serum insulin AUC was lower (p<0.05) following the HIGH (34,158±8,786 pmol·min·L−1) compared to the LOW (40,738±9,276 pmol·min·L−1) trial. No differences were observed when the LOW and HIGH trials were compared to HABITUAL. These data suggest that varying the PA level (from 50 to 150% of habitual PA) the day prior to an OGTT influences the insulin (but not blood glucose) response to an OGTT.
... We and others have studied different exercise methods (continuous vs. interval) to discern which result in the largest benefit for the health of MetS patients. Studies of 8-16 weeks of training using high intensity aerobic interval training (AIT) reveal that this type of training improves endothelial function above isocaloric continuous training [5], reduces BP [4], improves heart diastolic function [6], induces mitochondrial biogenesis [4,7], improves cardiorespiratory fitness [8] and insulin sensitivity [9]. ...
Objective:
To study if repeated yearly training programs consolidate the transient blood pressure (BP) improvements of one exercise program into durable adaptations.
Methods:
Obese middle-age individuals with metabolic syndrome (MetS) underwent high-intensity aerobic interval training during 16 weeks (November to mid-March) in 3 consecutive years [training group (TRAIN); N = 23]. Evolution of MetS components was compared with a matched-group that remained sedentary [control group (CONT); N = 26].
Results:
At the end of the first training program (0-4 months), TRAIN lowered systolic arterial pressure, blood glucose, waist circumference and MetS Z-score below CONT (-8.5 ± 2.5 mmHg; -19.9 ± 2.6 mg/dl; -3.8 ± 0.1 cm and -0.3 ± 0.1, respectively, all P < 0.05). With detraining (month 4-12) TRAIN adaptations relapsed to the levels of baseline (month 0) except for BP. A second exercise program (month 12-16) lowered blood glucose and waist circumference below CONT (-19.0 ± 2.0 mg/dl; -4.1 ± 0.1 cm). After detraining (month 16-24) BP, blood glucose and Z-score started below CONT values (-6.8 ± 0.9 mmHg; -24.6 ± 2.5 mg/dl and -0.4 ± 0.05, respectively, all P < 0.05) and those differences enlarged with the last training program (month 24-28). Ten-year atherosclerotic cardiovascular disease risk estimation increased only in CONT (8.6 ± 1.1-10.1 ± 1.3%; year 2-3; P < 0.05).
Conclusion:
At least two consecutive years of 4-month aerobic interval training are required to chronically improve MetS (Z-score). The chronic effect is mediated by BP that does not fully return to pretraining values allowing a cumulative improvement. On the other hand, sedentarism in MetS patients during 3 years increases their predicted atherosclerotic diseases risk. CLINICALTRIALS.
Gov identifier:
NCT03019796.
... We have recently found that shorter-interval exercise (i. e., 4 Wingate tests) improves insulin sensitivity 30 min after exercise [37] whereas isocaloric continuous moderate-intensity exercise does not. Thus, it is possible that the vasodilating effects of insulin are facilitated by HIIT but not by lower exercise intensity (i. ...
PurposeThe effectiveness of exercise to lower blood pressure may depend on the type and intensity of exercise. We study the short-term (i.e., 14-h) effects of a bout of high-intensity aerobic interval training (HIIT) on blood pressure in metabolic syndrome (MetS) patients. Methods
Nineteen MetS patients (55.2 ± 7.3 years, 6 women) entered the study. Eight of them were normotensive and eleven hypertensive according to MetS threshold (≥130 mmHg for SBP and/or ≥85 mmHg for DBP). In the morning of 3 separated days, they underwent a cycling exercise bout of HIIT (>90% of maximal heart rate, ~85% VO2max), or a bout of isocaloric moderate-intensity continuous training (MICT; ~70% of maximal heart rate, ~60% VO2max), or a control no-exercise trial (REST). After exercise, ambulatory blood pressure (ABP; 14 h) was monitored, while subjects continued their habitual daily activities wearing a wrist-band activity monitor. ResultsNo ABP differences were found for normotensive subjects. In hypertensive subjects, systolic ABP was reduced by 6.1 ± 2.2 mmHg after HIIT compared to MICT and REST (130.8 ± 3.9 vs. 137.4 ± 5.1 and 136.4 ± 3.8 mmHg, respectively; p < 0.05). However, diastolic ABP was similar in all three trials (77.2 ± 2.6 vs. 78.0 ± 2.6 and 78.9 ± 2.8 mmHg, respectively). Motion analysis revealed no differences among trials during the 14-h. Conclusion
This study suggests that the blood pressure reducing effect of a bout of exercise is influence by the intensity of exercise. A HIIT exercise bout is superior to an equivalent bout of continuous exercise when used as a non-pharmacological aid in the treatment of hypertension in MetS.
... We have recently found that shorter-interval exercise (i. e., 4 Wingate tests) improves insulin sensitivity 30 min after exercise [37] whereas isocaloric continuous moderate-intensity exercise does not. Thus, it is possible that the vasodilating effects of insulin are facilitated by HIIT but not by lower exercise intensity (i. ...
The purpose of this study was to compare the magnitude of post-exercise hypotension (PEH) after a bout of cycling exercise using high-intensity interval training (HIIT) in comparison to a bout of traditional moderate-intensity continuous exercise (CE). After supine rest 14 obese (31±1 kg·m(-2)) middle-age (57±2 y) metabolic syndrome patients (50% hypertensive) underwent a bout of HIIT or a bout of CE in a random order and then returned to supine recovery for another 45 min. Exercise trials were isocaloric and compared to a no-exercise trial (CONT) of supine rest for a total of 160 min. Before and after exercise we assessed blood pressure (BP), heart rate (HR), cardiac output (Q), systemic vascular resistance (SVR), intestinal temperature (TINT), forearm skin blood flow (SKBF) and percent dehydration. HIIT produced a larger post-exercise reduction in systolic blood pressure than CE in the hypertensive group (-20±6 vs. -5±3 mmHg) and in the normotensive group (-8±3 vs. -3±2 mmHg) while HIIT reduced SVR below CE (P<0.05). Percent dehydration was larger after HIIT, and post-exercise TINT and SKBF increased only after HIIT (all P<0.05). Our findings suggest that HIIT is a superior exercise method to CE to acutely reduce blood pressure in MSyn subjects.
... Exercise training intensity and duration in that study was in the lower end of the American College of Sports Med- icine prudent recommendations for exercise in deconditioned adults (i.e., 30-90 min at 50% of V ˙ O 2peak [14]). However, in the last decade, the use of a training mode reserved for im- proving athletic performance (i.e., HIIT) has spread following the findings that HIIT elicits similar or larger health benefits than moderate CE mode in healthy sedentary (15,29) and obese patients with metabolic syndrome (26,40). Aware of the increased use of HIIT for promoting health, we studied CDV drift not only during a constant exercise bout (70 min at 60% HR peak , CE trial) but also during an isocaloric bout of HIIT (45 min at 70%-90% HR peak , HIIT trial). ...
Purpose:
The health benefits of a training program are largely influenced by the exercise dose and intensity. We sought to determine if during a training bout of continuous vs. interval exercise the workload needs to be reduced to maintain the prescribed target heart rate.
Methods:
Fourteen obese (31±4 kg·m) middle-age (57±8 y) individuals with metabolic syndrome, underwent two exercise training bouts matched by energy expenditure (i.e., 70±5 min of continuous exercise; CE or 45 min of interval exercise; HIIT). All subjects completed both trials in a randomized order. Heart rate (HR), power output (W), percent dehydration, intestinal and skin temperature (TINT and TSK), mean blood pressure (MAP), cardiac output (CO), stroke volume (SV) and blood lactate concentration (La) were measured at the initial and latter stages of each trial to assess time-dependent drift.
Results:
During the HIIT trial power output was lowered by 30±16 W to maintain the target HR while a 10±11 W reduction was needed in the CE trial (P<0.05). Energy expenditure, cardiac output and stroke volume declined with exercise time only in the HIIT trial (15%, 10% and 13%, respectively). During HIIT, percent dehydration, TINT and TSK increased more than during the CE trial (all P=0.001). MAP and La were higher in HIIT without time drift in any trial.
Conclusion:
Our findings suggests that while CE results in mild power output reductions to maintain target HR, the increasingly popular HIIT results in significant reductions in power output, energy expenditure and cardiac output (21%; 15% and 10%, respectively). HIIT based on target HR may result in lower than expected training adaptations due to workload adjustments to avoid HR drift.
... In addition, insulin sensitivity improvements may depend on exercise modality. We have recently reported that a bout of HIIT resulted in greater improvements in insulin sensitivity when compared with a more "conventional" steady-state endurance exercise bout (28). In fact, a single session of HIIT in patients with MSyn improved insulin sensitivity to a similar extent as pharmacological treatment with metformin (29), emphasizing the utility of this exercise modality in this population. ...
Objective:
We studied the effects of exercise training alone or combined with dietary supplementation of omega-3 polyunsaturated fatty acids (Ω-3PUFA) and oleate on metabolic syndrome (MSyn) components and other markers of cardiometabolic health.
Methods:
Thirty-six patients with MSyn underwent 24 weeks of high-intensity interval training. In a double-blind randomized design, half of the group ingested 500 mL/day of semi-skim milk (8 g of fat; placebo milk) whereas the other half ingested 500 mL/day of skim milk enriched with 275 mg of Ω-3PUFA and 7.5 g of oleate (Ω-3 + OLE).
Results:
Ω-3 + OLE treatment elevated 30% plasma Ω-3PUFA but not significantly (P = 0.286). Improvements in VO2peak (12.8%), mean blood pressure (-7.1%), waist circumference (-1.8%), body fat mass (-2.9%), and trunk fat mass (-3.3%) were similar between groups. However, insulin sensitivity (measured by intravenous glucose tolerance test), serum concentration of C-reactive protein, and high-density lipoprotein improved only in the Ω-3 + OLE group by 31.5%, 32.1%, and 10.3%, respectively (all P < 0.05). Fasting serum triacylglycerol, glucose, and plasma fibrinogen concentrations did not improve in either group after 24 weeks of intervention.
Conclusions:
Diet supplementation with Ω-3PUFA and oleate enhanced cardiometabolic benefits of intense aerobic exercise training in patients with MSyn.
... CS I is highly correlated with the Minimal Model insulin sensitivity index (S I ) obtained from a 3-hour IVGTT, as well as the glucose infusion rate during a hyperinsulinemic-euglycemic clamp [19]. This method has also been used to assess insulin sensitivity in response to acute exercise [20,21], and has greater reproducibility than the Matsuda composite index (M ISI ) derived from an OGTT [20]. Briefly, CS I was calculated as follows: ...
Aims:
We investigated whether sprint interval training (SIT) was a time-efficient exercise strategy to improve insulin sensitivity and other indices of cardiometabolic health to the same extent as traditional moderate-intensity continuous training (MICT). SIT involved 1 minute of intense exercise within a 10-minute time commitment, whereas MICT involved 50 minutes of continuous exercise per session.
Methods:
Sedentary men (27±8y; BMI = 26±6kg/m2) performed three weekly sessions of SIT (n = 9) or MICT (n = 10) for 12 weeks or served as non-training controls (n = 6). SIT involved 3x20-second 'all-out' cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.
Results:
Peak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p<0.001 for both). Insulin sensitivity index (CSI), determined by intravenous glucose tolerance tests performed before and 72 hours after training, increased similarly after SIT (4.9±2.5 to 7.5±4.7, p = 0.002) and MICT (5.0±3.3 to 6.7±5.0 x 10-4 min-1 [μU/mL]-1, p = 0.013) (p<0.05). Skeletal muscle mitochondrial content also increased similarly after SIT and MICT, as primarily reflected by the maximal activity of citrate synthase (CS; P<0.001). The corresponding changes in the control group were small for VO2peak (p = 0.99), CSI (p = 0.63) and CS (p = 0.97).
Conclusions:
Twelve weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.
... Regular physical exercise improves lipid metabolism, blood pressure, insulin sensitivity, endothelial function and haemostatic factors, reducing the incidence of coronary heart disease independently of other changes in life style [1][2][3][4][5][6][7]. In animal models of atherosclerosis it has been shown that aerobic exercise training reduces the area of pre established atherosclerotic lesions, ameliorates plaque stability and improves mice survival rate [8,9]. ...
... Regular physical exercise improves lipid metabolism, blood pressure, insulin sensitivity, endothelial function and haemostatic factors, reducing the incidence of coronary heart disease independently of other changes in life style [1][2][3][4][5][6][7]. In animal models of atherosclerosis it has been shown that aerobic exercise training reduces the area of pre established atherosclerotic lesions, ameliorates plaque stability and improves mice survival rate [8,9]. ...
Background:
Regular exercise prevents and regresses atherosclerosis by improving lipid metabolism and antioxidant defenses. Exercise ameliorates the reverse cholesterol transport (RCT), an antiatherogenic system that drives cholesterol from arterial macrophages to the liver for excretion into bile and feces. In this study we analyzed the role of aerobic exercise on the in vivo RCT and expression of genes and proteins involved in lipid flux and inflammation in peritoneal macrophages, aortic arch and liver from wild type mice.
Methods:
Twelve-week-old male mice were divided into sedentary and trained groups. Exercise training was performed in a treadmill (15 m/min, 30 min/day, 5 days/week). Plasma lipids were determined by enzymatic methods and lipoprotein profile by fast protein liquid chromatography. After intraperitoneal injection of J774-macrophages the RCT was assessed by measuring the recovery of (3)H-cholesterol in plasma, feces and liver. The expression of liver receptors was determined by immunoblot, macrophages and aortic mRNAs by qRT-PCR. (14)C-cholesterol efflux mediated by apo A-I and HDL2 and the uptake of (3)H-cholesteryl oleoyl ether ((3)H-COE)-acetylated-LDL were determined in macrophages isolated from sedentary and trained animals 48 h after the last exercise session.
Results:
Body weight, plasma lipids, lipoprotein profile, glucose and blood pressure were not modified by exercise training. A greater amount of (3)H-cholesterol was recovered in plasma (24 h and 48 h) and liver (48 h) from trained animals in comparison to sedentary. No difference was found in (3)H-cholesterol excreted in feces between trained and sedentary mice. The hepatic expression of scavenger receptor class B type I (SR-BI) and LDL receptor (B-E) was enhanced by exercise. We observed 2.8 and 1.7 fold rise, respectively, in LXR and Cyp7a mRNA in the liver of trained as compared to sedentary mice. Macrophage and aortic expression of genes involved in lipid efflux was not systematically changed by physical exercise. In agreement, (14)C-cholestrol efflux and uptake of (3)H-COE-acetylated-LDL by macrophages was similar between sedentary and trained animals.
Conclusion:
Aerobic exercise in vivo accelerates the traffic of cholesterol from macrophages to the liver contributing to prevention and regression of atherosclerosis, independently of changes in macrophage and aorta gene expression.
Osteoglycin (OGN) and lipocalin-2 (LCN2) are hormones that can be secreted by bone and have been linked to glucose homeostasis in rodents. However, the endocrine role of these hormones in humans is contradictory and unclear. We examined the effects of exercise and meal ingestion on circulating serum OGN and LCN2 levels in eight healthy males (age: 28 [25, 30] years [median ± IQR] and BMI: 24.3 [23.6, 25.5] kg/m2). In a randomized crossover design, participants ingested a high-glucose (1.1 g glucose/kg body weight) mixed-nutrient meal (45% carbohydrate, 20% protein, and 35% fat) on a rest-control day and 3 h and 24 h after aerobic cycling exercise (1 h at 70-75% VO2peak). Acute aerobic exercise increased serum LCN2 levels immediately after exercise (~61%), which remained elevated 3 h post-exercise (~55%). In contrast, serum OGN remained similar to baseline levels throughout the 3 h post-exercise recovery period. The ingestion of a high-glucose mixed-nutrient meal led to a decrease in serum OGN at 90 min (~-17%) and 120 min postprandial (~-44%), and a decrease in LCN2 at 120 min postprandial (~-26%). Compared to the control meal, prior exercise elevated serum OGN and LCN2 levels at 120 min postprandial when the meal was ingested 3 h (OGN: ~74% and LCN2: ~68%) and 24 h post-exercise (OGN: ~56% and LCN2: ~16%). Acute exercise increases serum LCN2 and attenuates the postprandial decrease in OGN and LCN2 following high-glucose mixed-nutrient meal ingestion. The potential endocrine role of circulating OGN and LCN2 in humans warrants further investigation.
The interaction between insulin and exercise is an example of balancing and modifying the effects of two opposing metabolic regulatory forces under varying conditions. While insulin is secreted after food intake and is the primary hormone increasing glucose storage as glycogen and fatty acid storage as triglycerides, exercise is a condition where fuel stores need to be mobilized and oxidized. Thus, during physical activity the fuel storage effects of insulin need to be suppressed. This is done primarily by inhibiting insulin secretion during exercise as well as activating local and systemic fuel mobilizing processes. In contrast, following exercise there is a need for refilling the fuel depots mobilized during exercise, particularly the glycogen stores in muscle. This process is facilitated by an increase in insulin sensitivity of the muscles previously engaged in physical activity which directs glucose to glycogen resynthesis. In physically trained individuals, insulin sensitivity is also higher than in untrained individuals due to adaptations in the vasculature, skeletal muscle and adipose tissue. In this paper, we review the interactions between insulin and exercise during and after exercise, as well as the effects of regular exercise training on insulin action.
Regular exercise causes chronic adaptations in anatomy/physiology that provide first-line defense for disease prevention/treatment (‘exercise is medicine’). However, transient changes in function that occur following each exercise bout (acute effect) are also important to consider. For example, in contrast to chronic adaptations, the effect of exercise on insulin sensitivity is predominantly rooted in a prolonged acute effect (PAE) that can last up to 72 h. Untrained individuals and individuals with lower insulin sensitivity benefit more from this effect and even trained individuals with high insulin sensitivity restore most of a detraining-induced loss following one session of resumed training. Consequently, exercise to combat insulin resistance that begins the pathological journey to cardiometabolic diseases including type 2 diabetes (T2D) should be prescribed with precision to elicit a PAE on insulin sensitivity to serve as a first-line defense prior to pharmaceutical intervention or, when such intervention is necessary, a potential adjunct to it.
Video Abstract: http://links.lww.com/CAEN/A27
Key points
Exercise, insulin‐infusion and low‐glucose mixed‐nutrient meal ingestion increases muscle microvascular blood flow which in part facilitates glucose delivery and disposal. In contrast, high‐glucose ingestion impairs muscle microvascular blood flow which may contribute to impaired postprandial metabolism.
We investigated the effects of prior cycling exercise on postprandial muscle microvascular blood flow responses to a high‐glucose mixed‐nutrient meal ingested 3 and 24 h post‐exercise.
Prior exercise enhanced muscle microvascular blood flow and mitigated microvascular impairments induced by a high‐glucose mixed meal ingested 3 h post‐exercise, and to a lesser extent 24 h post‐exercise.
High‐glucose ingestion 3 h post‐exercise leads to greater postprandial blood glucose, non‐esterified fatty acids, and fat oxidation, and a delay in the insulin response to the meal compared to control.
Effects of acute exercise on muscle microvascular blood flow persist well after the cessation of exercise which may be beneficial for conditions characterized by microvascular and glycaemic dysfunction.
Abstract
Exercise, insulin‐infusion and low‐glucose mixed‐nutrient meal ingestion lead to increased muscle microvascular blood flow (MBF), whereas high‐glucose ingestion impairs MBF. We investigated whether prior cycling exercise could enhance postprandial muscle MBF and prevent MBF impairments induced by high‐glucose mixed‐nutrient meal ingestion. In a randomized cross‐over design, eight healthy young men ingested a high‐glucose mixed‐nutrient meal (1.1 g glucose/kg body weight; 45% carbohydrate, 20% protein and 35% fat) after an overnight fast (no‐exercise control) and 3 h and 24 h after moderate‐intensity cycling exercise (1 h at 70–75% V̇O2peak). Skeletal muscle MBF, measured directly by contrast‐enhanced ultrasound, was lower at 60 min and 120 min postprandially compared to baseline in all conditions (P < 0.05), with a greater decrease occurring from 60 min to 120 min in the control (no‐exercise) condition only (P < 0.001). Despite this meal‐induced decrease, MBF was still markedly higher compared to control in the 3 h post‐exercise condition at 0 min (pre‐meal; 74%, P = 0.004), 60 min (112%, P = 0.002) and 120 min (223%, P < 0.001), and in the 24 h post‐exercise condition at 120 min postprandially (132%, P < 0.001). We also report that in the 3 h post‐exercise condition postprandial blood glucose, non‐esterified fatty acids (NEFAs), and fat oxidation were substantially elevated, and the insulin response to the meal delayed compared to control. This probably reflects a combination of increased post‐exercise exogenous glucose appearance, substrate competition, and NEFA‐induced insulin resistance. We conclude that prior cycling exercise elicits long‐lasting effects on muscle MBF and partially mitigates MBF impairments induced by high‐glucose mixed‐nutrient meal ingestion.
Introduction: Skeletal muscle is the major site of insulin-stimulated glucose uptake and imparts the beneficial effects of exercise, and hence is an important site of insulin resistance in obesity and type 2 diabetes (T2D). Despite extensive molecular biology-oriented research the molecular mechanisms underlying insulin resistance in skeletal muscle remain to be established.
Areas covered: The proteomic capabilities have greatly improved over the last decades. This review summarizes the technical challenges in skeletal muscle proteomics studies as well as the results of quantitative proteomic studies of skeletal muscle in relation to obesity, T2D, and exercise.
Expert commentary: Current available proteomic studies contribute to the view that insulin resistance in obesity and T2D is associated with increased glycolysis and reduced mitochondrial oxidative metabolism in skeletal muscle, and that the latter can be improved by exercise. Future proteomics studies should be designed to markedly intensify the identification of abnormalities in metabolic and signaling pathways in skeletal muscle of insulin-resistant individuals to increase the understanding of the pathogenesis of T2D, but more importantly to identify multiple novel targets of treatment of which at least some can be safely targeted by novel drugs to treat and prevent T2D and reduce risk of cardiovascular disease.
Purpose and methods
This review presents established knowledge on the effects of physical activity (PA) on whole-body insulin sensitivity (SI) and summarises the findings of recent (2013–2016) studies.
Discussion and conclusions
Recent studies provide further evidence to support the notion that regular PA reduces the risk of insulin resistance, metabolic syndrome and type 2 diabetes, and SI improves when individuals comply with exercise and/or PA guidelines. Many studies indicate a dose response, with higher energy expenditures and higher exercise intensities, including high intensity interval training (HIIT), producing greater benefits on whole-body SI, although these findings are not unanimous. Aerobic exercise interventions can improve SI without an associated increase in cardiorespiratory fitness as measured by maximal or peak oxygen consumption. Both aerobic and resistance exercise can induce improvements in glycaemic regulation, with some suggestions that exercise regimens including both may be more efficacious than either exercise mode alone. Some studies report exercise-induced benefits to SI that are independent of habitual diet and weight loss, while others indicate an association with fat reduction, hence the debate over the relative importance of PA and weight loss continues. During exercise, muscle contraction stimulated improvements in SI are associated with increases in AMPK activity, which deactivates TCB1D1, promoting GLUT4 translocation to the cell membrane and thereby increasing glucose uptake. Postexercise, increases in Akt deactivate TCB1D4 and thereby increase GLUT4 translocation to the cell membrane. The reduction in intramuscular saturated fatty acids and concomitant reductions in ceramides, but not diacylglycerols, provide a potential link between intramuscular lipid content and SI. Increased skeletal muscle capillarisation provides another independent adaptation through which SI is improved, as does enhanced β cell activity. Recent studies are combining exercise interventions with dietary and feeding manipulations to investigate the potential for augmenting the exercise-induced improvements in SI and glycaemic control.
We have previously demonstrated that reduced-exertion high-intensity interval training (REHIT), requiring a maximum of two 20-s all out cycling sprints in a 10-min exercise session, improves insulin sensitivity in sedentary men over a 6-week training intervention. However, the acute effects of REHIT on insulin sensitivity have not previously been described. In this study fourteen men and women (mean±SD age: 23±5 y; BMI 22.7±4.7 kg•m-2; V̇O2max: 37.4±8.6 mL•kg-1•min-1) underwent oral glucose tolerance testing 14-16 hours after an acute bout of reduced-exertion high-intensity interval training (2 x 20-s all-out sprints; REHIT), moderate-vigorous aerobic exercise (45 minutes at ~75% VO2max; AER), and a resting control condition (REST). Neither REHIT nor AER were associated with significant changes in glucose AUC (REHIT 609±98 vs. AER 651±85 vs. REST 641±126 mmol•l-1•120 min), insulin AUC (REHIT 30.9±15.4 vs. AER 31.4±13.0 vs. REST 35.0±18.5 nmol•l-1•120 min) or insulin sensitivity estimated by the Cederholm index (REHIT 86±20 vs. AER 79±13 vs. REST 82±24 mg•l2•mmol-1•mU-1•min-1). These data suggest that improvements in insulin sensitivity following a chronic REHIT intervention are the result of training adaptations rather than acute effects of the last exercise session.
The aim of the present study was to determine which of the available glucose tolerance tests (oral (OGTT) vs. intravenous (IVGTT)) could more readily detect the insulin sensitizing effects of a bout of continuous exercise. Ten healthy moderately fit young men (V̇O2peak of 45.4 ± 1.8 mL·kg⁻¹·min⁻¹; age 27.5 ± 2.7 yr) underwent 4 OGTT and 4 IVGTT on different days following a standardized dinner and overnight fast. One test was performed immediately after 55 min of cycle-ergometer exercise at 60% V̇O2peak. Insulin sensitivity index was determined during a 50 min IVGTT according to Tura (CISI) and from a 120 min OGTT using the Matsuda composite index (MISI). After exercise, MISI improved 29 ± 10% without reaching statistical significance (p= 0.182) due to its low reproducibility (coefficient of variation 16 ± 3%; intra-class reliability 0.846). However, CISI significantly improved (50 ± 4%; p < 0.001) after exercise showing better reproducibility (coefficient of variation 13 ± 4%; intra-class reliability 0.955). Power calculation revealed that 6 participants were required for detecting the effects of exercise on insulin sensitivity when using IVGTT, whereas 54 were needed when using OGTT. The superior response of CISI compared with MISI suggests the preferential use of IVGTT to assess the effects of exercise on insulin sensitivity when using a glucose tolerance test.
Although physical activity (PA) is a key element in the prevention and management of type 2 diabetes mellitus (T2DM), many with this chronic disease do not become or remain regularly active. High-quality studies establishing the importance of exercise and fitness in diabetes were lacking until recently, but it is now well established that participation in regular PA improves blood glucose control and can prevent or delay T2DM, along with positively affecting lipids, blood pressure, cardiovascular events, mortality, and quality of life. Structured interventions combining PA and modest weight loss have been shown to lower T2DM risk by up to 58% in high-risk populations. Most benefits of PA on diabetes management are realized through acute and chronic improvements in insulin action, accomplished with both aerobic and resistance training. The benefits of physical training are discussed, along with recommendations for varying activities, PA-associated blood glucose management, diabetes prevention, gestational diabetes, and safe and effective practices for PA with diabetes-related complications.
Although physical activity (PA) is a key element in the prevention and management of type 2 diabetes, many with this chronic disease do not become or remain regularly active. High-quality studies establishing the importance of exercise and fitness in diabetes were lacking until recently, but it is now well established that participation in regular PA improves blood glucose control and can prevent or delay type 2 diabetes, along with positively affecting lipids, blood pressure, cardiovascular events, mortality, and quality of life. Structured interventions combining PA and modest weight loss have been shown to lower type 2 diabetes risk by up to 58% in high-risk populations. Most benefits of PA on diabetes management are realized through acute and chronic improvements in insulin action, accomplished with both aerobic and resistance training. The benefits of physical training are discussed, along with recommendations for varying activities, PA-associated blood glucose management, diabetes prevention, gestational diabetes mellitus, and safe and effective practices for PA with diabetes-related complications.
Skeletal muscle contraction increases intracellular ATP turnover, calcium flux, and mechanical stress, initiating signal transduction pathways that modulate peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha)-dependent transcriptional programmes. The purpose of this study was to determine if the intensity of exercise regulates PGC-1alpha expression in human skeletal muscle, coincident with activation of signalling cascades known to regulate PGC-1alpha transcription. Eight sedentary males expended 400 kcal (1674 kj) during a single bout of cycle ergometer exercise on two separate occasions at either 40% (LO) or 80% (HI) of . Skeletal muscle biopsies from the m. vastus lateralis were taken at rest and at +0, +3 and +19 h after exercise. Energy expenditure during exercise was similar between trials, but the high intensity bout was shorter in duration (LO, 69.9 +/- 4.0 min; HI, 36.0 +/- 2.2 min, P < 0.05) and had a higher rate of glycogen utilization (P < 0.05). PGC-1alpha mRNA abundance increased in an intensity-dependent manner +3 h after exercise (LO, 3.8-fold; HI, 10.2-fold, P < 0.05). AMP-activated protein kinase (AMPK) (2.8-fold, P < 0.05) and calcium/calmodulin-dependent protein kinase II (CaMKII) phosphorylation (84%, P < 0.05) increased immediately after HI but not LO. p38 mitogen-activated protein kinase (MAPK) phosphorylation increased after both trials (2.0-fold, P < 0.05), but phosphorylation of the downstream transcription factor, activating transcription factor-2 (ATF-2), increased only after HI (2.4-fold, P < 0.05). Cyclic-AMP response element binding protein (CREB) phosphorylation was elevated at +3 h after both trials (80%, P < 0.05) and class IIa histone deacetylase (HDAC) phosphorylation increased only after HI (2.0-fold, P < 0.05). In conclusion, exercise intensity regulates PGC-1alpha mRNA abundance in human skeletal muscle in response to a single bout of exercise. This effect is mediated by differential activation of multiple signalling pathways, with ATF-2 and HDAC phosphorylation proposed as key intensity-dependent mediators.
An acute bout of endurance exercise (EE) enhances insulin sensitivity, but the effects of sprint interval exercise (SIE) have not yet been described. We sought to compare insulin sensitivity at baseline and after an acute bout of EE and SIE in healthy men (n = 8) and women (n = 5) (age, 20.7 0.3years peak oxygen consumption (VO2 peak), 42.6 1.7mLkg¹min¹<1.5daysweek¹ structured exercise body fat, 21.1 1.9%). Subjects underwent 3 oral glucose tolerance tests (OGTTs) the day after each of the following 3 conditions: no exercise, baseline (OGTTB) SIE at ~125% VO2peak (OGTTSIE) and EE at ~75% VO2peak (OGTTEE). SIE and EE sessions were randomized for each subject. Subjects consumed identical meals the day preceding each OGTT. Two insulin sensitivity indices composite whole-body insulin sensitivity index (ISI-COMP) and ISI-hepatic insulin sensitivity (HOMA) were calculated, using previously validated formulas (ISI-COMP = 10000/(glucosefasting insulinfasting glucosemean OGTT insulinmeanOGTT) ISI-HOMA = 22.5/(insulinfasting glucosefasting)), and the plasma concentrations of cytokines interleukin-6 and tumor necrosis factor- were measured. There were no differences by sex for any condition (men vs. women, p> 0.05). Pearsons correlation coefficients between ISI-COMP and ISI-HOMA for each condition were highly correlated (p< 0.01), and followed similar patterns of response. ISI-COMPEE was 71.4% higher than ISI-COMPB (8.4 1.4 vs. 4.9 1.0; p< 0.01) and 40.0% higher than ISI-COMPSIE (8.4 1.4 vs. 6.0 1.5; p< 0.05), but there was no difference between ISI-COMPB and ISI-COMPSIE (p = 0.182). VO2 peak was highly correlated with both ISI-COMP and ISI-HOMA during baseline and SIE test conditions (p< 0.02). These findings demonstrate that an acute bout of EE, but not SIE, increases insulin sensitivity relative to a no-exercise control condition in healthy males and females. While these findings underscore the use of regular EE as an effective intervention strategy against insulin resistance, additional research examining repeated sessions of SIE on insulin sensitivity is warranted.
Traditional high volume aerobic exercise training reduces cardiovascular and metabolic disease risk but involves a substantial time commitment. Extremely low volume high-intensity interval training (HIT) has recently been demonstrated to produce improvements to aerobic function, but it is unknown whether HIT has the capacity to improve insulin action and hence glycemic control.
Sixteen young men (age: 21 +/- 2 y; BMI: 23.7 +/- 3.1 kg x m-2; VO2peak: 48 +/- 9 ml x kg-1 x min-1) performed 2 weeks of supervised HIT comprising of a total of 15 min of exercise (6 sessions; 4-6 x 30-s cycle sprints per session). Aerobic performance (250-kJ self-paced cycling time trial), and glucose, insulin and NEFA responses to a 75-g oral glucose load (oral glucose tolerance test; OGTT) were determined before and after training.
Following 2 weeks of HIT, the area under the plasma glucose, insulin and NEFA concentration-time curves were all reduced (12%, 37%, 26% respectively, all P < 0.001). Fasting plasma insulin and glucose concentrations remained unchanged, but there was a tendency for reduced fasting plasma NEFA concentrations post-training (pre: 350 +/- 36 v post: 290 +/- 39 micromol x l-1, P = 0.058). Insulin sensitivity, as measured by the Cederholm index, was improved by 23% (P < 0.01), while aerobic cycling performance improved by approximately 6% (P < 0.01).
The efficacy of a high intensity exercise protocol, involving only ~250 kcal of work each week, to substantially improve insulin action in young sedentary subjects is remarkable. This novel time-efficient training paradigm can be used as a strategy to reduce metabolic risk factors in young and middle aged sedentary populations who otherwise would not adhere to time consuming traditional aerobic exercise regimes.
To review current practice in centers that use the IVGTT for prediction of IDDM. To establish consensus protocol for performance of the test.
Postal questionnaires were delivered to 12 centers.
Eleven centers used a glucose dose of 0.5 g/kg and 1 used 0.3 g/kg; the dosage in adults was limited to a maximum of 25-50 g in some centers but others applied no upper limit. The glucose concentration of the infusate varied between 20 and 66%. Eight centers injected glucose manually, two used a syringe pump, and two used gravity infusion. The period of infusion ranged from 30 +/- 10 s to 4 +/- 2 min, and time zero was taken as the start (1 center), middle (1 center), or end (10 centers) of the infusion. The potential range in timing of the +1-min sample varied between 1 and 7 min from the start of the infusion. Quality-assurance standards for the insulin assays used were not always appropriate for the fasting and low stimulated range of insulin levels.
The first-phase insulin response to the IVGTT is widely measured as an index of risk of progression to IDDM. We established that methodology varies widely. Because of this, a new standard protocol for use in prediction of IDDM was agreed by an ICARUS working group and is described herein.
The effect of acute physical exercise on insulin sensitivity and responsiveness of glucose uptake and hepatic glucose production was studied. Seven untrained men were subjected to four sequential euglycemic hyperinsulinemic clamps after rest (R), immediately after exercise (E), as well as 48 h after 60 min of 150 W ergometer exercise (ER). Insulin-mediated glucose uptake was higher on E and ER days compared with R days. Apparent Km decreased after exercise (52 +/- 3 R vs. 43 +/- 4 E and 40 +/- 3 ER microU/ml, means +/- SE) and Vmax increased (9.5 +/- 0.8 R vs. 10.9 +/- 0.7 E and 10.7 +/- 0.8 ER mg.min-1.kg-1). Glucose oxidation increased with the increasing insulin infusion rate, and maximal glucose oxidation rate was lower on E days compared with R days. The maximal conversion rate of glucose to glycogen was higher on E and ER days (8.0 +/- 0.3 and 7.2 +/- 0.2, respectively) than on R days (5.7 +/- 0.6 mg.min-1 kg-1). Muscle glycogen synthase I activity was higher immediately after exercise and remained higher for the next 48 h. No change in any glucoregulatory hormone or metabolite could explain the increased insulin action seen after exercise. In additional experiments (n = 3), no remaining effect existed 5 days after exercise. Both insulin and exercise suppressed the pancreatic secretion of insulin and proinsulin. The conclusions drawn are that prolonged moderate exercise increases insulin action on glucose uptake in humans by reducing apparent Km and increasing Vmax. This effect lasts 48 h but not 5 days. The increased insulin action may be related to an exercise-induced increase in glycogen synthase activity.
In rats, muscle glycogen depletion has been associated with increased insulin action. Whether this also occurs in man has not been reported. After 4 d rest, 13 males (E Group) had a percutaneous muscle biopsy of the vastus lateralis muscle followed by a euglycemic clamp at plasma insulin ≃100 μU/ml and ≃1,900 μU/ml, with simultaneous indirect calorimetry. This was repeated 1 wk later, but after glycogen-depleting exercise the night before the euglycemic clamp. Seven subjects underwent the same protocol but were also re-fed 100 g carbohydrate (CHO) after the exercise (EF group). In both groups, the mean muscle glycogen content was ~40% lower (P < 0.01) after exercise compared with the muscle glycogen content measured after rest. In the E group, the mean muscle glycogen synthase activity (percent independent of glucose-6-phosphate) increased threefold (P < 0.001) after exercise, but increased only twofold in the EF group (P < 0.02 between groups). In both groups, the mean basal and insulin-stimulated CHO oxidation rates were lower in the post-exercise, glycogen-depleted condition compared with the rested, glycogen-replete condition. The mean insulin-stimulated CHO storage rate increased significantly in the E group after exercise but not in the EF group. In the E group, the total insulin-stimulated CHO disposal rate (M) was 17 (P < 0.04) and 10% (P < 0.03) higher after exercise during the low and high dose insulin infusion, respectively. No significant changes in M were observed in the EF group. For all subjects, after rest and exercise, the M correlated with the CHO storage rates during the low (r = 0.80, P < 0.001) and high dose (r = 0.77, P < 0.001) insulin infusions. After exercise, the muscle glycogen synthase activity correlated with the CHO storage rate (r = 0.73, P < 0.002; r = 0.75, P < 0.002) during the low and high dose insulin infusions, respectively, and also with M (r = 0.64, P < 0.008; r = 0.57; P < 0.02).
Stable isotope tracers and indirect calorimetry were used to evaluate the regulation of endogenous fat and glucose metabolism in relation to exercise intensity and duration. Five trained subjects were studied during exercise intensities of 25, 65, and 85% of maximal oxygen consumption (VO2max). Plasma glucose tissue uptake and muscle glycogen oxidation increased in relation to exercise intensity. In contrast, peripheral lipolysis was stimulated maximally at the lowest exercise intensity, and fatty acid release into plasma decreased with increasing exercise intensity. Muscle triglyceride lipolysis was stimulated only at higher intensities. During 2 h of exercise at 65% VO2max plasma-derived substrate oxidation progressively increased over time, whereas muscle glycogen and triglyceride oxidation decreased. In recovery from high-intensity exercise, although the rate of lipolysis immediately decreased, the rate of release of fatty acids into plasma increased, indicating release of fatty acids from previously hydrolyzed triglycerides. We conclude that, whereas carbohydrate availability is regulated directly in relation to exercise intensity, the regulation of lipid metabolism seems to be more complex.
To examine the mechanism by which lipids cause insulin resistance in humans, skeletal muscle glycogen and glucose-6-phosphate concentrations were measured every 15 min by simultaneous 13C and 31P nuclear magnetic resonance spectroscopy in nine healthy subjects in the presence of low (0.18 +/- 0.02 mM [mean +/- SEM]; control) or high (1.93 +/- 0.04 mM; lipid infusion) plasma free fatty acid levels under euglycemic (approximately 5.2 mM) hyperinsulinemic (approximately 400 pM) clamp conditions for 6 h. During the initial 3.5 h of the clamp the rate of whole-body glucose uptake was not affected by lipid infusion, but it then decreased continuously to be approximately 46% of control values after 6 h (P < 0.00001). Augmented lipid oxidation was accompanied by a approximately 40% reduction of oxidative glucose metabolism starting during the third hour of lipid infusion (P < 0.05). Rates of muscle glycogen synthesis were similar during the first 3 h of lipid and control infusion, but thereafter decreased to approximately 50% of control values (4.0 +/- 1.0 vs. 9.3 +/- 1.6 mumol/[kg.min], P < 0.05). Reduction of muscle glycogen synthesis by elevated plasma free fatty acids was preceded by a fall of muscle glucose-6-phosphate concentrations starting at approximately 1.5 h (195 +/- 25 vs. control: 237 +/- 26 mM; P < 0.01). Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.
This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10-and 30-s sprints. At the end of sprint 1, PCr was 16.9 ± 1.4% of the resting value, and muscle pH dropped to 6.69 ± 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 ± 0.03), but PCr was resynthesized to 78.7 ± 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 ± 9 mmol/kg dry muscle during the first sprint but was decreased to 139 ± 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a ~45% decrease in glycolysis. Despite this ~41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only ~18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 ± 0.10 vs. 3.17 ± 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part (~49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.
In intense exercise (>80% VO(2max)), unlike at lesser intensities, glucose is the exclusive muscle fuel. It must be mobilized from muscle and liver glycogen in both the fed and fasted states. Therefore, regulation of glucose production (GP) and glucose utilization (GU) have to be different from exercise at <60% VO(2max), in which it is established that the portal glucagon-to-insulin ratio causes the less than or equal to twofold increase in GP. GU is subject to complex regulation by insulin, plasma glucose, alternate substrates, other humoral factors, and muscle factors. At lower intensities, plasma glucose is constant during postabsorptive exercise and declines during postprandial exercise (and often in persons with diabetes). During such exercise, insulin secretion is inhibited by beta-cell alpha-adrenergic receptor activation. In contrast, in intense exercise, GP rises seven- to eightfold and GU rises three- to fourfold; therefore, glycemia increases and plasma insulin decreases minimally, if at all. Indeed, even an increase in insulin during alpha-blockade or during a pancreatic clamp does not prevent this response, nor does pre-exercise hyperinsulinemia due to a prior meal or glucose infusion. At exhaustion, GU initially decreases more than GP, which leads to greater hyperglycemia, requiring a substantial rise in insulin for 40--60 min to restore pre-exercise levels. Absence of this response in type 1 diabetes leads to sustained hyperglycemia, and mimicking it by intravenous infusion restores the normal response. Compelling evidence supports the conclusion that the marked catecholamine responses to intense exercise are responsible for both the GP increment (that occurs even during glucose infusion and postprandially) and the restrained increase of GU. These responses are normal in persons with type 1 diabetes, who often report exercise-induced hyperglycemia, and in whom the clinical challenge is to reproduce the recovery period hyperinsulinemia. Intense exercise in type 2 diabetes requires additional study.
Fatty acid oversupply is a key mediator of skeletal muscle insulin resistance in obesity, primarily via accumulation of fatty acid metabolites and activation of proinflammatory pathways. Herein, we demonstrate that fatty acid-induced insulin resistance in humans is completely prevented the day after 1 session of endurance exercise. Because skeletal muscle is the primary site for systemic glucose disposal and is highly susceptible to impaired insulin action by elevated fatty acid availability, we obtained skeletal muscle samples to investigate possible mechanisms mediating this protective effect of exercise. Prevention of fatty acid-induced insulin resistance after exercise accompanied enhanced skeletal muscle protein expression of key lipogenic enzymes and an increase in muscle triglyceride synthesis. Partitioning more fatty acids toward triglyceride synthesis within muscle reduced the accumulation of fatty acid metabolites and suppressed the proinflammatory response in skeletal muscle, as evidenced by decreased phosphorylation and activation of JNK and increased abundance of inhibitor of NF-kappaB alpha (I kappa B-alpha) and I kappa B-beta. We believe this is the first study to demonstrate that 1 session of exercise completely reverses fatty acid-induced insulin resistance in humans. Reversal of insulin resistance accompanied enhanced lipogenic capacity within skeletal muscle, reduced accumulation of highly bioactive fatty acid metabolites, and suppressed activation of proinflammatory pathways known to impair insulin action.
Knowledge of the within-subject variability of a parameter is required to properly design and calculate sample sizes for longitudinal studies. We sought to determine the day-to-day variability of measures of beta cell function derived from an OGTT.
Thirty-seven adults (13 with normal glucose tolerance, ten with impaired glucose tolerance, 14 with type 2 diabetes) underwent a standard 2 h 75 g OGTT on two separate days (median time between tests, 7 days; range, 5-14). From these data, the reproducibility of several indices of beta cell function were determined: insulinogenic index (DeltaI(0-30)/DeltaG(0-30)), early C-peptide response (DeltaCP(0-30)/DeltaG(0-30)), incremental AUC insulin to glucose response (incAUC(ins)/incAUC(glu)), integrated insulin secretion response from 0 to 120 min (IS/Glu(0-120)) and indices of beta cell function derived from a mathematical model.
Within-subject variability for DeltaI(0-30)/DeltaG(0-30) (CV 57.1%) was higher than DeltaCP(0-30)/DeltaG(0-30) (CV 34.7%). Measures integrated over the full 120 min of the OGTT, incAUC(ins)/incAUC(glu) (CV 24.9%) and IS/Glu(0-120) (CV 17.4%), demonstrated less variability. The mathematical model-derived measures of beta cell glucose sensitivity (CV 20.3%) and potentiation (CV 33.0%) showed moderate variability. The impact of the different measures' variability on sample size (30% change from baseline) is demonstrated by calculated sample sizes of 89 for DeltaI(0-30)/DeltaG(0-30), 37 for DeltaCP(0-30)/DeltaG(0-30), 21 for incAUC(ins)/incAUC(glu) and 11 for IS/Glu(0-120).
Some OGTT-derived indices of beta cell function, in particular the insulinogenic index, demonstrate high within-subject variability. Integrated measures that utilise multiple time points and measures that use C-peptide show less variability and may lead to a reduced sample size requirement.
PurposeThis study aimed to investigate the effects of a single session of sprint interval training (SIT) and a single extended sprint (ES), matched for total work, on metabolic health biomarkers.Methods
Ten overweight/obese men aged 26.9 ± 6.2 years participated. Following a pre-trial incremental exercise test and SIT familiarization, each participant undertook three 2-day trials in randomized order. On Day 1 participants either undertook no exercise (CON), four maximal 30-s sprints, with 4.5 min recovery between each (SIT), or a single maximal extended sprint (ES) matched with SIT for work done. On Day 2, participants had a fasting blood sample taken, undertook an oral glucose tolerance test to determine insulin sensitivity index (ISI), and had blood pressure measured.ResultsTotal work done during exercise did not differ between SIT and ES (61.7 ± 2.9 vs. 61.3 ± 2.8 kJ; p = 0.741). Mean power was higher in SIT than ES (518 ± 21 vs. 306 ± 16 W, p < 0.0005), resulting in a shorter high-intensity exercise duration in SIT (120 ± 0 vs. 198 ± 10 s, p < 0.0005). ISI was 44.6% higher following ES than CON (9.4 ± 2.1 vs. 6.5 ± 1.3; p = 0.022), but did not differ significantly between SIT and CON (6.6 ± 0.9 vs. 6.5 ± 1.3; p = 0.208). However, on the day following exercise fat oxidation in the fasted state was increased by 63% and 38%, compared to CON, in SIT and ES, respectively (p < 0.05 for both), with a concomitant reduction in carbohydrate oxidation (p < 0.05).ConclusionA single ES, which may represent a more time-efficient alternative to SIT, can increase insulin sensitivity and increase fat oxidation in overweight overweight/obese sedentary men.
Bergström needle muscle biopsies have been used by exercise physiologists for over 35 years but have been less accepted by neuromuscular clinicians due to size concerns.
We retrospectively reviewed over 13,500 muscle Bergström needle biopsies done over a 21-year period to determine sampling success, patient/subject experience, and complications. We compared sample yield between two different needles (Bergström vs. UCH), with and without suction modifications.
Needle biopsies adequate for histology and enzymology were obtainable from the vastus lateralis, deltoid, biceps brachii, soleus, and medial gastrocnemius muscles, with a success rate of >99.9% and a minor complication rate of 0.15%. Approximately 450 muscle fibers were submitted for histologic assessment; suction modification and use of the Bergström vs. UCH needle were associated with larger sample size (P < 0.05).
The suction-modified Bergström needle muscle biopsy technique is safe and provides an adequate sample size for histologic, ultrastructural, DNA, and enzyme analysis.
Sprint interval training (SIT) and traditional endurance training elicit similar physiological adaptations. From the perspective of metabolic function, superior glucose regulation is a common characteristic of endurance-trained adults. Accordingly, we have investigated the hypothesis that short-term SIT will increase insulin sensitivity in sedentary/recreationally active humans. Thirty one healthy adults were randomly assigned to one of three conditions: (1) SIT (n = 12): six sessions of repeated (4-7) 30 s bouts of very high-intensity cycle ergometer exercise over 14 days; (2) sedentary control (n = 10); (3) single-bout SIT (n = 9): one session of 4 x 30 s cycle ergometer sprints. Insulin sensitivity was determined (hyperinsulinaemic euglycaemic clamp) prior to and 72 h following each intervention. Compared with baseline, and sedentary and single-bout controls, SIT increased insulin sensitivity (glucose infusion rate: 6.3 +/- 0.6 vs. 8.0 +/- 0.8 mg kg(1) min(1); mean +/- s.e.m.; P = 0.04). In a separate study, we investigated the effect of SIT on the thermogenic response to beta-adrenergic receptor (beta-AR) stimulation, an important determinant of energy balance. Compared with baseline, and sedentary and single-bout control groups, SIT did not affect resting energy expenditure (EE: ventilated hood technique; 6274 +/- 226 vs. 6079 +/- 297 kJ day(1); P = 0.51) or the thermogenic response to isoproterenol (6, 12 and 24 ng (kg fat-free mass)(1) min(1): %EE 11 +/- 2, 14 +/- 3, 23 +/- 2 vs. 11 +/- 1, 16 +/- 2, 25 +/- 3; P = 0.79). Combined data from both studies revealed no effect of SIT on fasted circulating concentrations of glucose, insulin, adiponectin, pigment epithelial-derived factor, non-esterified fatty acids or noradrenaline (all P > 0.05). Sixteen minutes of high-intensity exercise over 14 days augments insulin sensitivity but does not affect the thermogenic response to beta-AR stimulation.
Minimal model analysis for insulin sensitivity has been validated against the glucose clamp and is an accepted method for estimating insulin sensitivity from IVGTT. However minimal model analysis requires a 3 h test and relevant expertise to run the mathematical model. The aim of this study was to suggest a simple predictor of minimal model analysis index using only 1 h IVGTT.
We studied participants with different clinical characteristics who underwent 3 h regular (n = 336) or insulin-modified (n = 160) IVGTT, or 1 h IVGTT and euglycaemic-hyperinsulinaemic clamp (n = 247). Measures of insulin sensitivity were insulin sensitivity index estimated by minimal model analysis (S(I)) and the mean glucose infusion rate (clamp) (M). A calculated S(I) (CS(I)) predictor, CS(I) = Alpha X K(G)/(DeltaAUC(INS)/T), was suggested, based on the calculation of the rate of glucose disappearance K(G) and the suprabasal AUC of insulin concentration DeltaAUC(INS) over T = 40 min. For all the participants, alpha was assumed equal to the regression line slope between K(G)/(DeltaAUC(INS)/T) and S(I) in control participants.
CS(I) and S(I) showed high correlation (R(2) = 0.68-0.96) and regression line slopes of approximately one in the majority of groups. CS(I) tended to overestimate S(I) in type 2 diabetic participants, but results were more reliable when CS(I) was computed with insulin-modified rather than regular IVGTT. CS(I) showed behaviours similar to S(I) as regards relationships with BMI, acute insulin response and sex. CS(I) showed good correlation with M (R(2) = 0.82).
A short test can achieve a good approximation of minimal model analysis and clamp insulin sensitivity. The importance of a method such as CS(I) is that it allows analysis of IVGTT datasets with samples limited to 1 h.
Glucose turnover and its regulation were studied during and after two identical bouts of intense exhaustive exercise separated by 1 h to define differences in response. Six lean young postabsorptive male subjects exercised at approximately 100% maximal O2 uptake (3.7 +/- 0.3 l/min) for 13.0 +/- 0.7 min for the first (EX1) and 13.2 +/- 0.8 min for the second (EX2) bout. Plasma glucose increased during EX1 and peaked at 7.0 +/- 0.6 mmol/l in early recovery but to 5.8 +/- 0.5 mmol/l (P less than 0.05) after EX2, and both the hyperglycemic and the hyperinsulinemic responses were less after EX2 (P less than 0.015, analysis of variance). The hyperglycemia was due to lesser increments in glucose utilization (Rd) (3-fold resting) than glucose production (Ra) (7-fold) toward exhaustion and for 7 min of recovery. The rise in Rd was more rapid (P less than 0.05) and metabolic clearance rate was greater during (P = 0.015) and from 9 to 60 min after EX2, and Ra also remained higher during recovery (P less than 0.05). Marked and similar increments in plasma norepinephrine (18-fold) and epinephrine (14-fold) occurred with both bouts. Plasma glucagon increments were small and not different. Therefore, 1) more circulating glucose was used with EX2, 2) greater metabolic clearance rate during and after EX2 suggests local muscle adaptations due to EX1, and 3) significant correlations (P less than 0.002) between plasma norepinephrine and Ra (r = 0.82) and Ra - Rd (r = 0.52) and between epinephrine and Ra (r = 0.71) and Ra - Rd (r = 0.48) suggest a major regulatory role for the catecholamine responses.
The effects of prior high-intensity cycle exercise (85% VO2 max) to muscular exhaustion on basal and insulinstimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Six obese (30.4% fat) and six lean (14.5% fat) adult males underwent two separate, two-level hyperinsulinemic-euglycemic clamp studies (100-min infusions at 40 and 400 mU/m2/min), with and without exercise 12 h earlier. Carbohydrate oxidation was estimated by indirect calorimetry using a ventilated hood system, and endogenous glucose production by D-(3-3H)-glucose infusion. Glycogen content and glycogen synthase activity (GS %l) were measured in vastus lateralis muscle biopsies before and at the end of each insulin clamp procedure.
After exercise, the obese and lean subjects had comparably low muscle glycogen concentrations (0.10 versus 0.08 mg/g protein, respectively), and equal activation of muscle GS activity (54.4 versus 45.3 GS %l, respectively). In the obese subjects, insulin-stimulated glucose disposal was increased significantly, but not totally corrected to normal. In both groups there was a comparable increase in nonoxidative glucose disposal (NOGD), whereas glucose oxidation was decreased and lipid oxidation was increased. Thus, the major effect of prior exercise was to increase insulin-stimulated glucose disposal in the obese subjects and to alter the pathways of glucose metabolism to favor NOGD and decrease glucose oxidation.
No correlation was found between the exercise-induced increase in GS %l and NOGD, except in the normal subjects during maximal insulin stimulation. Thus, glycogen synthase activity does not appear to be ratelimiting fpr NOGD at physiologic insulin concentrations. Our findings suggest that a single bout of glycogendepleting exercise can increase glucose disposal for at least 12–14 h in obese subjects with insulin resistance.
Three methods have been used for analysis of glycogen in tissue homogenates: hydrolysis of the tissue in acid and followed by enzymic analysis of the resulting glucose; enzymic hydrolysis with amylo-α-1,4-α-1,6-glucosidase, again followed by enzymic measurement of glucose; and degradation of the glycogen with phosphorylase and debrancher complex coupled to measurement of the resulting glucose-1-P. The two enzymic procedures yielded equivalent results with all tissues examined (brain, liver, muscle and polymorphonuclear leucocytes). Acid hydrolysis of the tissues resulted in higher values for brain tissue only, presumably due to the hydrolysis of the gangliosides and cerebrosides present in brain.
After exercise, glucose uptake in tissues increases by insulin-dependent and -independent mechanisms. We evaluated whether these two effects of exercise on glucose disposal can be detected with the minimal model technique. Seven healthy volunteers were submitted at random order to two frequently sampled intravenous glucose tolerance test (FSIVGTTs), one at rest and the other 25 minutes after a 15-minute exercise test. This exercise included 5 minutes of increasing workload on a cycloergometer followed by 10 minutes at 85% of the maximal theoretic heart rate. Bergman's minimal model of insulin action was used to analyze the two FSIVGTTs and produced the following parameters: coefficient of glucose tolerance (Kg), ie, the slope of the exponential decrease in glycemia between 4 and 19 minutes after intravenous glucose; insulin sensitivity (Sl); and glucose effectiveness at basal insulin (Sg). Sg was divided into its two components: basal insulin effectiveness ([BIE] Sl x basal insulin) and glucose effectiveness at zero insulin ([GEZI] Sg-BIE). After the exercise bout, subjects had an increased Kg (3.44 +/- 0.44 v 2.06 +/- 0.28 x 10(-2).min-1, P < .02), Sl (11.43 +/- 1.27 v 6.23 +/- 0.97 x 10(-4) microU/mL.min-1, P < .01), and Sg (4.40 +/- 0.55 v 2.81 +/- 0.36 x 10(-2).min-1, P < .02). The increase in Sg was mainly explained by a 60% increase in GEZI (3.6 +/- 0.57 v 2.25 +/- 0.36 x 10(-2).min-1, P < .02), but also by an increase in BIE (0.80 +/- 0.12 v 0.47 +/- 0.08 x 10(-2).min-1, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Measures of substrate oxidation have traditionally been calculated from indirect calorimetry measurements using stoichiometric equations. Although this has proven to be a solid technique and it has become one of the standard techniques to measure whole body substrate metabolism, there are also several limitations that have to be considered. When indirect calorimetry is used during exercise most of the assumptions on which the method is based hold true although changes in the size of the bicarbonate pool at higher exercise intensities may invalidate the calculations of carbohydrate and fat oxidation. Most of the existing equations are based on stoichiometric equations of glucose oxidation and the oxidation of a triacylglycerol that is representative of human adipose tissue. However, in many exercise conditions, glycogen and not glucose is the predominant carbohydrate substrate. Therefore we propose slightly modified equations for the calculation of carbohydrate and fat oxidation for use during low to high intensity exercise. Studies that investigated fat oxidation over a wide range of intensities and that determined the exercise intensity at which fat oxidation is maximal have provided useful insights in the variation in fat oxidation between individuals and in the factors that affect fat oxidation. Fat oxidation during exercise can be influenced by exercise intensity and duration, diet, exercise training, exercise mode and gender. Although a number of important factors regulating fat oxidation have been identified, it is apparent that a considerable degree of inter-subject variability in substrate utilization persists and cannot be explained by the aforementioned factors. Future research should investigate the causes of the large inter-individual differences in fat metabolism between individuals and their links with various disease states.
Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 +/- 1 yr; peak oxygen uptake = 50 +/- 2 ml.kg(-1).min(-1)) performed 4-6 x 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by approximately 35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining (P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained approximately 20% higher compared with baseline during detraining (P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.
Low-volume 'sprint' interval training (SIT) stimulates rapid improvements in muscle oxidative capacity that are comparable to levels reached following traditional endurance training (ET) but no study has examined metabolic adaptations during exercise after these different training strategies. We hypothesized that SIT and ET would induce similar adaptations in markers of skeletal muscle carbohydrate (CHO) and lipid metabolism and metabolic control during exercise despite large differences in training volume and time commitment. Active but untrained subjects (23 +/- 1 years) performed a constant-load cycling challenge (1 h at 65% of peak oxygen uptake (.VO(2peak)) before and after 6 weeks of either SIT or ET (n = 5 men and 5 women per group). SIT consisted of four to six repeats of a 30 s 'all out' Wingate Test (mean power output approximately 500 W) with 4.5 min recovery between repeats, 3 days per week. ET consisted of 40-60 min of continuous cycling at a workload that elicited approximately 65% (mean power output approximately 150 W) per day, 5 days per week. Weekly time commitment (approximately 1.5 versus approximately 4.5 h) and total training volume (approximately 225 versus approximately 2250 kJ week(-1)) were substantially lower in SIT versus ET. Despite these differences, both protocols induced similar increases (P < 0.05) in mitochondrial markers for skeletal muscle CHO (pyruvate dehydrogenase E1alpha protein content) and lipid oxidation (3-hydroxyacyl CoA dehydrogenase maximal activity) and protein content of peroxisome proliferator-activated receptor-gamma coactivator-1alpha. Glycogen and phosphocreatine utilization during exercise were reduced after training, and calculated rates of whole-body CHO and lipid oxidation were decreased and increased, respectively, with no differences between groups (all main effects, P < 0.05). Given the markedly lower training volume in the SIT group, these data suggest that high-intensity interval training is a time-efficient strategy to increase skeletal muscle oxidative capacity and induce specific metabolic adaptations during exercise that are comparable to traditional ET.
High-intensity interval training (HIT) is a potent time-efficient strategy to induce numerous metabolic adaptations usually associated with traditional endurance training. As little as six sessions of HIT over 2 wk or a total of only approximately 15 min of very intense exercise (approximately 600 kJ), can increase skeletal muscle oxidative capacity and endurance performance and alter metabolic control during aerobic-based exercise.
The aim of this work was to quantify the magnitude of changes in insulin sensitivity (S(I)) and glucose effectiveness (S(G)) in response to acute exercise in type 2 diabetic (T2D) patients, as previously studied in non-diabetic subjects.
Seven T2D patients and seven non-diabetic controls participated in the study. Two intravenous glucose tolerance tests (0.5 g/kg) with frequent blood sampling over 180 minutes and mathematical modelling were carried out in a randomized fashion, one at rest and the other immediately following 15 minutes of exercise at 50% of the maximum theoretical heart rate (HR(max)) followed by five minutes at 85% of the HR(max). S(I) and S(G) were calculated using Bergman's minimal model.
After exercise, S(I) was increased by 773% (from 0.62+/-0.16 to 5.41+/-1.59 min(-1) x 10(-4)/(microU/mL) and even reached the zone of control values at rest (5.52+/-2.28), whereas S(G) remained unchanged. The disposition index acute insulin response (AIR(G)) x S(I) and the product of fasting insulin (I(B)) x S(I) also increased after exercise.
A single bout of exercise at moderate intensity in type 2 diabetics did not improve S(G), but markedly improved the low S(I) values found in these patients, indicating that the acute effects of exercise on S(I) are quantitatively important in the interpretation of training-related S(I) changes and may even be therapeutically useful on their own. Surrogates such as homoeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) were not sensitive enough to detect this increase in S(I) and should probably be used with caution in the follow-up of exercise protocols in diabetic patients.
Higher Insulin-sensitizing Response after
- Ortega
- Jf
Ortega JF et al. Higher Insulin-sensitizing Response after … Int J Sports Med 2015; 36: 209–214 21
- S R Colberg
- A L Albright
- B J Blissmer
- B Braun
- L Chasan-Taber
- B Fernhall
- J G Regensteiner
- R R Rubin
- R J Sigal
Colberg S R, Albright A L, Blissmer B J, Braun B, Chasan-Taber L, Fernhall
B, Regensteiner J G, Rubin R R, Sigal R J. Exercise and type 2 diabetes:
American College of Sports Medicine and the American Diabetes Association: joint position statement. Exercise and type 2 diabetes. Med
Sci Sports Exerc 2010 ; 42 : 2282-2303
Exercise intensitydependent regulation of peroxisome proliferator-activated receptor coactivator-1 mRNA abundance is associated with diff erential activation of upstream signalling kinases in human skeletal muscle
- B Egan
- B P Carson
- P M Garcia-Roves
- A V Chibalin
- Sarsfi Eld F M
- N Barron
- N Mccaff Rey
- N M Moyna
- J R Zierath
- O 'gorman
Egan B, Carson B P, Garcia-Roves P M, Chibalin A V, Sarsfi eld F M, Barron
N, McCaff rey N, Moyna N M, Zierath J R, O'Gorman D J. Exercise intensitydependent regulation of peroxisome proliferator-activated receptor
coactivator-1 mRNA abundance is associated with diff erential activation of upstream signalling kinases in human skeletal muscle. J Physiol
2010 ; 588 : 1779 -1790