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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.

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... GXT requires participants exercising to the point of volitional fatigue which results in marked elevations in BP, heart rate, cardiac output, high muscle metabolite, and heat accumulation. Those are responses that we recently reported to be increased during HIIT in comparison to MICT in MetS patients (Morales-Palomo et al. 2016). Alternatively, Tjønna and associate's (2011) work supports that a bout of HIIT is superior to MICT in lowering blood pressure because of its larger effect on improving endothelial mediated vasodilation. ...
... It is unclear if HIIT resulted in lower systolic blood pressure than MICT during those digestion hours. However, HIIT results in higher elevations in blood lactate than MICT (Morales-Palomo et al. 2016) which clearance involves the splanchnic circulation. ...
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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.
... Thus, caloric intake underreporting might have occurred. On average, caloric expenditure of the training bouts exceeded 400 kcals [39], which might not be feasible for all individuals. It is uncertain if a lesser dose of exercise would accomplish similar results. ...
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: Individuals with abdominal obesity and metabolic syndrome (MetS) have augmented risk of all-cause mortality. Lifestyle interventions are effective to treat MetS, however, there are periods during the year in which exercise programs are discontinued and improper dietary habits reappear (e.g., Christmas holidays). We aimed to analyze if exercise-training during Christmas holidays would avoid body-weight gains and cardiometabolic deterioration in MetS individuals, using a randomized control trial. Thirty-eight men with MetS undergoing exercise training were randomly allocated to either continue (TRAIN group, n = 16) or discontinue (HOLID group, n = 22) training, during the three weeks of Christmas. Anthropometrics (body weight, fat, and waist circumference), fasting blood metabolites (glucose, insulin, triglycerides, and cholesterol concentrations) and exercise maximal fat oxidation (FOMAX) and oxygen uptake (VO2PEAK) were determined before and after Christmas. Both groups were similar at baseline in all parameters (p > 0.05). HOLID group increased body weight (91.3 ± 13.0 to 92.0 ± 13.4 kg, p = 0.004), mean arterial pressure (94.0 ± 10.6 to 97.1 ± 8.9 mmHg, p = 0.026), blood insulin (10.2 ± 3.8 to 12.5 ± 5.4 µIU·mL−1, p = 0.003) and HOMA (3.2 ± 1.3 to 4.1 ± 2.3, p = 0.003). In contrast, TRAIN prevented those disarrangements and reduced total (170.6 ± 30.6 to 161.3 ± 31.3 mg·dL−1, p = 0.026) and low-density lipoprotein cholesterol (i.e., LDL-C, 104.8 ± 26.1 to 95.6 ± 21.7 mg·dL−1, p = 0.013). TRAIN also prevented the reductions in exercise FOMAX and VO2PEAK that was observed in the HOLID group (p = 0.002). In conclusion, exercise training during Christmas, prevents body weight gains and the associated cardiovascular (increase in blood pressure and LDL-C) and metabolic (reduced insulin sensitivity) health risks are an optimal non-pharmacological therapy for that period of the year.
... HR maintenance is affected by a phenomenon known as cardiovascular drift. Recent data from our laboratory with MetS individuals (41) suggest that to maintain HR target during 43 min of an HIIT session, PO and EExp must be reduced (21% and 15%, respectively) to prevent HR drift. Therefore, 4HIIT based on target HR may result in lower than expected training adaptations because of workload adjustments to avoid HR drift. ...
Article
Purpose: Continuous and interval are the two types of aerobic exercise training commonly used for health promotion. We sought to determine which aerobic exercise training program results in larger health improvements in metabolic syndrome (MetS) individuals. Methods: One hundred twenty-one MetS patients (age, 57 ± 8 yr; weight, 92 ± 15 kg; and MetS factors, 3.8 ± 0.8 components) with low initial cardiorespiratory fitness (CRF) (V˙O2peak, 24.0 ± 5.5 mL·kg·min) were randomized to undergo one of the following 16-wk exercise program: (a) 4 × 4-min high-intensity interval training at 90% of HRMAX (4HIIT group; n = 32), (b) 50-min moderate-intensity continuous training at 70% of HRMAX (MICT group; n = 35), (c) 10 × 1-min HIIT at 100% of HRMAX (1HIIT group; n = 32), or (d) no exercise control group (CONT; n = 22). We measured the evolution of all five MetS components (i.e., MetS Z Score) and CRF (assessed by V˙O2peak) before and after intervention. Results: MetS Z score decreased 41% after 4HIIT (95% confidence interval [CI], 0.25-0.06; P < 0.01) and 52% in MICT (95% CI, 0.24-0.06; P < 0.01), whereas it did not change in 1HIIT (decreased 24%; 95% CI, -0.16 to 0.03; P = 0.21) and CONT (increased 20%; 95% CI, -0.19 to 0.04; P = 0.22). However, the three exercise groups improved similarly their V˙O2peak (4HIIT, 11%; 95% CI, 0.14-0.33; MICT, 12%; 95% CI, 0.18-0.36; and 1HIIT, 14%; 95% CI, 0.21-0.40 L·min; all P < 0.001). Conclusions: Our findings suggest that in sedentary individuals with MetS and low initial CRF level any aerobic training program of 16 wk with a frequency of three times per week is sufficient stimulus to raise CRF. However, the more intense but shorter 1HIIT training program is not effective on improving MetS Z score, and thus we caution its recommendation for health promotion purposes in this population.
... The TRAIN group underwent 45 min of pedaling 3 days per week for a total of 75 sessions in 6 months. In every exercise session participants wore a heart rate monitor and workloads were self-adjusted to reach four bouts of 90% HR MAX during 4 min alternated with 3 min of active recovery periods at 70% HR MAX as described previously (Morales-Palomo et al. 2017). This AIT protocol was previously shown to both improve CRF and be tolerable in this population (Mora-Rodriguez et al. 2014Stensvold et al. 2010). ...
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PurposeThe aim of this study was to determine the effects of high-intensity aerobic interval training (AIT) on exercise hemodynamics in metabolic syndrome (MetS) volunteers. Methods Thirty-eight, MetS participants were randomly assigned to a training (TRAIN) or to a non-training control (CONT) group. TRAIN consisted of stationary interval cycling alternating bouts at 70–90% of maximal heart rate during 45 min day−1 for 6 months. ResultsCONT maintained baseline physical activity and no changes in cardiovascular function or MetS factors were detected. In contrast, TRAIN increased cardiorespiratory fitness (14% in VO2PEAK; 95% CI 9–18%) and improved metabolic syndrome (−42% in Z score; 95% CI 83–1%). After TRAIN, the workload that elicited a VO2 of 1500 ml min−1 increased 15% (95% CI 5–25%; P < 0.001). After TRAIN when subjects pedaled at an identical submaximal rate of oxygen consumption, cardiac output increased by 8% (95% CI 4–11%; P < 0.01) and stroke volume by 10% (95% CI, 6–14%; P < 0.005) being above the CONT group values at that time point. TRAIN reduced submaximal exercise heart rate (109 ± 15–106 ± 13 beats min−1; P < 0.05), diastolic blood pressure (83 ± 8–75 ± 8 mmHg; P < 0.001) and systemic vascular resistances (P < 0.01) below CONT values. Double product was reduced only after TRAIN (18.2 ± 3.2–17.4 ± 2.4 bt min−1 mmHg 10−3; P < 0.05). Conclusions The data suggest that intense aerobic interval training improves hemodynamics during submaximal exercise in MetS patients. Specifically, it reduces diastolic blood pressure, systemic vascular resistances, and the double product. The reduction in double product, suggests decreased myocardial oxygen demands which could prevent the occurrence of adverse cardiovascular events during exercise in this population. Clinicaltrials.gov identifierNCT03019796.
... Training consisted on pedaling for 10 min as warm up at 70% of maximal heart rate (HR max ) followed by 4 Â 4-min intervals at 90% of HR max interspersed with 3-min active recovery at 70% HR max and a 5-min cool-down period for a total of 43-min workout. Exercise intensity was increased as training adaptations developed to maintain target heart rate (HR) ( [20], Seego; Realtrack Systems, Almeria, Spain). Participants were required to attend at least 90% of all the exercise sessions. ...
Article
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.
Article
Background Statins reduce atherogenic dyslipidemia and cardiovascular disease (CVD) risk in metabolic syndrome individuals (MetS). Exercise-training could also contribute to reduce CVD by improving cardiorespiratory fitness and fat oxidation. However, statin use could interfere with training adaptations. Methods One hundred and six MetS were divided into statin users (STATIN group, n=46) and statin-naïve (CONTROL group, n=60). Groups were matched by age, weight, and MetS components. Subjects completed 16 weeks of high intensity interval training (HIIT). Before and after HIIT, muscle biopsies were collected to assess mitochondrial content (citrate synthase (CS) activity) and the activity of the rate limiting β-oxidation enzyme (3-hydroxyacyl-CoA-dehydrogenase (HAD)). Fasting plasma glucose, insulin, TG, HDL-c and LDL-c concentrations were measured. Exercise maximal fat oxidation (FOMAX) and oxygen uptake (VO2PEAK) were determined. Results Training improved MetS similarly in both groups (MetS Z-score -0.26±0.38 vs -0.22±0.31; P<0.001 for time and P=0.60 for time x group). Before training, STATIN had reduced muscle HAD activity and whole body FOMAX compared to CONTROL. However, 16-weeks of HIIT increased HAD and FOMAX in both groups (P<0.03, time-effect). STATIN did not prevent the increases in CS with HIIT observed in CONTROL (38% vs 64%, respectively; P<0.001, time-effect). Conversely, with training VO2PEAK improved less in STATIN than in CONTROL (12% vs 19%, respectively; P=0.013, time x group effect). Conclusion Chronic statin use in MetS does not interfere with exercise training improvements in MetS components, FOMAX or mitochondrial muscle enzymes (i.e., CS and HAD). However, STATIN attenuated the improvements in VO2PEAK with training.
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An increased "dose" of endurance exercise training is associated with a greater maximal oxygen uptake (VO2max), a larger left ventricular (LV) mass, and improved heart rate and blood pressure control. However, the effect of lifelong exercise dose on metabolic and hemodynamic response during exercise has not been previously examined. Methods and Results: We performed a cross-sectional study on 101 (69 men) seniors (60 yr and older) focusing on lifelong exercise frequency as an index of exercise dose. These included 27 who had performed ≤2 exercise sessions/wk (sedentary), 25 who performed 2-3 sessions/wk (casual), 24 who performed 4-5 sessions/wk (committed) and 25 who performed ≥6 sessions/wk plus regular competitions (Masters athletes) over at least the last 25 yr. Oxygen uptake and hemodynamics (cardiac output [Qc], stroke volume [SV]) were collected at rest, two levels of steady-state submaximal exercise and maximal exercise. Doppler ultrasound measures of LV diastolic filling were assessed at rest and during LV loading (saline infusion) to simulate increased LV filling. Body composition, total blood volume, and heart-rate recovery after maximal exercise were also examined. VO2max increased in a dose-dependent manner (P<0.05). At maximal exercise, Qc and SV were largest in committed exercisers and Masters athletes (P<0.05), while arteriovenous oxygen difference was greater in all trained groups (P<0.05). At maximal exercise, effective arterial elastance, an index of ventricular-arterial coupling, was lower in committed exercisers and Masters athletes (P<0.05). Doppler measures of LV filling were not enhanced at any condition irrespective of lifelong exercise frequency. Conclusion: These data suggest that performing 4 or more weekly endurance exercise sessions over a lifetime results in significant gains in VO2max, SV and heart rate regulation during exercise; however, improved SV regulation during exercise is not coupled with favorable effects on LV filling, even when the heart is fully loaded.
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Different muscle recruitment patterns during cycling and walking may influence the magnitude of cardiovascular drift (CV drift) during these respective modes of exercise, but whether this also influences the magnitude of reduced maximal oxygen uptake (Vo2max) associated with CV drift is unknown.This study tested the hypothesis that cycling results in greater CV drift and a greater decrement in Vo2max than walking in a temperate environment. CV drift was measured in nine recreationally active women (ages = 23 +/- 2 yr, Vo2max = 43.0 +/- 5.5 ml x kg(-1) x min(-1)) between 15 and 45 min of cycling or walking at 60% Vo2max on Separate occasions in 22 degrees C, 44% relative humidity. A graded exercise test to measure Vo2max was performed immediately after the submaximal exercise bout with no cessation of exercise. During separate trials involving each exercise mode, Vo2max was measured after 15 min of submaximal exercise so that changes in Vo2max between 15 and 45 min of exercise could be assessed between the same points in time in which CV drift occurred. Across both conditions, heart rate (HR) increased 5.4% and stroke volume (SV) decreased 11% from 15 to 45 min, but Vo2max was not significantly affected (7% reduction; 2.70 +/- 0.5 L min(-1) vs. 2.52 +/- 0.6 L min(-1)). In a temperate environment, a small CV drift corresponds to a small, non-significant decrease in Vo2max, regardless of whether the exercise performed is cycling or walking.
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The purpose of this Position Stand is to provide guidance to professionals who counsel and prescribe individualized exercise to apparently healthy adults of all ages. These recommendations also may apply to adults with certain chronic diseases or disabilities, when appropriately evaluated and advised by a health professional. This document supersedes the 1998 American College of Sports Medicine (ACSM) Position Stand, "The Recommended Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory and Muscular Fitness, and Flexibility in Healthy Adults." The scientific evidence demonstrating the beneficial effects of exercise is indisputable, and the benefits of exercise far outweigh the risks in most adults. A program of regular exercise that includes cardiorespiratory, resistance, flexibility, and neuromotor exercise training beyond activities of daily living to improve and maintain physical fitness and health is essential for most adults. The ACSM recommends that most adults engage in moderate-intensity cardiorespiratory exercise training for ≥30 min·d on ≥5 d·wk for a total of ≥150 min·wk, vigorous-intensity cardiorespiratory exercise training for ≥20 min·d on ≥3 d·wk (≥75 min·wk), or a combination of moderate- and vigorous-intensity exercise to achieve a total energy expenditure of ≥500-1000 MET·min·wk. On 2-3 d·wk, adults should also perform resistance exercises for each of the major muscle groups, and neuromotor exercise involving balance, agility, and coordination. Crucial to maintaining joint range of movement, completing a series of flexibility exercises for each the major muscle-tendon groups (a total of 60 s per exercise) on ≥2 d·wk is recommended. The exercise program should be modified according to an individual's habitual physical activity, physical function, health status, exercise responses, and stated goals. Adults who are unable or unwilling to meet the exercise targets outlined here still can benefit from engaging in amounts of exercise less than recommended. In addition to exercising regularly, there are health benefits in concurrently reducing total time engaged in sedentary pursuits and also by interspersing frequent, short bouts of standing and physical activity between periods of sedentary activity, even in physically active adults. Behaviorally based exercise interventions, the use of behavior change strategies, supervision by an experienced fitness instructor, and exercise that is pleasant and enjoyable can improve adoption and adherence to prescribed exercise programs. Educating adults about and screening for signs and symptoms of CHD and gradual progression of exercise intensity and volume may reduce the risks of exercise. Consultations with a medical professional and diagnostic exercise testing for CHD are useful when clinically indicated but are not recommended for universal screening to enhance the safety of exercise.
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Our purpose was to examine the effects of sprint interval training on muscle glycolytic and oxidative enzyme activity and exercise performance. Twelve healthy men (22 +/- 2 yr of age) underwent intense interval training on a cycle ergometer for 7 wk. Training consisted of 30-s maximum sprint efforts (Wingate protocol) interspersed by 2-4 min of recovery, performed three times per week. The program began with four intervals with 4 min of recovery per session in week 1 and progressed to 10 intervals with 2.5 min of recovery per session by week 7. Peak power output and total work over repeated maximal 30-s efforts and maximal oxygen consumption (VO2 max) were measured before and after the training program. Needle biopsies were taken from vastus lateralis of nine subjects before and after the program and assayed for the maximal activity of hexokinase, total glycogen phosphorylase, phosphofructokinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase. The training program resulted in significant increases in peak power output, total work over 30 s, and VO2 max. Maximal enzyme activity of hexokinase, phosphofructokinase, citrate synthase, succinate dehydrogenase, and malate dehydrogenase was also significantly (P < 0.05) higher after training. It was concluded that relatively brief but intense sprint training can result in an increase in both glycolytic and oxidative enzyme activity, maximum short-term power output, and VO2 max.
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This Position Stand provides guidance on fluid replacement to sustain appropriate hydration of individuals performing physical activity. The goal of prehydrating is to start the activity euhydrated and with normal plasma electrolyte levels. Prehydrating with beverages, in addition to normal meals and fluid intake, should be initiated when needed at least several hours before the activity to enable fluid absorption and allow urine output to return to normal levels. The goal of drinking during exercise is to prevent excessive (>2% body weight loss from water deficit) dehydration and excessive changes in electrolyte balance to avert compromised performance. Because there is considerable variability in sweating rates and sweat electrolyte content between individuals, customized fluid replacement programs are recommended. Individual sweat rates can be estimated by measuring body weight before and after exercise. During exercise, consuming beverages containing electrolytes and carbohydrates can provide benefits over water alone under certain circumstances. After exercise, the goal is to replace any fluid electrolyte deficit. The speed with which rehydration is needed and the magnitude of fluid electrolyte deficits will determine if an aggressive replacement program is merited.
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Individuals with the metabolic syndrome are 3 times more likely to die of heart disease than healthy counterparts. Exercise training reduces several of the symptoms of the syndrome, but the exercise intensity that yields the maximal beneficial adaptations is in dispute. We compared moderate and high exercise intensity with regard to variables associated with cardiovascular function and prognosis in patients with the metabolic syndrome. Thirty-two metabolic syndrome patients (age, 52.3+/-3.7 years; maximal oxygen uptake [o(2)max], 34 mL x kg(-1) x min(-1)) were randomized to equal volumes of either moderate continuous moderate exercise (CME; 70% of highest measured heart rate [Hfmax]) or aerobic interval training (AIT; 90% of Hfmax) 3 times a week for 16 weeks or to a control group. o(2)max increased more after AIT than CME (35% versus 16%; P<0.01) and was associated with removal of more risk factors that constitute the metabolic syndrome (number of factors: AIT, 5.9 before versus 4.0 after; P<0.01; CME, 5.7 before versus 5.0 after; group difference, P<0.05). AIT was superior to CME in enhancing endothelial function (9% versus 5%; P<0.001), insulin signaling in fat and skeletal muscle, skeletal muscle biogenesis, and excitation-contraction coupling and in reducing blood glucose and lipogenesis in adipose tissue. The 2 exercise programs were equally effective at lowering mean arterial blood pressure and reducing body weight (-2.3 and -3.6 kg in AIT and CME, respectively) and fat. Exercise intensity was an important factor for improving aerobic capacity and reversing the risk factors of the metabolic syndrome. These findings may have important implications for exercise training in rehabilitation programs and future studies.
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Exercise intensity can be prescribed using a variety of indices, such as rating of perceived exertion, heart rate, levels of absolute intensity (e.g., metabolic equivalents), and levels of relative intensity [e.g., percentage of maximal aerobic capacity (% V ˙ O 2 m a x ) or percentage of oxygen uptake reserve (% V ˙ O 2 R )]. Heart rate has a linear relationship with oxygen uptake, is easy to measure, and requires relatively inexpensive monitoring equipment, so it is commonly used to monitor exercise intensity. During heat stress, however, cardiovascular adjustments - including a rise in heart rate that is disproportionate to absolute intensity - result in diminished aerobic capacity and performance. These adjustments include cardiovascular drift, the progressive rise in heart rate and fall in stroke volume over time during prolonged, constant-rate exercise. A variety of factors have been shown to modulate the magnitude of cardiovascular drift, e.g., hyperthermia, dehydration, exercise intensity, and ambient temperature. Regardless of the mode of manipulation, decreases in stroke volume with cardiovascular drift are associated with proportionally similar decreases in V ˙ O 2 m a x , which affects the relationship between heart rate and relative metabolic intensity (% V ˙ O 2 m a x or % V ˙ O 2 R ). This review summarizes the current state of knowledge regarding the influence of cardiovascular drift and reduced V ˙ O 2 m a x on exercise intensity prescription in hot conditions. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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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.
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Several techniques assessing cardiac output (Q) during exercise are available. The extent to which the measurements obtained from each respective technique compares to one another, however, is unclear. We quantified Q simultaneously using four methods: the Fick method with blood obtained from the right atrium (QFick-M), Innocor (inert gas rebreathing; QInn), Physioflow (impedance cardiography; QPhys), and Nexfin (pulse contour analysis; QPulse) in 12 male subjects during incremental cycling exercise to exhaustion in normoxia and hypoxia (FiO2 = 12%). While all four methods reported a progressive increase in Q with exercise intensity, the slopes of the Q/oxygen uptake (VO2) relationship differed by up to 50% between methods in both normoxia [4.9 ± 0.3, 3.9 ± 0.2, 6.0 ± 0.4, 4.8 ± 0.2 L/min per L/min (mean ± SE) for QFick-M, QInn, QPhys and QPulse, respectively; P = 0.001] and hypoxia (7.2 ± 0.7, 4.9 ± 0.5, 6.4 ± 0.8 and 5.1 ± 0.4 L/min per L/min; P = 0.04). In hypoxia, the increase in the Q/VO2 slope was not detected by Nexfin. In normoxia, Q increases by 5–6 L/min per L/min increase in VO2, which is within the 95% confidence interval of the Q/VO2 slopes determined by the modified Fick method, Physioflow, and Nexfin apparatus while Innocor provided a lower value, potentially reflecting recirculation of the test gas into the pulmonary circulation. Thus, determination of Q during exercise depends significantly on the applied method.
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Background and Aims Exercise training can improve health of patients with metabolic syndrome (MetS). However, which MetS factors are most responsive to exercise training remains unclear. We studied the time-course of changes in MetS factors in response to training and detraining. Methods and Results Forty eight MetS patients (52±8.8 yrs old; 33±4 BMI) underwent 4 months (3 days/week) of supervised aerobic interval training (AIT) program. After 1 month of training, there were progressive increases in high density lipoprotein cholesterol (HDL-c) and reductions in waist circumference and blood pressure (12±3%, -3.9±0.4, and -12±1, respectively after 4 months; all P<0.05). However, fasting plasma concentration of triglycerides and glucose were not reduced by training. Insulin sensitivity (HOMA), cardiorespiratory fitness (VO2peak) and exercise maximal fat oxidation (FOMAX) also progressively improved with training (-17±5; 21±2 and 31±8%, respectively, after 4 months; all P<0.05). Vastus lateralis samples from seven subjects revealed that mitochondrial O2 flux was markedly increased with training (71±11%) due to increased mitochondrial content. After 1 month of detraining, the training-induced improvements in waist circumference and blood pressure were maintained. HDL-c and VO2peak returned to the values found after 1-2 months of training while HOMA and FOMAX returned to pre-training values. Conclusions The health related variables most responsive to aerobic interval training in MetS patients are waist circumference, blood pressure and the muscle and systemic adaptations to consume oxygen and fat. However, the latter reverse with detraining while blood pressure and waist circumference are persistent to one month of detraining.
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To obtain optimal training effects and avoid overtraining, it is necessary to monitor the intensity of training. In cycling, speed is not an accurate indicator of exercise intensity, and therefore alternatives have to be found to monitor exercise intensity during training and competition. Power output may be the most direct indicator, but heart rate is easier to monitor and measure. There are, however, limitations that have to be taken into account when using a heart rate monitor. For example, the position on the bicycle may change heart rate at a given exercise intensity. More important, however, is the increase in heart rate over time, a phenomenon described as 'cardiac drift'. Cardiac drift can change the heart rate-power output relationship drastically, especially in hot environments or at altitude. It is important to determine whether one is interested in monitoring exercise intensity per se or measuring whole-body stress. Power output may be a better indicator of the former and heart rate may, under many conditions, be a better indicator of the latter. Heart rate can be used to evaluate a cyclist after training or competition, or to determine the exercise intensity during training. Heart rate monitoring is very useful in the detection of early overtraining, especially in combination with lactate curves and questionnaires. During overtraining, maximal heart rates as well as submaximal heart rates may be decreased, while resting and, in particular, sleeping - heart rates may be increased.
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It has been proposed that self-paced exercise in the heat is regulated by an anticipatory reduction in work rate based on the rate of heat storage. However, performance may be impaired by the development of hyperthermia and concomitant rise in cardiovascular strain increasing relative exercise intensity. This study evaluated the influence of thermal strain on cardiovascular function and power output during self-paced exercise in the heat. Eight endurance-trained cyclists performed a 40 km simulated time trial in hot (35°C) and thermoneutral conditions (20°C), while power output, mean arterial pressure, heart rate, oxygen uptake and cardiac output were measured. Time trial duration was 64.3 ± 2.8 min (242.1 W) in the hot condition and 59.8 ± 2.6 min (279.4 W) in the thermoneutral condition (P < 0.01). Power output in the heat was depressed from 20 min onwards compared with exercise in the thermoneutral condition (P < 0.05). Rectal temperature reached 39.8 ± 0.3 (hot) and 38.9 ± 0.2°C (thermoneutral; P < 0.01). From 10 min onwards, mean skin temperature was ~7.5°C higher in the heat, and skin blood flow was significantly elevated (P < 0.01). Heart rate was ~8 beats min(-1) higher throughout hot exercise, while stroke volume, cardiac output and mean arterial pressure were significantly depressed compared with the thermoneutral condition (P < 0.05). Peak oxygen uptake measured during the final kilometre of exercise at maximal effort reached 77 (hot) and 95% (thermoneutral) of pre-experimental control values (P < 0.01). We conclude that a thermoregulatory-mediated rise in cardiovascular strain is associated with reductions in sustainable power output, peak oxygen uptake and maximal power output during prolonged, intense self-paced exercise in the heat.
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Exercise testing remains a remarkably durable and versatile tool that provides valuable diagnostic and prognostic information regarding patients with cardiovascular and pulmonary disease. Exercise testing has been available for more than a half century and, like many other cardiovascular procedures, has evolved in its technology and scope. When combined with exercise testing, adjunctive imaging modalities offer greater diagnostic accuracy, additional information regarding cardiac structure and function, and additional prognostic information. Similarly, the addition of ventilatory gas exchange measurements during exercise testing provides a wide array of unique and clinically useful incremental information that heretofore has been poorly understood and underutilized by the practicing clinician. The reasons for this are many and include the requirement for additional equipment (cardiopulmonary exercise testing [CPX] systems), personnel who are proficient in the administration and interpretation of these tests, limited or absence of training of cardiovascular specialists and limited training by pulmonary specialists in this technique, and the lack of understanding of the value of CPX by practicing clinicians. Modern CPX systems allow for the analysis of gas exchange at rest, during exercise, and during recovery and yield breath-by-breath measures of oxygen uptake (V̇o2), carbon dioxide output (V̇co2), and ventilation (V̇e). These advanced computerized systems provide both simple and complex analyses of these data that are easy to retrieve and store, which makes CPX available for widespread use. These data can be readily integrated with standard variables measured during exercise testing, including heart rate, blood pressure, work rate, electrocardiography findings, and symptoms, to provide a comprehensive assessment of exercise tolerance and exercise responses. CPX can even be performed with adjunctive imaging modalities for additional diagnostic assessment. Hence, CPX offers the clinician the ability to obtain a wealth of information beyond standard exercise electrocardiography testing that when appropriately applied and interpreted …
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Cardiac output represents the primary determinant of cardiovascular function. Therefore, understanding how cardiac output is regulated during exercise is crucial. A recently developed tool for determining cardiac output is the Innocor rebreathing system, which also incorporates an ergospirometry unit. So far, Innocor's test-retest reliability under exercise conditions has not been determined in healthy participants. Therefore, 15 male and 15 female healthy participants [30.6 y (SD 4.5); 68.0 kg (SD 10.5)] performed 2 test sessions, each consisting of 2 graded exercise tests to volitional exhaustion. We determined intra- and inter-session reliability of cardiac output, oxygen consumption, carbon dioxide output, and ventilation at 130 W and at peak exercise. For cardiac output, we found averaged coefficients of variation ranging from 4.3 (intra-session, 130 W) to 10.0% (inter-session, rest). For oxygen consumption, coefficients of variation ranged from 3.4 (intra-session, peak) to 5.7% (inter-session, peak). Coefficients of variation for carbon dioxide output were between 4.4 (intra-session, peak) and 6.6% (inter-session, peak), and for ventilation between 5.1 (intra-session, 130 W) and 7.0% (intra-session, peak). Innocor delivers safe and reliable measurements of cardiac output, gas exchange, and ventilation. Therefore, Innocor can be used to assess these parameters in exercise physiology studies as well as in performance diagnostics.
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In previously sedentary individuals, regularly performed aerobic exercise results in significant improvements in exercise capacity. The development of peak exercise performance, as typified by competitive endurance athletes, is dependent upon several months to years of aerobic training. The physiological adaptations associated with these improvements in both maximal exercise performance, as reflected by increases in maximal oxygen uptake (V̇O2max), and submaximal exercise endurance include increases in both cardiovascular function and skeletal muscle oxidative capacity. Despite prolonged periods of aerobic training, reductions in maximal and submaximal exercise performance occur within weeks after the cessation of training. These losses in exercise performance coincide with declines in cardiovascular function and muscle metabolic potential. Significant reductions in V̇O2max have been reported to occur within 2 to 4 weeks of detraining. This initial rapid decline in V̇O2max is likely related to a corresponding fall in maximal cardiac output which, in turn, appears to be mediated by a reduced stroke volume with little or no change in maximal heart rate. A loss in blood volume appears to, at least partially, account for the decline in stroke volume and V̇O2max during the initial weeks of detraining, although changes in cardiac hypertrophy, total haemoglobin content, skeletal muscle capillarisation and temperature regulation have been suggested as possible mediating factors. When detraining continues beyond 2 to 4 weeks, further declines in V̇O2max appear to be a function of corresponding reductions in maximal arterial-venous (mixed) oxygen difference. Whether reductions in oxygen delivery to and/or extraction by working muscle regulates this progressive decline is not readily apparent. Changes in maximal oxygen delivery may result from decreases in total haemoglobin content and/or maximal muscle blood flow and vascular conductance. The declines in skeletal muscle oxidative enzyme activity observed with detraining are not causally linked to changes in V̇O2max but appear to be functionally related to the accelerated carbohydrate oxidation and lactate production observed during exercise at a given intensity. Alternatively, reductions in submaximal exercise performance may be related to changes in the mean transit time of blood flow through the active muscle and/or the thermore-gulatory response (i.e. degree of thermal strain) to exercise. In contrast to the responses observed with detraining, currently available research indicates that the adaptations to aerobic training may be retained for at least several months when training is maintained at a reduced level. Reductions of one- to two-thirds in training frequency and/or duration do not significantly alter V̇O2max or submaximal endurance time provided the intensity of each exercise session is maintained. Conversely, a decrease of one- to two-thirds in exercise training intensity, despite a maintenance of training frequency and duration, reduces both V̇O2max and submaximal endurance time. Thus, it appears that exercise intensity is the principal component necessary to maintain a training-induced increase in V̇O2max and submaximal exercise endurance during periods of reduced training. It is suggested that the maintenance of V̇O2max with reduced training frequency and/or duration may be related to a retention of blood volume. When exercise training intensity is reduced, however, it is possible that the stimulus mediating the relative hypervolaemia observed with aerobic training may be attenuated, thereby accounting for the corresponding decrease in V̇O2max. However, the interactions of possible changes in cardiac hypertrophy and contractility, thermoregulatory strain, total haemoglobin content, capillary density, mean transit time, and skeletal muscle oxidative capacity in relation to changes in V̇O2max and submaximal endurance time with reduced training and detraining warrant further study.
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The purpose of this study was to compare the effects of exercise and/or caloric restriction for 12 wk on body composition, maximal aerobic power (VO2max), and serum lipids and lipoproteins in overweight individuals. Forty-eight males and 48 females (means age = 36.6 yr), 120-140% of ideal body weight, were randomly assigned to groups (N = 12 each) of diet-exercise (DE), diet (D), exercise (E), and sedentary control (C). The dietary regimen consisted of 1,200 kcal X d-1, while exercise consisted of 5 d X wk-1 of 30 min of walk/running. For the males, body weight (BW) and fat weight loss in the DE group (-11.8 and 23%, respectively) were significantly greater than in the D group (-9.1 and -18%), with both groups significantly greater than for E and C. In the females, BW and fat weight loss for DE (-10.4 and -24%) were significantly greater than for D (-7.8 and -20%), with both groups significantly greater than E and C. Both DE and D males and females had a decrease in fat-free weight of -4.5 and -2.4%, respectively. In both sexes, the increase in VO2max-BW (ml X kg -1 X min-1) in DE (25%) was significantly greater than for E (15%), D (11%), and C (0%), with differences between E and D nonsignificant. However, increases in absolute VO2max (1 X min-1) and VO2max-fat-free weight (ml X kg-1 X min-1) were similar (P greater than 0.05) for DE and E (14%) but significantly greater compared to D and C (2%).(ABSTRACT TRUNCATED AT 250 WORDS)
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The involvement of changes in sympathetic activity, changes in cardiac efferent vagal activity, and nonautonomic mechanisms in producing the rise in heart rate (HR) during heat stress-induced hyperthermia was studied in seven unanesthetized, chronically instrumented baboons (Papio anubis and P. cynocephalus). The experimental protocol consisted of subjecting the baboon to environmental heating (EH) of sufficient intensity (40-45 degrees C) to raise arterial blood temperature (Tbl) 2-3 degrees C in 1-2 h while in one of four states: 1) normal (control), 2) beta-adrenergic receptor blockade induced by propranolol, 3) cholinergic receptor blockade induced by atropine, and 4) combined beta- and cholinergic receptor blockade induced by propranolol and atropine together. HR rose linearly with Tbl during EH in all four states (correlation coefficient greater than or equal to 0.97 in all cases) with average HR-Tbl regression coefficients (slopes) being 20.5 +/- 1.2 (SE) beats X min-1 . degrees C for the normal state, 12.2 +/- 0.5 beats X min-1 . degrees C-1 for the beta-blockade state, 13.3 +/- 1.1 beats X min-1 . degrees C for the cholinergic blockade state, and 8.4 +/- 0.8 beats X min-1 . degrees C-1 for the combined beta- and cholinergic receptor blockade state. Thus nonautonomic mechanisms account for about 40% of the tachycardia in heat-stressed baboons with the remaining 60% produced by combined vagal withdrawal and sympathetic activation. Furthermore application of a multiplicative model of autonomic control of HR to these data suggests that about 75% of the autonomic component is produced by vagal withdrawal.
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This study determined whether the decline in stroke volume (SV) during prolonged exercise is related to an increase in heart rate (HR) and/or an increase in cutaneous blood flow (CBF). Seven active men cycled for 60 min at approximately 57% peak O2 uptake in a neutral environment (i.e., 27 degrees C, <40% relative humidity). They received a placebo control (CON) or a small oral dose (i.e., approximately 7 mg) of the beta1-adrenoceptor blocker atenolol (BB) at the onset of exercise. At 15 min, HR and SV were similar during CON and BB. From 15 to 55 min during CON, a 13% decline in SV was associated with an 11% increase in HR and not with an increase in CBF. CBF increased mainly from 5 to 15 min and remained stable from 20 to 60 min of exercise in both treatments. However, from 15 to 55 min during BB, when the increase in HR was prevented by atenolol, the decline in SV was also prevented, despite a normal CBF response (i.e., similar to CON). Cardiac output was similar in both treatments and stable throughout the exercise bouts. We conclude that during prolonged exercise in a neutral environment the decline in SV is related to the increase in HR and is not affected by CBF.
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Recent investigations have demonstrated that at the onset of low-to-moderate-intensity leg cycling exercise (L) the carotid baroreflex (CBR) was classically reset in direct relation to the intensity of exercise. On the basis of these data, we proposed that the CBR would also be classically reset at the onset of moderate- to maximal-intensity L exercise. Therefore, CBR stimulus-response relationships were compared in seven male volunteers by using the neck pressure-neck suction technique during dynamic exercise that ranged in intensity from 50 to 100% of maximal oxygen uptake (VO(2 max)). L exercise alone was performed at 50 and 75% VO(2 max), and L exercise combined with arm (A) exercise (L + A) was performed at 75 and 100% VO(2 max). O(2) consumption and heart rate (HR) increased in direct relation with the increases in exercise intensity. The threshold and saturation pressures of the carotid-cardiac reflex at 100% VO(2 max) were >75% VO(2 max), which were in turn >50% VO(2 max) (P < 0.05), without a change in the maximal reflex gain (G(max)). In addition, the HR response value at threshold and saturation at 75% VO(2 max) was >50% VO(2 max) (P < 0.05) and 100% VO(2 max) was >75% VO(2 max) (P < 0.07). Similar changes were observed for the carotid-vasomotor reflex. In addition, as exercise intensity increased, the operating point (the prestimulus blood pressure) of the CBR was significantly relocated further from the centering point (G(max)) of the stimulus-response curve and was at threshold during 100% VO(2 max). These findings identify the continuous classic rightward and upward resetting of the CBR, without a change in G(max), during increases in dynamic exercise intensity to maximal effort.
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This study was designed to evaluate the stability of target heart rate (HR) values corresponding to performance markers such as lactate threshold (LT) and the first and second ventilatory thresholds (VT1, VT2) in a group of 13 professional road cyclists (VO2max, approximately 75.0 mL x kg(-1) x min(-1)) during the course of a complete sports season. Each subject performed a progressive exercise test on a bicycle ergometer (ramp protocol with workload increases of 25 W x min(-1)) three times during the season corresponding to the "active" rest (fall: November), precompetition (winter: January), and competition periods (spring: May) to determine HR values at LT, VT1 and VT2. Despite a significant improvement in performance throughout the training season (i.e., increases in the power output eliciting LT, VT1, or VT2), target HR values were overall stable (HR at LT: 154 +/- 3, 152 +/- 3, and 154 +/- 2 beats x min(-1); HR at VT1: 155 +/- 3, 156 +/- 3, and 159 +/- 3 beats x min(-1); and at VT2: 178 +/- 2, 173 +/- 3, and 176 +/- 2 beats x min(-1) during rest, precompetition, and competition periods, respectively). A single laboratory testing session at the beginning of the season might be sufficient to adequately prescribe training loads based on HR data in elite endurance athletes such as professional cyclists. This would simplify the testing schedule generally used for this type of athlete.
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On the basis of an analysis of the skin temperature data on three resting human subjects from 112 experiments, a simple weighting system for computing the mean skin temperature from observations on four areas of the body, namely, chest, arms, thighs, and legs, has been proposed. The proposed system of weighting yields mean skin temperature values identical with the elaborate Hardy-Dubois weighting formula. The value of the medial thigh temperature as an index of the mean skin temperature has also been investigated and discussed. skin temperature measurement Submitted on May 20, 1963
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Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint-interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 +/- 1 years, ) were assigned to a SIT or ET group (n = 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s 'all out' cycling at approximately 250% with 4 min recovery (SIT) or 90-120 min continuous cycling at approximately 65% (ET). Training time commitment over 2 weeks was approximately 2.5 h for SIT and approximately 10.5 h for ET, and total training volume was approximately 90% lower for SIT versus ET ( approximately 630 versus approximately 6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P </= 0.05). Biopsy samples obtained before and after training revealed similar increases in muscle oxidative capacity, as reflected by the maximal activity of cytochrome c oxidase (COX) and COX subunits II and IV protein content (main effects, P </= 0.05), but COX II and IV mRNAs were unchanged. Training-induced increases in muscle buffering capacity and glycogen content were also similar between groups (main effects, P </= 0.05). Given the large difference in training volume, these data demonstrate that SIT is a time-efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance that are comparable to ET in young active men.
Article
The present study compared the effects of aerobic endurance training at different intensities and with different methods matched for total work and frequency. Responses in maximal oxygen uptake (VO2max), stroke volume of the heart (SV), blood volume, lactate threshold (LT), and running economy (CR) were examined. Forty healthy, nonsmoking, moderately trained male subjects were randomly assigned to one of four groups:1) long slow distance (70% maximal heart rate; HRmax); 2)lactate threshold (85% HRmax); 3) 15/15 interval running (15 s of running at 90-95% HRmax followed by 15 s of active resting at 70% HRmax); and 4) 4 x 4 min of interval running (4 min of running at 90-95% HRmax followed by 3 min of active resting at 70%HRmax). All four training protocols resulted in similar total oxygen consumption and were performed 3 d.wk for 8 wk. High-intensity aerobic interval training resulted in significantly increased VO2max compared with long slow distance and lactate-threshold training intensities (P<0.01). The percentage increases for the 15/15 and 4 x 4 min groups were 5.5 and 7.2%, respectively, reflecting increases in V O2max from 60.5 to 64.4 mL x kg(-1) x min(-1) and 55.5 to 60.4 mL x kg(-1) x min(-1). SV increased significantly by approximately 10% after interval training (P<0.05). : High-aerobic intensity endurance interval training is significantly more effective than performing the same total work at either lactate threshold or at 70% HRmax, in improving VO2max. The changes in VO2max correspond with changes in SV, indicating a close link between the two.
Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention
  • K G Alberti
  • R H Eckel
  • S M Grundy
Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute;
American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity
American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):1640-5.