Literature examining the effects of aerobic exercise training on excess postexercise oxygen consumption (EPOC) is sparse. In this study, 9 male participants (19–32 yr) trained (EX) for 12 wk, and 10 in a control group (CON) maintained normal activity. VO2max, rectal temperature (Tre), epinephrine, norepinephrine, free fatty acids (FFA), insulin, glucose, blood lactate (BLA), and EPOC were measured before (PRE) and after (POST) the intervention. EPOC at PRE was measured for 120 min after 30 min of treadmill running at 70% VO2max. EX completed 2 EPOC trials at POST, i.e., at the same absolute (ABS) and relative (REL) intensity; 1 EPOC test for CON served as both the ABS and REL trial because no significant change in VO2max was noted. During the ABS trial, total EPOC decreased significantly (p < .01) from PRE (39.4 ± 3.6 kcal) to POST (31.7 ± 2.2 kcal). Tre, epinephrine, insulin, glucose, and BLA at end-exercise or during recovery were significantly lower and FFA significantly higher after training. Training did not significantly affect EPOC during the REL trial; however, epinephrine was significantly lower, and norepinephrine and FFA, significantly higher, at endexercise after training. Results indicate that EPOC varies as a function of relative rather than absolute metabolic stress and that training improves the efficiency of metabolic regulation during recovery from exercise. Mechanisms for the decreased magnitude of EPOC in the ABS trial include decreases in BLA, Tre, and perhaps epinephrine-mediated hepatic glucose production and insulin-mediated glucose uptake.
Darlene A. Sedlock, Man-Gyoon Lee, Michael G. Flynn, Kyung-Shin Park and Gary H. Kamimori
Amy Warren, Erin J. Howden, Andrew D. Williams, James W. Fell and Nathan A. Johnson
Postexercise fat oxidation may be important for exercise prescription aimed at optimizing fat loss. The authors examined the effects of exercise intensity, duration, and modality on postexercise oxygen consumption (VO2) and substrate selection/respiratory-exchange ratio (RER) in healthy individuals. Three experiments (n = 7 for each) compared (a) short- (SD) vs. long-duration (LD) ergometer cycling exercise (30 min vs. 90 min) matched for intensity, (b) low- (LI) vs. high-intensity (HI) cycling (50% vs. 85% of VO2max) matched for energy expenditure, and (c) continuous (CON) vs. interval (INT) cycling matched for energy expenditure and mean intensity. All experiments were administered by crossover design. Altering exercise duration did not affect postexercise VO2 or RER kinetics (p > .05). However, RER was lower and fat oxidation was higher during the postexercise period in LD vs. SD (p < .05). HI vs. LI resulted in a significant increase in total postexercise energy expenditure and fat oxidation (p < .01). Altering exercise modality (CON vs. INT) did not affect postexercise VO2, RER, or fat oxidation (p > .05). These results demonstrate that postexercise energy expenditure and fat oxidation can be augmented by increasing exercise intensity, but these benefits cannot be exploited by undertaking interval exercise (1:2-min work:recovery ratio) when total energy expenditure, duration, and mean intensity remain unchanged. In spite of the apparent benefit of these strategies, the amount of fat oxidized after exercise may be inconsequential compared with that oxidized during the exercise bout.
Jean Gutierrez, Andrei Gribok, William Rumpler, Avinash Chandran and Loretta DiPietro
People with a family history of type 2 diabetes have lower energy expenditure (EE) and more obesity than those having no such family history. Resistance exercise (RE) may induce excess postexercise energy expenditure (EPEE) and reduce long-term risk for obesity in this susceptible group.
To determine the effect of RE on EPEE for 15 hr after a single exercise bout in healthy, untrained young men having a family history of type 2 diabetes.
Seven untrained men (23 ± 1.2 years, BMI 24 ± 1.1) completed a 48-hr protocol in a whole room calorimeter. The first day served as a control day, with a moderate 40-min RE bout occurring on the second day. Differences in postexercise EE were compared with matched periods from the control day for cumulative 15-min intervals (up to 150 min) and 15 hr after the RE bout was completed.
The most robust difference in EPEE between the experimental and control days was observed in the first 15-min postexercise period (M = 1.4Kcal/min; SD = 0.7; p < .05). No statistically significant differences in EPEE were noted beyond 90-min of continuous measurement.
Young people with a family history of type 2 diabetes may not show EPEE after a single RE bout when observed for 15 hr after RE and long-term resistance training may be required to promote EPEE.
Darlene A. Sedlock
This study is a comparison of both the magnitude and duration of excess postexercise oxygen consumption (EPOC) between women and men. Eighteen (9 women, 9 men) physically active, young adult volunteers performed a moderate exercise in the early morning after having refrained from any strenuous activity for the previous 36-48 hr. Baseline oxygen uptake (VO2) and heart rate (HR) were measured for the last 15 min of a 45 min seated rest. The 30 min cycle ergometer exercise was performed at 60% of each subject’s previously determined peak VO2. Subjects sat quietly in a chair during recovery until VO2 returned to baseline. The women had a significantly lower (t=4.22, p<0.01) resting VO2(0.22±0.03 L min−1) than the men (0.31±0.06 L min−1), however no significant difference was observed when resting VO2 was expressed relative to body weight. VO2 values during exercise were also significantly lower in the women compared to the men (t=4.85, p<0.01). Duration of EPOC was similar between the two groups (women=27.6±15.6, men=28.2±15.9 min). The 38% difference in magnitude of EPOC between the women (9.4±4.7 kcal) and men (13.0±4.6 kcal) was not statistically significant and approximated 5% of the exercise energy expenditure in each group. It was concluded that there was no sex difference in EPOC duration following moderate exercise conditions. Magnitude of EPOC was small for both groups, with women having a slightly lower value.
William McGarvey, Richard Jones and Stewart Petersen
The purpose of this investigation was to examine the effect of interval (INT) and continuous (CON) cycle exercise on excess post-exercise oxygen consumption (EPOC). Twelve males first completed a graded exercise test for VO2max and then the two exercise challenges in random order on separate days approximately 1 wk apart. The INT challenge consisted of seven 2 min work intervals at 90% VO2max, each followed by 3 min of relief at 30% VO2max. The CON exercise consisted of 30 to 32 min of continuous cycling at 65% VO2max. Gas exchange and heart rate (HR) were measured for 30 min before, during, and for 2 h post-exercise. Three methods were used to analyze post-exercise oxygen consumption and all produced similar results. There were no significant differences in either the magnitude or duration of EPOC between the CON and INT protocols. HR, however, was higher (P < 0.05) while respiratory exchange ratio (RER) was lower (P < 0.05) following INT. These results indicate that when total work was similar, the magnitude and duration of EPOC were similar following CON or INT exercise. The differences in HR and RER during recovery suggest differential physiological responses to the exercise challenges.
Jason C. Bartram, Dominic Thewlis, David T. Martin and Kevin I. Norton
differences in elevated postexercise oxygen consumption (EPOC). In a review article, Tomlin and Wenger 13 explored a number of studies demonstrating that trained individuals show a greater EPOC response immediately following high-intensity work bouts than their lesser trained peers. Presumably this increased
Monica Klungland Torstveit, Ida Fahrenholtz, Thomas B. Stenqvist, Øystein Sylta and Anna Melin
.83 × supine HR) Crouter et al. ( 2008 ) Brage et al. ( 2005 ) EPOC Defined as 5% of EEE the first hour postexercise plus 3% of EEE the second hour postexercise Phelain, Reinke, Harris, and Melby ( 1997 ) Fahrenholtz et al. ( 2018 ) RMR The pRMR used to calculate WDEB was calculated using the Cunningham
Richard Latzel, Olaf Hoos, Sebastian Stier, Sebastian Kaufmann, Volker Fresz, Dominik Reim and Ralph Beneke
EPOC ) using the following formula: VO 2 EPOC ( mL · kg − 1 ) = a * exp ( − t / tau a ) + b * exp( − t / tau b ) + c with VO 2 PCr ( mL · kg − 1 ) = a * e xp( − t / tau a ) W tot was calculated as W tot = W PCr + W blc + W aer . P tot and fractions derived from W PCr , W blc , and W aer
Sebastian Kaufmann, Olaf Hoos, Timo Kuehl, Thomas Tietz, Dominik Reim, Kai Fehske, Richard Latzel and Ralph Beneke
component of postexercise oxygen uptake (VO 2PCr ) calculated from the latter and body mass by: W PCr (kJ·kg −1 ) = VO 2PCr (mL·kg −1 ) × caloric equivalent (J·mL −1 ) × body mass (kg) × 1000 −1 . A biexponential model [ VO 2 EPOC ( mL · kg − 1 ) = a e ( − t ÷ τ a ) + b e ( − t ÷ τ b ) + c with VO 2
Scott Cocking, Mathew G. Wilson, David Nichols, N. Timothy Cable, Daniel J. Green, Dick H. J. Thijssen and Helen Jones
exercise while, during recovery, it produced higher amplitude of blood lactate kinetics and increased excess postexercise oxygen consumption (EPOC) compared with sham exercise. This, in combination with our data, suggests that the potential ergogenic mechanisms relating to IPC-induced metabolic alteration