Effect of duration of exercise on excess postexercise O2 consumption

1987 ◽  
Vol 62 (2) ◽  
pp. 485-490 ◽  
Author(s):  
R. Bahr ◽  
I. Ingnes ◽  
O. Vaage ◽  
O. M. Sejersted ◽  
E. A. Newsholme

This study was undertaken to determine the effect of exercise duration on the time course and magnitude of excess postexercise O2 consumption (EPOC). Six healthy male subjects exercised on separate days for 80, 40, and 20 min at 70% of maximal O2 consumption on a cycle ergometer. A control experiment without exercise was performed. O2 uptake, respiratory exchange ratio (R), and rectal temperature were monitored while the subjects rested in bed 24 h postexercise. An increase in O2 uptake lasting 12 h was observed for all exercise durations, but no increase was seen after 24 h. The magnitude of 12-h EPOC was proportional to exercise duration and equaled 14.4 +/- 1.2, 6.8 +/- 1.7, and 5.1 +/- 1.2% after 80, 40, and 20 min of exercise, respectively. On the average, 12-h EPOC equaled 15.2 +/- 2.0% of total exercise O2 consumption (EOC). There was no difference in EPOC:EOC for different exercise durations. A linear decrease with exercise duration was observed in R between 2 and 24 h postexercise. No change was observed in recovery rectal temperature. It is concluded that EPOC increases linearly with exercise duration at a work intensity of 70% of maximal O2 consumption.

1991 ◽  
Vol 71 (3) ◽  
pp. 993-998 ◽  
Author(s):  
S. Zanconato ◽  
D. M. Cooper ◽  
Y. Armon

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7–11 yr) and 13 adults (26–42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.


1989 ◽  
Vol 66 (6) ◽  
pp. 2733-2738 ◽  
Author(s):  
P. R. Bender ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
S. Y. Huang ◽  
P. D. Wagner ◽  
...  

Arterial O2 saturation (Sao2) decreases in hypoxia in the transition from rest to moderate exercise, but it is unknown whether other several weeks at high altitude SaO2 in submaximal exercise follows the same time course and pattern as that of ventilatory acclimatization in resting subjects. Ventilatory acclimatization is essentially complete after approximately 1 wk at 4,300 m, such that improvement in submaximal exercise SaO2 would then require other mechanisms. On days 2, 8, and 22 on Pikes Peak (4,300 m), 6 male subjects performed prolonged steady-state cycle exercise at 79% maximal O2 uptake (VO2 max). Resting SaO2 rose from day 1 (78.4 +/- 1.6%) to day 8 (87.5 +/- 1.4%) and then did not increase further by day 20 (86.4 +/- 0.6%). During exercise, SaO2 values (mean of 5-, 15-, and 30-min measurements) were 72.7% (day 2), 78.6% (day 8), and 82.3% (day 22), meaning that all of the increase in resting SaO2 occurred from day 1 to day 8, but exercise SaO2 increased from day 2 to day 8 (5.9%) and then increased further from day 8 to day 22 (3.7%). On day 22, the exercise SaO2 was higher than on day 8 despite an unchanged ventilation and O2 consumption. The increased exercise SaO2 was accompanied by decreased CO2 production. The mechanisms responsible for the increased exercise SaO2 require further investigation.


1988 ◽  
Vol 65 (3) ◽  
pp. 1045-1049 ◽  
Author(s):  
D. A. Roth ◽  
W. C. Stanley ◽  
G. A. Brooks

To study the effects of circulatory occlusion on the time course and magnitude of postexercise O2 consumption (VO2) and blood lactate responses, nine male subjects were studied twice for 50 min on a cycle ergometer. On one occasion, leg blood flow was occluded with surgical thigh cuffs placed below the buttocks and inflated to 200 mmHg. The protocol consisted of a 10-min rest, 12 min of exercise at 40% peak O2 consumption (VO2 peak), and a 28-min resting recovery while respiratory gas exchange was determined breath by breath. Occlusion (OCC) spanned min 6-8 during the 12-min work bout and elicited mean blood lactate of 5.2 +/- 0.8 mM, which was 380% greater than control (CON). During 18 min of recovery, blood lactate after OCC remained significantly above CON values. VO2 was significantly lower during exercise with OCC compared with CON but was significantly higher during the 4 min of exercise after cuff release. VO2 was higher after OCC during the first 4 min of recovery but was not significantly different thereafter. Neither total recovery VO2 (gross recovery VO2 with no base-line subtraction) nor excess postexercise VO2 (net recovery VO2 above an asymptotic base line) was significantly different for OCC and CON conditions (13.71 +/- 0.45 vs. 13.44 +/- 0.61 liters and 4.93 +/- 0.26 vs. 4.17 +/- 0.35 liters, respectively). Manipulation of exercise blood lactate levels had no significant effect on the slow ("lactacid") component of the recovery VO2.


1986 ◽  
Vol 61 (1) ◽  
pp. 155-159 ◽  
Author(s):  
D. D. Hatcher ◽  
O. D. Srb

This study presents the comparison of two different noninvasive techniques for the estimation of cardiac output (Q). The two techniques used were transthoracic impedance plethysmography (Z) and the indirect Fick CO2 rebreathing (RB) method. Paired estimates of Q were made on 60 different male subjects at rest and during graded increments of work on a cycle ergometer. The mean resting Q as measured by the Z technique (COZ) was 7.46 +/- 0.35 and 5.96 +/- 0.43 l/min using the RB (CORB) technique. At 200 W the mean COZ was 18.67 +/- 0.72 l/min and the CORB was 23.73 +/- 0.84 l/min. Both the techniques were linearly correlated (R) with O2 consumption; i.e., RZ = 0.752, RRB = 0.855. The difference between these two R values is statistically significant (P less than 0.001). A linear relationship was found between the Z and RB techniques at all work loads (R = 0.75). This study suggests that both techniques are equally as reliable over a large range of work loads, with the Z technique being the simplest and most efficient to implement. It was also found that lung volume had no effect on the calculated COZ.


1985 ◽  
Vol 59 (4) ◽  
pp. 1061-1067 ◽  
Author(s):  
M. Kjaer ◽  
N. J. Christensen ◽  
B. Sonne ◽  
E. A. Richter ◽  
H. Galbo

The kinetics underlying plasma epinephrine concentrations were studied. Six athletes (T) and six sedentary males (C) were given intravenous infusions of 3H-labeled epinephrine, after which arterial blood was drawn. They rested sitting and bicycled continuously to exhaustion (60 min at 125 W, 60 min at 160 W, 40 min at 200 W, and 240 W to the end). Work time was 154 +/- 13 (SE) (T) and 75 +/- 6 (C) min. At rest, epinephrine clearance was identical [28.4 +/- 1.3 (T) vs. 29.2 +/- 1.8 (C) ml . kg-1 . min-1], but plasma concentration [1.42 +/- 0.27 (T) vs. 0.71 +/- 0.16 (C) nmol . l-1] and, accordingly, secretion [2.9 +/- 0.7 vs. 1.5 +/- 0.4 nmol . min-1] were higher (P less than 0.05) in T than C subjects. Epinephrine clearance was closely related to relative work load, decreasing from 15% above the basal level at 30% of maximal O2 uptake (VO2 max) to 22% below at 76% of VO2 max. Epinephrine concentrations increased much more with work intensity than could be accounted for by changes in clearance and were, at exhaustion, higher (P less than 0.05) in T (7.2 +/- 1.6) than in C (2.5 +/- 0.7 nmol . l-1) subjects despite similar glucose, heart rate, and hematocrit values. At a given load, epinephrine clearance rapidly became constant, whereas concentration increased continuously. Forearm extraction of epinephrine invalidated use of blood from a cubital vein or a hand vein arterialized by hot water in turnover measurements. During exercise, changes in epinephrine concentrations reflect changes in secretion rather than in clearance. Training may increase adrenal medullary secretory capacity.


1985 ◽  
Vol 59 (5) ◽  
pp. 1350-1354 ◽  
Author(s):  
D. S. King ◽  
D. L. Costill ◽  
W. J. Fink ◽  
M. Hargreaves ◽  
R. A. Fielding

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.


1994 ◽  
Vol 76 (6) ◽  
pp. 2541-2545 ◽  
Author(s):  
F. Yamazaki ◽  
R. Sone ◽  
H. Ikegami

This study determined the phase response and amplitude response (delta) of esophageal temperature (T(es)), mean skin temperature (Tsk), and forearm sweating rate (Msw) to sinusoidal work. Six healthy male subjects exercised on a cycle ergometer with a constant load (approximately 35% maximal O2 uptake) for a 30-min period; for the next 40 min they exercised with a sinusoidal load at 25 degrees C at 35% relative humidity. The sinusoidal load varied between approximately 10 and 60% maximal O2 uptake, and three different time periods (1.3, 4, and 8 min) were selected. Each subject performed three experiments that differed only in the timing of sinusoidal work. During the 4- and 8-min periods, T(es), Tsk, and Msw changed almost sinusoidally. The phase of Msw change significantly preceded those of T(es) and Tsk changes (P < 0.05). During the 1.3-min period, the level of T(es) and Tsk remained almost constant (delta T(es) 0.01 +/- 0.00 degrees C, delta Tsk 0.03 +/- 0.01 degrees C), whereas Msw showed a clear sinusoidal pattern. We conclude that the sweating response during sinusoidal work depends on both thermal and nonthermal factors, the latter being emotional, mental, or sensory stimulation. The contribution of the nonthermal factors to the general sweating response during exercise can be separated from that of the thermal factors by using sinusoidal work during a short period (e.g., 1.3 min).


1995 ◽  
Vol 79 (3) ◽  
pp. 838-845 ◽  
Author(s):  
C. J. Womack ◽  
S. E. Davis ◽  
J. L. Blumer ◽  
E. Barrett ◽  
A. L. Weltman ◽  
...  

Seven untrained male subjects [age 25.6 +/- 1.5 (SE) yr, peak O2 uptake (VO2) 3.20 +/- 0.19 l/min] trained on a cycle ergometer 4 days/wk for 6 wk, with the absolute training workload held constant for the duration of training. Before and at the end of each week of training, the subjects performed 20 min of constant-power exercise at a power designed to elicit a pronounced slow component of VO2 (end-exercise VO2-VO2 at minute 3 of exercise) in the pretraining session. An additional 20-min exercise bout was performed after training at this same absolute power output during which epinephrine (Epi) was infused at a rate of 100 ng.kg-1.min-1 between minutes 10 and 20. After 2 wk of training, significant decreases in VO2 slow component, end-exercise VO2, blood lactate ([La-] and glucose concentrations, plasma Epi ([Epi]) and norepinephrine concentrations, ventilation (VE), and heart rate (HR) were observed (P < 0.05). Although the rapid attenuation of the VO2 slow component coincided temporally with reductions in plasma [Epi], blood [La-], and VE, the infusion of Epi after training significantly increased plasma [Epi] (delta 2.22 ng/ml), blood [La-] (delta 2.4 mmol/l) and VE (delta 10.0 l/min) without any change in exercise VO2. We therefore conclude that diminution of the VO2 slow component with training is attributable to factors other than the reduction in plasma [Epi], blood [La-] and VE.


1982 ◽  
Vol 53 (2) ◽  
pp. 436-439 ◽  
Author(s):  
M. J. Buono ◽  
F. B. Roby

Acid-base, metabolic, and ventilatory responses to repeated bouts of exercise were examined. Ten male subjects performed two (T1, T2) 5-min work tests, on a cycle ergometer, separated by a 25-min rest. The results indicate the following. 1) T2 appears to have a larger aerobic energy component than T1, due to the fact that cumulative O2 uptake (Vo2) was significantly larger for T2 and that the immediate postexercise lactic acid (HLa) and delta HLa values were both significantly smaller for T2.2) CO2 production (Vco2) and the respiratory exchange ratio were both significantly lower for T2. This is probably due to greater fat metabolism and less nonmetabolic CO2 being produced from bicarbonate (HCO-3) buffering of HLa during T2.3) Even though Vco2 was significantly lower during T2, minute ventilation (VE) was not significantly different between T1 and T2. This suggests that the ventilatory response during exercise cannot be solely mediated via CO2 flux to the lungs. 4) HLa removal and (HCO-3) regeneration appear to be sequentially linked together as indicated by the almost identical mirror image and significant -0.93 correlation. In conclusion, it appears that a bout of high-intensity exercise (T1) can alter the acid-base and metabolic responses seen during subsequent performance (T2).


1991 ◽  
Vol 71 (6) ◽  
pp. 2088-2093 ◽  
Author(s):  
R. Bahr ◽  
O. M. Sejersted

This study was undertaken to determine the effect of fasting on the magnitude and time course of the excess postexercise O2 consumption (EPOC). Six lean untrained subjects were studied in the fasted state for 7 h after a previous strenuous exercise bout (80 min at 75% of maximal O2 uptake) and in a control experiment. The results were compared with identical control and exercise experiments where the subjects were fed a 4.5-MJ test meal after 2 h of rest. EPOC was calculated as the difference in O2 uptake between the corresponding control and exercise experiments. The total EPOC (0–7 h postexercise) was 20.9 +/- 4.5 (fasting) and 21.1 +/- 3.6 liters (food, NS). A significant prolonged EPOC component was observed in the fasted and in the fed state. The thermic effect of food (TEF) was calculated from O2 consumption and respiratory exchange ratio as the difference in energy expenditure between the corresponding food and fasting experiments. The total TEF (0–5 h postprandial) was 321 +/- 32.0 (control) and 280 +/- 37.7 kJ/5 h (exercise, NS). It is concluded that the prolonged component of EPOC is present in the fasting state. Furthermore, no major interaction effects between food intake and exercise on the postexercise O2 consumption could be detected.


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