scholarly journals Oxygen cost and oxygen uptake dynamics and recovery with 1 min of exercise in children and adults

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.

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.


1993 ◽  
Vol 75 (3) ◽  
pp. 1419-1422 ◽  
Author(s):  
F. Peronnet ◽  
E. Adopo ◽  
D. Massicotte ◽  
G. R. Brisson ◽  
C. Hillaire-Marcel

This study presents a method for computing the respective amounts of two simultaneously ingested exogenous substrates (A and B) that are oxidized during a period of prolonged exercise by use of 13C labeling. This method is based on the observation that the total volume of 13CO2 produced (V13CO2tot) is the sum of 1) V13CO2 arising from the oxidation of endogenous substrates (V13CO2endo), 2) V13CO2 arising from the oxidation of substrate A (V13CO2A), and 3) V13CO2 arising from the oxidation of substrate B (V13CO2B). The equation, V13CO2tot = V13CO2endo+V13CO2A+V13CO2B, with three unknowns, can be solved from the results of three experiments conducted under the same conditions but with at least two values for the isotopic composition of A and B. This method has been used on five healthy male subjects to compute the amounts of glucose and fructose oxidized when a mixture of 15 g of glucose and 15 g of fructose is ingested (in 300 ml of water) over 60 min of cycle ergometer exercise at 65% of maximal O2 uptake. Results from three experiments indicated that 9.8 +/- 3.1 and 5.7 +/- 2.1 g of glucose and fructose, respectively, were oxidized. The total amount of exogenous carbohydrates oxidized (15.5 +/- 4.3 g) is in agreement with the oxidation rates of exogenous glucose computed in similar conditions when 30 g of glucose were ingested (13 g; Peronnet et al. Med. Sci. Sports Exercise 25: 297–302, 1993). The difference between the oxidation rates of exogenous glucose and fructose is also in line with data from the literature.


1991 ◽  
Vol 70 (2) ◽  
pp. 841-848 ◽  
Author(s):  
Y. Armon ◽  
D. M. Cooper ◽  
R. Flores ◽  
S. Zanconato ◽  
T. J. Barstow

We hypothesized that the O2 uptake (Vo2) response to high-intensity exercise would be different in children than in adults. To test this hypothesis, 22 children (6-12 yr old) and 7 adults (27-40 yr old) performed 6 min of constant-work-rate cycle-ergometer exercise. Sixteen children performed a single test above their anaerobic threshold (AT). In a separate protocol, six children and all adults exercised at low and high intensity. Low-intensity exercise corresponded to the work rate at 80% of each subject's AT. High-intensity exercise (above the AT) was determined first by calculating the difference in work rate between the AT and the maximal Vo2 (delta). Twenty-five, 50, and 75% of this difference were added to the work rate at the subject's AT, and these work rates were referred to as 25% delta, 50% delta, and 75% delta. For exercise at 50% delta and 75% delta, Vo2 increased throughout exercise (O2 drift, linear regression slope of Vo2 as a function of time from 3 to 6 min) in all the adults, and the magnitude of the drift was correlated with increasing work rates in the above-AT range (r = 0.91, P less than 0.0001). In contrast, no O2 drift was observed in over half of the children during above-AT exercise. The O2 drifts were much higher in adults (1.76 +/- 0.63 ml O2.kg-1.min-2 at 75% delta) than in children (0.20 +/- 0.42, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


1976 ◽  
Vol 40 (6) ◽  
pp. 864-867 ◽  
Author(s):  
S. N. Koyal ◽  
B. J. Whipp ◽  
D. Huntsman ◽  
G. A. Bray ◽  
K. Wasserman

Ventilation and acid-base responses were studied at comparable levels of O2 uptake during cycle ergometer and treadmill exercise, to determine the extent to which the type of exercise affects these responses. Twenty male subjects performed 50-, 100-, and 150-W cycle ergometer exercise and three work rates of similar O2 uptake on a treadmill. At comparable oxygen uptakes, arterial lactate and VE were higher and arterial pH and bicarbonate were lower for cycle ergometer than treadmill exercise. These differences could be accounted for by the greater degree of metabolic acidosis during cycle ergometer work. The increment in VE over that predicted (from an extrapolation of the linear relationship of the VE-VO2 relationship for low work rates) was linearly related to the decrease in arterial bicarbonate; VE was increased by approximately 4 1/min for each meq/1 of bicarbonate decrease for both treadmill and cycle ergometry.


1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 76 (3) ◽  
pp. 1346-1349 ◽  
Author(s):  
L. Kaijser ◽  
J. Pernow ◽  
B. Berglund ◽  
J. Grubbstrom ◽  
J. M. Lundberg

To evaluate the effect of hypoxemia on cardiac release of neuropeptide Y-like immunoreactivity (NPY-LI) and norepinephrine (NE), arterial and coronary sinus blood was sampled and coronary sinus blood flow was measured by thermodilution in nine healthy volunteers at rest and during supine cycle ergometer exercise while they breathed air and 12% O2, which reduced arterial O2 saturation to approximately 68%. Five subjects started to exercise for 30 min breathing air and continued for 30 min breathing 12% O2; four subjects breathed 12% O2 and air in the reverse order. The load was adjusted to give the same heart rate during O2 and air breathing. No significant cardiac net release of NPY-LI or NE was seen at rest. Exercise induced release of NPY-LI and NE. The net release of NPY-LI was 0.7 +/- 0.4 pmol/min during air breathing (average 12 and 30 min) and 2.8 +/- 0.6 pmol/min during 12% O2 breathing. The difference was not influenced by the order of the breathing periods. The NE coronary sinus-arterial difference was not significantly different between 12% O2 and air breathing, whereas the net release was significantly larger during 12% O2 breathing (0.6 +/- 0.1 vs. 0.4 +/- 0.1 nmol/min). Thus, NPY is released with NE from the heart during exercise. Arterial hypoxemia seems to be an additional stimulus of preferential NPY release.


1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)


2004 ◽  
Vol 96 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Timothy P. Gavin ◽  
Christopher B. Robinson ◽  
Robert C. Yeager ◽  
Justin A. England ◽  
L. Wiley Nifong ◽  
...  

We investigated whether acute systemic exercise increases vascular endothelial growth factor (VEGF), VEGF receptor (KDR and Flt-1) mRNA, and VEGF protein in sedentary humans. Twelve sedentary subjects were recruited and performed 1 h of acute, cycle ergometer exercise at 50% of maximal oxygen consumption. Muscle biopsies were obtained from the vastus lateralis before exercise and at 0, 2, and 4 h postexercise. Acute exercise significantly increased VEGF mRNA at 2 and 4 h and increased KDR and Flt-1 mRNA at 4 h postexercise. The sustained increase in VEGF mRNA through 4 h and the increases in KDR and Flt-1 at 4 h are different from their respective time course responses in rats. In contrast to the increase in VEGF mRNA postexercise, VEGF protein levels were decreased at 0 h postexercise. These results provide evidence in humans that 1) VEGF, KDR, and Flt-1 mRNA are increased by acute systemic exercise; 2) the time course of the VEGF, KDR, and Flt-1 mRNA responses are different from those previously reported in rats (Gavin TP and Wagner PD. Acta Physiol Scand 175: 201–209, 2002); and 3) VEGF protein is decreased immediately after exercise.


1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.


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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