Response of respiratory exchange ratio (R) to sinusoidal work load in humans

An examination was made of the response of respiratory exchange ratio (R), carbon dioxide output (VCO2) and oxygen uptake (VO2) to sinusoidal work load with periods (T) of 1-16 min in six healthy men to determine whether R response is sinusoidal. The influence of the ratio of the amplitude of VCO2 to that of VO2 and the phase lag between them on R response was also studied by computer simulation. The results and conclusions obtained are as follows: 1) With decrease in the period, the amplitudes of VO2 and VCO2 dropped exponentially, becoming least at T of 1 min (T = 1 min). In contrast, the amplitude of R was largest at T = 4 min and subsequently decreased progressively. 2) The peak amplitude of R at T = 4 min can be explained by the larger phase lag and relatively low of amplitude of VCO2 to VO2. 3) The smallest amplitude of R at T = 1 min was due not to the ratio of amplitude or phase lag, but to remarkably smaller amplitudes of VO2 and VCO2. 4) The phase lag of VO2 to sinusoidal work load was smaller than that of VCO2. Phase lag of R was considerably larger than that of VO2 or VCO2. 5) The response curve of VO2 and VCO2 is a sinusoidal curve with the same period as exercise. However, the response of R is not a real sinusoidal but a deformed biphasic curve with a high crest and low trough. The deformity is determined by the phase lag between VO2 and VCO2 response and also the ratio of amplitude of VCO2 to that of VO2.     

Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.

We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)     

VO2 kinetics in subjects differing in aerobic capacity: investigation by spectral analysis

The power-VO2 transfer functions of 38 subjects differing in aerobic capacity have been determined on the basis of breath-by-breath total oxygen uptake (VO2,t) measurements during light cycle ergometer exercise (lactic acid concentrations below 2 mmol.l-1). At constant pedalling frequency (1 Hz) pseudorandom binary sequences (PRBS) of workload were used as the testing signal. The VO2,t response was analysed by autocorrelating the ergometer power input and crosscorrelating the power input and VO2,t output. From the spectra of these functions the amplitude ratios and phase relationships were computed for the first six harmonics of the PRBS fundamental (14 mrad X s-1). We found that differences in aerobic capacity are associated with significant differences in the amplitude plots of the VO2 transfer function.     

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.     

Dynamic linearity of VO2 responses during aerobic exercise.

The multifrequent pseudorandom binary sequence (PRBS) technique is a useful tool for studying oxygen uptake (VO2) kinetics within the aerobic range. However, the validity of this multifrequent test may be limited by nonlinearities generated by the circulatory and pulmonary system. To check for such nonlinear effects, we compared the frequency responses computed from two PRBS protocols with the results of pure sinusoidal frequencies varying in amplitude and mean values (periods between 50 s and 450 s). According to our results the VO2 frequency response does not seem to depend on the type of testing--PRBS or sine--or the changes within each test, i.e. mean power and power amplitude of the sine tests and the switching frequency of the PRBS. In the range of higher frequencies small differences between the test conditions may have been obscured by the greater scatter of dynamic responses. It was concluded that the VO2 frequency response was quasi-linear for periods down to the least 100 s. However, even in this range nonlinearities can be provoked by rest-exercise transitions, by a varying contribution of lactate or by an insufficient noise reduction.     

Kinetics of .VO2 and femoral artery blood flow during heavy-intensity, knee-extension exercise.

It has been suggested that, during heavy-intensity exercise, O(2) delivery may limit oxygen uptake (.VO2) kinetics; however, there are limited data regarding the relationship of blood flow and .VO2 kinetics for heavy-intensity exercise. The purpose was to determine the exercise on-transient time course of femoral artery blood flow (Q(leg)) in relation to .VO2 during heavy-intensity, single-leg, knee-extension exercise. Five young subjects performed five to eight repeats of heavy-intensity exercise with measures of breath-by-breath pulmonary .VO2 and Doppler ultrasound femoral artery mean blood velocity and vessel diameter. The phase 2 time frame for .VO2 and Q(leg) was isolated and fit with a monoexponent to characterize the amplitude and time course of the responses. Amplitude of the phase 3 response was also determined. The phase 2 time constant for .VO2 of 29.0 s and time constant for Q(leg) of 24.5 s were not different. The change (Delta) in .VO2 response to the end of phase 2 of 0.317 l/min was accompanied by a DeltaQ(leg) of 2.35 l/min, giving a DeltaQ(leg)-to-Delta.VO2 ratio of 7.4. A slow-component .VO2 of 0.098 l/min was accompanied by a further Q(leg) increase of 0.72 l/min (DeltaQ(leg)-to-Delta.VO2 ratio = 7.3). Thus the time course of Q(leg) was similar to that of muscle .VO2 (as measured by the phase 2 .VO2 kinetics), and throughout the on-transient the amplitude of the Q(leg) increase achieved (or exceeded) the Q(leg)-to-.VO2 ratio steady-state relationship (ratio approximately 4.9). Additionally, the .VO2 slow component was accompanied by a relatively large rise in Q(leg), with the increased O(2) delivery meeting the increased Vo(2). Thus, in heavy-intensity, single-leg, knee-extension exercise, the amplitude and kinetics of blood flow to the exercising limb appear to be closely linked to the .VO2 kinetics.     

Study of the circadian variation of different circulatory and respiratory functions at submaximal and maximal ergometer work (author's transl)]

The maximal aerobic power of six highly trained young cyclist, mean age 16.3 years and mean VO2max 4.9 l/min, was directly measured at intervals of 4 hrs. A Latin square design was used for the test order. At submaximal work of O2-consumption 2.4 to 4.4 l/min no circadian variation of any single function was found. However, at maximal work load the differences between the maxima and minima values were 12.4% for maximal work output (W max), 7.8% for expiratory minute volume (V Emax), 5.7% for maximal aerobic power (VO2max) and 3.4% for maximal heart rate (H Rmax). All the functions--with the exception of VO2max-had their minima at 0300 hrs; the minima of VO2max was reached already at 2300 hours. The maxima-values of V Emax and VO2max were measured at 1500 hrs, of W max and H Rmax at 0700 and of H Rrest at 1900 hrs correspondingly. A one-tailed test showed significant differences between the maxima and minima values of all variables (P less than 0.05). The results suggest a decreased cardiopulmonary working capacity at night. However, this impairment is only of practical importance if the work will be done near the limit of endurance capacity. Besides it will suggest, that the indirect methods for assessing the cardiopulmonary capacity based on VO2max and W170 are not useful at nighttime, because the presuppositions for these methods are limited of the time of day.     

Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.

We tested the hypothesis that heavy-exercise phase II oxygen uptake (VO(2)) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The VO(2) responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 +/- 4.1 to 47.0 +/- 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 +/- 1.9 to 25.3 +/- 2.9 s) of the VO(2) response in phase II. Instead, this "speeding" was due to a significant reduction in the amplitude of the VO(2) slow component. These results suggest phase II VO(2) kinetics are not speeded by prior heavy exercise.     

Kinetics of oxygen uptake during supine and upright heavy exercise.

It is presently unclear how the fast and slow components of pulmonary oxygen uptake (VO(2)) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (VO(2) equal to 50% of the difference between LT and peak VO(2)) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in VO(2) was similar in the two positions, but VO(2) kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of VO(2) to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component of VO(2), without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise VO(2) was the same in the two positions. The changes in VO(2) kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for VO(2) but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.     

Parameters of ventilatory and gas exchange dynamics during exercise

To determine the precise nonsteady-state characteristics of ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) during moderate-intensity exercise, six subjects each underwent eight repetitions of 100-W constant-load cycling. The tests were preceded either by rest or unloaded cycling ("0" W). An early component of VE, VO2, and VCO2 responses, which was obscured on any single test by the breath-to-breath fluctuations, became apparent when the several repetitions were averaged. These early responses were abrupt when the work was instituted from rest but were much slower and smaller from the 0-W base line and corresponded to the phase of cardiodynamic gas exchange. Some 20 s after the onset of the work a further monoexponential increase to steady state occurred in all three variables, the time constants of which did not differ between the two types of test. Consequently, the exponential behavior of VE, VO2, and VCO2 in response to moderate exercise is best described by a model that incorporates only the second phase of the response.     

Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise.

Prior heavy exercise markedly alters the O2 uptake (VO2) response to subsequent heavy exercise. However, the time required for VO2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the VO2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second VO2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary VO2 time constant (from 25.9 +/- 4.7 s to 23.9 +/- 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary VO2 amplitude (from 2.42 +/- 0.39 to 2.53 +/- 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the VO2 slow component (from 0.44 +/- 0.13 to 0.21 +/- 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20-45 min, but not after 60 min, of recovery. The increase in the primary VO2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 +/- 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20-60 min of recovery. The priming effect of prior heavy exercise on the VO2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.     

Influence of work rate on ventilatory and gas exchange kinetics

A linear system has the property that the kinetics of response do not depend on the stimulus amplitude. We sought to determine whether the responses of O2 uptake (VO2), CO2 output (VCO2), and ventilation (VE) in the transition between loadless pedaling and higher work rates are linear in this respect. Four healthy subjects performed a total of 158 cycle ergometer tests in which 10 min of exercise followed unloaded pedaling. Each subject performed three to nine tests at each of seven work rates, spaced evenly below the maximum the subject could sustain. VO2, VCO2, and VE were measured breath by breath, and studies at the same work rate were time aligned and averaged. Computerized nonlinear regression techniques were used to fit a single exponential and two more complex expressions to each response time course. End-exercise blood lactate was determined at each work rate. Both VE and VO2 kinetics were markedly slower at work rates associated with sustained blood lactate elevations. A tendency was also detected for VO2 (but not VE) kinetics to be slower as work rate increased for exercise intensities not associated with lactic acidosis (P less than 0.01). VO2 kinetics at high work rates were well characterized by the addition of a slower exponential component to the faster component, which was seen at lower work rates. In contrast, VCO2 kinetics did not slow at the higher exercise intensities; this may be the result of the coincident influence of several sources of CO2 related to lactic acidosis. These findings provide guidance for interpretation of ventilatory and gas exchange kinetics.     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

A model for studying the distortion of muscle oxygen uptake patterns by circulation parameters

The transmission of muscle oxygen uptake (VO2) patterns to the pulmonary site is a basically nonlinear process during unsteady state exercise. We were mainly interested in three questions concerning the dynamic relationship between power input and pulmonary VO2 output: 1. To what extent can linear system analysis be applied? 2. What is the relative influence of muscle VO2 on pulmonary VO2 as compared to other parameters such as muscle perfusion kinetics? 3. To what extent does pulmonary VO2 reflect muscle VO2? Investigations were performed by means of a mathematical model including a muscle compartment and two serial, flow-varying time delays. The non-exercising parts of the body were incorporated as one term for perfusion and one for VO2. Parameters were adjusted so as to represent a reference state of aerobic exercise while monofrequent sinusoidal changes in aerobic metabolism were used as forcing signals. The following answers were derived from the simulations: 1. Non-linear distortions of the VO2 signals are negligible provided that analyses are not driven too far into the higher frequency range (periods shorter than about 1 min). 2. Variations of muscle VO2 kinetics have greater effects on pulmonary VO2 than changes of perfusion kinetics or venous volume. This finding applies irrespective of whether or not pulmonary VO2 closely reflects muscle VO2. 3. Small differences in the time constants for muscle perfusion and muscle VO2 are a major prerequisite if pulmonary VO2 kinetics are to be taken as correct estimates of muscle VO2 kinetics. High basal muscle perfusion, small perfusion changes and small venous volumes between muscle and lungs are further factors reducing dynamic distortions of the muscle VO2 signal.     

Breath-by-breath gas exchange kinetics during constant-load work

In order to study respiratory transients during exercise, we examined breath-by-breath gas exchange kinetics during constant-load work. Five male subjects performed cycle ergometer tests which 6 min of constant-load work (150, 200, 250W) followed 50W base-line work. VCO2 and VO2 measured at the mouth ((VCO2)E, (VO2)E) and estimated at the alveolar level ((VCO2)A, (VO2)A) were computed breath-by-breath. The kinetic parameter (time constant) of first- and second-order exponential model was estimated using non-linear least-squares method. Our results demonstrated that a relative stability of PETO2, PETCO2, and R at their control values in the first phase. Independent of work intensities, breath-by-breath variation in gas exchange measured at the mouth was larger than those in gas exchange estimated at the alveolar level both at a non-steady state and a steady state. The time constants of (VO2)A and (VO2)E were varied with increase of work load intensity.     

Maximal aerobic capacity at several ambient concentrations of CO at several altitudes

To assess the nature of the combined effect of the hypoxias of altitude (ALT) and CO exposure, 11 men and 12 women nonsmokers served as subjects in a double-blind experiment. The exposure conditions were four ambient CO levels (0, 50, 100, and 150 ppm) at each of four ALT (55, 1,524, 2,134, and 3,048 m). Each subject, after attaining the required ALT and ambient CO level, performed a maximal aerobic capacity test (VO2max). Blood samples were obtained before, at 50-W, 100-W, 150-W, and maximum work loads and at the 5th min of recovery. Blood were analyzed for hemoglobin, hematocrit, plasma proteins, lactates, and carboxyhemoglobin (HbCO). VO2max was similar at 55 and 1,524 m and decreased by 4 and 8% from the 55-m value at 2,134 and 3,048 m, respectively. On the basis of all statistical analyses, we concluded that VO2max values measured in men were only slightly diminished due to increased ambient CO. HbCO attained at maximum was highest at 55 m and lowest at 3,048 m. Women's HbCO concentrations were lower than men's. At maximal work loads CO shifted into extravascular spaces and returned to the vascular space within 5 min after exercise stopped. The independence of altitude and CO hypoxias on parameters of the maximum aerobic capacity test and a decrease in the CO to HbCO uptake with increasing altitude were demonstrated and attributed in part to the decrease in driving pressure of CO at altitude.     

Assessment of aerobic and anaerobic capacity of athletes in treadmill running tests.

The criteria of max VO2 and max O2D which are traditionally used in studying aerobic and anaerobic work capacity, have the different dimensions. While max VO2 is an index of the power of aerobic energy output, max O2D assesses the capacity of anaerobic sources. For a comprehensive assessment of physical working capacity of athletes, both aerobic and anaerobic capabilities should be represented in three dimensions, i.e. in indexes of power, capacity and efficiency. Experimental procedures have been developed for assessing these three parameters in treadmill running tests. It is proposed to assess anaerobic power by measuring excess CO2, concurrently with determination of max VO2. Maximal aerobic capacity is established as the product of max VO2 by the time of max VO2 maintenance determined in a special test with running at critical speed. The erogmetric criteria derived on the basis of the tests proposed, may be used for systematization of various physical work loads.     

Frequency domain analysis of ventilation and gas exchange kinetics in hypoxic exercise.

The kinetics of O2 up-take (VO2), CO2 output (VCO2), ventilation (VE), and heart rate (HR) were studied during exercise in normoxia and hypoxia [inspired O2 fraction (FIO2) 0.14]. Eight male subjects each completed 6 on- and off-step transitions in work rate (WR) from low (25 W) to moderate (100-125 W) levels and a pseudorandom binary sequence (PRBS) exercise test in which WR was varied between the same WRs. Breath-by-breath data were linearly interpolated to yield 1-s values. After the first PRBS cycle had been omitted as a warm-up, five cycles were ensemble-averaged before frequency domain analysis by standard Fourier methods. The step data were fit by a two-component (three for HR) exponential model to estimate kinetic parameters. In the steady state of low and moderate WRs, each value of VO2, VCO2, VE, and HR was significantly greater during hypoxic than normoxic exercise (P less than 0.05) with the exception of VCO2 (low WR). Hypoxia slowed the kinetics of VO2 and HR in on- and off-step transitions and speeded up the kinetics of VCO2 and VE in the on-transition and of VE in the off-transition. Frequency domain analysis confined to the range of 0.003-0.019 Hz for the PRBS tests indicated reductions in amplitude and greater phase shifts in the hypoxic tests for VO2 and HR at specific frequencies, whereas amplitude tended to be greater with little change in phase shift for VCO2 and VE during hypoxic tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Phosphate supplementation, cardiovascular function, and exercise performance in humans

The use of oral phosphate (Pi) supplements to improve muscular work performance has long been proposed without substantiating data. In a double-blind, crossover experiment 11 male runners ingested calcium Pi (176 mmol/day) or placebo for 4 days. On the 3rd treatment day, subjects ran an incremental maximal aerobic capacity test (VO2 max) on a treadmill, and on the 4th day a treadmill run to exhaustion at approximately 70% VO2max. By the 4th day of Pi loading, plasma Pi was significantly higher than control (P less than 0.05); however, erythrocyte Pi, 2,3-diphosphoglycerate, and O2 half-saturation pressure of hemoglobin (P50) were not elevated. VO2 max was not changed by the treatments (mean 62.9, 64.2, 64.9 ml.kg-1.min-1 for control, Pi, and placebo bouts, respectively) nor was submaximal run time to exhaustion (61.6 min for Pi, 65.5 min for placebo). Stroke volume at steady-state VO2 was decreased with Pi (P less than 0.05), whereas cardiac output tended (P = 0.07) to be lower. Greater arteriovenous O2 difference (P less than 0.05) with Pi suggested a peripheral effect that increased O2 extraction. We concluded that in healthy individuals Pi loading produced no improvement in work tolerance or aerobic capacity but did alter some aspects of cardiovascular function.     

Exercise intensity and glucose tolerance in trained and nontrained subjects

The improved glucose tolerance and increased insulin sensitivity associated with regular exercise appear to be the result, in large part, of the residual effects of the last bout of exercise. To determine the effects of exercise intensity on this response, glucose tolerance and the insulin response to a glucose load were determined in seven well-trained male subjects [maximal O2 uptake (VO2max) = 58 ml.kg-1.min-1] and in seven nontrained male subjects (VO2max = 49 ml.kg-1.min-1) in the morning after an overnight fast 1) 40 h after the last training session (control), 2) 14 h after 40 min of exercise on a cycle ergometer at 40% VO2max, and 3) 14 h after 40 min of exercise at 80% VO2max. Subjects replicated their diets for 3 days before each test and ate a standard meal the evening before the oral glucose tolerance test. No differences in the 3-h insulin or glucose response were observed between the control trial and before exercise at either 40 or 80% VO2max in the trained subjects. In the nontrained subjects the plasma insulin response was decreased by 40% after a single bout of exercise at either 40 or 80% VO2max (7.0 X 10(3) vs. 5.0 X 10(3), P less than 0.05; 3.8 X 10(3) microU.ml-1.180 min-1, P less than 0.01). The insulin response after a single bout of exercise in the nontrained subjects was comparable with the insulin responses found in the trained subjects for the control and exercise trials.(ABSTRACT TRUNCATED AT 250 WORDS)