Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

Effect of endurance training on oxygen uptake kinetics during treadmill running.

The purpose of this study was to examine the effect of endurance training on oxygen uptake (VO(2)) kinetics during moderate [below the lactate threshold (LT)] and heavy (above LT) treadmill running. Twenty-three healthy physical education students undertook 6 wk of endurance training that involved continuous and interval running training 3-5 days per week for 20-30 min per session. Before and after the training program, the subjects performed an incremental treadmill test to exhaustion for determination of the LT and the VO(2 max) and a series of 6-min square-wave transitions from rest to running speeds calculated to require 80% of the LT and 50% of the difference between LT and maximal VO(2). The training program caused small (3-4%) but significant increases in LT and maximal VO(2) (P<0.05). The VO(2) kinetics for moderate exercise were not significantly affected by training. For heavy exercise, the time constant and amplitude of the fast component were not significantly affected by training, but the amplitude of the VO(2) slow component was significantly reduced from 321+/-32 to 217+/-23 ml/min (P<0.05). The reduction in the slow component was not significantly correlated to the reduction in blood lactate concentration (r = 0. 39). Although the reduction in the slow component was significantly related to the reduction in minute ventilation (r = 0.46; P<0.05), it was calculated that only 9-14% of the slow component could be attributed to the change in minute ventilation. We conclude that the VO(2) slow component during treadmill running can be attenuated with a short-term program of endurance running training.     

Oxygen uptake kinetics in treadmill running and cycle ergometry: a comparison.

The purpose of the present study was to comprehensively examine oxygen consumption (VO(2)) kinetics during running and cycling through mathematical modeling of the breath-by-breath gas exchange responses to moderate and heavy exercise. After determination of the lactate threshold (LT) and maximal oxygen consumption (VO(2 max)) in both cycling and running exercise, seven subjects (age 26.6 +/- 5.1 yr) completed a series of "square-wave" rest-to-exercise transitions at running speeds and cycling power outputs that corresponded to 80% LT and 25, 50, and 75%Delta (Delta being the difference between LT and VO(2 max)). VO(2) responses were fit with either a two- (LT) exponential model. The parameters of the VO(2) kinetic response were similar between exercise modes, except for the VO(2) slow component, which was significantly (P < 0.05) greater for cycling than for running at 50 and 75%Delta (334 +/- 183 and 430 +/- 159 ml/min vs. 205 +/- 84 and 302 +/- 154 ml/min, respectively). We speculate that the differences between the modes are related to the higher intramuscular tension development in heavy cycle exercise and the higher eccentric exercise component in running. This may cause a relatively greater recruitment of the less efficient type II muscle fibers in cycling.     

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.     

Oxygen uptake kinetics during treadmill running in boys and men.

The purpose of this study was to compare the kinetics of the oxygen uptake (VO(2)) response of boys to men during treadmill running using a three-phase exponential modeling procedure. Eight boys (11-12 yr) and eight men (21-36 yr) completed an incremental treadmill test to determine lactate threshold (LT) and maximum VO(2). Subsequently, the subjects exercised for 6 min at two different running speeds corresponding to 80% of VO(2) at LT (moderate exercise) and 50% of the difference between VO(2) at LT and maximum VO(2) (heavy exercise). For moderate exercise, the time constant for the primary response was not significantly different between boys [10.2 +/- 1.0 (SE) s] and men (14.7 +/- 2.8 s). The gain of the primary response was significantly greater in boys than men (239.1 +/- 7.5 vs. 167.7 +/- 5.4 ml. kg(-1). km(-1); P < 0.05). For heavy exercise, the VO(2) on-kinetics were significantly faster in boys than men (primary response time constant = 14.9 +/- 1.1 vs. 19.0 +/- 1.6 s; P < 0.05), and the primary gain was significantly greater in boys than men (209.8 +/- 4.3 vs. 167.2 +/- 4.6 ml. kg(-1). km(-1); P < 0.05). The amplitude of the VO(2) slow component was significantly smaller in boys than men (19 +/- 19 vs. 289 +/- 40 ml/min; P < 0.05). The VO(2) responses at the onset of moderate and heavy treadmill exercise are different between boys and men, with a tendency for boys to have faster on-kinetics and a greater initial increase in VO(2) for a given increase in running speed.     

Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline.

It has been suggested that the slower O2 uptake (VO2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that "priming" exercise would significantly reduce the phase II time constant (tau) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak VO2 from a moderate-intensity baseline (90% GET) on three occasions in each of the "unprimed" and "primed" conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II VO2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean+/-SD tau, 42+/-15 vs. 33+/-8 s; P<0.05), but were not accelerated by priming exercise (42+/-17 s; P>0.05). The amplitude of the VO2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (VO2 slow component: from 0.47+/-0.09 to 0.27+/-0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51+/-35 to 26+/-43% of baseline; P<0.05 for both comparisons). These results indicate that the slower phase II VO2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced VO2 slow component may be linked to changes in muscle fiber activation.     

Kinetics of ventilation and gas exchange during supine and upright cycle exercise.

The dynamics of ventilation (VE), oxygen uptake (VO2), carbon dioxide output (VCO2), and heart rate (fc) were studied in 12 healthy young men during upright and supine exercise. Responses to maximal and to two different types of submaximal exercise tests were contrasted. During incremental exercise to exhaustion, the maximal work rate, VO2max, VEmax, fc,max, and ventilatory threshold were all significantly reduced in supine compared to upright exercise (P less than 0.01-0.001). Following step increases or decreases in work rate between 25 W and 105 W, both VO2 and VCO2 responded more slowly in supine than upright exercise. Dynamics were also studied in two different pseudorandom binary-sequence (PRBS) exercise tests, with the work rate varying between 25 W and 105 W with either 5-s or 30-s durations of each PRBS unit. In both of these tests, there were no differences caused by body position in the amplitude or phase shifts obtained from Fourier analysis for any observed variable. These data show that the body position alters the dynamic response to the more traditional step increase in work rate, but not during PRBS exercise. It is speculated that the elevation of cardiac output observed with supine exercise in combination with the continuously varying work-rate pattern of the PRBS exercise allowed adequate, perhaps near steady-state, perfusion of the working muscles in these tests, whereas at the onset of a step increase in work rate, greater demands were placed on the mechanisms of blood flow redistribution.     

Blood flow to contracting human muscles: influence of increased sympathetic activity

The purpose of this study was to examine the effects of the increased sympathetic activity elicited by the upright posture on blood flow to exercising human forearm muscles. Six subjects performed light and heavy rhythmic forearm exercise. Trials were conducted with the subjects supine and standing. Forearm blood flow (FBF, plethysmography) and skin blood flow (laser Doppler) were measured during brief pauses in the contractions. Arterial blood pressure and heart rate were also measured. During the first 6 min of light exercise, blood flow was similar in the supine and standing positions (approximately 15 ml.min-1.100 ml-1); from minutes 7 to 20 FBF was approximately 3-7 ml.min-1.100 ml-1 less in the standing position (P less than 0.05). When 5 min of heavy exercise immediately followed the light exercise, FBF was approximately 30-35 ml.min-1.100 ml-1 in the supine position. These values were approximately 8-12 ml.min-1.100 ml-1 greater than those observed in the upright position (P less than 0.05). When light exercise did not precede 8 min of heavy exercise, the blood flow at the end of minute 1 was similar in the supine and standing positions but was approximately 6-9 ml.min-1.100 ml-1 lower in the standing position during minutes 2-8. Heart rate was always approximately 10-20 beats higher in the upright position (P less than 0.05). Forearm skin blood flow and mean arterial pressure were similar in the two positions, indicating that the changes in FBF resulted from differences in the caliber of the resistance vessels in the forearm muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

VO(2) kinetics in heavy exercise is not altered by prior exercise with a different muscle group.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O(2) uptake (VO(2)) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO(2)) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of VO(2) with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the VO(2) kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) VO(2) kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the VO(2) slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO(2) kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.     

Physiological background of the change point in VO2 and the slow component of oxygen uptake kinetics.

It is generally believed that oxygen uptake during incremental exercise--until VO2max, increases linearly with power output (see eg. Astrand & Rodahl, 1986). On the other hand, it is well established that the oxygen uptake reaches a steady state only during a low power output exercise, but during a high power output exercise, performed above the lactate threshold (LT), the oxygen uptake shows a continuous increase until the end of the exercise. This effect has been called the slow component of VO2 kinetics (Whipp & Wasserman, 1972). The presence of a slow component in VO2 kinetics implies that during an incremental exercise test, after the LT has been exceeded, the VO2 to power output relationship has to become curvilinear. Indeed, it has recently been shown that during the incremental exercise, the exceeding of the power output, at which blood lactate begins to accumulate (LT), causes a non-proportional increase in VO2 (Zoladz et al. 1995) which indicates a drop in muscle mechanical efficiency. The power output at which VO2 starts to rise non-proportionally to the power output has been called "the change point in VO2" (Zoladz et al. 1998). In this paper, the significance of the factors most likely involved in the physiological mechanism responsible for the change point in oxygen uptake (CP-VO2) and for the slow component of VO2 kinetics, including: increase of activation of additional muscle groups, intensification of the respiratory muscle activity, recruitment of type II muscle fibres, increase of muscle temperature, increase of the basal metabolic rate, lactate and hydrogen ion accumulation, proton leak through the inner mitochondrial membrane, slipping of the ATP synthase and a decrease in the cytosolic phosphorylation potential, are discussed. Finally, an original own model describing the sequence of events leading to the non-proportional increase of oxygen cost of work at a high exercise intensity is presented.     

Influence of body position and pre-exercise activity on cardiac output and oxygen uptake following step changes in exercise intensity.

Parallel measurements of breath-by-breath oxygen uptake, cardiac output (Doppler technique), blood pressure (Finapres technique) and heart rate were performed in nine subjects during cycle ergometer exercise in the upright and supine positions. Transients were monitored during power steps starting from and leading to either rest or lower levels of exercise intensity. Oxygen uptake (VO2) and cardiac output kinetics were markedly faster than in all other conditions when exercise was started from rest. In contrast to exercise-exercise on steps, the computed arteriovenous difference in O2 content increased almost immediately in this situation, indicating that not only the additional energy expenditure due to the acceleration of the flywheel but also an increased venous admixture from non-exercising parts of the body contributed to the early kinetics. The off kinetics generally showed a more uniform pattern and did not simply mirror the on transients. The present findings indicate that transitions from rest should be avoided when muscle VO2 kinetics are to be assessed on the basis of VO2 measurements at the mouth.     

Interactive effects of body posture and exercise training on maximal oxygen uptake

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.     

Oxygen uptake kinetics for moderate exercise are speeded in older humans by prior heavy exercise.

This study examined the effect of heavy-intensity warm-up exercise on O(2) uptake (VO(2)) kinetics at the onset of moderate-intensity (80% ventilation threshold), constant-work rate exercise in eight older (65 +/- 2 yr) and seven younger adults (26 +/- 1 yr). Step increases in work rate from loadless cycling to moderate exercise (Mod(1)), heavy exercise, and moderate exercise (Mod(2)) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling. VO(2) kinetics were modeled from the onset of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single exponential model. During Mod(1), the time constant (tau) for the predominant rise in VO(2) (tau VO(2)) was slower (P < 0.05) in the older adults (50 +/- 10 s) than in young adults (19 +/- 5 s). The older adults demonstrated a speeding (P < 0.05) of VO(2) kinetics when moderate-intensity exercise (Mod(2)) was preceded by high-intensity warm-up exercise (tau VO(2), 27 +/- 3 s), whereas young adults showed no speeding of VO(2) kinetics (tau VO(2), 17 +/- 3 s). In the older and younger adults, baseline HR preceding Mod(2) was elevated compared with Mod(1), but the tau for HR kinetics was slowed (P < 0.05) in Mod(2) only for the older adults. Prior heavy-intensity exercise in old, but not young, adults speeded VO(2) kinetics during Mod(2). Despite slowed HR kinetics in Mod(2) in the older adults, an elevated baseline HR before the onset of Mod(2) may have led to sufficient muscle perfusion and O(2) delivery. These results suggest that, when muscle blood flow and O(2) delivery are adequate, muscle O(2) consumption in both old and young adults is limited by intracellular processes within the exercising muscle.     

Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake.

We tested the hypothesis that kinetics of O(2) uptake (VO(2)) measured in the transition to exercise near or above peak VO(2) (VO(2 peak)) would be slower than those for subventilatory threshold exercise. Eight healthy young men exercised at approximately 57, approximately 96, and approximately 125% VO(2 peak). Data were fit by a two- or three-component exponential model and with a semilogarithmic transformation that tested the difference between required VO(2) and measured VO(2). With the exponential model, phase 2 kinetics appeared to be faster at 125% VO(2 peak) [time constant (tau(2)) = 16.3 +/- 8.8 (SE) s] than at 57% VO(2 peak) (tau(2) = 29. 4 +/- 4.0 s) but were not different from that at 96% VO(2 peak) exercise (tau(2) = 22.1 +/- 2.1 s). VO(2) at the completion of phase 2 was 77 and 80% VO(2 peak) in tests predicted to require 96 and 125% VO(2 peak). When VO(2) kinetics were calculated with the semilogarithmic model, the estimated tau(2) at 96% VO(2 peak) (49.7 +/- 5.1 s) and 125% VO(2 peak) (40.2 +/- 5.1 s) were slower than with the exponential model. These results are consistent with our hypothesis and with a model in which the cardiovascular system is compromised during very heavy exercise.     

Exercise with and without gravitational gradient: evaluation with the new random access mass spectrometer (RAMS)

Gravity adds about 40-50 mmHg perfusion pressure to the arterial supply of the quadriceps muscles in the upright posture. This could have important implications in supply of blood flow during exercise. Recently, we have shown that when subjects exercise in the supine posture the rate of increase in VO2 is considerably slower then when cycling exercise takes place in the upright posture. The most probable explanation for this slower adaptation was the altered perfusion gradient. Indeed, when the perfusion gradient from heart to legs was restored by placing the lower part of the body of supine subjects in a negative pressure chamber, the rate of increase in VO2 returned to upright values. The hypothesis advanced from these studies was that skeletal muscle blood flow was reduced at the onset of supine exercise. Exercise in the microgravity environment of space should be similar to that in the supine posture. The only experiments conducted in space to this date that have addressed the question of cardiorespiratory adaptation to changing work rates were performed on the German D2 mission using the methodology proposed by Stegemann and colleagues. To conduct these experiments, it is necessary to utilize sensitive breath-by-breath technology. Recently, NASA and the Russian space programs have commissioned a new mass spectrometer based system as part of the GASMAP project. It was the purpose of this study to evaluate the new mass spectrometer under conditions in which the gravitational effects on the cardiorespiratory response were being challenged.     

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.     

Comparison of oxygen uptake kinetics during concentric and eccentric cycle exercise.

O2 uptake (VO2) kinetics and electromyographic (EMG) activity from the vastus medialis, rectus femoris, biceps femoris, and medial gastrocnemius muscles were studied during constant-load concentric and eccentric cycling. Six healthy men performed transitions from baseline to high-intensity eccentric (HE) exercise and to high-intensity (HC), moderate-intensity (MC), and low-intensity (LC) concentric exercise. For HE and HC exercise, absolute work rate was equivalent. For HE and LC exercise, VO2 was equivalent. VO2 data were fit by a two- or three-component exponential model. Surface EMG was recorded during the last 12 s of each minute of exercise to obtain integrated EMG and mean power frequency. Only in the HC exercise did VO2 increase progressively with evidence of a slow component (phase 3), and only in HC exercise was there evidence of a coincident increase with time in integrated EMG of the vastus medialis and rectus femoris muscles (P < 0.05) with no change in mean power frequency. The phase 2 time constant was slower in HC [24.0 +/- 1.7 (SE) s] than in HE (14.7 +/- 2.8 s) and LC (16.7 +/- 2.2 s) exercise, while it was not different from MC exercise (20.6 +/- 2.1 s). These results show that the rate of increase in VO2 at the onset of exercise was not different between HE and LC exercise, where the metabolic demand was similar, but both had significantly faster kinetics for VO2 than HC exercise. The VO2 slow component might be related to increased muscle activation, which is a function of metabolic demand and not absolute work rate.     

VO(2) kinetics of mild exercise are altered by RER.

We propose that variations in fat and carbohydrate (CHO) oxidation by working muscle alter O(2) uptake (VO(2)) kinetics. This hypothesis provides two predictions: 1) the kinetics should comprise two exponential components, one fast and the other slow, and 2) their contribution should change with variations in fat and CHO oxidation, as predicted by steady-state respiratory exchange ratio (RER). The purpose of this study was to test these predictions by evaluating the VO(2) kinetic model: VO(2)(t) = alpha(R) + alpha(F)(1 - exp[(t - TD)/-tau(F)]) + alpha(C)(1 - exp[(t - TD)/-tau(C)]) for short-term, mild leg cycling in 38 women and 44 men, where VO(2)(t) describes the time course, alpha(R) is resting VO(2), t is time after onset of exercise, TD is time delay, alpha(F) and tau(F) are asymptote and time constant, respectively, for the fast (fat) oxidative term, and alpha(C) and tau(C) are the corresponding parameters for the slow (CHO) oxidative term. We found that 1) this biexponential model accurately described the VO(2) kinetics over a wide range of RERs, 2) the contribution of the fast (alpha(F), fat) component was inversely related to RER, whereas the slow (alpha(C), CHO) component was positively related to RER, and 3) this assignment of the fast and slow terms accurately predicted steady-state respiratory quotient and CO(2) output. Therefore, the kinetic model can quantify the dynamics of fat and CHO oxidation over the first 5-10 min of mild exercise in young adult men and women.