Aortic-cardiac reflex during dynamic exercise.

We investigated the aortic-cardiac reflex during low-intensity cycling in 10 healthy volunteers. Baroreflex function was assessed by the ratio of change in heart rate to mean arterial pressure (delta HR/delta MAP) during phenylephrine (PE) infusion. The ratio obtained during PE combined with low-level lower body negative pressure (LBNP) and calculated neck pressure (NP) was assessed as the gain of the aortic-cardiac reflex. Exercise (approximately 25% maximal O2 uptake or 25 +/- 2 W) significantly increased HR from 64 +/- 2 to 98 +/- 2 beats/min, MAP from 90 +/- 3 to 98 +/- 3 mmHg, cardiac output from 6.6 +/- 0.5 to 12.0 +/- 1.4 l/min, and O2 uptake from 3.8 +/- 0.2 to 10.4 +/- 0.6 ml.min-1.kg-1. However, delta MAP (+11.8 +/- 0.4 vs. + 11.3 +/- 0.8 mmHg), delta HR (-12.7 +/- 2 vs. -12.9 +/- 2 beats/min), and delta HR/delta MAP (1.10 +/- 0.19 vs. 1.15 +/- 0.15 beats.min-1.mmHg-1) were not statistically different between rest and exercise during PE. Although PE significantly increased central venous pressure in both supine rest (from 6.7 +/- 0.7 to 10.4 +/- 0.7 mmHg) and exercise (5.8 +/- 0.8 to 8.6 +/- 0.9 mmHg) conditions, when LBNP (-15 +/- 2 vs. -16 +/- 1 Torr for rest vs. exercise) was applied, both rest and exercise central venous pressures were returned to the preinfusion baseline values, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic baroreflex control of heart rate after 15 days of simulated microgravity exposure.

To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects (mean age 38 +/- 3 yr) to 15 days of bed rest in the 6 degrees head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex (from 0.45 +/- 0.07 to 0.84 +/- 0.18 beats.min-1.mmHg-1; P = 0.03). Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.

Brain activation by central command during actual and imagined handgrip under hypnosis.

The purpose was to compare patterns of brain activation during imagined handgrip exercise and identify cerebral cortical structures participating in "central" cardiovascular regulation. Subjects screened for hypnotizability, five with higher (HH) and four with lower hypnotizability (LH) scores, were tested under two conditions involving 3 min of 1) static handgrip exercise (HG) at 30% of maximal voluntary contraction (MVC) and 2) imagined HG (I-HG) at 30% MVC. Force (kg), forearm integrated electromyography, rating of perceived exertion, heart rate (HR), mean blood pressure (MBP), and differences in regional cerebral blood flow distributions were compared using an ANOVA. During HG, both groups showed similar increases in HR (+13 +/- 5 beats/min) and MBP (+17 +/- 3 mmHg) after 3 min. However, during I-HG, only the HH group showed increases in HR (+10 +/- 2 beats/min; P < 0.05) and MBP (+12 +/- 2 mmHg; P < 0.05). There were no significant increases or differences in force or integrated electromyographic activity between groups during I-HG. The rating of perceived exertion was significantly increased for the HH group during I-HG, but not for the LH group. In comparison of regional cerebral blood flow, the LH showed significantly lower activity in the anterior cingulate (-6 +/- 2%) and insular cortexes (-9 +/- 4%) during I-HG. These findings suggest that cardiovascular responses elicited during imagined exercise involve central activation of insular and anterior cingulate cortexes, independent of muscle afferent feedback; these structures appear to have key roles in the central modulation of cardiovascular responses.

Altered thermoregulatory responses after 15 days of head-down tilt.

To determine whether extended exposure to a simulation of microgravity alters thermoregulatory reflex control of skin blood flow, six adult males (mean age 40 +/- 2 yr) were exposed to 15 days of 6 degrees head-down tilt (HDT). On an ambulatory control day before HDT exposure and on HDT day 15, the core temperature of each subject was increased by 0.5-1.0 degree C by whole body heating with a water-perfused suit. Mean skin temperature, oral temperature (Tor), mean arterial pressure, and forearm blood flow were measured throughout the protocol. Forearm vascular conductance (FVC) was calculated from the ratio of forearm blood flow to mean arterial pressure. After HDT exposure, the Tor threshold at which reflex thermally induced increases in FVC began was elevated (36.87 +/- 0.06 to 37.00 +/- 0.09 degrees C; P = 0.043), whereas the slope of the Tor-FVC relationship after this threshold was reduced (13.7 +/- 2.3 to 9.5 +/- 1.1 FVC units/degrees C; P = 0.038). Moreover, normothermic FVC and FVC at the highest common Tor between pre- and post-HDT trials were reduced after HDT (normothermic: 4.2 +/- 0.5 to 3.0 +/- 0.4 ml.100 ml-1.min-1.100 mmHg-1, P = 0.04; hyperthermic: 12.4 +/- 1.0 to 7.8 +/- 0.7 ml.100 ml-1.min-1.100 mmHg-1, P < 0.001). These data suggest that HDT exposure reduces thermoregulatory responses to heat stress. The mechanisms resulting in such an impaired thermoregulatory response are unknown but are likely related to the relative dehydration that accompanies this exposure.

Resetting of the carotid arterial baroreflex during dynamic exercise in humans.

Recent investigations have demonstrated that at the onset of low-to-moderate-intensity leg cycling exercise (L) the carotid baroreflex (CBR) was classically reset in direct relation to the intensity of exercise. On the basis of these data, we proposed that the CBR would also be classically reset at the onset of moderate- to maximal-intensity L exercise. Therefore, CBR stimulus-response relationships were compared in seven male volunteers by using the neck pressure-neck suction technique during dynamic exercise that ranged in intensity from 50 to 100% of maximal oxygen uptake (VO(2 max)). L exercise alone was performed at 50 and 75% VO(2 max), and L exercise combined with arm (A) exercise (L + A) was performed at 75 and 100% VO(2 max). O(2) consumption and heart rate (HR) increased in direct relation with the increases in exercise intensity. The threshold and saturation pressures of the carotid-cardiac reflex at 100% VO(2 max) were >75% VO(2 max), which were in turn >50% VO(2 max) (P < 0.05), without a change in the maximal reflex gain (G(max)). In addition, the HR response value at threshold and saturation at 75% VO(2 max) was >50% VO(2 max) (P < 0.05) and 100% VO(2 max) was >75% VO(2 max) (P < 0.07). Similar changes were observed for the carotid-vasomotor reflex. In addition, as exercise intensity increased, the operating point (the prestimulus blood pressure) of the CBR was significantly relocated further from the centering point (G(max)) of the stimulus-response curve and was at threshold during 100% VO(2 max). These findings identify the continuous classic rightward and upward resetting of the CBR, without a change in G(max), during increases in dynamic exercise intensity to maximal effort.

Blood pressure regulation during cardiac autonomic blockade: effect of fitness.

The purpose of this study was to determine the role of the autonomic nervous system's control of the heart in fitness-related differences in blood pressure regulation. The cardiovascular responses to progressive lower-body negative pressure (LBNP) were studied during unblocked (control) and full blockade (experimental) conditions in 10 endurance-trained (T) and 10 untrained (UT) men, aged 20-31 yr. The experimental conditions included beta 1-adrenergic blockade (metoprolol tartrate), parasympathetic blockade (atropine sulfate), or complete blockade (metoprolol and atropine). Heart rate, blood pressure, forearm blood flow, and cardiac output were measured at rest and -16 and -40 Torr LBNP. Forearm vascular resistance, peripheral vascular resistance, and stroke volume were calculated from these measurements at each stage of LBNP. Blood pressure was maintained, primarily by augmented vasoconstriction, equally in T and UT subjects during complete and atropine blockade. The fall in systolic and mean pressure from 0 to -40 Torr was greater (P less than 0.05) in the T subjects during the unblocked and metoprolol blockade conditions. This reduced blood pressure control during unblocked condition was attributable to attenuated vaso-constrictor and chronotropic responses in the T subjects. We hypothesize that an autonomic imbalance (elevated base-line parasympathetic activity) in highly trained subjects restricts reflex cardiac responses, which accompanied by an attenuated vasoconstrictor response, results in attenuated blood pressure control during a steady-state hypotensive stress.

Hypnotic manipulation of effort sense during dynamic exercise: cardiovascular responses and brain activation.

The purpose of this investigation was to hypnotically manipulate effort sense during dynamic exercise and determine whether cerebral cortical structures previously implicated in the central modulation of cardiovascular responses were activated. Six healthy volunteers (4 women, 2 men) screened for high hypnotizability were studied on 3 separate days during constant-load exercise under three hypnotic conditions involving cycling on a 1) perceived level grade, 2) perceived downhill grade, and 3) perceived uphill grade. Ratings of perceived exertion (RPE), heart rate (HR), blood pressure (BP), and regional cerebral blood flow (rCBF) distributions for several sites were compared across conditions using an analysis of variance. The suggestion of downhill cycling decreased both the RPE [from 13 +/- 2 to 11 +/- 2 (SD) units; P < 0.05] and rCBF in the left insular cortex and anterior cingulate cortex, but it did not alter exercise HR or BP responses. Perceived uphill cycling elicited significant increases in RPE (from 13 +/- 2 to 14 +/- 1 units), HR (+16 beats/min), mean BP (+7 mmHg), right insular activation (+7.7 +/- 4%), and right thalamus activation (+9.2 +/- 5%). There were no differences in rCBF for leg sensorimotor regions across conditions. These findings show that an increase in effort sense during constant-load exercise can activate both insular and thalamic regions and elevate cardiovascular responses but that decreases in effort sense do not reduce cardiovascular responses below the level required to sustain metabolic needs.

Baroreflex function in endurance- and static exercise-trained men.

The effect of exercise training mode on reflex cardiovascular control was studied in a cross-sectional design. We examined the cardiovascular responses to progressive incremental phenylephrine (PE) infusion to maximal rates of 120 micrograms/min and the delta heart rate/delta blood pressure responses to lower body negative pressure (LBNP) to -50 Torr in 30 men who were either endurance exercise trained (ET), untrained (UT), or weight trained (WT). During PE infusion, measures of blood pressures, forearm blood flow, heart rate and cardiac output, and calculations of forearm vascular resistance, stroke volume, and peripheral vascular resistance were made at each infusion rate when steady-state blood pressure was attained. No significant differences (P less than 0.05) in forearm blood flow or resistance were observed between the groups at any dose of PE, suggesting that the vasoconstrictor response was similar among the groups. Regression analyses of heart rate against mean blood pressure during the PE infusion were performed to evaluate baroreflex function. A linear model was used and correlation coefficients ranging from 0.82 to 0.96 were obtained (P less than 0.05). The slope of the line of best fit for the ET subjects (-0.57) was significantly less (P less than 0.05) than the slopes obtained for either the UT (-0.91) or WT (-0.88) subjects. In addition, the delta heart rate/delta blood pressure measurements obtained during LBNP reflected a similarly significant attenuation of reflex chronotropic control in the ET subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic baroreflex control of heart rate during hypertensive stimuli: effect of fitness.

We examined the aortic baroreflex control of heart rate (HR) in seven healthy young men of average fitness (AF) and seven of high fitness (HF). The fitness level was determined by maximal oxygen uptake (AF = 42.9 +/- 1.1, HF = 62.3 +/- 1.8 ml.kg-1.min-1). Aortic baroreflex control of HR was determined during a steady-state increase of mean arterial pressure (MAP; AF, +15.0 +/- 2.1 and HF, +18.3 +/- 0.8 mmHg) with phenylephrine (PE) infusion combined with positive neck pressure (NP; AF, 18 +/- 2.0 and HF, 20 +/- 0.8 mmHg) to counteract the increased carotid sinus pressure and with low levels of lower body negative pressure to counteract the increased central venous pressure. There was no group difference in the increased MAP or NP, nor was there stage difference in MAP within either group during PE infusion. However, the isolated cardiac-aortic baroreflex gains (i.e., delta HR/delta MAP) were significantly less in the HF (0.16 +/- 0.02 and 0.14 +/- 0.03 beats.min-1.mmHg-1) than in the AF (0.52 +/- 0.08 and 0.59 +/- 0.07 beats.min-1.mmHg-1) subjects at PE + NP and PE + NP + lower body negative pressure. We concluded that during steady-state increases in MAP, the sensitivity of aortic baroreflex control of HR was significantly less in the HF than in the AF subjects.

Carotid baroreflex function during prolonged exercise.

The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 +/- 1.8 vs. 11.6+/- 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.

Increases in intramuscular pressure raise arterial blood pressure during dynamic exercise.

This investigation was designed to determine the role of intramuscular pressure-sensitive mechanoreceptors and chemically sensitive metaboreceptors in affecting the blood pressure response to dynamic exercise in humans. Sixteen subjects performed incremental (20 W/min) cycle exercise to fatigue under four conditions: control, exercise with thigh cuff occlusion of 90 Torr (Cuff occlusion), exercise with lower body positive pressure (LBPP) of 45 Torr, and a combination of thigh cuff occlusion and LBPP (combination). Indexes of central command (heart rate, oxygen uptake, ratings of perceived exertion, and electromyographic activity), cardiac output, stroke volume, and total peripheral resistance were not significantly different between the four conditions. Mechanical stimulation during LBPP and combination conditions resulted in significant elevations in intramuscular pressure and mean arterial pressure from control at rest and throughout the incremental exercise protocol (P < 0.05). Conversely, there existed no significant changes in mean arterial pressure when the metaboreflex was stimulated by cuff occlusion. These findings suggest that under normal conditions the mechanoreflex is tonically active and is the primary mediator of exercise pressor reflex-induced alterations in arterial blood pressure during submaximal dynamic exercise in humans.

An overview of the problem: exercise training and orthostatic intolerance.

The questions, whether endurance exercise training (a) induces orthostatic intolerance and (b) alters blood pressure regulation during orthostasis, have been debated since the early 1970s. This symposium presents data that both support and discount the concepts. In addition, data were presented that document invasive and noninvasive techniques of measurement used during investigations of baroreflex and hemodynamic mechanisms of blood pressure regulation during lower body negative pressure (LBNP), a laboratory technique that simulates orthostasis. These techniques and the results obtained enabled the formulation of a hypothetical mechanism of explanation of the "pro and con" of the debated questions.

Chronic endurance exercise training: a condition of inadequate blood pressure regulation and reduced tolerance to LBNP.

We review the hypotheses presented to account for the anecdotal and literature-based reports that chronic endurance exercise training reduces orthostatic tolerance. The findings from cross-sectional investigations of unfit subjects and endurance athletes are examined, as well as limited data from recent investigations of the changes in orthostatic tolerance and blood pressure regulation that occur after 8 d to 8 months of endurance exercise training. Statistical models have not found wide variations in maximal aerobic power (VO2max) to contribute to the prediction of orthostatic responses. However, research data are generally consistent that the orthostatic tolerance of athletes whose VO2max exceeds 65 ml.kg-1.min-1 is lower than that of sedentary control subjects. These two findings suggest that it is exercise training, rather than VO2max, that reduces orthostatic tolerance. Findings from a recent longitudinal investigation corroborate this theory. We conclude that at least four factors associated with exercise training contribute to the development of orthostatic intolerance. These include: a) increased limb compliance (although its effect is likely to be trivial), b) eccentric ventricular hypertrophy, and c) increases in total blood volume, which may attenuate cardiopulmonary baroreflex responsiveness, shift ventricular function to a steeper portion of the ventricular compliance curve, and increase the inhibitory effect of cardiopulmonary baroreceptors on carotid baroreflex responsiveness; and d) an independent effect that reduces carotid and aortic baroreflex responsiveness. These mechanisms mimic changes observed in pathological states such as heart failure and hypertension. Our conclusions are best summarized by Greenleaf et al. (J. Appl. Physiol. 51:298-305, 1981): ""Trained men can run, but they cannot stand.''

Unilateral carotid-cardiac baroreflex responses in exercise trained and untrained men.

To determine effects of aerobic exercise training on individual contributions of the right and left carotid sinus baroreflex control of the cardiac interval, heart rate [expressed as R-R Interval (RRI)] and mean arterial pressure (MAP) responses were elicited by pulsed trains of neck suction and pressure in exercise trained (ET = 8) and untrained (UT = 8) men. ET subjects had a greater (mean +/- SD) maximal oxygen uptake (VO2max) than UT subjects (ET = 64.5 +/- 2.4 ml.kg.min-1 vs UT = 39.8 +/- 3.7 ml.kg.min-1; P < 0.001). A neck collar device was modified for delivery of suction and pressure pulses to only one side of the neck. Carotid-cardiac gains for right, left, and bilateral baroreflexes were determined from the logistic function of RRI responses to changes in estimated carotid sinus pressure (ECSP). There were no significant differences in the maximal gains for bilateral (ET = 6.4 +/- 1.8 vs UT = 5.9 +/- 1.3 ms.mm Hg-1 ECSP), right sided (ET = 5.3 +/- 1.2 vs UT = 4.5 +/- 1.2 ms.mm Hg-1 ECSP) or left sided (ET = 3.3 +/- 1.8 vs UT = 3.6 +/- 1.8 ms.mm Hg-1 ECSP) responses between groups and both groups demonstrated an inhibitory summation of reflexes. We suggest that right and left carotid-cardiac responses, as well as the summation of these reflexes, are quantitatively similar in exercise trained and untrained subjects.

Cardiovascular responses to lower body negative pressure in endurance and static exercise-trained men.

The cardiovascular responses to lower body negative pressure (LBNP) (to -50 torr) were examined in 8 sedentary control (UT), 8 endurance-trained (ET), and 8 weight-trained (WT) human subjects. The results were used to compare and contrast the blood pressure control system of the three subject groups. The primary differences in response included a more effective maintenance of blood pressure, by reason of greater stroke volume and cardiac indices of the WT subjects during LBNP (P less than 0.05). Peripheral vascular resistances were not different (P greater than 0.05) throughout LBN P between the three groups. Therefore, the improved blood pressure maintenance of the WT subjects was attributed to a cardiac effect. The ET subjects were less effective in maintaining blood pressure than UT or WT subjects. This finding was apparently due to an attenuated baroreflex sensitivity, as evidenced by a significantly (P less than 0.05) lower delta heart rate/delta systemic blood pressure ratio, 0.99 for ET vs 1.51 and 1.38 or the UT and WT groups respectively, calculated from the responses observed from 0 to -50 torr of LBNP.

The effects of oral smokeless tobacco on the cardiorespiratory response to exercise.

The purpose of this investigation was to determine the effects of oral smokeless tobacco (OST) usage on oxygen uptake (VO2), cardiac output (Qc), stroke volume (SV), heart rate (HR), and plasma lactate concentration (Lc) during rest and exercise. Fifteen asymptomatic subjects were recruited from 18 to 33-yr-old male users of OST. Comparisons of the responses of VO2, Qc, SV, HR, and Lc were made between 2.5-g OST and placebo experimental conditions during rest and at 60% and 85% maximal VO2 treadmill exercise. Plasma nicotine concentrations (Nc) were determined by radioimmunoassay. There were significant increases in HR and Lc and a decrease in SV during rest and at 60% and 85% maximal exercise (P less than 0.05). Furthermore, there were no significant differences in maximal HR, Lc, and VO2 (P greater than 0.05). In conclusion, these data indicate that the increased Nc incurred by OST usage increases anaerobic energy production and produces an increased tachycardiac response to a given relative submaximal workload.

Evaluation of the Cosmed K2 portable telemetric oxygen uptake analyzer.

The purpose of this study was to determine the validity and evaluate the accuracy of a portable telemetric oxygen uptake analyzer (K2). Two experiments were carried out: a) using a mechanical lung, the accuracy of the K2 to measure oxygen fractions and minute ventilation following 10 and 60 min of warm-up was determined; and b) two maximal graded exercise tests (GXT) on 15 subjects, one with the K2 system and the other with a standardized breath-by-breath (BBB) system, while heart rate (HR), minute ventilation (VE), and oxygen uptake (VO2) were compared. Following 10-min warm-up prior to calibration, the K2 underestimated the true oxygen fraction as early as 5 min into the test, and this value continued to decrease throughout the 30-min test. After 60 min of warm-up prior to calibration, the K2 accurately measured the true oxygen fraction for the first 15 min; at minute 20, and on to minute 30, the K2 underestimated the oxygen fraction. Ventilation volumes were not affected by warm-up time. Minute ventilation during the K2 GXT was significantly higher than VE for the BBB test. No significant differences were found between the HRs obtained with the BBB or K2 systems. No differences in VO2 for any stage of the GXT were identified between the K2 device, BBB device or when a respiratory exchange ratio (RER) correction factor was applied to the K2 derived values. However, the RER correction factor did minimize the VO2 differences between the BBB and K2 systems. Therefore, we conclude that the K2 accurately measures VO2 during a GXT; however, its accuracy can be compromised by limitations inherent to the system.

Benefits of aerobic exercise for the paraplegic: a brief review.

The importance of exercise for the general population is emphasized widely; therefore, it must be even more important for paralegics who are already threatened with poor health due to the sedentary nature of their lifestyle. The effects of functional degeneration are vast and greatly reduce the overall health of paraplegics, particularly within the musculoskeletal and cardiovascular systems, thereby increasing their risk for cardiovascular disease. Recent investigations suggest that this process may be reversible through exercise training and that paraplegics respond to exercise training in essentially the same manner as the non-handicapped individual. In addition, exercise training has been reported to decrease the resorptive process of the skeleton by decreasing bone and collagen catabolism and possibly aiding in new bone formation. This review attempts to summarize the available literature on the effects of exercise on the paraplegic and will hopefully provide some direction not only for further research but also recommendations for practitioners working in the field.

Effect of pedal rate on cardiorespiratory responses during continuous exercise.

The role of cycle ergometer pedal rate on the gradual increase in ventilation (VE), heart rate (HR), and oxygen uptake (VO2) accompanying continuous submaximal exercise is unknown. To examine this problem, five trained males (VO2peak = 4.00 +/- 0.27 l.min-1) performed 45 min of moderate intensity (MI, 127 W) and high-moderate intensity (HMI, 166 W) cycle ergometry both at pedal rates of 60 rpm and 90 rpm. Power output and pedal rate had an additive effect on the overall mean responses for VE, HR, and VO2, producing significantly higher values as power output and pedal rate increased. During continuous exercise, VE, HR, and VO2 increased progressively from the 10th to the 45th minute for all tests. However, the rates of increase and factors modifying the VE, HR, and VO2 responses were different. HR increased during all exercise tests an average of 10.8% independent of power output and pedal rate. VE increased 7.4% during MI exercise and 10% during HMI exercise independent of pedal rate. Similar power output dependent responses were observed for rectal temperature (Tr) and blood lactate. VO2 increased 4.4% for MI and HMI exercise at 60 rpm, and 8.2% for the same power outputs at 90 rpm, respectively. Increases in Tr, the oxygen cost of pulmonary ventilation and fat oxidation, and lactate removal were estimated to account for only 31-36% of the slow rise in VO2 for any single test. This suggests that 64-69% of the rise in VO2 was due to factors related to muscle use.(ABSTRACT TRUNCATED AT 250 WORDS)