Aerobic fitness, endurance training, and orthostatic intolerance.
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Aerobiosis↗
Biomedical subjects
V A Convertino
Publications and source records attributed to V A Convertino.
Exercise training-induced hypervolemia in the horse.
The purpose of this study was to determine if a chronic hypervolemia would accompany endurance exercise training in the horse. Six mature previously inactive horses were utilized for this study. During the 5-wk experiment, five of the horses were trained for 14 d on a treadmill ergometer at a constant treadmill speed of 5.6 km X hr-1 and a constant grade of 12.5% for graduated lengths of time. One horse was trained by lunging at a trotting pace in a round pen. Following training, plasma volume increased by 4.7 1 (29.1%, P less than 0.05). Although the rate of daily water intake did not change during the training period, 24-h urine output decreased by an average of 3.5 1 X d-1 (-24.5%, P less than 0.05). Resting glomerular filtration rate and the rate of sodium clearance were not altered by training. However, urea, potassium, and osmotic clearance were decreased by training (P less than 0.05) while free water clearance was increased (P less than 0.05). Resting plasma aldosterone and arginine vasopressin concentrations were not altered by training. Plasma potassium concentration was significantly decreased (P less than 0.05) following the 2 wk of training. These data would appear to suggest that renal control mechanisms affecting water reabsorption via the re-absorption of urea and osmotically active substances other than sodium provide the primary route for the training-induced hypervolemia seen in horses.
Aldosterone↗
Potential benefits of maximal exercise just prior to return from weightlessness.
The purpose of this study was to determine whether performance of a single maximal bout of exercise during weightlessness within hours of return to earth would enhance recovery of aerobic fitness and physical work capacities under a 1G environment. Ten healthy men (36-51 yr) underwent maximal supine exercise followed by upright maximal exercise before and after a 10-d bedrest period in the 6 degrees headdown position. A graded maximal supine cycle ergometer test was performed before and at the end of bedrest to simulate exercise during weightlessness. Following 3 h of resumption of the upright posture from the supine exercise test, a second maximal exercise test was performed on a treadmill to measure work capacity under conditions of 1G. Compared to before bedrest, peak VO2 decreased (p less than 0.05) by 8.7% and peak HR increased (p less than 0.05) by 5.6% in the supine cycle test at the end of bedrest. However, there were no significant changes in peak VO2 and peak HR in the upright treadmill test following bedrest. These data, based on a simulation, suggest that one bout of maximal leg exercise prior to return from 10 d of weightlessness may be adequate to restore preflight aerobic fitness and physical work capacity.
Adult↗
Logistic risk model for the unique effects of inherent aerobic capacity on +Gz tolerance before and after simulated weightlessness.
Small sample size (n less than 10) and inappropriate analysis of multivariate data have hindered previous attempts to describe which physiologic and demographic variables are most important in determining how long humans can tolerate acceleration. Data from previous centrifuge studies conducted at NASA/Ames Research Center, utilizing a 7-14 d bed rest protocol to simulate weightlessness, were included in the current investigation. After review, data on 25 women and 22 men were available for analysis. Study variables included gender, age, weight, height, percent body fat, resting heart rate, mean arterial pressure, VO2max, and plasma volume. Since the dependent variable was time to greyout (failure), two contemporary biostatistical modeling procedures (proportional hazard and logistic discriminant function) were used to estimate risk, given a particular subject's profile. After adjusting for pre-bed-rest tolerance time, none of the profile variables remained in the risk equation for post-bed-rest tolerance greyout. However, prior to bed rest, risk of greyout could be predicted with 91% accuracy. All of the profile variables except weight, MAP, and those related to inherent aerobic capacity (VO2max, percent body fat, resting heart rate) entered the risk equation for pre-bed-rest greyout. A cross-validation using 24 new subjects indicated a very stable model for risk prediction, accurate within 5% of the original equation. The result for the inherent fitness variables is significant in that a consensus as to whether an increased aerobic capacity is beneficial or detrimental has not been satisfactorily established. We conclude that tolerance to +Gz acceleration before and after simulated weightlessness is independent of inherent aerobic fitness.
Acceleration↗
Plasma aldosterone and sweat sodium concentrations after exercise and heat acclimation.
This investigation was designed to determine the relationship between the levels of plasma aldosterone and eccrine sweat gland sodium excretion following exercise and heat acclimation. Ten subjects exercised at 45% of their maximal O2 uptake in a hot (40 degrees C), moderately humid (45% relative humidity) environment for 2 h/day on ten consecutive days. Acclimation was verified by significant reductions in exercise heart rate, rectal temperature, and heat storage, as well as significant elevation of resting plasma volume (12%, P less than 0.05) and exercise sweat rate on day 10 compared with day 1 of acclimation. During exercise, the concentration and total content of sodium in sweat as well as plasma aldosterone were significantly decreased from day 1 to day 10. The ratio of sweat sodium reabsorbed to plasma aldosterone concentration was significantly increased from day 1 to day 10 after both 1 and 2 h of exercise. These data indicate that plasma aldosterone concentrations decrease following heat acclimation; and eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augumented through exercise and heat acclimation.
Acclimatization↗
Cardiovascular dynamics associated with tolerance to lower body negative pressure.
The purpose of this investigation was to identify cardiovascular responses associated with tolerance to lower body negative pressure (LBNP). In this study, 18 men, ages 29-51 years, were categorized as high (HT) or low (LT) LBNP tolerant based on a graded presyncopal-limited LBNP exposure criterion of -60 mm Hg relative to ambient pressure. Groups were matched for physical characteristics and preLBNP cardiovascular measurements, with the exceptions of greater (p less than 0.05) end-diastolic volume and cardiac output in the HT group. During peak LBNP, cardiac output was similar (NS) in both groups, although the HT group displayed a greater heart rate (p less than 0.05). In both groups, venous return appeared to limit cardiac output resulting in decreased arterial pressure. Tolerance to LBNP did not appear solely dependent on the absolute amount of blood pooled in the legs since the HT group demonstrated a greater (p less than 0.05) peak LBNP-induced increase in midthigh-leg volume. Greater tolerance to LBNP was associated with a larger preLBNP cardiac output reserve and higher compensatory increases in heart rate and peripheral resistance.
Adult↗
Plasma viscosity elevations with simulated weightlessness.
Bed rest studies which simulate weightlessness have demonstrated marked changes in the state of hydration of subjects as well as decrements in aerobic capacity. These two phenomena may be linked through increases in blood viscosity which is altered by a loss of free water and which, in turn, influences blood flow needed for aerobic muscular work. This study examines changes in the rheologic properties of blood which attend changes in plasma volume with bed rest in humans and correlates these changes with alterations in aerobic capacity. Eight healthy human subjects were studied on the 6th day of bed rest during two consecutive 10-d bed rest periods separated by a 14-d recovery interval designed to simulate the flight-layover schedule of shuttle astronauts. Plasma viscosity was measured with a Wells-Brookfield viscometer, plasma volume by dye dilution, and maximal aerobic capacity (VO2max) by recumbent cycle ergometry. Bed rest resulted in significant increases in hematocrit and in total plasma protein concentration and fibrinogen concentration, both of which contribute to an elevation in plasma viscosity. The greater than 20% increase in fibrinogen concentration was much greater than could be explained by hemoconcentration. VO2max decreased significantly in the first but not the second bed rest cycle. In many individuals, a decrease in plasma volume and aerobic capacity was coupled with elevated plasma viscosity and hematocrit; however, significant correlations between these variables were lacking. Although significant rheologic perturbations do occur with bed rest, in this study, blood viscosity elevation failed to directly correlate with the reduction in VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Aerobic fitness does not contribute to prediction of orthostatic intolerance.
Several investigations have suggested that orthostatic tolerance may be inversely related to aerobic fitness (VO2max). To test this hypothesis, 18 males (age 29 to 51 yr) underwent both treadmill VO2max determination and graded lower body negative pressures (LBNP) exposure to tolerance. VO2max was measured during the last minute of a Bruce treadmill protocol. LBNP was terminated based on pre-syncopal symptoms, and LBNP tolerance (peak LBNP) was expressed as the cumulative product of LBNP and time (torr-min). Changes in heart rate, stroke volume, cardiac output, blood pressure, and impedance rheographic indices of mid-thigh-leg fluid accumulation were measured at rest and during the final minute of LBNP. For all 18 subjects, mean (+/- SE) fluid accumulation index and leg venous compliance index at peak LBNP were 139 +/- 22 ml and 3.9 +/- 0.4 ml . 100 ml . torr-min-2 x 10(3), respectively. Pearson product-moment correlations and step-wise linear regression were used to investigate relationships with peak LBNP. Variables associated with endurance training, such as VO2max and percent body fat, were not found to correlate significantly (P less than 0.05) with peak LBNP and did not add sufficiently to the prediction of peak LBNP to be included in the step-wise regression model. The step-wise regression model included only fluid accumulation index, leg venous compliance index, and blood volume, and resulted in a squared multiple correlation coefficient of 0.978. These data do not support the hypothesis that orthostatic tolerance as measured by LBNP is lower in individuals with high aerobic fitness.
Adult↗
Bedrest-induced peak VO2 reduction associated with age, gender, and aerobic capacity.
To compare the factors of age and gender on aerobic work capacity following bedrest-induced deconditioning, peak oxygen uptake (peak VO2), heart rate (peak HR), and exercise tolerance time were measured in 15 middle-aged men (55 +/- 2 yr) and 17 middle-aged women (55 +/- 1 yr) before and after 10 d of continuous bedrest (BR). The average body weight following BR was unchanged in both men and women. Following BR, peak VO2 decreased from 35.6 +/- 2.0 to 32.6 +/- 1.1 ml . kg-1 . min-1 (-8.4%, p less than 0.05) in the men and from 26.5 +/- 1.4 to 24.7 +/- 1.3 ml . kg-1 . min-1 (-6.8%, p less than 0.05) in the women, while total exercise tolerance time was reduced by 8.1% (p less than 0.05) and 7.3% (p less than 0.05) in the men and women, respectively. The peak HR was elevated by BR from 158 +/- 4 to 165 +/- 4 bpm (+4.4%, p less than 0.05) in the men and from 157 +/- 4 to 159 +/- 4 bpm (+1.3%, NS) in the women. The percent changes in peak VO2, peak HR, and exercise tolerance time measured in the men were not significantly different compared to those of the women. The reduction in peak VO2 in the middle-aged men and women in the present study were comparable to the reductions of 9.3% and 7.8% observed in our earlier studies with 15 young men (21 +/- 1 yr) and 8 young women (28 +/- 2 yr), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adaptation, Physiological↗
Effect of simulated weightlessness on exercise-induced anaerobic threshold.
Ventilation (VE), CO2 output (VCO2), oxygen uptake (VO2), respiratory exchange ratio (R), and the ventilatory equivalents for VO2 and VCO2 were measured during graded exercise before and after 10 d of continuous bed rest (BR) in the -6 degrees head-down position to determine the effect of deconditioning on the anaerobic threshold (AT), i.e., the highest workrate or VO2 which was achieved without evidence of lactic acidosis, as judged from the profile of ventilatory and gas exchange responses. Ten healthy male subjects performed a supine graded cycle ergometer test before (pre) and after (post) BR which consisted of 4 min of unloaded pedaling at 60 rpm followed by an increased workrate of 15 W X min-1 until volitional fatigue (max). VE, VCO2, VO2, R, VE/VO2 and VE/VCO2 were measured every 30 s and used collectively to identify the AT. Plasma (PV) and blood (BV) volumes were measured pre- and post-BR by T-1824. Following BR, VO2max decreased from 2.42 +/- 0.17 to 2.25 +/- 0.13 L X min-1 (7.0%, p less than 0.05). BR significantly (p less than 0.05) reduced the AT from 1.26 +/- 0.09 to 0.95 +/- 0.05 L X min-1 VO2; from 52.2 +/- 2.0 to 42.6 +/- 1.6% VO2max; and from 93 +/- 9 to 65 +/- 6 W. A correlation coefficient (r) of -0.11 (NS) was found between the change in VO2max and change in AT. A decrease in BV of 8.8% (p less than 0.05) was due to the 11.0% reduction in PV; red cell volume remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)
Acidosis↗
Exercise training-induced hypervolemia in greyhounds: role of water intake and renal mechanisms.
The purpose of this study was to determine if the chronic hypervolemia that accompanies endurance exercise training is due only to an increase in the rate of water intake or if there were contributions from renal mechanisms. Four greyhound dogs, previously sedentary for 3 yr, were utilized. During the 28-day experiment each dog was trained on a treadmill ergometer for 14 consecutive days at 65% of its pretraining maximal work intensity. After training, plasma volume increased 472 ml (27.5%, P less than 0.05). The rate of water intake increased 328 ml/day (33%, P less than 0.05), whereas urine output increased 87 ml/day (20.8%, P less than 0.05). The mean resting 24-h values for clearance of sodium increased 0.29 ml/min (90.3%, P less than 0.05), and clearance of potassium decreased 1.51 ml/min (16.1%, NS). Glomerular filtration rate, free water clearance, and osmotic clearance were not significantly altered. These data suggest that the primary mechanism for the exercise training-induced hypervolemia in dogs is a net positive water balance via increased water consumption without significant contribution from an increase in renal water reabsorption.
Animals↗
Response to muscular exercise following repeated simulated weightlessness.
The effect of repeated weightlessness exposures on maximal aerobic capacity was determined when seven healthy men (36-48 yr) underwent two 10-d bedrest (BR) periods in the -6 degrees headdown position, which were separated by a 14-d recovery period. No prescribed exercise was performed by the subjects during the course of the experiment. A graded supine cycle ergometer test consisting of 4 min of unloaded pedaling at 60 rpm followed by increased work rate of 15 W X min-1 until volitional fatigue (max) was performed before (pre) and after (post) the first and second BR periods, i.e., BR1 and BR2, and again 14 d after BR2 (REC). During exercise, submaximal and maximal oxygen uptake (VO2), ventilation (VE), heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures were measured and the gas exchange anaerobic threshold (AT) was determined. Plasma volume (Vp, T-1824) and body composition were measured pre- and post-BR1 and BR2 and following REC. Compared to the respective pre-BR control values, VO2max decreased (p less than 0.05) by 8.7% after BR1 and 5.2% after BR2 but returned to pre-BR values following 14 d REC. Submaximal and maximal HR increased (p less than 0.05) post-BR1 and BR2 but returned to pre-BR levels after REC. The AT and Vp decreased (p less than 0.05) post-BR1 and BR2 but returned to pre-BR levels after REC. Body weight increased (p less than 0.05) gradually during the experiment and did not return to control values.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
VO2 kinetics of constant-load exercise following bed-rest-induced deconditioning.
The purpose of this study was to determine the effects of bed-rest-induced deconditioning on changes in O2 uptake (VO2) kinetics, O2 deficit, steady-state VO2, and recovery VO2 during the performance of constant-load exercise. Five male subjects (36-40 yr) underwent 7 days of continuous bed rest (BR) in the head-down (-6 degrees) position. Two days before (pre) and the day after (post) BR each subject performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min of rest, 5 min of cycle ergometer exercise at 700 kg.m/min, and 10 min of recovery from exercise. VO2 was measured continuously in all tests from 2-liter aliquot gas samples collected every 30 s. Following BR steady-state VO2 was unchanged in supine and upright exercise. In the supine position BR did not change total exercise VO2, O2 deficit, or total recovery VO2. However, compared with pre-BR, total exercise VO2 decreased (P less than 0.05) from 7.41 +/- 0.11 to 7.23 +/- 0.17 liters, O2 deficit increased (P less than 0.05) from 1.15 +/- 0.05 to 1.41 +/- 0.07 liters, and total recovery VO2 increased (P less than 0.05) from 5.17 +/- 0.11 to 5.47 +/- 0.17 liters during the post-BR upright test. Despite the ability to attain similar steady-state VO2 within 5 min, bed-rest-induced deconditioning resulted in a reduction of total VO2 capacity and an increase in the O2 deficit during submaximal constant-load exercise. This change in VO2 kinetics is found only with exercise in the upright rather than supine position implicating orthostatic mechanisms in the delayed response to submaximal exercise.
Adult↗
Role of cardiac volume receptors in the control of ADH release during acute simulated weightlessness in man.
Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce central blood volume shifts in ten cardiac and one heart-lung transplant recipients to assess the contribution of cardiac volume receptors in the control of ADH release during the initial acute phase of exposure to weightlessness. Each subject underwent 15 min of a sitting-control period (C) followed by 30 min of -6 degrees headdown tilt (T) and 30 min of resumed sitting (S). Venous blood samples and cardiac dimensions were taken at 0 and 15 min of C; 5, 15, and 30 min of T; and, 5, 15, and 30 min of S. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Heart rate (HR) and blood pressure (BP) were recorded every two min. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P < .05) from 90 ml in C to 106 ml in T and returned to 87 ml in S. Plasma ADH was reduced by 20% (P < .05) with T and returned to control levels with S. These responses were similar in six normal cardiac-innervated control subjects. These data may suggest that cardiac volume receptors are not the primary mechanism for the control of ADH release during acute central volume shifts in man.
Adult↗
Oxygen uptake kinetics of constant-load work: upright vs. supine exercise.
The purpose of this study was to compare oxygen uptake (VO2), O2 deficit, steady-state VO2, and recovery VO2 during the performance of a constant-load exercise in the supine and upright position. Ten male subjects (36-40 yr) performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min rest, 5 min cycle ergometer exercise at 700 kg X min-1 and 10 min of recovery from exercise. The VO2 was measured continuously in all tests from 2-L aliquot air samples collected every 30 s. Steady-state VO2 was similar during supine and upright exercise. However, total VO2 during upright exercise was 0.30 L greater (p less than 0.05) than during supine exercise while O2 deficit and recovery VO2 in the upright position were 0.64 L and 0.22 L less (p less than 0.05) compared to the supine test. The larger O2 deficit during supine exercise resulted from a significantly greater VO2 halftime compared to that of the upright response. Despite the ability to eventually attain similar steady-state VO2, supine exercise results in a reduction of total VO2 capacity associated with an increase in the O2 deficit during submaximal constant-load exercise and manifested by elevated recovery VO2.
Adult↗
Cardiovascular responses during orthostasis: effect of an increase in VO2max.
Cardiovascular responses to orthostasis were assessed in eight men (18-29 years old) before and after an 8-d cycle ergometer exercise training (E) regimen for 2 h . d-1 at 65% maximal O2 uptake (VO2 max). Each subject underwent 60 degrees head-up tilt (60 min max) before (T1) and after (T2) E. Heart rate (HR), systolic (SBP), and diastolic (DBP) pressures were measured each min before, during, and after tilt; pulse pressure (PP), mean arterial pressure (MAP), and rate-pressure-product (RPP) were calculated. Changes in plasma renin activity (PRA), vasopressin (pVP), hematocrit, hemoglobin, and plasma volume (PV, T-1824) were measured from venous blood samples taken pre- and immediately post-tilt. Following E, VO2 max increased by 8.3% (p less than 0.05), resting HR decreased by 8.1% (p less than 0.05), and PV increased by 430 ml (12.2%, p less than 0.05). Mean (+/- S.E.) tilt duration went from 40.0 +/- 5.1 min during T1 to 46.7 +/- 3.4 min during T2 (NS); mean tilt HR decreased from 86 +/- 4 bpm to 77 +/- 3 bpm (p less than 0.05), RPP decreased from 10,320 +/- 390 to 9,317 +/- 310 mm Hg . bpm (p less than 0.05), while mean SBP, DBP, PP, and MAP were unchanged. Plasma volume decreased during tilt by 479 ml in T1 compared to 544 ml in T2 (p less than 0.05), while % delta PV were similar: -13.6% and -13.9%, respectively. Peak fluid-accumulation in the calf and total leg during tilt increased (p less than 0.05) following E.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Mechanisms for decreased exercise capacity after bed rest in normal middle-aged men.
The mechanisms responsible for the decrease in exercise capacity after bed rest were assessed in 12 apparently healthy men aged 50 +/- 4 years who underwent equilibrium gated blood pool scintigraphy during supine and upright multistage bicycle ergometry before and after 10 days of bed rest. After bed rest, echocardiographically measured supine resting left ventricular end-diastolic volume decreased by 16% (p less than 0.05). Peak oxygen uptake during supine effort after bed rest was diminished by 6% (p = not significant [NS]), whereas peak oxygen uptake during upright effort declined by 15% (p less than 0.05). After bed rest, increases in heart rate were also greater during exercise in the upright than in the supine position (p less than 0.05). Values of left ventricular ejection fraction increased normally during both supine and upright effort after bed rest and were higher than corresponding values before bed rest (p less than 0.05). After bed rest, increased left ventricular ejection fraction and heart rate largely compensated for the reduced cardiac volume during supine effort, but these mechanisms were insufficient to maintain oxygen transport capacity at levels during upright effort before bed rest. These results indicate that orthostatically induced cardiac underfilling, not physical deconditioning or left ventricular dysfunction, is the major cause of reduced effort tolerance after 10 days of bed rest in normal middle-aged men.
Bed Rest↗
Plasma volume, renin, and vasopressin responses to graded exercise after training.
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Adult↗