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Convertino, V. A.

Publications and source records attributed to Convertino, V. A..

At least 73 records · Page 4

Interaction of the carotid baroreflex, the muscle chemoreflex and the cardiopulmonary baroreflex in man during exercise

The interaction of the muscle chemoreflex and the cardiopulmonary baroreflex with the carotid baroreflex in humans performing exercise was investigated in healthy subjects using specially designed exercise regimen and apparatus. Stimulation of the muscle chemoreflex was achieved by restricting blood flow in the exercising muscles by means of applying a pressure of 50 mm Hg, whereas cardiopulmonary baroreceptors were unloaded by employing LBNP of -20 mm Hg. The carotid baroreceptors were unloaded and stimulated by neck-pressure maneuvers (Sprenkle et al., 1986). Results showed that the cardiodecelerating capacity of the carotid baroreflex remains active during exercise, and may even be sensitized by the chemoreflex-induced increase in arterial pressure; but it is not affected by the cardiopulmonary baroreceptor activity.

Eiken, O.

Elevated central venous pressure: a consequence of exercise training-induced hypervolemia?

Resting blood volumes and arterial and central venous pressures (CVP) were measured in 14 men before and after exercise training to determine whether training-induced hypervolemia is accompanied by a change in total vascular capacitance. In addition, resting levels of plasma arginine vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (Ald), and norepinephrine (NE) were measured. The same measurements were conducted in seven subjects who did not undergo exercise and acted as controls. Exercise training consisted of 10 wk of controlled cycle exercise for 30 min/day, 4 days/wk at 75-80% of maximal O2 uptake (VO2max). A training effect was verified by a 20% increase in VO2max, a resting bradycardia, and a 9% increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased by 16% (P less than 0.05). The percent change in blood volume from before to after training was linearly related to the percent change in CVP (r = 0.903, P less than 0.05). As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was unchanged after exercise training. Plasma AVP, ANP, Ald, and NE were unaltered. Our results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance.

NASA Program Space Physiology and Countermeasures

Baroreflex responses and LBNP tolerance following exercise training

The hypothesis that endurance exercise training designed to increase aerobic capacity results in reduced orthostatic tolerance due to alterations of blood-pressure controlling mechanisms was reexamined using a specially designed training in which tolerance to orthostasis and the primary mechanisms associated with the blood-pressure control could be measured before and after the increase in aerobic capacity. Results demonstrate that maximal oxygen uptake can be significantly elevated in individuals of average fit without reducing lower body negative pressure tolerance. The exercise training was found to cause a resting bradycardia, which had no effect on the cardiac vagal reflex response.

Convertino, V. A.

Hemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans

Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in ten cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 deg head down tilt (HDT) followed by 20 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15, and 30 min of HDT, and 5, 15, and 30 min of seated recovery. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Resting plasma volume (PV) was measured by Evans blue dye and percent changes in PV during posture changes were calculated from changes in hematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. Results indicate that cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

Convertino, V. A.

Carotid baroreflex response following 30 days exposure to simulated microgravity

The mechanism of the carotid-baroreflex response to weightlessness was investigated in human subjects exposed to simulated microgravity (30 days of 6-day head-down bed rest followed by 5 days of recovery). Baroreceptor-cardiac reflex responses were elicited by a complex sequence of pressure changes delivered to a neck chamber device. The shape of the sigmoid baroreceptor-cardiac response curve was examined for alterations and the occurrence of resetting, as well as for a possible association of the impaired baroreflex function with hypotension during the postexposure orthostatic stress. It was found that the exposure to head-down bed rest caused a significant shift on the R-R interval axis, which paralleled reductions and elevations in baseline HR such that the baseline R-R (operational point) remained in the same position on the response curve. This shift in the location of the reflex relation indicates a significant resetting of the carotid baroreceptors, which may represent an appropriate adaptation which contributes to the maintenance of a constant resting arterial blood pressure before, during, and after bed rest, observed in these study.

Convertino, V. A.

Plasma aldosterone and sweat sodium concentrations after exercise and heat acclimation

The relationship between plasma aldosterone levels and sweat sodium excretion after chronic exercise and heat acclimation was investigated, using subjects exercised, at 40 C and 45 percent humidity, for 2 h/day on ten consecutive days at 45 percent of their maximal oxygen uptake. The data indicate that, following heat acclimation, plasma aldosterone concentrations decrease, and that the eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augmented through exercise and heat acclimation.

Kirby, C. R.

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). Eighteen 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 pre-LBNP 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 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 pre-LBNP cardiac output reserve and higher compensatory increases in heart rate and peripheral resistance.

Sather, T. M.

Plasma viscosity elevations with simulated weightlessness

A hypothesis correlating an increase in blood viscosity during bed rest to a decrease in aerobic capacity during simulated weightlessness is tested. Eight human subjects were studied on the sixth 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 and volume were measured, together with maximal aerobic capacity (VO2max). An increase in hematocrit, plasma protein, and fibrinogen concentrations was found, contributing to an elevation in plasma viscosity. VO2max decreased significantly in the first, but not the second bed rest cycle, and though many individuals exhibited a decrease in plasma volume and aerobic capacity coupled with elevated plasma viscosity, correlations between these variables were lacking. It is concluded that the decrease in VO2max observed following simulated weightlessness cannot be attributed to alterations in muscle blood flow resulting from increased blood viscosity.

Martin, D. G.

Effect of simulated weightlessness on exercise-induced anaerobic threshold

The effect of simulated weightlessness, induced by ten days of continuous bedrest (BR) in the -6 deg head-down position, on the exercise-induced anaerobic threshold (AT) was determined by comparing specific ventilatory and gas-exchange measurements during an incremental ergometer test performed before and after BR. The primary index for determining the exercise-induced AT values of each subject was visual identification of the workrate or oxygen uptake (VO2) at which the ratio of the expired minute ventilation volume (VE) to VO2 exhibited a systematic increase without a concomitant increase in the VE/VCO2 value. Following BR, the mean VO2max of the subjects decreased by 7.0 percent, and the AT decreased from a mean of 1.26 L/min VO2 before BR to 0.95 L/min VO2 after BR. The decrease in AT was manifested by a decrease in both absolute and relative workrates. The change in AT correlated significantly with the change in plasma volume but not with the change in VO2max. The results suggest that the reduction in AT cannot be completely explained by the reduction in VO2, and that the AT decrease is associated with the reduction in intravascular fluid volume.

Convertino, V. A.

Bedrest-induced peak VO2 reduction associated with age, gender, and aerobic capacity

A study measuring the peak oxygen uptake (V02), heart rate (HR), and exercise tolerance time of 15 men of 55 + or - 2 yr and 17 women of 55 + or - 1 yr after 10 days of continuous bed rest (BR) is presented. The experimental conditions and procedures are described. Following BR a decrease in peak VO2 of 8.4 percent in men and 6.8 percent in women, a reduction in exercise tolerance time by 8.1 percent in men and 7.3 percent in women, and an increse in HR of 4.4 percent and 1.3 percent for men and women, respectively, are observed. These data are compared with data from Convertino et al. (1977) for men 21 + or - 1 yr and women 28 + or - 2yr. It is concluded that BR-induced aerobic deconditioning is independent of age and sex, since the relative decrease in peak V02 in the older and younger subjects and men and women are similar.

Convertino, V. A.

Response to muscular exercise following repeated simulated weightlessness

The effects of 10-d 6-deg-head-down bed rest (BR1), 14 d of recovery, another 10 d bed rest (BR2), and another 14-d recovery on the cardiovascular response to a graded supine cycle ergometer test (4 min unloaded 60-rpm pedaling followed by 15-W/min increasing work load to volitional fatigue) are investigated experimentally in seven male nonsmokers of mean age 41 yrs, mean weight 80.2 kg, mean height 178 cm, and mean body fat content 22.3 percent. Ergometer tests are performed before BR1, after BR1 and BR2, and 14 d after BR2. The results are presented in tables, and it is found that the significantly decreased maximum-O2-uptake, gas-exchange-aerobic-threshold, and plasma-volume responses and the increased submaximal and maximal heart rates observed (relative to pre-BR1 levels) after BR1 and BR2 return to pre-BR1 values 14 d after BR2. It is inferred that 14 d of mild exercise are adequate for recovery from even repeated exposure to this type of simulated weightlessness.

Convertino, V. A.

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 deg 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 and blood pressure were recorded every two min. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 ml in C to 106 ml in T and returned to 87 ml in S. Plasma ADH was reduced by 20 percent (P less than 0.05) 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.

Convertino, V. A.

VO2 kinetics of constant-load exercise following bed-rest-induced deconditioning

Previous studies have shown that the oxygen uptake kinetics during exercise and recovery may be changed by alterations in work intensity, prior exercise, muscle group involvement, ambient conditions, posture, disease state, and level of physical conditioning. However, the effects of detraining on oxygen uptake kinetics have not been determined. The present investigation has the objective to determine the effects of deconditioning following seven days of continuous head-down bed rest on changes in steady-state oxygen uptake, O2 deficit, and recovery oxygen uptake during the performance of constant-load exercise. The obtained results may provide support for previous proposals that submaximal oxygen uptake was significantly reduced following bed rest. The major finding was that bed-rest deconditioning resulted in a reduction of total O2 transport/utilization capacity during the transient phase of upright but not supine exercise.

Convertino, V. A.

Cardiovascular responses during orthostasis - Effect of an increase in maximal O2 uptake

A study is described which tests the hypothesis that changes in aerobic activity (increases in maximum oxygen uptake) will reduce the effectiveness of cardiovascular reflexes to regulate blood pressure during orthostasis. The hypothesis was tested by measuring heart rate, blood pressure and blood volume responses in eight healthy male subjects before and after an eight-day endurance regimen. The results of the study suggest that the physiologic responses to orthostasis are dependent upon the rate of plasma volume loss and pooling, and are associated with training-induced hypervolemia. It is indicated that endurance type exercise training enhances cardiovascular adjustments during tilt. The implications of these results for the use of exercise training as a countermeasure and/or therapeutic method for the prevention of cardiovascular instability during orthostatic stress are discussed.

Convertino, V. A.

Oxygen uptake kinetics of constant-load work - Upright vs. supine exercise

Supine and upright positions were used in a comparitive study of the effects of constant load exercise on oxygen uptake (VO2), O2 deficit, steady-state VO2 and VO2 following recovery from constant load work. Ten male subjects (36-40 yr.) performed one submaximal exercise test in the supine and one test in the upright position consisting of 5 min rest and 5 min cycle ergometer exercise at 700 kg/min followed by ten minutes of recovery. It is found that the significant difference in VO2 kinetics during exercise in the upright compared to supine position resulted from changes in oxygen transport and utilization mechanisms rather than changes in mechanical efficiency. To the extent that data measured in the supine position can be used to estimate physiological responses to zero gravity, it is suggested that limitation of systemic O2 consumption may be the result of slow rates of oxygen uptake during transient periods of muscular work. Significant reductions in the rate of steady-state VO2 attainment at submaximal work intensities may produce an onset of muscle fatigue and exhaustion.

Convertino, V. A.

Handgrip and general muscular strength and endurance during prolonged bedrest with isometric and isotonic leg exercise training

Measurements of maximal grip strength and endurance at 40 percent max strength were obtained for 7 men 19-21 years of age, 1-2 days before and on the first recovery day during three 2-week bedrest (BR) periods, each separated by a 3-week ambulatory recovery period. The subjects performed isometric exercise (IME) for 1 hr/day, isotonic exercise (ITE) for 1 hr/day, and no exercise (NOE) in the three BR periods. It was found that the mean maximal grip strength was unchanged after all three BR periods. Mean grip endurance was found to be unchanged after IME and ITE training, but was significantly reduced after NOE. These results indicate that IME and ITE training during BR do not increase or decrease maximal grip strength, alghough they prevent loss of grip endurance, while the maximal strength of all other major muscle groups decreases in proportion to the length of BR to 70 days. The maximal strength reduction of the large muscle groups was found to be about twice that of the small muscle groups during BR. In addition, it is shown that changes in maximal strength after spaceflight, BR, or water immersion deconditioning cannot be predicted from changes in submaximal or maximal oxygen uptake values.

Greenleaf, J. E.

Plasma volume, renin, and vasopressin responses to graded exercise after training

Four male subjects underwent a series of ergometer trials to test the hypothesis that training-induced hypervolemia produces a reduction in the relative change of plasma volume, vasopressin, and renin activity levels. Sitting ergometer exercise was performed for 2 hr per day for 8 consecutive days and the VO2 was monitored. A second phase involved a graded exercise and recording of the VO2 and HR, as well as the taking of blood samples to measure the plasma osmolality, the vasopressin content, and the renin activity. The training was found to reduce the plasma volume levels for a given work load. Hypervolemia was induced by a training-produced plasma volume expansion. The osmolality, vasopressin content, and renin activity increased with training. A threshold work intensity of 50 percent was identified for changes in the osmolality and the stimulation of renin activity and vasopressin increase. The maintenance of a certain level of intensity during training is concluded necessary to stimulate the hypervolemic response.

Convertino, V. A.

VO2 kinetics during submaximal exercise following simulated weightlessness

A study is presented of the effects of deconditioning following 7 days of continuous head-down (-6 degrees) bedrest on changes in steady-state VO2, O2, and recovery VO2 during the performance of constant-load exercises. The deconditioning effects of bedrest on the physical working capacity were manifested in the subjects by significant changes in VO2 kinetics following the 7 days of head-down bedrest. While the subjects demonstrated the ability to attain similar steady-state VO2, simulated weightlessness using head-down bedrest resulted in a reduction of total VO2 capacity and an increase in the O2 deficit and VO2 halftime during submaximal constant-load exercise. It is concluded that this change in VO2 kinetics was induced by reexposure of the cardiovascular system to the +1 Gz (upright) environment.

Convertino, V. A.