Effects of increased muscle perfusion pressure on responses to dynamic leg exercise in man

Summary Ventilatory, cardiovascular and metabolic functions and work performance were studied in men performing incremental-load dynamic leg exercise until exhaustion.Part I: Responses to supine exercise were investigated in 8 subjects during exposure of the lower body to subatmospheric pressure at –6.67 kPa (–50 mm Hg) (Lower Body Negative Pressure, LBNP). Due to curtailment of stroke volume, cardiac output was reduced by LBNP over a wide range of work intensities, including heavy loads: ventilation, oxygen uptake and blood lactate concentrations increased with work load, but at lower rates than in the control condition.Part II: In 9 subjects, work performance was compared in three conditions: supine exercise with and without LBNP, and upright exercise. Performance in supine exercise was enhanced by LBNP, and was further improved in upright exercise. In supine exercise, the LBNP-induced reduction in blood lactate and enhancement of work performance are attributed to a more efficient muscle blood flow resulting from increased local perfusion pressure. This strongly suggests that the primary limitation of work performance was set by the peripheral circulation in working muscles rather than by cardiac performance. A similar mechanism may, in part, explain why work performance in dynamic leg exercise was greater in the upright than in the supine posture. It is also concluded that supine leg exercise during LBNP is a useful model of upright exercise, with regard to the central circulation and the circulation in working muscles.     

Evaluation of Mechanisms of Postflight Orthostatic Intolerance with a Simple Cardiovascular System Model

A significant fraction of astronauts experience postflight orthostatic intolerance (POI) during 10-min stand tests conducted on landing day. The average time that nonfinishers can stand is about 7 min. This phenomenon, including the delay in occurrence of presyncope, was studied with a five-compartment model of the cardiovascular system incorporating compartments for the heart/lungs, systemic arteries and cephalic, central, and caudal veins. The model included 28 independent parameters, including factors characterizing cardiac performance, vascular resistance, intrathoracic pressure, nonlinear venous compliance and circulating blood volume, and 13 dependent parameters, including cardiac output and cardiac and vascular compartment pressures and volumes. First, a sensitivity analysis of hemodynamic indicators of presyncope to independent parameters was performed. Results demonstrated that both cardiac output and arterial pressure were most sensitive to volume-related parameters, particularly total blood volume, and less sensitive to peripheral resistance. Next, a simulated postflight stand test confirmed that fluid loss due to capillary filtration, particularly from the caudal region where transmural pressure is high during standing, is a plausible mechanism of POI that also explains the delayed onset of symptoms in most astronauts. An accumulated drop in arterial pressure sufficient to compromise cerebral perfusion and, therefore, cause syncope was reached in about 7 min with a fluid loss of 280 mL. Finally, additional simulations showed that a 75% increase in peripheral resistance, similar to finishers of stand tests, was insufficient to overcome the loss of circulating fluid associated with capillary filtration, and extended the time that the modeled astronaut could stand by only about 1 min. It is therefore concluded that capillary filtration may play a key role in producing POI and that development of countermeasures should perhaps focus on reducing postflight capillary permeability or on stimulating volume-compensating mechanisms.     

Hemodynamic and neurohumoral responses to the restriction of femoral blood flow by KAATSU in healthy subjects

The application of an orthostatic stress such as lower body negative pressure (LBNP) has been proposed to minimize the effects of weightlessness on the cardiovascular system and subsequently to reduce the cardiovascular deconditioning. The KAATSU training is a novel method to induce muscle strength and hypertrophy with blood pooling in capacitance vessels by restricting venous return. Here, we studied the hemodynamic, autonomic nervous and hormonal responses to the restriction of femoral blood flow by KAATSU in healthy male subjects, using the ultrasonography and impedance cardiography. The pressurization on both thighs induced pooling of blood into the legs with pressure-dependent reduction of femoral arterial blood flow. The application of 200 mmHg KAATSU significantly decreased left ventricular diastolic dimension (LVDd), cardiac output (CO) and diameter of inferior vena cava (IVC). Similarly, 200 mmHg KAATSU also decreased stroke volume (SV), which was almost equal to the value in standing. Heart rate (HR) and total peripheral resistance (TPR) increased in a similar manner to standing with slight change of mean blood pressure (mBP). High-frequency power (HF_RR) decreased during both 200 mmHg KAATSU and standing, while low-frequency/high-frequency power (LF_RR/HF_RR) increased significantly. During KAATSU and standing, the concentration of noradrenaline (NA) and vasopressin (ADH) and plasma renin activity (PRA) increased. These results indicate that KAATSU in supine subjects reproduces the effects of standing on HR, SV, TPR, etc., thus stimulating an orthostatic stimulus. And, KAATSU training appears to be a useful method for potential countermeasure like LBNP against orthostatic intolerance after spaceflight.     

Cardiovascular effects of anti-G suit inflation at 1 and 2 G

We sought to determine to which pressure a full-coverage anti-G suit needs to be inflated in order to obtain the same stroke volume during a brief exposure to twice the normal gravity (2 G) as that at 1 G without anti-G suit inflation. Nine sitting subjects were studied at normal (1 G) and during 20 s of exposure to 2 G. They wore anti-G suits, which were inflated at both G-levels to the following target pressures: 0, 70, 140 and 210 mmHg. Stroke volume was computed from cardiac output, which was measured by rebreathing. Heart rate and mean arterial pressure at heart level were recorded. Inflation to 70 mmHg compensated for the decrease in stroke volume and cardiac output caused by hypergravity. Mean arterial pressure at heart level was comparable at 1 G and at 2 G and increased gradually and similarly with inflation (P<0.001) at both gravity levels. Thus, anti-G suits act by increasing both preload and afterload but the two effects counteract each other in terms of cardiac output, so that cardiac output at 2 G is maintained at its 1 G level. This effect is reached already at 70 mmHg of inflation. Greater inflation pressure further increases mean arterial pressure at heart level and compensates for the increased difference in hydrostatic pressure between heart and head in moderate hypergravity.     

Increased hypoxic ventilatory response during hypovolemic stress imposed through head-up-tilt and lower-body negative pressure

The aim of this study was to quantify the influence of head-up-tilt (HUT) on the isocapnic hypoxic ventilatory response (HVR) in man, and to investigate the effect of orthostatic blood shifts separately from other gravitational effects by the application of lower-body negative pressure (LBNP) with subjects in a horizontal position. HVR was measured in 15 subjects during passive HUT from 0° to 85° as well as during −7° head-down-tilt and while they were in a sitting position. In a subgroup of eight subjects the effect of 85° HUT was compared to a corresponding LBNP of −70 mbar on HVR. Moreover, by imposing graded HUT (7°, 15°, 30°, 50°) and LBNP (−15, −30 mbar) we studied the effect of low-level orthostatic stress on HVR. Ventilation, end-tidal partial pressure of CO₂, heart rate and blood pressure were recorded continuously for 1 min before, and during HVR. HVR was significantly increased by ≅50% through both 85° HUT and −70 mbar LBNP as compared to 0° and 0 mbar, respectively, at unchanged mean arterial pressure. Low-level HUT and LBNP had no effect on HVR. It was concluded that the orthostatic HVR increase may be attributable to caudal blood shifts (i.e., central hypovolemia). This HVR increase requires a pronounced hypovolemic stress but no decrease in arterial blood pressure. It is suggested that a central interaction of arterial and cardiopulmonary baroreceptors is underlying this response. Their separate contribution remains to be assessed. Accepted: 14 October 1999     

Forced expiratory flow-volume curves during the application of lower-body negative pressure

Ten normal subjects were studied during supine rest and quiet standing, and when exposed, supine, to lower-body negative pressure (LBNP) of 30, 40 and 50 mmHg, each for a period of 7 min, in random order. Their partial and complete flow-volume curves, heart rate and blood pressure were recorded during the last 3 min in each condition. The expected reflex cardiovascular responses to the decrease in central blood volume during standing and during LBNP were seen. The forced vital capacity was somewhat greater during standing and during LBNP than while supine. The airflow variables measured from the flow-volume curve-except MEF25% (partial)--were significantly increased during progressive LBNP but did not reach the raised values found when the posture changed from supine to standing. The observations suggest that besides the redistribution of the central blood volume to the periphery, other factors must contribute to the increase in airflows during standing.     

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (f _c), stroke volume (SV), cardiac output (Q˙ _c), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of f _c, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at ?30 torr (LBNP ?30, where 1 torr?=?133.32?N/m²), and (3) for PARA only, LBNP ?30 with ES-induced leg muscle contractions (LBNP?+?ES). LBNP ?30 elicited a decrease in SV (by 23% and 22%), Q˙ _c (by 15% and 18%) and the PNS indicator, but an increase in f _c (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP ?30, LBNP?+?ES increased SV (by 20%) and Q˙ _c (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP ?30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP ?30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.     

Lower Body Negative Pressure and Effects of Autonomic Heart Blockade on Cardiovascular Responses

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48 % of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

Lower body negative pressure and effects of autonomic heart blockade on cardiovascular responses.

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48% of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

Comparison of supine and sitting body position during a triangular exercise test

Summary A comparison of haemodynamic parameters is performed during a triangular exercise test on bicycle ergometer in respect of studying the influence of supine and sitting body position.At the maximal symptom-limited work load reached the heart rate is on the average 9.2% higher, the arterial systolic pressure 16.1% and the cardiac output 17.2% less in the sitting body position (P<0.001).On the opposite the pulmonary artery pressure during work is of slightly but not significantly higher level in the sitting position than in the supine. This phenomenon is explained by a prevailing of the beta-adrenergic tonus in our untrained subjects, while total sympathetic stimulation seems to be comparable in both body positions.     

Circulatory effects of carotid sinus stimulation and changes in blood volume distribution in hypertensive man

In 8 patients with moderate hypertension and 8 normotensive subjects an attempt was made to study the circulatory effects of high and low pressure baroreceptor stimulation. Intrathoracic low pressure receptors were stimulated by changes in blood volume distribution using lower body negative pressure (LBNP) and lower body positive pressure (LBPP). The carotid sinus was stimulated by sinusoidal neck suction. Blood pressure, central venous pressure, heart rate, cardiac output and forearm blood flow were recorded. During LBNP and LBPP changes in central blood volume, reflected in changes in central venous pressure, induced significantly greater changes in cardiac output and forearm blood flow in the hypertensive subjects. In both normotensive and hypertensive subjects mean arterial blood pressure was essentially unchanged during LBNP and a slight increase was found during LBPP. Heart rate and blood pressure response to stimulation of the carotid sinus decreased with increasing resting mean arterial pressure. The results suggest impairment of reflex adjustments, via arterial baroreceptors, possibly in particular to dynamic stimuli, rather than via intrathoracic “low pressure” baroreceptors in subjects with moderate hypertension.     

Cardiac responses to the Valsalva manoeuvre in different body positions

Summary A standardized Valsalva manoeuvre (VM) with a 15-s straining period was repeated in each of four postures by six male subjects. The postures were supine (SUP), sitting leaning back (LB), sitting leaning forward (LF) and standing (ST). During straining, the increase in heart rate (f _c) was different between LB and LF (+50% and +23%, respectively P<0.05). The decrease in stroke volume (SV), which was monitored by means of impedance cardiography, was different (63%, 68%, 39%, and 72%, P<0.001) as well as the decrease in cardiac output (CO) (55%, 53%, 26%, and 61%, P<0.001) in SUP, LB, LF, and ST, respectively. Accordingly, after pressure release the smallest changes of SV, f _c and CO were found in LF. In conclusion, cardiovascular stability during straining was increased during LF. Consequently, this posture would appear to be superior to other postures during unavoidable VM (weight lifting and defaecation). To perform tests on autonomic function LB would appear to be superior to the other postures because of the large autonomic responses, combined with minimum risk for the subject. The impedance method provided simple and reproducible determinations of SV changes during VM.     

Cardiac responses to lower body negative pressure and dynamic leg exercise

Summary Cardiac responses to dynamic leg exercise at 0, 50, and 100 W in the supine position were investigated with and without the lower portion of the body exposed to a pressure of –6.6 kPa (Lower Body Negative Pressure, LBNP). Resting values for heart rate (HR) and stroke volume (SV) were considerably higher and lower, respectively, during LBNP than in the control condition. At the transition from rest to the mildest exercise during LBNP SV showed a prompt increase by about 40%, but no significant change in the control condition. HR, which increased by 17 beats · min^–1 in the control condition, showed during LBNP no change initially and subsequently a small but significant drop below its resting value. Steady-state values for HR at the various levels of exercise were not significantly affected by LBNP, whereas corresponding values for SV were considerably lowered, so that exercise values for cardiac output were about 3 l · min^–1 less during LBNP than in the control condition. The reductions in SV and cardiac output indicate residual pooling of blood in intra- and extramuscular capacitance vessels of the legs. With a change from rest to exercise at 100 W during LBNP mean systolic ejection rate (MSER) increased by 67%, the relations between SV and MSER suggesting that ventricular performance was maintained by a combination of the Frank-Starling mechanism and enhanced contractile strength.     

Effects of microgravity on interstitial muscle receptors affecting heart rate and blood pressure during static exercise

Summary Afferent nerve fibers from receptors situated in the interstitium of skeletal muscles can induce cardiovascular reflexes. It has been shown that these interstitial muscle receptors are also sensitive to the local state of hydration: increased heart rates and blood pressure values were seen during dynamic and static exercise after local dehydration on earth. Since weightlessness leads to a persisting fluid loss in the lower part of the body, we hypothesized that leg exercise in space would augment heart rate and blood pressure responses to a similar extent as during local, interstitial dehydration on earth. Initial measurements during weightlessness were obtained in one subject after 6 days of space flight. Heart rate and blood pressure responses to light static foot plantar flexion (18% of maximal voluntary contraction) were recorded in two sessions. To eliminate the influence of muscle perfusion, exercise was performed during a period of arterial occlusion obtained by means of pneumatic cuffs at mid-thigh level. Identical protocols were used in the pre- and postflight controls, which were performed both in the sitting posture and in a –90° tilted sitting posture assumed 30–40 min before arterial occlusion. During weightlessness the exercise responses of heart rate and systolic and diastolic blood pressure closely followed the tracings obtained with the tilted sitting posture on ground. The response amplitudes in these states of reduced lower limb volumes (about 20/min and 20 mmHg, respectively) exceeded the responses in the supine position by a factor of at least 2. Enhancement of cardiovascular reflexes following local fluid losses of skeletal muscles appears to be a general phenomenon that can also be seen during weightlessness.Abbreviations EMG Electromyogram - LBNP Lower body negative pressure - MVC Maximal voluntary contraction     

Simulation study of the effects of hypovolaemia on cardiovascular response to orthostatic stress

To investigate the role played by hypovolaemia in the mechanism of orthostatic intolerance, a mathematical model was developed. The model consisted of seven sub-models that describe: the redistribution of blood induced by lower body negative pressure (LBNP); filling of the left ventricle; contracting of the left ventricle; interaction between the left ventricle and peripheral circulation; and baroreflex regulation. The model was evaluated using experimental data. Using the model, computer simulations were performed to investigate the effects of hypovolaemia on the cardiovascular response to LBNP. The simulation results indicated that, first, when the blood loss is less than 5%, blood pressure can be maintained in the normal range by the baroreflex regulatory mechanism, even with high LBNP application; secondly, when the blood loss is between 15 and 20%, heart rate and blood pressure can be kept in the normal range if LBNP is not applied, but blood pressure falls sharply with LBNP application; and, thirdly, when the blood loss is 25%, the cardiovascular system is in an unstable state (heart rate: 116beat min⁻¹, systolic blood pressure: 97 mmHg; diastolic blood pressure: 77 mmHg), even without any LBNP, and becomes more unstable with LBNP. The simulation results support the hypothesis that hypovolaemia is a cause of orthostatic intolerance.     

Effect of Changes in Blood Volume Distribution on Circulatory Variables and Plasma Renin Activity in Man

In 8 healthy subjects the pressure around the lower body was changed to 40 mmHg above (LBPP) and below (LBNP) atmospheric, thereby altering the amount of blood pooled in the lower body. Heart rate, intraarterial blood pressure, central venous pressure, cardiac output (dye dilution technique) and forearm blood flow (venous occlusion plethysmography) were measured. Plasma renin activity was determined with a radioimmunological method. 6 subjects maintained a relative circulatory steady state during LBNP. LBNP caused significant decreases in central venous pressure (CVP), stroke volume and cardiac output (0) with an unchanged mean arterial pressure (MAP). Heart rate (HR) increased significantly. Calculated total peripheral vascular resistance (TPVR) and regional vascular resistance (RVR) in the forearm were significantly increased when measured 5–9 min after the onset of LBNP, whereas plasma renin activity (PRA) showed a definite increase only after 19 min of LBNP stimulation. No correlation was found between the changes in PRA and TPVR or RVR. Increasing the pressure around the lower body (LBPP) resulted in a slight but significant increase in MAP as well as a significant but transient increase in CVP. No significant changes were found in HR, Q or TPVR. In the forearm a decrease in RVR was demonstrated. PRA was not significantly changed. The results demonstrate that peripheral vascular resistance and PRA are both influenced by changes in blood volume distribution, possibly elicited via intrathoracic receptors sensitive to changes in central blood volume and/or CVP. The results also suggest that PRA does not play any significant part in the vasoconstriction during LBNP stimulation.     

Subclinical orthostatic pulse pressure confirms mothers' ratings of ADHD in preschoolers

Subclinical levels of orthostatic hypotension (OH) have been linked to a variety of emotional and behavioral outcomes across the life span. These connections are not surprising, given the multitude of correlated conditions, including autonomic control, cardiovascular functioning, baroreceptor activity, and dopamine and serotonin. The current study assessed blood pressure regulation in healthy preschool children ages 3–5 (n = 61). The Conner's Parent Rating Scale Revised was used to assess indexes of attention deficit hyperactivity disorder (ADHD). With the difference between standing and supine pulse pressure as the index of orthostatic blood pressure regulation, the results indicated that efficient pulse pressure regulation was significantly correlated with lower ADHD scores. Poorer orthostatic pulse pressure regulation in response to an orthostatic challenge may be a risk for symptoms of ADHD.     

Simulated Stand Tests and Centrifuge Training to Prevent Orthostatic Intolerance on Earth,Moon, and Mars

One proposed method to overcome postflight orthostatic intolerance is for astronauts to undergo inflight centrifugation. Cardiovascular responses were compared between centrifuge and gravitational conditions using a seven-compartment cardiovascular model. Vascular resistance, heart rate, and stroke volume values were adopted from literature, while compartmental volumes and compliances were derived from impedance plethysmography of subjects (n = 8) riding on a centrifuge. Three different models were developed to represent the typical male subject who completed a 10-min postflight stand test (“male finisher”), “non-finishing male” and “female” (all non-finishers). A sensitivity analysis found that both cardiac output and arterial pressure were most sensitive to total blood volume. Simulated stand tests showed that female astronauts were more susceptible to orthostatic intolerance due to lower initial blood pressure and higher pressure threshold for presyncope. Rates of blood volume loss by capillary filtration were found to be equivalent in female and male non-finishers, but four times smaller in male finishers. For equivalent times to presyncope during centrifugation as those during constant gravity, lower G forces at the level of the heart were required. Centrifuge G levels to match other cardiovascular parameters varied depending on the parameter, centrifuge arm length, and the gravity level being matched.     

Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake ( O_2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6°) head-down tilt (HDT), each subject underwent graded LBNP to –6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither O_2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.     

Resistance exercise training and the orthostatic response

Resistance exercise has been suggested to increase blood volume, increase the sensitivity of the carotid baroreceptor cardiac reflex response (BARO), and decrease leg compliance, all factors that are expected to improve orthostatic tolerance. To further test these hypotheses, cardiovascular responses to standing and to pre-syncopal limited lower body negative pressure (LBNP) were measured in two groups of sedentary men before and after a 12-week period of either exercise (n = 10) or no exercise (control, n = 9). Resistance exercise training consisted of nine isotonic exercises, four sets of each, 3 days per week, stressing all major muscle groups. After exercise training, leg muscle volumes increased (P?P = 0.00) by 2.0 (0.5)?kg, leg compliance and BARO were not significantly altered, and the maximal LBNP tolerated without pre-syncope was not significantly different. Supine resting heart rate was reduced (P = 0.03) without attenuating the heart rate or blood pressure responses during the stand test or LBNP. Also, blood volume (¹²⁵I and ⁵¹Cr) and red cell mass were increased (P?相似文献