Does heat acclimation improve exercise capacity at altitude? A cross-tolerance model.

New approaches to inducing altitude acclimation in a relatively short timeframe are needed, as it is not practical for many soldiers and athletes to gain access to specialized training facilities. Acclimation to one environmental stressor could enhance adaptation to various other stressors in animals and humans. This phenomenon has been described as cross-tolerance and involves the activation of common protective pathways. The purpose of this review is to discuss possible mechanisms involved in the cross-tolerance between heat and hypoxia. Future data could potentially support the use of a cross-tolerance model as a means for military personnel to prepare for deployment to high-altitude environments, as well as for athletes competing at high altitude.

Variations in exercise ventilation in hypoxia will affect oxygen uptake.

Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42-87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE-VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

VESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia.

This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈4,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the VESTPD at RER <1.0 was significantly lower and the VEBTPS was higher because of higher breathing frequency; at VO2max, both VESTPD and VEBTPS were not significantly different. As percent of VO2max, the VEBTPS was nearly identical and VESTPD was 30% lower throughout the exercise at 455 mmHg. The lower VESTPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where VESTPD at submaximal workloads was maintained or increased above that at sea level. The lower VESTPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO2 (≈0.17 pHa units), reduction in PACO2 (≈5 mmHg) and higher PAO2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict VESTPD from VO2 and PB in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in VESTPD at low workloads after arrival at altitude.

Plasma volume after heat acclimation: Variations due to season, fitness and methods of measurement.

PURPOSE: The reported magnitude of plasma volume increase (Δ%PV) following heat acclimation (HA) varies widely. Variations may result from differences in measurement techniques, season and subjects' fitness. This report compares direct and indirect measurements of Δ%PV after 10 days of HA from studies in winter (WIN, n = 8) and summer (SUM, n = 10) in men, age 21-43 yr, at two fitness levels (VO(2)max: 35 and 51 ml/min/kg). Direct measurements were made before and after HA (cycling at 30% of VO(2)max at 50 °C, for 100 min/day) by carbon monoxide (CO) rebreathing and compared with indirect estimates from changes in hematocrit, hemoglobin and plasma protein concentration. RESULTS: Overall, Δ%PV by CO was small (2.9%) and greater in SUM than WIN (5.0 vs. 0.3%). Red cell, blood and plasma volumes/kg lean body mass increased in SUM and decreased in WIN, the difference being significant, and Δ%PV by CO was similar for high and low VO(2)max. CONCLUSION: Overall, indirect estimates of Δ%PV by hemoglobin and hematocrit were similar to CO, but tended to differentiate by fitness and not season. The difference in THb increase in SUM and decrease in WIN was significant. This probably accounts for the differences from the seasonal and fitness results by the direct CO method.

Abnormal cerebrovascular responses to CO2 in sleep apnea patients.

The responses of common carotid blood flow (CCF), pressure (BP), and resistance (R) to variations in respiratory gases were compared during waking periods in 10 sleep apnea patients (SA) and 10 healthy controls (N) of similar age. Respiratory gases were altered by 3-min CO2 rebreathing (RB), 3-min hyperventilation (HV), and 4-min hypoxia (HYP) procedures. CCF was measured continuously by a 5-MHz pulsed Doppler duplex scanner and R was calculated using brachial BP. During RB, which increased end-tidal PCO2 (PACO2) by 15 mm Hg, SA had a lower CCF and greater BP response and therefore a significantly different (positive) change in R compared with N. The ventilatory responses to CO2 were not significantly different. With HV the PACO2 fell by 13 mm Hg in both groups and CCF fell more markedly in SA than N with the same change in BP; therefore, R was increased significantly more in SA. The HYP results did not demonstrate a difference between groups. These results suggest that abnormal cerebrovascular responses to PACO2, initiated either by unusual vasoactive properties of cerebral resistance vessels or peculiar venous outlow patterns, may initiate or potentiate periodic breathing in SA by prolonging lung-to-brain circulation time.

Sleep apnea and autonomic cerebrovascular dysfunction.

Changes in common carotid blood flow (CCF) and resistance index (RI), calculated from velocity waveforms by a noninvasive pulsed Doppler technique, were measured during apneic episodes and voluntary breath holding in five sleep apnea patients (SA) and during breath holding in five normal subjects (N). During apneic episodes averaging 27 s, CCF was reduced by 9% and RI increased by 4%, both trends being related to apneic duration. Internal carotid artery measurements in one SA indicated more dramatic changes in blood flow and RI than noted in CCF. During breath holding, CCF decreased significantly in SA but not in N, and RI showed a smaller reduction in SA. These changes in CCF and RI during sleep apnea are similar to those noted in anesthetized dogs where vasomotor waves and associated apneas were induced by elevating intracranial pressure. Previously reported recordings of ventilatory and systemic cardiovascular responses in SA are similar to these recordings in dogs, and it is therefore proposed that vasomotor responses to intermittent cerebral ischemia and hypercapnia may be the principle event in SA and periodic breathing only a secondary consequence of the prevailing autonomic dysfunction.

Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia.

Acute mountain sickness (AMS) strikes those in the mountains who go too high too fast. Although AMS has been long assumed to be due solely to the hypoxia of high altitude, recent evidence suggests that hypobaria may also make a significant contribution to the pathophysiology of AMS. We studied nine healthy men exposed to simulated altitude, normobaric hypoxia, and normoxic hypobaria in an environmental chamber for 9 h on separate occasions. To simulate altitude, the barometric pressure was lowered to 432 +/- 2 (SE) mmHg (simulated terrestrial altitude 4,564 m). Normobaric hypoxia resulted from adding nitrogen to the chamber (maintained near normobaric conditions) to match the inspired PO2 of the altitude exposure. By lowering the barometric pressure and adding oxygen, we achieved normoxic hypobaria with the same inspired PO2 as in our laboratory at normal pressure. AMS symptom scores (average scores from 6 and 9 h of exposure) were higher during simulated altitude (3.7 +/- 0.8) compared with either normobaric hypoxia (2.0 +/- 0.8; P < 0.01) or normoxic hypobaria (0.4 +/- 0.2; P < 0.01). In conclusion, simulated altitude induces AMS to a greater extent than does either normobaric hypoxia or normoxic hypobaria, although normobaric hypoxia induced some AMS.

Arterial-alveolar CO2 equilibration in exercising dogs during prolonged rebreathing.

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30-68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.

Effects of acid-base status on acute hypoxic pulmonary vasoconstriction and gas exchange.

To investigate the relationship between hypoxic pulmonary vasoconstriction and respiratory and metabolic acidosis and respiratory alkalosis, the pulmonary gas exchange and pulmonary hemodynamic responses were measured in anesthetized, paralyzed, and mechanically ventilated dogs in two sets of experiments (series A, n = 6; series B, n = 10). The animals were treated with acute hypoxia, CO2 inhalation, hyperventilation, and dinitrophenol in various combinations. Multiple regression analysis indicated that mean pulmonary arterial pressure (Ppa) was significantly correlated with end-tidal PO2, mixed venous PO2, and the mean pulmonary capillary pH (average of arterial and mixed venous pH) as independent variables [series A: r = +0.999, standard error of estimate (SEE) = 0.4 mmHg; series B: r = +0.98, SEE = 1.4 mmHg]. Similar analyses of mean values published by other authors from an acute study on humans with exercise at sea level and simulated altitudes of 10,000 and 15,000 ft also indicated a good relationship (n = 14, r = +0.98, SEE = 2.1 mmHg). The mean data (n = 19) obtained in Operation Everest II at various exercise loads and simulated altitudes gave a correlation of r = +0.87, SEE = 6.1 mmHg. These empirical analyses suggest that variations in the rise of Ppa with hypoxia can be accounted for in vivo by the superimposed acid-base status. Furthermore, ventilation-perfusion inhomogeneity, as estimated in the dogs from end-tidal and arterial O2 and CO2 differences and assuming no true shunt or diffusion impairment, was highly correlated with Ppa and mean pulmonary capillary pH (r = +0.999 in series A, r = +0.77 in series B). The human data from the above studies also showed significant correlations between Ppa and directly measured ventilation-perfusion (standard deviation of perfusion obtained from inert gas measurements). These observations indicate that the beneficial effects of hyperventilation during hypoxia may be related to the marked alkalosis that serves to reduce Ppa and improve pulmonary gas exchange efficiency.

Exercise exacerbates acute mountain sickness at simulated high altitude.

We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, approximately 4,800 m (J. B. West, J. Appl. Physiol. 81: 1850-1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (VE), pulmonary function, arterial oxygen saturation (Sa(O(2))), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 +/- 1.0 and 1.3 +/- 0.4 in Ex and Sed, respectively (P < 0.01); but resting VE and Sa(O(2)) were not different between trials. However, Sa(O(2)) during the exercise bouts in Ex was at 76.3 +/- 1.7%, lower than during either Sed or at rest in Ex (81.4 +/- 1.8 and 82.2 +/- 2.6%, respectively, P < 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3-6 h (P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

Acute effects of head-down tilt and hypoxia on modulators of fluid homeostasis.

In an effort to understand the interaction between acute postural fluid shifts and hypoxia on hormonal regulation of fluid homeostasis, the authors measured the responses to head-down tilt with and without acute exposure to normobaric hypoxia. Plasma atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), cyclic adenosine monophosphate (cAMP), plasma aldosterone (ALD), and plasma renin activity (PRA) were measured in six healthy male volunteers who were exposed to a head-down tilt protocol during normoxia and hypoxia. The tilt protocol consisted of a 17 degrees head-up phase (30 minutes), a 28 degrees head-down phase (1 hour), and a 17 degrees head-up recovery period (2 hours, with the last hour normoxic in both experiments). Altitude equivalent to 14,828 ft was simulated by having the subjects breathe an inspired gas mixture with 13.9% oxygen. The results indicate that the postural fluid redistribution associated with a 60-minute head-down tilt induces the release of ANP and cGMP during both hypoxia and normoxia. Hypoxia increased cGMP, cAMP, ALD, and PRA throughout the protocol and significantly potentiated the increase in cGMP during head-down tilt. Hypoxia had no overall effect on the release of ANP, but appeared to attenuate the increase with head-down tilt. This study describes the acute effects of hypoxia on the endocrine response during fluid redistribution and suggests that the magnitude, but not the direction, of these changes with posture is affected by hypoxia.

Circulation and respiration response to arm exercise and lower body negative pressure.

The effects of supine arm exercise and lower body negative pressure (LBNP) were studied in six subjects with 10 min of LBNP at -40 mmHg (L), arm cranking for 8 min at a work load of 225 kpm/min (E) and both combined (L + E) preceded by 2 min of LBNP. Initial responses of ventilation (VI) and VO2 were curtailed and heart rate was significantly higher after the first min of L + E than E, reflecting the less accessible venous reservoir and reduced stroke volume due to L. Leg volume was significantly reduced after 30 s of E and continued to decline and remained below baseline during 6 min of recovery. With L + E, leg volume remained constant after E began, indicating both a shift of blood from legs to arms and reduced extra-vasation with LBNP. End-tidal PO2, VI and VI/VO2 were higher and PCO2 lower during the latter stages of L + E than during E, indicating less effective lung perfusion and greater alveolar deadspace caused by LBNP. The release of pooled blood from the lower body after L + E caused a greater VI, VO2 and lower RE than after E and produced marked transients in PCO2 and PO2, thereby slowing the recovery of gas exchange.

The effects of low levels of CO2 on ventilation during rest and exercise.

BACKGROUND: Measurements of pulmonary gas exchange are especially sensitive to low levels of CO2 in the environment; this is an important consideration in measurements in enclosed spaces. METHODS: In order to determine the responses to these low levels, subjects were exposed in five studies to partial pressures of inspired CO2 (PICO2) of 5.7 and 7.5 mmHg for 30 min during basal conditions at rest and to 5.4, 9.4 and 15 mmHg during a progressive exercise to VO2max on a cycle ergometer. RESULTS: In the two resting studies, total pulmonary ventilation and alveolar ventilation were increased by 19% at 7.5 mmHg (1.1% sea level equivalent) and 10% at 5.4 mmHg (0.8% equivalent), with clear evidence of CO2 retention in both studies. During exercise at 15 mmHg the VO2max was reduced significantly by 13%, compared with air at about the same maximal ventilation, but VO2max was not reduced at 9.4 mmHg. A 6% decrease in VO2max at a PICO2 of 5.4 mmHg may have resulted from these subjects being less fit. The maximal CO2 output and respiratory exchange ratio in the three exercise studies was always lower with CO2 than corresponding air measurements, indicating CO2 storage. Evaluation of submaximal measurements provided an equation for predicting ventilation as a function of PICO2 and VO2/VO2max and demonstrated that ventilation during submaximal exercise is increased significantly by the lowest CO2 level. BP and heart rate responses during submaximal and maximal work were not predictably altered by CO2 at these levels. CONCLUSION: These studies demonstrate that minimal CO2 levels have significant influences on pulmonary ventilation during rest and exercise and must be considered in acute studies in confined spaces such as space cabins. The inspired CO2 should be stated when ventilation measurements are reported under these conditions.

Cardiorespiratory responses to orthostasis and the effects of propranolol.

Cardiac output and gas exchange were determined serially using the single-breath method of Kim et al. before, during, and after orthostasis on six subjects after beta-adrenergic blockade and in duplicate controls. In the latter, heart rate increased and pulse pressure dropped immediately on tilting to 60 degrees and remained stable while cardiac output and stroke volume declined gradually over 21 min upright. On propranolol, heart rate was 10 bpm lower supine and 20 bpm less at 60 degrees but cardiac output was only slightly lower before and following tilt-up. However, after 15 min upright, stroke volume and cardiac output recovered on propranolol exceeding the controls after 21 min without change in heart rate. Returning to supine, heart rate dropped in all tests with a transitory increase in stroke volume, cardiac output and arterio-venous O2 difference. At the same time, apparent O2 uptake increased temporarily, reflecting the return of pooled venous blood to the lungs. Orthostatic tolerance did not appear to be affected by beta-adrenergic blockade.

Work capacity, exercise responses and body composition of professional pilots in relation to age.

Body composition and submaximal and maximal cardiorespiratory responses during a progressive upright bicycle ergometer test were measured in 410 professional male pilots, aged 20 to 68 years, and divided into four groups (30, 39, 49, and 59 years). Fat-free weight by hydrostatic weighing was not significantly different between groups and fat increased linearly with age, while height was lower and weight levelled off in the oldest group. Aerobic work capacity (VO2max) fell at a rate of 0.25 ml.min-1.kg-1 per year in this unique population of healthy, but generally sedentary men. A subgroup of 10 pilots, tested annually from age 31 to 47, demonstrated a reversal of the age-related decline in VO2max. This was attributable to regular physical activity, short of athletic training, and changes in personal health habits stimulated by self-assessment available from the repeated tests incorporated into the medical prevention program. These data considered in relation to more recent reports of stroke volume during similar maximal exercise protocols suggest that VO2max is limited during aging by a reduction in tissue diffusing capacity or increased maldistribution of perfusion in relation to O2 uptake in muscle and this can be partially prevented by training. Reference standards for heart rate, blood pressure and ventilation during submaximal and maximal exercise levels are presented in relation to energy requirements and work intensity at various ages.

Acute ventilatory response to simulated altitude, normobaric hypoxia, and hypobaria.

BACKGROUND: Some reports claim that ventilation (VE) is greater in human subjects in normobaric hypoxia than at altitude following an equivalent drop in inspired PO2 (PIO2). It has been suggested that reduced barometric pressure (PB) may decrease chemoreceptor sensitivity and account for these results. In this pilot study we tested the hypothesis that VE and hypoxic chemoresponsiveness would not be different after 30 min of normobaric hypoxia and altitude. METHODS: We exposed three male and three female subjects to four conditions in an environmental chamber, varying the order. The four conditions were: air (PB = 640, FIO2 = 0.204), hypobaria (434, 0.298), hypoxia (640, 0.141) and altitude (434, 0.203). We measured VE, end-tidal O2 and CO2 and arterial O2 saturation (SpO2) after 30 min in each environment, and while breathing 100% O2 for 1 min immediately thereafter. RESULTS: The mean increase in VE relative to air was 14%, 20% and 26% for hypobaria, hypoxia and altitude, respectively, with corresponding reductions in PETCO2 in the three conditions. The reduction in VE with 100% O2 was inversely proportional to the rise in SpO2 in all cases, indicating that chemoresponsiveness was unchanged by PB. When hypobaria preceded altitude, the VE at altitude increased less, relative to air, than when altitude was given first (not significant). CONCLUSIONS: The VE and chemosensitivity are about the same after 30 min of altitude and equivalent hypoxia. However, when the drop in PIO2 is not synchronous with the drop in PB, like at altitude, the VE values may be altered. Air density, hypoxic pulmonary vasoconstriction and circulating microbubbles may interact to account for the observed findings.

Blood volume and cardiorespiratory responses to lower body negative pressure.

Breath-by-breath measurements of pulmonary capillary O2 transfer and ventilation were made on three subjects during and after 10 min of lower body negative pressure (LBNP) at -20, -40, and -60 torr. Loss in blood O2 stores (O2B) during and replenishment after LBNP were directly related to the intensity of LBNP. The peak rise in pulmonary capillary O2 transfer after release of LBNP was always preceded by a decrease in leg volume, indicating that O2B changes were related to blood volume shifts. The return of O2-depleted, pooled blood to the central circulation during the first minute of recovery caused significant hyperpnea. Three compartment lung model analyses from alveolar and arterial blood samples at -60 torr showed an increase in the alveolar deadspace fraction from 0.09 to 0.17, and a decline in the effective compartment from 0.83 to 0.77. The less effective lung perfusion during LBNP may explain a 30% increase in ventilation equivalent for O2.

Effects of regional hemoconcentration during LBNP on plasma volume determinations.

Blood samples were obtained from forearm vein or artery with indwelling cannula I. before, II. during the last min, and III. about 2 min after lower body negative pressure (LBNP) in 16 experiments to determine whether plasma volume (PV) estimates were affected by regional hemoconcentration in the lower body. Total hemoglobin (THb) was estimated with the CO method prior to LBNP. Hemoglobin (Hb) and hematocrit (Hct) values from II gave only a 3% (87 ml) loss in PV due to LBNP, assuming no change in THb. However, Hb and Hct values from III showed an 11% loss in PV (313 ml). This 72% underestimation of PV loss with II must have resulted from the sequestration of blood and subsequent hemoconcentration in the lower body during LBNP. The effects of LBNP on PV should be estimated 1-3 min after exposure, after mixing but before extravascular fluid returns to the circulation.

The effects of head-down tilt on carotid blood flow and pulmonary gas exchange.

Common carotid artery blood flow (CCF), pulmonary gas exchange and ventilation were measured in six subjects in the supine posture (SUP I), serially during 20 min of head-down tilt at -30 degrees (HDT) and after returning to the supine posture (SUP II). CCF was approximately 6% lower during HDT, with a transient increase during the second minute, and was about 7% higher during SUP II than during SUP I. The transition from SUP I to HDT caused increases in O2 uptake (VO2), CO2 output, respiratory exchange ratio and tidal volume in the first minute. Similar responses were apparent following the HDT to SUP II transition, except for VO2, which changed little. Correction of VO2 for changes in estimated lung O2 stores indicated that about 200 ml of blood were shifted within the circulation by the tilt transitions which provided a ventilatory stimulus. HDT can cause a loss in blood and tissue O2 stores and gain in CO2 stores by shifting blood volume toward and blood flow away from the dependent headward vascular compartment and perhaps by producing ischemia in the elevated lower extremities. Cerebral venous congestion during HDT appears to cause periodic breathing and reduce CCF, the latter being partially offset by reduced flow resistance in the carotid artery.

Effects of acute hypoxia on cardiopulmonary responses to head-down tilt.

Six male subjects were exposed on two separate occasions to simulated microgravity with 28 degrees head-down tilt (HD) for 1 h with baseline followed by recovery at + 17 degrees head-up. Pulmonary ventilation, gas exchange, spirometry, and central and cerebral blood flow characteristics were compared while breathing ambient air (PIO2 = 122 mm Hg) and reduced FIO2 equivalent to 14,828 ft (PIO2 = 81 mm Hg). With hypoxia (HY), the increased tidal volume served to attenuate the drop in arterial saturation by reducing deadspace ventilation. Arterial and mixed venous PO2 values, estimated from peripheral venous samples and cardiac output (CO), were both maintained during HD in HY. Mixed venous PO2 was elevated by an increase in CO associated with a reduction in systemic resistance. Changes in spirometric indices during HD were not accentuated by HY, making the presence of interstitial edema unlikely. Cerebral flow and resistance showed minor reductions with HD. Tissue oxygenation and cardiopulmonary function were not notably effected by HD during HY, but a combination of these two stressors may predispose subjects to subsequent orthostatic intolerance during initial recovery.