Heterogeneity of responses to orthostatic stress in homozygous twins.

Early analysis into the role of genetics on cardiovascular regulation has been accomplished by comparing blood pressure and heart rate in homozygous twins during unstressed, resting physiological conditions. However, many variables, including cognitive and environmental factors, contribute to the regulation of cardiovascular hemodynamics. Therefore, the purpose of this study was to determine the hemodynamic response of identical twins to an orthostatic stress, ranging from supine rest to presyncope. Heart rate, arterial blood pressure, middle cerebral artery blood velocity, an index of cerebrovascular resistance, cardiac output, total peripheral resistance, and end-tidal carbon dioxide were measured in 16 healthy monozygotic twin pairs. Five minutes of supine resting baseline data were collected, followed by 5 min of 60 degrees head-up tilt. After 5 min of head-up tilt, lower body negative pressure was applied in increments of 10 mmHg every 3 min until the onset of presyncope, at which time the subject was returned to the supine position for a 5-min recovery period. The data indicate that cardiovascular regulation under orthostatic stress demonstrates a significant degree of variance between identical twins, despite similar orthostatic tolerance. As the level of stress increases, so does the difference in the cardiovascular response within a twin pair. The elevated variance with increasing stress may be due to an increase in the role of environmental factors, as the influential role of genetics nears a functional limit. Therefore, although orthostatic tolerance times were very similar between identical twins, the mechanism involved in sustaining cardiovascular function during increasing stress was different.

Lumbar spine disc height and curvature responses to an axial load generated by a compression device compatible with magnetic resonance imaging.

STUDY DESIGN: Axial load-dependent changes in the lumbar spine of supine healthy volunteers were examined using a compression device compatible with magnetic resonance imaging. OBJECTIVE: To test two hypotheses: Axial loading of 50% body weight from shoulder to feet in supine posture 1) simulates the upright lumbar spine alignment and 2) decreases disc height significantly. SUMMARY OF BACKGROUND DATA: Axial compression on the lumbar spine has significantly narrowed the lumbar dural sac in patients with sciatica, neurogenic claudication or both. METHODS: Using a device compatible with magnetic resonance imaging, the lumbar spine of eight young volunteers, ages 22 to 36 years, was axially compressed with a force equivalent to 50% of body weight, approximating the normal load on the lumbar spine in upright posture. Sagittal lumbar magnetic resonance imaging was performed to measure intervertebral angle and disc height before and during compression. RESULTS: Each intervertebral angle before and during compression was as follows: T12-L1 (-0.8 degrees +/- 2.5 degrees and -1.5 degrees +/- 2.6 degrees ), L1-L2 (0.7 degrees +/- 1.4 degrees and 3.3 degrees +/- 2.9 degrees ), L2-L3 (4.7 degrees +/- 3.5 degrees and 7.3 degrees +/- 6 degrees ), L3-L4 (7.9 degrees +/- 2.4 degrees and 11.1 degrees +/- 4.6 degrees ), L4-L5 (14.3 degrees +/- 3.3 degrees and 14.9 degrees +/- 1.7 degrees ), L5-S1 (25.8 degrees +/- 5.2 degrees and 20.8 degrees +/- 6 degrees ), and L1-S1 (53.4 degrees +/- 11.9 degrees and 57.3 degrees +/- 16.7 degrees ). Negative values reflect kyphosis, and positive values reflect lordosis. A significant difference between values before and during compression was obtained at L3-L4 and L5-S1. There was a significant decrease in disc height only at L4-L5 during compression. CONCLUSIONS: The axial force of 50% body weight in supine posture simulates the upright lumbar spine morphologically. No change in intervertebral angle occurred at L4-L5. However, disc height at L4-L5 decreased significantly during compression.

Fluid volume control during short-term space flight and implications for human performance.

Space flight exerts substantial effects on fluid volume control in humans. Cardiac distension occurs during the first 1-2 days of space flight relative to supine and especially upright 1g conditions. Plasma volume contraction occurs quickly in microgravity, probably as a result of transcapillary fluid filtration into upper-body interstitial spaces. No natriuresis or diuresis has been observed in microgravity, such that diuresis cannot explain microgravity-induced hypovolemia. Reduction of fluid intake occurs irrespective of space motion sickness and leads to hypovolemia. The fourfold elevation of urinary antidiuretic hormone (ADH) levels on flight day 1 probably results from acceleration exposures and other stresses of launch. Nevertheless, it is fascinating that elevated ADH levels and reduced fluid intake occur simultaneously early in flight. Extracellular fluid volume decreases by 10-15% in microgravity, and intracellular fluid volume appears to increase. Total red blood cell mass decreases by approximately 10% within 1 week in space. Inflight Na(+) and volume excretory responses to saline infusion are approximately half those seen in pre-flight supine conditions. Fluid volume acclimation to microgravity sets the central circulation to homeostatic conditions similar to those found in an upright sitting posture on Earth. Fluid loss in space contributes to reduced exercise performance upon return to 1g, although not necessarily in flight. In-flight exercise training may help prevent microgravity-induced losses of fluid and, therefore, preserve the capacity for upright exercise post-flight. Protection of orthostatic tolerance during space flight probably requires stimulation of orthostatic blood pressure control systems in addition to fluid maintenance or replacement.

Gender differences in cardiovascular regulation during recovery from exercise.

Are women more susceptible to acute postexercise orthostatic hypotension compared with men? We hypothesized that decreases in arterial pressure during recovery from dynamic exercise are greater in women compared with men. We studied 8 men and 11 women during inactive and active recovery from cycling exercise. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured during and after 3 min of exercise at 60% of calculated maximum heart rate. At 1 min after exercise, MAP decreased less (P < 0.05) during inactive recovery in men (-18 +/- 2 mmHg) compared with women (-30 +/- 2 mmHg). This difference was due to greater decreases in SV and less increase in TPR during inactive recovery from exercise in women compared with men. These differences persisted for 5 min after exercise. MAP decreased less during active recovery in men compared with women. These findings suggest that women may have increased risk of postexercise orthostatic hypotension and that active recovery from exercise may reduce this risk.

Effects of spaceflight on human calf hemodynamics.

Chronic microgravity may modify adaptations of the leg circulation to gravitational pressures. We measured resting calf compliance and blood flow with venous occlusion plethysmography, and arterial blood pressure with sphygmomanometry, in seven subjects before, during, and after spaceflight. Calf vascular resistance equaled mean arterial pressure divided by calf flow. Compliance equaled the slope of the calf volume change and venous occlusion pressure relationship for thigh cuff pressures of 20, 40, 60, and 80 mmHg held for 1, 2, 3, and 4 min, respectively, with 1-min breaks between occlusions. Calf blood flow decreased 41% in microgravity (to 1.15 +/- 0.16 ml x 100 ml(-1) x min(-1)) relative to 1-G supine conditions (1.94 +/- 0.19 ml x 100 ml(-1) x min(-1), P = 0.01), and arterial pressure tended to increase (P = 0.05), such that calf vascular resistance doubled in microgravity (preflight: 43 +/- 4 units; in-flight: 83 +/- 13 units; P < 0.001) yet returned to preflight levels after flight. Calf compliance remained unchanged in microgravity but tended to increase during the first week postflight (P > 0.2). Calf vasoconstriction in microgravity qualitatively agrees with the "upright set-point" hypothesis: the circulation seeks conditions approximating upright posture on Earth. No calf hemodynamic result exhibited obvious mechanistic implications for postflight orthostatic intolerance.

Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans.

We sought to determine whether carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) was altered during dynamic exercise. In five men and three women, 23.8 +/- 0.7 (SE) yr of age, CBR function was evaluated at rest and during 20 min of arm cycling at 50% peak O(2) uptake using 5-s periods of neck pressure and neck suction. From rest to steady-state arm cycling, mean arterial pressure (MAP) was significantly increased from 90.0 +/- 2.7 to 118.7 +/- 3.6 mmHg and MSNA burst frequency (microneurography at the peroneal nerve) was elevated by 51 +/- 14% (P < 0.01). However, despite the marked increases in MAP and MSNA during exercise, CBR-Delta%MSNA responses elicited by the application of various levels of neck pressure and neck suction ranging from +45 to -80 Torr were not significantly different from those at rest. Furthermore, estimated baroreflex sensitivity for the control of MSNA at rest was the same as during exercise (P = 0.74) across the range of neck chamber pressures. Thus CBR control of sympathetic nerve activity appears to be preserved during moderate-intensity dynamic exercise.

Cerebrovascular responses during lower body negative pressure-induced presyncope.

BACKGROUND: Reduced orthostatic tolerance is commonly observed after spaceflight, occasionally causing presyncopal symptoms which may be due to low cerebral blood flow (CBF). It has been suggested that CBF decreases in early stages of exposure to orthostatic stress. The purpose of this study was to investigate cerebrovascular responses during presyncope induced by lower body negative pressure (LBNP). HYPOTHESIS: Although CBF decreases during LBNP exposure, blood pressure (BP) or heart rate (HR) contributes more to induce presyncopal conditions. METHODS: Eight healthy male volunteers were exposed to LBNP in steps of 10 mm Hg every 3 min until presyncopal symptoms were detected. Electrocardiogram (ECG) was monitored continuously and arterial BP was measured by arterial tonometry. CBF velocity at the middle cerebral artery was measured by transcranial Doppler sonography (TCD). Cerebral tissue oxygenation was detected using near-infrared spectroscopy (NIRS). We focused our investigation on the data obtained during the final 2 min before the presyncopal endpoint. RESULTS: BP gradually decreased from 2 min to 10 s before the endpoint, and fell more rapidly during the final 10 s. HR did not change significantly during presyncope. CBF velocity did not change significantly, while cerebral tissue oxygenation decreased prior to the presyncopal endpoint in concert with BP. Our results suggest that CBF is maintained in the middle cerebral artery during presyncope, while BP decreases rapidly. CONCLUSIONS: Cerebrovascular hemodynamics are relatively well maintained while arterial hypotension occurs just prior to syncope.

Does gender influence human cardiovascular and renal responses to water immersion?

We hypothesized that women and men exhibit similar cardiovascular and renal responses to thermoneutral water immersion (WI) to the neck. Ten women and nine men underwent two sessions in random order: 1) seated nonimmersed for 5.5 h (control) and 2) WI for 3 h, with subjects seated nonimmersed for 1.5 h pre- and 1 h postimmersion. We measured left atrial diameter, heart rate, arterial pressure, urine volume and osmolality, and urinary endothelin, urodilatin, sodium, and potassium excretion. No significant difference existed between groups in cardiovascular responses. The groups also exhibited mostly similar renal responses to immersion after adjustment for body mass. However, female urodilatin excretion per kilogram during immersion was over twofold that of men, and the female kaliuretic response to immersion was delayed and less pronounced relative to that in men. Men may excrete more potassium than women during immersion because men possess greater lean body mass (potassium per kilogram). Results obtained in men during WI may be cautiously extrapolated to women, yet urodilatin and potassium responses exhibit gender differences.

Supine lower body negative pressure exercise simulates metabolic and kinetic features of upright exercise.

Exercise within an artificial gravity environment may help prevent microgravity-induced deconditioning. We hypothesized that supine lower body negative pressure (LBNP) exercise simulates physiological and biomechanical features of upright exercise. Walking (4.5 +/- 0.3 km/h) and running (8.0 +/- 1.0 km/h) while supine within a LBNP exerciser were compared with walking and running while upright. Eight healthy subjects exercised for 5 min at each of the four posture/gait conditions. LBNP of 52 +/- 4 mmHg generated one body weight of supine ground reaction force (GRF). Gait parameters and GRFs were measured during the third minute of exercise, and heart rate and oxygen consumption were measured during the fifth minute. Oxygen consumption during supine LBNP treadmill exercise [walking: 14.6 +/- 0.9; running: 32.2 +/- 1.6 (SE) ml. min(-1). kg(-1)] was similar to that during upright treadmill exercise (walking: 15.1 +/- 0.9; running: 34.0 +/- 1.9 ml. min(-1). kg(-1)). Heart rate for supine LBNP exercise (grand mean: 133 +/- 11 beats/min) was also similar to that for upright exercise (136 +/- 11 beats/min). Footward forces integrated over each stride (330.5 +/- 34.4 vs. 319. 1 +/- 29.6 N. s) and rate of force generation (26,483 +/- 4,310 vs. 25,634 +/- 4,434 N/s) were similar for upright and LBNP exercise, respectively. Our collective results indicate that supine exercise within LBNP can simulate the physiological stress and GRFs that are generated during upright gait.

Supine lower body negative pressure exercise during bed rest maintains upright exercise capacity.

Bed rest and spaceflight reduce exercise fitness. Supine lower body negative pressure (LBNP) treadmill exercise provides integrated cardiovascular and musculoskeletal stimulation similar to that imposed by upright exercise in Earth gravity. We hypothesized that 40 min of supine exercise per day in a LBNP chamber at 1.0-1.2 body wt (58 +/- 2 mmHg LBNP) maintains aerobic fitness and sprint speed during 15 days of 6 degrees head-down bed rest (simulated microgravity). Seven male subjects underwent two such bed-rest studies in random order: one as a control study (no exercise) and one with daily supine LBNP treadmill exercise. After controlled bed-rest, time to exhaustion during an upright treadmill exercise test decreased 10%, peak oxygen consumption during the test decreased 14%, and sprint speed decreased 16% (all P < 0.05). Supine LBNP exercise during bed rest maintained all the above variables at pre-bed-rest levels. Our findings support further evaluation of LBNP exercise as a countermeasure against long-term microgravity-induced deconditioning.

Effect of sleep restriction on orthostatic cardiovascular control in humans.

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction (P > 0.3). Systolic pressure was greater at -60 mmHg LBNP after sleep restriction than before sleep restriction (110 +/- 6 and 124 +/- 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 +/- 8 and 99 +/- 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

Muscle pump and central command during recovery from exercise in humans.

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.

Post-apneic inhalation reverses apnea-induced sympathoexcitation before restoration of blood oxygen levels.

Sleep apneas acutely increase sympathetic nerve activity (SNA) and thus arterial blood pressure. We hypothesized that after apnea, sympathoexcitation decreases before recovery of blood oxygen levels because of the predominant inhibitory effect respiratory factors exert over sympathetic nervous system activation. Seven healthy subjects were instrumented for arterial oxygen saturation (pulse oximetry, SaO2), leg muscle SNA (microneurography), and arterial pressure (Finapres). Supine subjects breathed 12% oxygen, 3% carbon dioxide, and 85% nitrogen for one min prior to apnea at the end of a normal tidal expiration. We accounted for circulatory delay in SaO2 measurement (5.4 +/- 0.4 s, mean +/- SE) as the time from the termination of apnea to the midpoint of the nadir of SaO2. SaO2 decreased to average 84 +/- 3% over the final 10 seconds of apnea, and recovered only partially to average 87 +/- 3% over the 10 seconds immediately following apnea. End-expiratory apnea increased SNA 14-fold from baseline levels of 217 +/- 37 units/10 seconds to 3063 +/- 442 units/10 seconds. However, SNA decreased to 93 +/- 32 units/10 s during the first 10 seconds after apnea. These findings indicate that sympathoinhibitory effects of respiratory signals, either lung inflation receptors or central respiratory inputs, predominate over sympathoexcitatory inputs from chemoreceptors to produce immediate and complete sympathoinhibition at the termination of a voluntary apnea. Arterial baroreflexes probably also contribute to sympathoinhibition after apnea.

Self-generated lower body negative pressure exercise.

BACKGROUND: Exercise during spaceflight helps prevent musculoskeletal and cardiovascular deconditioning to Earth gravity. This report evaluates the aerobic and anaerobic exercise stimulus provided by self-generated lower body negative pressure. METHODS: A lower body negative pressure cylinder expands and collapses longitudinally, but not radially. As the legs push footward to expand the cylinder, the air pressure in the cylinder decreases, increasing the force required to continue expanding the cylinder. In addition, valves control air flow into and out of the cylinder, and thus workload. In seven supine subjects, knee bend exercise was performed at 19 cycles per minute for 6 min. Footward force was measured with load cells, cylinder pressure with a transducer, heart rate from ECG, and oxygen consumption with turbine volumetry and gas analysis. RESULTS: Maximum footward force at the peak of the exercise cycle averaged 1120+/-88 N (114+/-9 kg), and pressure within the cylinder concomitantly decreased 26+/-3 mmHg below ambient. Heart rate and oxygen consumption increased 75+/-4 bpm and 26.3+/-1.4 ml O2/kg x min(-1) from supine resting values, respectively. CONCLUSIONS: With the air inlet valve nearly closed, exercise with this device approximates a resistance-type leg press. With more inflow of air, more rapid, aerobic knee bends can be performed. This exercise device/concept provides simultaneous dynamic musculoskeletal and cardiovascular stresses without an external power source.

Measurement of net whole-body transcapillary fluid transport and effective vascular compliance in humans.

BACKGROUND: Net whole-body transcapillary fluid transport (TFT) between the circulation and the interstitial (extravascular) space may be calculated as: IV - deltaPV - UV - IL, where IV=infused or ingested volume (when applicable), deltaPV = change in plasma volume, UV=urine volume, and IL=insensible loss. RESULTS: Infusion of 30 mL/kg isotonic saline over 25 minutes increased supine TFT from a basal capillary reabsorption of -106+/-24 mL/h (mean+/-SE) to a net filtration of 1,229+/-124 mL/h. One hour after infusion, reabsorption of -236+/-102 mL/h was seen, and control reabsorption levels returned by 3 hours. Four hours of 30 mm Hg lower body negative pressure (LBNP) elicited no net TFT, probably because of upper body reabsorptive compensation for lower body capillary filtration. When ingestion of 1 L of isotonic saline accompanied LBNP, filtration of 145+/-10 mL/h occurred. Reabsorption of extravascular fluid into the circulation always followed LBNP. CONCLUSION: Application of this technique could aid understanding of physiologic conditions, experimental interventions, disease states, and therapies that cause or are influenced by fluid shifts between intravascular and interstitial compartments.

Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand.

Peripheral vasoconstriction decreases thermal conductance of hypothermic individuals, making it difficult to transfer externally applied heat to the body core. We hypothesized that increasing blood flow to the skin of a hypothermic individual would enhance the transfer of exogenous heat to the body core, thereby increasing the rate of rewarming. External auditory meatus temperature (TEAM) was monitored in hypothermic subjects during recovery from general anesthesia. In 10 subjects, heat (45-46 degreesC, water-perfused blanket) was applied to a single forearm and hand that had been placed in a subatmospheric pressure environment (-30 to -40 mmHg) to distend the blood vessels. Heat alone was applied to control subjects (n = 6). The application of subatmospheric pressure resulted in a 10-fold increase in rewarming rates as determined by changes in TEAM [13.6 +/- 2.1 (SE) degreesC/h in the experimental group vs. 1.4 +/- 0.1 degreesC/h in the control group; P < 0.001]. In the experimental subjects, the rate of change of TEAM decreased sharply as TEAM neared the normothermic range.

Leg intramuscular pressures during locomotion in humans.

To assess the usefulness of intramuscular pressure (IMP) measurement for studying muscle function during gait, IMP was recorded in the soleus and tibialis anterior muscles of 10 volunteers during treadmill walking and running by using transducer-tipped catheters. Soleus IMP exhibited single peaks during late-stance phase of walking [181 +/- 69 (SE) mmHg] and running (269 +/- 95 mmHg). Tibialis anterior IMP showed a biphasic response, with the largest peak (90 +/- 15 mmHg during walking and 151 +/- 25 mmHg during running) occurring shortly after heel strike. IMP magnitude increased with gait speed in both muscles. Linear regression of soleus IMP against ankle joint torque obtained by a dynamometer produced linear relationships (n = 2, r = 0.97 for both). Application of these relationships to IMP data yielded estimated peak soleus moment contributions of 0.95-1.65 N . m/kg during walking, and 1.43-2.70 N . m/kg during running. Phasic elevations of IMP during exercise are probably generated by local muscle tissue deformations due to muscle force development. Thus profiles of IMP provide a direct, reproducible index of muscle function during locomotion in humans.

Human cardiovascular acclimation to microgravity.

This brief review provides an update on recent studies of human cardiovascular responses to spaceflight. This report complements prior reviews of the acute responses and chronic acclimation of the cardiovascular system to actual and simulated microgravity.