Orthostatic intolerance and motion sickness after parabolic flight.

Because it is not clear that the induction of orthostatic intolerance in returning astronauts always requires prolonged exposure to microgravity, we investigated orthostatic tolerance and autonomic cardiovascular function in 16 healthy subjects before and after the brief micro- and hypergravity of parabolic flight. Concomitantly, we investigated the effect of parabolic flight-induced vomiting on orthostatic tolerance, R-wave-R-wave interval and arterial pressure power spectra, and carotid-cardiac baroreflex and Valsalva responses. After parabolic flight 1) 8 of 16 subjects could not tolerate 30 min of upright tilt (compared to 2 of 16 before flight); 2) 6 of 16 subjects vomited; 3) new intolerance to upright tilt was associated with exaggerated falls in total peripheral resistance, whereas vomiting was associated with increased R-wave-R-wave interval variability and carotid-cardiac baroreflex responsiveness; and 4) the proximate mode of new orthostatic failure differed in subjects who did and did not vomit, with vomiters experiencing comparatively isolated upright hypocapnia and cerebral vasoconstriction and nonvomiters experiencing signs and symptoms reminiscent of the clinical postural tachycardia syndrome. Results suggest, first, that syndromes of orthostatic intolerance resembling those developing after space flight can develop after a brief (i.e., 2-h) parabolic flight and, second, that recent vomiting can influence the results of tests of autonomic cardiovascular function commonly utilized in returning astronauts.

Inflight exercise affects stand test responses after space flight.

PURPOSE: The purpose of this study was to determine whether exercise performed by Space Shuttle crew members during short-duration space flights (9-16 d) affects the heart rate (HR) and blood pressure (BP) responses to standing within 2-4 h of landing. METHODS: Thirty crew members performed self-selected inflight exercise and maintained exercise logs to monitor their exercise intensity and duration. Two subjects participated in this investigation during two different flights. A 10-min stand test, preceded by at least 6 min of quiet supine rest, was completed 10-15 d before launch (PRE) and within 4 h of landing (POST). Based upon their inflight exercise records, subjects were grouped as either high (HIex: > or = 3 times/week, HR > or = 70% HRmax, > or = 20 min/session, N = 11), medium (MEDex: > or = 3 times/week, HR < 70% HRmax, > or = 20 min/session, N = 10), or low (LOex: < or = 3 times/week, HR and duration variable, N = 11) exercisers. HR and BP responses to standing were compared between groups (ANOVA, P < or = 0.05). RESULTS: There were no PRE differences between the groups in supine or standing HR and BP. Although POST supine HR was similar to PRE, all groups had an increased standing HR compared with PRE. The increase in HR upon standing was significantly greater after flight in the LOex group (36 +/- 5 bpm) compared with HIex or MEDex groups (25 +/- 1 bpm; 22 +/- 2 bpm). Similarly, the decrease in pulse pressure (PP) from supine to standing was unchanged after space flight in the MEDex and HIex groups but was significantly greater in the LOex group (PRE: -9 +/- 3; POST: -19 +/- 4 mm Hg). CONCLUSIONS: Thus, moderate to high levels of inflight exercise attenuated HR and PP responses to standing after space flight.

Acute manipulations of plasma volume alter arterial pressure responses during Valsalva maneuvers.

The effects of changes in blood volume on arterial pressure patterns during the Valsalva maneuver are incompletely understood. In the present study we measured beat-to-beat arterial pressure and heart rate responses to supine Valsalva maneuvers during normovolemia, hypovolemia induced with intravenous furosemide, and hypervolemia induced with ingestion of isotonic saline. Valsalva responses were analyzed according to the four phases as previously described (W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. JAMA 107: 853-856, 1936; W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. Am. J. Physiol. 141: 42-50, 1944). Phase I is the initial onset of straining, which elicits a rise in arterial pressure; phase II is the period of straining, during which venous return is impeded and pressure falls (early) and then partially recovers (late); phase III is the initial release of straining; and phase IV consists of a rapid "overshoot" of arterial pressure after the release. During hypervolemia, early phase II arterial pressure decreases were significantly less than those during hypovolemia, thus making the response more "square." Systolic pressure hypervolemic vs. hypovolemic falls were -7.4 +/- 2.1 vs. -30.7 +/- 7 mmHg (P = 0.005). Diastolic pressure hypervolemic vs. hypovolemic falls were -2.4 +/- 1.6 vs. -15.2 +/- 2.6 mmHg (P = 0.05). A significant direct correlation was found between plasma volume and phase II systolic pressure falls, and a significant inverse correlation was found between plasma volume and phase III-IV systolic pressure overshoots. Heart rate responses to systolic pressure falls during phase II were significantly less during hypovolemia than during hypervolemia (0.7 +/- 0.2 vs. 2.82 +/- 0.2 beats. min-1. mmHg-1; P = 0.05) but were not different during phase III-IV overshoots. We conclude that acute changes in intravascular volume from hypovolemia to hypervolemia affect cardiovascular responses, particularly arterial pressure changes, to the Valsalva maneuver and should be considered in both clinical and research applications of this maneuver.

An episode of ventricular tachycardia during long-duration spaceflight.

An episode of nonsustained ventricular tachycardia was recorded from a crew member during the second month aboard the MIR space station. Although asymptomatic, this cardiac event increases the concern that serious cardiac dysrhythmias may be a limiting factor during long-duration spaceflight.

Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight.

Postflight orthostatic intolerance is experienced by virtually all astronauts but differs greatly in degree of severity. We studied cardiovascular responses to upright posture in 40 astronauts before and after spaceflights lasting up to 16 days. We separated individuals according to their ability to remain standing without assistance for 10 min on landing day. Astronauts who could not remain standing on landing day had significantly smaller increases in plasma norepinephrine levels with standing than did those who could remain standing (105 +/- 41 vs. 340 +/- 62 pg/ml; P = 0.05). In addition, they had significantly lower standing peripheral vascular resistance (23 +/- 3 vs. 34 +/- 3 mmHg.1l-1).min; P = 0.02) and greater decreases in systolic (-28 +/- 4 vs. -11 +/- 3 mmHg; P = 0.002) and diastolic (-14 +/- 7 vs. 3 +/- 2 mmHg; P = 0.0003) pressures. The presyncopal group also had significantly lower supine (16 +/- 1 vs. 21 +/- 2 mmHg.1l-1).min; P = 0.04) and standing (23 +/- 2 vs. 32 +/- 2 mmHg.1l-1).min; P = 0.038) vascular resistance, supine (66 +/- 2 vs. 73 +/- 2 mmHg; P = 0.008) and standing (69 +/- 4 vs. 77 +/- 2 mmHg; P = 0.007) diastolic pressure, and supine (109 +/- 3 vs. 114 +/- 2 mmHg; P = 0.05) and standing (99 +/- 4 vs. 108 +/- 3 mmHg; P = 0.006) systolic pressures before flight. This is the first study to clearly document these differences among presyncopal and nonpresyncopal astronauts after spaceflight and also offer the possibility of preflight prediction of postflight susceptibility. These results clearly point to hypoadrenergic responsiveness, possibly centrally mediated, as a contributing factor in postflight orthostatic intolerance. They may provide insights into autonomic dysfunction in Earthbound patients.

Valsalva's maneuver revisited: a quantitative method yielding insights into human autonomic control.

Seventeen healthy supine subjects performed graded Valsalva maneuvers. In four subjects, transesophageal echographic aortic cross-sectional areas decreased during and increased after straining. During the first seconds of straining, when aortic cross-sectional area was declining and peripheral arterial pressure was rising, peroneal sympathetic muscle neurons were nearly silent. Then, as aortic cross-sectional area and peripheral pressure both declined, sympathetic muscle nerve activity increased, in proportion to the intensity of straining. Poststraining arterial pressure elevations were proportional to preceding increases of sympathetic activity. Sympathetic inhibition after straining persisted much longer than arterial and right atrial pressure elevations. Similarly, R-R intervals changed in parallel with peripheral arterial pressure, until approximately 45 s after the onset of straining, when R-R intervals were greater and arterial pressures were smaller than prestraining levels. Our conclusions are as follows: opposing changes of carotid and aortic baroreceptor inputs reduce sympathetic muscle and increase vagal cardiac motor neuronal firing; parallel changes of barorsensory inputs provoke reciprocal changes of sympathetic and direct changes of vagal firing; and pressure transients lasting only seconds reset arterial pressure-sympathetic and -vagal response relations.

Microgravity decreases heart rate and arterial pressure in humans.

Spaceflight causes adaptive changes in cardiovascular physiology, such as postflight orthostatic intolerance, that can have deleterious effects on astronauts. In-flight cardiovascular data are difficult to obtain, and results have been inconsistent. To determine normative in-flight changes in Shuttle astronauts, we measured heart rate, arterial pressure, and cardiac rhythm disturbances for 24-h periods before, during, and after spaceflight on Shuttle astronauts performing their normal routines. We found that heart rate, diastolic pressure, variability of heart rate and diastolic pressure, and premature ventricular contractions all were significantly reduced in flight. Systolic pressure and premature atrial contractions also tended to be reduced in flight. These data constitute the first systematic evaluation of in-flight changes in basic cardiovascular variables in Shuttle astronauts and suggest that a microgravity environment itself does not present a chronic stress to the cardiovascular system.

Modulation of human sympathetic periodicity by mild, brief hypoxia and hypercapnia.

We determined the influence of brief mild normocapnic hyperoxia, hypoxia, and hyperoxic hypercapnia on human muscle sympathetic nerve activity and R-R intervals, as quantified by both time- and frequency-domain analyses. We obtained measurements in nine healthy young adult men and women during uncontrolled and frequency (but not tidal volume) controlled breathing. Responses were evaluated with forward selection and backward elimination statistical models, with muscle sympathetic nerve activity as the dependent variable, and power spectral techniques. Hyperoxia and hypoxia did not alter arterial pressure; hypercapnia increased diastolic pressure modestly. Average R-R intervals tended to increase during hyperoxia, and decrease during hypoxia and hypercapnia. During uncontrolled breathing, changes of inspiratory gases exerted only minor effects on muscle sympathetic nerve activity; during controlled breathing, both hypoxia and hypercapnia tended to increase muscle sympathetic nerve activity. Statistical modeling suggested that chemoreceptor stimulation increased muscle sympathetic neural outflows, but that increases of sympathetic traffic were opposed by secondary increases of ventilation. Inspiratory gases modulated the frequency distribution of muscle sympathetic nerve activity strikingly: hypoxia increased sympathetic power at respiratory frequencies and hypercapnia increased sympathetic power at both respiratory and (primarily in one subject) cardiac frequencies. Our data suggest that mild brief hypoxia and hypercapnia increase human muscle sympathetic nerve activity, but that this tendency is opposed by chemoreflex-induced increases of ventilation. Our results suggest also that chemoreceptor activity exerts important influences on the frequency content, as well as the quantity of sympathetic neural outflow.

Spaceflight alters autonomic regulation of arterial pressure in humans.

Spaceflight is associated with decreased orthostatic tolerance after landing. Short-duration spaceflight (4-5 days) impairs one neural mechanism: the carotid baroreceptor-cardiac reflex. To understand the effects of longer-duration spaceflight on baroreflex function, we measured R-R interval power spectra, antecubital vein plasma catecholamine levels, carotid baroreceptor-cardiac reflex responses, responses to Valsalva maneuvers, and orthostatic tolerance in 16 astronauts before and after shuttle missions lasting 8-14 days. We found the following changes between preflight and landing day: 1) orthostatic tolerance decreased; 2) R-R interval spectral power in the 0.05 to 0.15-Hz band increased; 3) plasma norepinephrine and epinephrine levels increased; 4) the slope, range, and operational point of the carotid baroreceptor cardiac reflex response decreased; and 5) blood pressure and heart rate responses to Valsalva maneuvers were altered. Autonomic changes persisted for several days after landing. These results provide further evidence of functionally relevant reductions in parasympathetic and increases in sympathetic influences on arterial pressure control after spaceflight.