| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas; 2Department of Community Health Sciences, Brock University, St. Catharines, Ontario, Canada; 3University of New Mexico, Albuquerque, New Mexico; 4Wyle Laboratories, Houston, Texas; 5Department of Orthopaedic Surgery, University of California, San Diego, California; 6Department of Physiology, Gifu University, Gifu, Japan; and 7University of Waterloo, Waterloo, Ontario, Canada
Submitted 7 January 2007 ; accepted in final form 12 October 2007
 |
ABSTRACT |
|---|
 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
human; microgravity; spaceflight; countermeasure; cerebral blood flow
Hypovolemia constitutes the most established cause of postflight orthostatic intolerance (65). Some investigators postulate that the chronic stroke volume (SV) reduction secondary to hypovolemia causes cardiac remodeling and atrophy (65), which in turn contributes to intolerance (40). The cardiac baroreflex appears to function appropriately in response to postflight hypovolemia because all astronauts exhibit accentuated postural tachycardia after flight (6, 39, 65). No increase occurs in leg compliance after spaceflight (6, 62), but some evidence suggests that problems with the vascular baroreflex arm contribute to postflight orthostatic intolerance (23, 24, 66). In weightlessness, gravitational pressure gradients never arise in the circulation, so cerebral blood flow continues unchallenged, and baroreflexive vasoconstriction remains chronically understimulated. Also, chronic lack of gravitational pressures in the lower body circulation may compromise local arteriolar structure and function (16, 65).
Most literature indicates that exercise training during bed rest does not protect orthostatic tolerance (20, 27, 29). However, based on the mechanistic information above, our laboratory previously hypothesized that addition of a gravity-like stress such as lower body negative pressure (LBNP) during exercise would be effective (38, 64). Control subjects (no exercise) were compared with subjects who performed daily LBNP exercise during 5 days of bed rest. LBNP exercise consisted of 30 min/day of supine interval treadmill exercise at intensities up to 90% of maximum heart rate (HR), followed immediately by 5 min of resting LBNP (i.e., ongoing LBNP during recovery from the LBNP exercise) (38). We added the 5-min postexercise LBNP period as a pilot study of postexercise hypotension during bed rest; at the time of the study, it was not intended as a formal part of the countermeasure (S. M. C. Lee, unpublished observations).
Tilt tolerance time in control subjects decreased significantly (18%), yet tolerance tended to increase in LBNP exercisers (9%, not significant). Hematocrit increased in controls, indicating substantial hemoconcentration; hematocrit did not increase in the exercisers. The countermeasure was then evaluated during 15 days of bed rest (53, 59). For this study, LBNP exercise was prolonged to 40 min, but the 5-min postexercise LBNP period was deleted: we assumed such a short period of LBNP did not contribute to the positive results from the 5-day bed rest study. Supine LBNP assessed orthostatic tolerance. Surprisingly, orthostatic tolerance decreased identically (24%) after bed rest alone and bed rest with LBNP exercise, despite some protection of subtolerance HR and blood pressure responses by LBNP exercise (53). As in the 5-day study, the countermeasure maintained blood volume.
We confronted the possibility that a short resting LBNP period immediately following LBNP exercise may challenge orthostatic blood pressure control mechanisms enough to maintain tolerance during bed rest. For a variety of reasons, orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise (11, 15, 22, 30, 31, 52). For example, Bjurstedt and coworkers (3) reported that five of six subjects experienced presyncope during 6 min of 70° head-up tilt (HUT) after exhausting exercise, whereas all six tolerated the test in preexercise conditions. Also, people sometimes faint when standing still after strenuous exercise when they otherwise have no such trouble (68). These findings imply that orthostatic stimulation imposed immediately following exercise may more efficiently train orthostatic cardiovascular control mechanisms than stimulation without prior exercise, because of the greater cardiovascular stress. Given the collective observations above, we hypothesized that daily exposure to short periods of simulated orthostatic stress immediately following vigorous dynamic exercise maintains orthostatic tolerance during bed rest. The countermeasure protocol again included 5 min of resting LBNP immediately following supine LBNP treadmill exercise.
|
METHODS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Experimental design and conditions. The UCSD Hillcrest Hospital General Clinical Research Center housed, fed, and cared for subjects throughout their participation. The study occupied 6 days of familiarization and baseline data collection, 30 days of bed rest, and 3 days of post-bed rest testing and recovery. Siblings shared rooms and received diets containing 180 mmol Na/day. Water intake was ad libitum. Subjects abstained from caffeine and alcohol throughout the study. No subject used tobacco. Nonprescription medications such as analgesics and stool softeners were given as needed. Some female subjects used oral contraceptives. Menstrual cycle phase was not controlled or accounted for except that female subjects were at approximately the same phase of their cycle during pre- and post-bed rest testing because of the 30-day bed rest period.
Before baseline (pre-bed rest) data collection, subjects experienced all testing procedures to become fully familiarized with the study. All tests took place at the same time of day pre- vs. post-bed rest for a given subject, and all were at least 2-h postprandial. After completion of baseline data collection, twin siblings were randomly assigned to control or countermeasure groups. Group assignment after baseline data collection eliminated any possibility of group assignment influencing pre-bed rest results. Body weight did not vary significantly between groups or across bed rest. During the entire bed rest period, subjects remained at 6° head-down tilt except during periods for showers and training (0.5–1.5 h/day), when they were horizontal (0°). No training occurred on the day before end-bed rest orthostatic tolerance testing. All training and testing sessions occurred at room temperature (21–23°C).
LBNP exercise and orthostatic training.
The LBNP exercise device consists of a vacuum control system connected to a rectangular chamber containing a vertically oriented treadmill. Earlier reports detail chamber construction and operation (21, 38, 59), and Fig. 1 further illustrates waist seal hardware and integration. Waist seal area was set to equal approximately twice a given subject's waist cross-sectional area, such that the negative pressure necessary to produce one body weight equals 
50–60 mmHg (6.65–7.98 kPa). This larger waist seal reduces orthostatic stress and risks of LBNP (petechiae, hernia, syncope) by decreasing the LBNP necessary to generate a given level of footward force (58). Subjects wore inelastic shorts during countermeasure sessions to prevent abnormal LBNP-induced lower abdominal distension (4, 38, 59). The shorts held a 12 x 30-cm air bladder in place over the lower abdomen. A tube from the air bladder passed through the LBNP waist seal to outside the chamber. Therefore, the bladder automatically inflated to compress the lower abdomen in direct proportion to the magnitude of LBNP.
|
|
Orthostatic tolerance testing. Orthostatic tolerance tests consisted of combined HUT and LBNP (17). A semicylindrical Plexiglas LBNP chamber was attached to a tilt table. Subjects underwent three tests: familiarization, pre-bed rest baseline data collection, and post-bed rest data collection. After instrumentation for the orthostatic tolerance test, 5 min of supine resting cardiovascular data were collected. HUT to 60° (+0.87 Gz) then began and continued for 5 min. Thereafter, LBNP ensued at 10 mmHg (1.33 kPa) for 3 min, followed by stepwise 10-mmHg decrements for 3 min each until presyncope. We defined presyncope as drop of systolic pressure below 70 mmHg; sudden and progressive blood pressure reduction; sudden, obvious, and sustained drop in HR; sudden appearance or rapid worsening of presyncopal signs and symptoms (nausea, dizziness, tingling, clamminess, sweating, ashen face, weak legs, anxiety, unresponsiveness); or any combination of the above. Subjects stood on a footplate inside the LBNP chamber during HUT, and they were instructed and reminded as necessary to remain quiet, still, and relaxed throughout the test. Orthostatic tolerance time equaled the time from onset of HUT to presyncope. The same medical monitor judged presyncopal symptoms and called test endpoints pre- and post-bed rest. Baseline (pre-bed rest) data from this test were previously employed to investigate heritability of orthostatic cardiovascular function (46).
Orthostatic tolerance test instrumentation. Electrocardiography allowed determination of HR and monitoring for dysrhythmias. Doppler ultrasound from the suprasternal notch yielded beat-by-beat aortic outflow tract blood flow velocity (2-MHz probe, CFM750, GE/Vingmed, Horten, Norway), such that the integral of this signal provided cardiac SV. Aortic flow (cardiac output) was then calculated using outflow tract diameter as determined with standard echocardiography (Hewlett Packard, Palo Alto, CA) (47). We measured finger arterial blood pressure continuously with a Finapres device (Ohmeda 2300, Englewood, CO) on the right hand, and left arm blood pressure was measured each minute with manual sphygmomanometric auscultation. The Finapres was adjusted before testing such that finger diastolic pressure was within 5 mmHg of arm diastolic pressure. Transcranial Doppler ultrasound permitted measurement of middle cerebral arterial blood flow velocity from a temporal cranial window (Transpect TCD, Medasonics, Mountain View, CA) (37, 47). Because of its influence on cerebral hemodynamics, end-tidal carbon dioxide was monitored (Ohmeda 5200, Englewood, CO) via nasal cannulas. Total peripheral resistance was calculated as mean arterial pressure divided by cardiac output. SV and cardiac output were converted to indexes by dividing by calculated body surface area. We calculated cerebral vascular resistance (CVR) as mean arterial pressure at eye level divided by cerebral blood flow velocity. This approach assumes minimal change in middle cerebral arterial diameter occurred such that velocity provided a reliable quantitative indicator of blood flow (47).
Statistical analyses. Multifactor repeated-measures ANOVA assessed independent and interactive effects of bed rest and the countermeasure for orthostatic tolerance test time. For physiological variables during the test, an additional factor (time) was included to analyze data from the three levels of orthostatic stress that all subjects achieved both pre- and post-bed rest: supine rest, HUT, and presyncope. Dependent variables were averaged over the fifth minute of supine rest, the fifth minute of HUT, and the minute before presyncope. Technical problems with aortic Doppler in specific subjects and during HUT plus LBNP led to significant loss of SV and thus blood flow and TPR data, so n = 10 for these variables (5 per sex), and they are not represented at presyncope. The sample size for sex comparisons was marginal, and they were deemed beyond the scope of this work. Tukey's honestly significant difference post hoc tests determined which specific mean values differed from others for each variable. We accepted a finding as significant if P < 0.05. SAS software performed all statistical analyses (SAS Institute, Cary, NC). Values are expressed as means (SD) unless noted otherwise.
|
RESULTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Subjects tolerated LBNP exercise very well after resolution of any initial comfort problems (e.g., ankle and leg chafing from suspension system, waist chafing from seal, waist seal sizing, shoulder strap vs. waist seal pressure distribution, etc.). Less-fit subjects tended to spend the first few exercise sessions acclimating to regular vigorous activity. LBNP was stopped occasionally during postexercise LBNP periods because of presyncopal symptoms. This occurred more for women than for men, and more toward the beginning of the bed rest period than toward the end. At these stoppages, subjects enacted the remedies described above (see METHODS) until presyncopal symptoms resolved, after which they continued the protocol to completion.
Orthostatic tolerance time. For this and other dependent variables, no significant control vs. countermeasure group differences existed prior to bed rest (F < 2.39; P > 0.132). Bed rest reduced orthostatic tolerance time in both groups (F = 64.84; P < 0.001; Fig. 3). However, countermeasure use attenuated loss of orthostatic tolerance during bed rest: the 13% (20) reduction of tolerance time seen in countermeasure subjects was significantly less than the 34% (10) reduction exhibited by control subjects (F > 10.20; P < 0.004). Figure 4 illustrates individual orthostatic tolerance data.
|
|
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Acute responses to training sessions. Previous work discusses responses to LBNP exercise per se (4, 59, 60). The present data confirm that the exercise portion of the protocol provides a vigorous workout (Fig. 2): peak HR averaged 86% of maximal levels. HR at a given treadmill speed and LBNP level at the end of an exercise session exceeded by 20% HR at the same speed and LBNP near the start of the session (after the 7-min warm-up). As discussed previously (59), multiple factors explain this cardiovascular drift, including 1) incomplete recovery from prior exercise at higher workloads, 2) fluid losses via respiration and sweat, 3) progressive LBNP-induced blood and extravascular fluid accumulation in the lower body (2, 60, 69), 4) cutaneous vasodilation from metabolic and LBNP chamber heat accumulation (59), and 5) synergistic interactions between the above factors. These acute responses to LBNP exercise set-up conditions for exaggeration of subsequent orthostatic stress.
Mechanisms of current observations. We sought to exploit postexercise hemodynamic conditions to train orthostatic blood pressure control mechanisms efficiently. Static upright posture immediately after strenuous exercise provides a substantially greater cardiovascular stress than orthostasis without prior exercise (68). Factors contributing to this observation include exercise-induced blood and extracellular fluid volume reduction (31), cessation of skeletal muscle pumping (10, 11), reduction of respiratory pumping (52), postexercise reduction of vasoconstrictive sympathetic nerve activity (15, 30), ongoing skeletal muscle vasodilation to meet metabolic demands of exercise recovery (52), and cutaneous vasodilation to dissipate residual heat from exercise (22).
Bjurstedt and colleagues (3) blamed low systemic resistance for postexercise orthostatic intolerance, because central venous pressure and thus cardiac filling remained at preexercise values during postexercise HUT. Indeed, Halliwill and coworkers (30) noted reduced sensitivity of both the arterial-sympathovascular baroreflex and the vasoconstrictive transduction of sympathetic activity following dynamic exercise. Therefore, ongoing vasodilation during recovery from dynamic exercise accentuates the cardiovascular challenge imposed by orthostatic stress. In some ways, the postexercise condition mimics the hypovolemia and limited ability to vasoconstrict seen after spaceflight.
Plasma and blood volume results from the present study are presented elsewhere, and they agree with earlier evaluations (38, 64): LBNP treadmill exercise prevents intravascular fluid volume loss during bed rest. This in turn helps normalize cardiac filling pressure during orthostasis and thus facilitates maintenance of orthostatic tolerance (13, 20, 48, 65). However, as noted above, maintenance of blood volume with LBNP exercise alone failed to prevent bed rest-induced loss of tolerance (53). The clearest physiological difference between the present control and countermeasure groups is the post-bed rest SV reduction and HR elevation in controls. This did not occur in countermeasure subjects. This maintenance of SV during bed rest suggests that the countermeasure prevented any cardiac remodeling that may contribute to loss of orthostatic tolerance (48, 65).
We saw no significant control vs. countermeasure group differences in TPR during HUT, but intersubject variability seemed to increase post-bed rest (Fig. 6), and technical problems limited sample size for these data. The countermeasure group exhibited an interesting trend toward reduced CVR after bed rest relative to pre-bed rest and control group values, including at presyncope (Fig. 6). Some evidence suggests that bed rest and spaceflight affect the cerebral circulation in ways that compromise brain blood flow during orthostasis, perhaps secondary to chronic elevation of cerebral circulatory and/or intracranial pressures (37, 65, 67, 71, 72). If so, the brief but strong stimulus offered by postexercise LBNP during bed rest may have reduced perfusion pressure and challenged autoregulation enough to help prevent maladaptive cerebral circulatory changes.
The present orthostatic tolerance results confirm and extend findings from our laboratory's previous 5-day bed-rest study (38, 64). In that work, 5 min of postexercise LBNP applied daily appeared to fully preserve orthostatic tolerance during the relatively short bed rest period. Although the 5-min stimulus did not prevent degradation of orthostatic tolerance fully during 30 days of bed rest, it roughly halved the magnitude of degradation. We speculate that increasing postexercise LBNP duration may fully protect orthostatic tolerance during prolonged bed rest.
Alternatively, more accurate simulation of gravity may be necessary for full protection of tolerance. LBNP does not create a gradient of pressure in the circulation as does gravity, nor does it apply static +Gz vestibular stimulation (61, 65). Full preservation of orthostatic function may somehow depend on reproducing the gravitational pressure gradient between the cerebral circulation, carotid, and aortic baroreceptors. A literature search yielded no investigations of this idea. Vestibulovascular control mechanisms provide a more studied example of how gravity affects the circulation in ways tht LBNP cannot duplicate. Many works suggest vestibular inputs to circulatory control may importantly influence orthostatic cardiovascular function (36, 43, 51, 70), whereas other findings question this contention (63). If future work confirms need for +Gz vestibular stimulation to protect orthostatic tolerance during bed rest, such results would suggest superiority of long-arm centrifugation over LBNP as a countermeasure.
Comparison to other countermeasures. Most current countermeasures against orthostatic intolerance either prove inadequate or take too much crew time. Toward the end of flights lasting months, astronauts on Mir spent 2–3 h/day exercising, yet they wore anti-G suits for up to 4 days postflight (26, 65). Vernikos and coworkers (57) reported that standing 4 h/day completely prevented, and 2 h/day partially prevented, reduction of orthostatic tolerance after 4 days of bed rest. Hyatt and West (33) found that 4 h of 30 mmHg (3.99 kPa) LBNP plus ingestion of 1 liter of isotonic beverage at the end of 7 days of bed rest restored LBNP responses to pre-bed rest levels.
Vernikos and coworkers (57) also reported that walking 2 or 4 h/day did not alleviate orthostatic intolerance. This and multiple other studies (20, 27, 29, 39), along with our laboratory's results (53), document that exercise by itself offers little or no protection against loss of orthostatic tolerance during bed rest. Cerebral blood flow continues uncompromised or increases during even intense upright dynamic exercise (49), because of blood pressure elevation from sympathoexcitation and the skeletal muscle and respiratory pumps. Therefore, dynamic exercise by itself does little or nothing to train resting blood pressure control mechanisms for their task of maintaining cerebral blood flow during gravitational stress. These collective observations suggest that protection of orthostatic tolerance during bed rest requires stimulation of orthostatic (resting) blood pressure control mechanisms. In this regard, our laboratory's prior 15-day bed rest results (53) effectively provide an exercise-only control condition for the present study, because if LBNP exercise alone failed to protect orthostatic tolerance during 15 days of bed rest, no basis exists to expect it to protect tolerance during 30 days of bed rest.
A study by Engelke and colleagues (18) refutes the contention that exercise offers little benefit for orthostatic function. Their subjects performed a single bout of supine maximal cycling exercise after 15 days of bed rest. When LBNP tolerance was measured 24 h later (end of bed rest), subjects experienced less loss of tolerance after they had exercised than in control conditions. Although these findings are scientifically interesting, it is probably unrealistic to expect all crew members on a given flight to perform maximal exercise within 24 h before return from space, especially if return was unexpectedly urgent. Also, it may be unreasonable to expect occasional maximal exercise to counter the scope and degree of deconditioning seen after months in space (25, 45).
The simplicity of a pharmacological remedy for postflight orthostatic intolerance offers obvious advantages. Isotonic beverages provide limited and inconsistent benefit (6, 7) except when given in conjunction with prolonged LBNP (33). Fludrocortisone (55, 56) and midodrine (50) each proved effective for restoring orthostatic tolerance when given alone before the end of bed rest, but postflight results for fludrocortisone taken late in-flight were less promising (54). Although medications may perform well for orthostatic tolerance, they may not offer similar benefit for other systems and functions degraded by bed rest or spaceflight, and protected by LBNP exercise, such as spinal biomechanics (9), anti-G muscle strength, and upright exercise capacity (38, 59). Although a "drug cocktail" of agents could conceivably protect against all debilitating effects of spaceflight, no such combination of medications currently exists. Moreover, a LBNP treadmill system integrated with virtual environments offers recreation and other utility: such a system could be programmed to simulate the gravitational force and possibly even local terrain features of destinations such as Earth's moon or Mars (42, 65).
Similarly, adjustment of centrifugation rate allows simulation of variable gravity. Also, centrifugation applies +Gz force to the otoliths unless the head is at the center of rotation, and centrifugation more accurately duplicates gravitational pressure gradients in the circulation than LBNP (61). Neurolab shuttle flight results imply that even short-arm centrifugation may impose sufficient vestibular stimulation to aid postflight orthostatic function (44). Several interesting bed rest studies from Japan demonstrate that cycling exercise during short-arm centrifugation defends against cardiovascular deconditioning, including orthostatic intolerance (34), with efficacy rivaling LBNP exercise (1, 35). Also, Evans and colleagues (19) demonstrated that centrifuge training increases orthostatic tolerance in ambulatory subjects. Other works review the promise (8, 14) and recent progress (12, 14) of centrifugation as a countermeasure.
Safety and operational considerations. The muscle pumping and sympathoexcitatory stimuli practically always reversed the rare presyncope seen during postexercise LBNP. For operational implementation, a more proactive approach may employ brief scheduled applications of such stimuli. LBNP exercisers may easily and instantly stop LBNP by disengaging the waist skirt from the chamber, opening a vacuum release valve, or turning off the vacuum source. System operation could depend on physiologic feedback and/or active subject participation (e.g., a handgrip switch). Finally, the large chamber orifice over which the waist seal lies provides failsafe protection: a user who faints or is otherwise incapacitated would be drawn into the chamber, breaking the seal and thus stopping LBNP.
Although evidence suggests LBNP and centrifugation offer similar effectiveness as countermeasures, practical considerations favor LBNP. A human centrifuge on a spacecraft or a spinning spacecraft would be much larger, more complex, and expensive. The forces created by periodic operation of a human centrifuge would impose significant energy requirements and challenges to a spacecraft's orientation control systems. LBNP exercise would require minimal purpose-built hardware and control systems: the spacecraft airlock could serve as a LBNP exercise chamber with existing pressure controls, vacuum vented to the spacecraft cabin, a waist seal installation, and a stowable treadmill inside (59).
We used treadmill exercise, as opposed to alternatives such as cycling, for multiple reasons presented previously (59). The present findings do not exclude other forms of exercise, and orthostatic training after shorter bouts of exercise than 40 min may also prove feasible. Concerning postexercise orthostatic training, methods other than LBNP exist to impose such stimulation in weightlessness, and our results do not exclude these options. Such methods include centrifugation (1, 8, 12, 28, 61) and thigh venous occlusion (32, 41). Thigh venous occlusion in particular offers the potential for immediate implementation: one simply applies venous occlusion pressure cuffs to the upper thighs following in-flight aerobic leg exercise and then inflates the cuffs to subdiastolic pressure for the prescribed time.
Limitations. In some subjects, signal quality problems prevented quantification of SV using aortic Doppler ultrasound. In others, as LBNP increased during orthostatic tolerance tests, insonation of the aortic outflow tract became unreliable. These problems limited the number of data points for SV, blood flow, and TPR data through HUT, and they disallowed inclusion of SV, blood flow, and TPR data at presyncope. Therefore, our ability to interpret and conclude from these data is restricted.
We employed identical twin subjects to minimize genetic variability between control and countermeasure groups. Hypothetically, this experimental design maximized our ability to detect and quantify effects of the countermeasure (5). However, despite their genetic identity, physiological and psychological differences between twin siblings occasionally emerged during baseline testing (46). Therefore, it did not seem appropriate to treat each twin pair as a single "subject" for statistical purposes, so we utilized the same statistical approach as one would with unrelated subjects. In these respects, the degree to which use of twins helped us test our hypotheses remains unclear but may have been overestimated. Twin subjects bring instant roommate rapport and an established support system to challenging studies such as this, which offers an advantage over use of unrelated strangers. In one case, the psychological support provided by a twin probably kept their sibling from dropping out of the study.
Our study design left out an LBNP-alone condition because 45 min of 50–60 mmHg resting LBNP exceeds the tolerance of most subjects (60, 69). Subjects tolerate sustained 50–60 mmHg LBNP with concomitant exercise because exercise increases LBNP tolerance (60). Bed rest is not physiologically identical to spaceflight (20, 65), so in-flight studies offer the only way to test whether post-exercise LBNP maintains orthostatic tolerance during spaceflight.
Conclusions. These results demonstrate that daily brief post-exercise orthostatic stress during bed rest attenuates bed rest-induced loss of orthostatic tolerance. Vigorous exercise followed by brief orthostatic stimulation appears capable of maintaining blood volume and orthostatic cardiovascular function near baseline levels. This strategy reduces the daily duration of orthostatic stress necessary for protecting orthostatic tolerance during bed rest from hours to minutes, and it appends time for orthostatic training to that already used for exercise countermeasures. Taken together with prior related work, these results support spaceflight study of orthostatic stimulation during recovery from exercise. Hardware currently exist in-flight to apply safely such stimulation in some form (32).
|
GRANTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
ACKNOWLEDGMENTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
FOOTNOTES |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
|
REFERENCES |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. M. C. Lee, S. M. Schneider, W. L. Boda, D. E. Watenpaugh, B. R. Macias, R. S. Meyer, and A. R. Hargens LBNP exercise protects aerobic capacity and sprint speed of female twins during 30 days of bed rest J Appl Physiol, March 1, 2009; 106(3): 919 - 928. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
O2pk, peak oxygen consumption.
, men; 
, women). Pre, before bed rest; Post, after bed rest. All control subjects exhibited reduced orthostatic tolerance after 30 days of bed rest. Tolerance increased post-bed rest in 4 of the 15 countermeasure subjects.
, countermeasure (CM) group. Values are means ± SD; n = 15 except for stroke volume and cardiac indexes, where n = 10, and no data appear at PS because of technical problems. *Control group exhibited reduced stroke volume and elevated heart rate after bed rest relative to pre-bed rest (P < 0.03); no such changes occurred in the countermeasure group (P > 0.82). #After bed rest, control group heart rate exceeded countermeasure group heart rate (P < 0.005).