Skin Surface Cooling Improves Orthostatic Tolerance After Prolonged Head-Down Bed Rest

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S324
Author(s):  
David M. Keller ◽  
David A. Low ◽  
Scott L. Davis ◽  
Kenichi Kimura ◽  
Jonathan Wingo ◽  
...  
2011 ◽  
Vol 110 (6) ◽  
pp. 1592-1597 ◽  
Author(s):  
David M. Keller ◽  
David A. Low ◽  
Scott L. Davis ◽  
Jeff Hastings ◽  
Craig G. Crandall

Prolonged exposure to microgravity, as well as its ground-based analog, head-down bed rest (HDBR), reduces orthostatic tolerance in humans. While skin surface cooling improves orthostatic tolerance, it remains unknown whether this could be an effective countermeasure to preserve orthostatic tolerance following HDBR. We therefore tested the hypothesis that skin surface cooling improves orthostatic tolerance after prolonged HDBR. Eight subjects (six men and two women) participated in the investigation. Orthostatic tolerance was determined using a progressive lower-body negative pressure (LBNP) tolerance test before HDBR during normothermic conditions and on day 16 or day 18 of 6° HDBR during normothermic and skin surface cooling conditions (randomized order post-HDBR). The thermal conditions were achieved by perfusing water (normothermia ∼34°C and skin surface cooling ∼12–15°C) through a tube-lined suit worn by each subject. Tolerance tests were performed after ∼30 min of the respective thermal stimulus. A cumulative stress index (CSI; mmHg LBNP·min) was determined for each LBNP protocol by summing the product of the applied negative pressure and the duration of LBNP at each stage. HDBR reduced normothermic orthostatic tolerance as indexed by a reduction in the CSI from 1,037 ± 96 mmHg·min to 574 ± 63 mmHg·min ( P < 0.05). After HDBR, skin surface cooling increased orthostatic tolerance (797 ± 77 mmHg·min) compared with normothermia ( P < 0.05). While the reduction in orthostatic tolerance following prolonged HDBR was not completely reversed by acute skin surface cooling, the identified improvements may serve as an important and effective countermeasure for individuals exposed to microgravity, as well as immobilized and bed-stricken individuals.


2004 ◽  
Vol 286 (1) ◽  
pp. R199-R205 ◽  
Author(s):  
S. Durand ◽  
J. Cui ◽  
K. D. Williams ◽  
C. G. Crandall

Previous studies suggest that skin surface cooling (SSC) preserves orthostatic tolerance; however, this hypothesis has not been experimentally tested. Thus the purpose of this project was to identify whether SSC improves orthostatic tolerance in otherwise normothermic individuals. Eight subjects underwent two presyncope limited graded lower-body negative pressure (LBNP) tolerance tests. On different days, and randomly assigned, LBNP tolerance was assessed under control conditions and during SSC (perfused 16°C water through tube-lined suit worn by each subject). Orthostatic tolerance was significantly elevated in each individual due to SSC, as evidenced by a significant increase in a standardized cumulative stress index (normothermia 564 ± 58 mmHg·min; SSC 752 ± 58 mmHg·min; P < 0.05). At most levels of LBNP, blood pressure during the SSC tolerance test was significantly greater than during the control test. Furthermore, the reduction in cerebral blood flow velocity was attenuated during some of the early stages of LBNP for the SSC trial. Plasma norepinephrine concentrations were significantly higher during LBNP with SSC, suggesting that SSC may improve orthostatic tolerance through increased sympathetic activity. These data demonstrate that SSC is effective in improving orthostatic tolerance in otherwise normothermic individuals.


2005 ◽  
Vol 289 (6) ◽  
pp. H2429-H2433 ◽  
Author(s):  
Jian Cui ◽  
Sylvain Durand ◽  
Benjamin D. Levine ◽  
Craig G. Crandall

Orthostatic stress leads to a reduction in central venous pressure (CVP), which is an index of cardiac preload. Skin surface cooling has been shown to improve orthostatic tolerance, although the mechanism resulting in this outcome is unclear. One possible mechanism may be that skin surface cooling attenuates the drop in CVP during an orthostatic challenge, thereby preserving cardiac filling. To test this hypothesis, CVP, arterial blood pressure, heart rate, and skin blood flow, as well as skin and sublingual temperatures, were recorded in nine healthy subjects during lower body negative pressure (LBNP) in both normothermic and skin surface cooling conditions. Cardiac output was also measured via acetylene rebreathing. Progressive LBNP was applied at −10, −15, −20, and −40 mmHg at 5 min/stage. Before LBNP, skin surface cooling lowered mean skin temperature, increased CVP, and increased mean arterial blood pressure (all P < 0.001) but did not change mean heart rate ( P = 0.38). Compared with normothermic conditions, arterial blood pressure remained elevated throughout progressive LBNP. Although progressive LBNP decreased CVP under both thermal conditions, during cooling CVP at each stage of LBNP was significantly greater relative to normothermia. Moreover, at higher levels of LBNP with skin cooling, stroke volume was significantly greater relative to normothermic conditions. These data indicate that skin surface cooling induced an upward shift in CVP throughout LBNP, which may be a key factor for preserving preload, stroke volume, and blood pressure and improving orthostatic tolerance.


2002 ◽  
Vol 93 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Rong Zhang ◽  
Sarah Witkowski ◽  
Craig G. Crandall

Orthostatic tolerance is reduced in the heat-stressed human. The purpose of this project was to identify whether skin-surface cooling improves orthostatic tolerance. Nine subjects were exposed to 10 min of 60° head-up tilting in each of four conditions: normothermia (NT-tilt), heat stress (HT-tilt), normothermia plus skin-surface cooling 1 min before and throughout tilting (NT-tiltcool), and heat stress plus skin-surface cooling 1 min before and throughout tilting (HT-tiltcool). Heating and cooling were accomplished by perfusing 46 and 15°C water, respectively, though a tube-lined suit worn by each subject. During HT-tilt, four of nine subjects developed presyncopal symptoms resulting in the termination of the tilt test. In contrast, no subject experienced presyncopal symptoms during NT-tilt, NT-tiltcool, or HT-tiltcool. During the HT-tilt procedure, mean arterial blood pressure (MAP) and cerebral blood flow velocity (CBFV) decreased. However, during HT-tiltcool, MAP, total peripheral resistance, and CBFV were significantly greater relative to HT-tilt (all P< 0.01). No differences were observed in calculated cerebral vascular resistance between the four conditions. These data suggest that skin-surface cooling prevents the fall in CBFV during upright tilting and improves orthostatic tolerance, presumably via maintenance of MAP. Hence, skin-surface cooling may be a potent countermeasure to protect against orthostatic intolerance observed in heat-stressed humans.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jeffrey Hastings ◽  
Eric Pacini ◽  
Felix Krainski ◽  
Shigeki Shibata ◽  
Manish Jain ◽  
...  

We propose to prevent the cardiac atrophy and orthostatic intolerance associated with prolonged bed rest using rowing ergometry/resistance training with aggressive volume loading on the day of testing. We hypothesize that prevention of cardiac atrophy will forestall cardiovascular deconditioning, leading to preserved exercise capacity and orthostatic tolerance. Twenty-four healthy subjects, ages 20 –55, were enrolled with 8 randomized to training (EX), 8 with training and volume loading (VOL), and 8 as sedentary (SED) controls. Testing included maximal upright exercise, orthostatic tolerance via graded lower body negative pressure (LBNP), cardiac MRI, as well as invasive cardiac pressure-volume measurements, performed at baseline and at the end of 5 weeks of 6° head down bedrest. Upright exercise capacity was preserved with training as measured by peak workrate and VO2max (EX/VOL: pre 195±46W, 34±7 ml/kg/min; post 202±42W, 33±4 ml/kg/min) but deteriorated in SED group (pre 171±55W, 34±8 ml/kg/min; post 145±51W, 27±7 ml/kg/min). MRI derived mass (% change: +6.3±9.9% EX/VOL vs. −5.5±3.7% SED) was increased by training. Exercise training appears to preserve LV chamber compliance (stiffness constants: EX/VOL: pre= 0.035±0.021, post = 0.036±0.029; SED: pre= 0.020±0.011, post = 0.028±0.007). Training also preserves hemodynamic variables measured at −40mmHg of LBNP, including stroke volume (EX: pre 44±12; post 38±9 ml, VOL: pre 49±30; post 45±29 ml, SED: pre 35±5; post 24±8 ml ). These preliminary data support our hypothesis that an optimized training program consisting of dynamic and resistance exercise can prevent part of the multisystem atrophy and orthostatic intolerance associated with prolonged bed rest. This defines a specific countermeasure that is practical, safe, and effective against the cardiovascular, muscle and bone deconditioning associated with prolonged bed rest. This information is relevant not only for astronauts exposed to long duration spaceflight, but also for patients with chronic reductions in physical activity, and those with disease processes that alter cardiac stiffness such as obesity, hypertension, heart failure or ischemic heart disease, plus normal aging and osteoporosis. This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).


2020 ◽  
Author(s):  
VP Katuntsev ◽  
TV Sukhostavtseva ◽  
AN Kotov ◽  
MV Baranov

Reduced orthostatic tolerance (OT) is a serious concern facing space medicine. This work sought to evaluate the effects of intermittent hypoxic training (IHT) on OT in humans before and after 3 days of head-down bed rest (HDBR) used to model microgravity. The study was carried out in 16 male volunteers aged 18 to 40 years and included 2 series of experiments with 11-day and 21-day IHT administered on a daily basis. During the first IHT session, the concentration of oxygen in the inspired gas mixture was 10%; for other sessions it was adjusted to 9%. OT was assessed by a 20-minute-long orthostatic tilt test (OTT) conducted before and after HDBR. Before HDBR, orthostatic intolerance was observed in 3 participants, while after HDBR, it was observed in 9 of 16 volunteers (p < 0.05). During OTT conducted after HDBR, the heart rate (HR) exceeded control values by 26.8% (p < 0.01). Preexposure to any of the applied IHT regimens led to a reduction in the number of volunteers with orthostatic intolerance. After the 11-day IHT program, there was a less pronounced increase in HR during OTT before HDBR; with the extended IHT regimen, less pronounced changes were observed for HR, systolic, diastolic and mean blood pressure (BP). The increase in HR during OTT after HDBR was significantly lower in the group that had completed the 11-day IHT program, while BP remained stable. The changes in HR and systolic BP were less pronounced in the group that had completed the 21-day IHT program than in the control group (p < 0.05). Thus, IHT reduced the risk of orthostatic disorders and mitigated changes in cardiovascular parameters during the orthostatic test.


2004 ◽  
Vol 96 (3) ◽  
pp. 840-847 ◽  
Author(s):  
M. W. P. Bleeker ◽  
P. C. E. De Groot ◽  
J. A. Pawelczyk ◽  
M. T. E. Hopman ◽  
B. D. Levine

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6° head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 ± 0.007 ml·100 ml-1·mmHg-1, post: 0.033 ± 0.007 ml·100 ml-1·mmHg-1; P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 ± 1.08 mmHg·ml-1·100 ml·min, post: 3.10 ± 1.00 mmHg·ml-1·100 ml·min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure·time), decreased in all subjects after bed rest (pre: 932 mmHg·min, post: 747 mmHg·min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.


2007 ◽  
Vol 103 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Jian Cui ◽  
Sylvain Durand ◽  
Craig G. Crandall

Skin surface cooling improves orthostatic tolerance through a yet to be identified mechanism. One possibility is that skin surface cooling increases the gain of baroreflex control of efferent responses contributing to the maintenance of blood pressure. To test this hypothesis, muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate were recorded in nine healthy subjects during both normothermic and skin surface cooling conditions, while baroreflex control of MSNA and heart rate were assessed during rapid pharmacologically induced changes in arterial blood pressure. Skin surface cooling decreased mean skin temperature (34.9 ± 0.2 to 29.8 ± 0.6°C; P < 0.001) and increased mean arterial blood pressure (85 ± 2 to 93 ± 3 mmHg; P < 0.001) without changing MSNA ( P = 0.47) or heart rate ( P = 0.21). The slope of the relationship between MSNA and diastolic blood pressure during skin surface cooling (−3.54 ± 0.29 units·beat−1·mmHg−1) was not significantly different from normothermic conditions (−2.94 ± 0.21 units·beat−1·mmHg−1; P = 0.19). The slope depicting baroreflex control of heart rate was also not altered by skin surface cooling. However, skin surface cooling shifted the “operating point” of both baroreflex curves to high arterial blood pressures (i.e., rightward shift). Resetting baroreflex curves to higher pressure might contribute to the elevations in orthostatic tolerance associated with skin surface cooling.


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