Effects of whole-body and local thermal stress on hydrostatic volume changes in the human calf

Yamazaki, Fumio; Okuno, Chitose; Nagamatsu, Shoko; Sone, Ryoko

doi:10.1007/s00421-002-0688-z

Cited by 10 publications

(12 citation statements)

References 21 publications

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“…We (4) and others (11) have shown that the increase in leg circumference during LBNP is significantly smaller with skin surface cooling compared with normothermic conditions. Similar responses have also been reported during head-up tilt with cooling (19). These data suggest that central blood volume under cooling conditions may remain relatively higher during orthostatic stress.…”

Section: Discussionsupporting

confidence: 73%

Effect of skin surface cooling on central venous pressure during orthostatic challenge

Cui¹,

Durand²,

Levine³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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(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 Ϫ10, Ϫ15, Ϫ20, and Ϫ40 mmHg at 5 min/stage. Before LBNP, skin surface cooling lowered mean skin temperature, increased CVP, and increased mean arterial blood pressure (all P Ͻ 0.001) but did not change mean heart rate (P ϭ 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. thermoregulation; cardiovascular regulation; orthostatic tolerance; lower body negative pressure ORTHOSTATIC INTOLERANCE is a common occurrence after spaceflight (2, 6), after long-term bed rest (5), and in over 500,000 Americans who suffer from idiopathic orthostatic intolerance (13,14). We recently showed (4, 18) that skin surface cooling improves orthostatic tolerance in normothermic and heatstressed individuals. Although increases in orthostatic tolerance with skin surface cooling are clearly a result of attenuated decreases in arterial blood pressure and cerebral blood flow velocity (4,10,11,18), the mechanism(s) by which skin cooling causes these responses remains unclear. One possible mechanism is that skin surface cooling increases central blood volume and central venous pressure (CVP) and in turn elevates stroke volume, arterial blood pressure, and cerebral perfusion during orthostasis. Raven et al. (10,11) showed that skin surface cooling attenuates the reduction in stroke volume during progressive lower body negative pressure (LBNP). They proposed that elevated cardiac preload was the primary mechanism for heightened stroke volumes with cooling (10, 11). However, indicators of cardiac preload (e.g., CVP) were not measured in those studies, and changes in CVP and stroke volume are not consistently well correlated (8,17). Therefore, it is necessary to evaluate the combined effects of skin surface cooling and orthostatic stress on CVP. Such information will provide insight into mechanisms o...

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Section: Discussionsupporting

confidence: 73%

Effect of skin surface cooling on central venous pressure during orthostatic challenge

Cui¹,

Durand²,

Levine³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Whole-body heating induces cutaneous venodilatation in the legs and arms 46,47) and decreases muscle venous volume as a percentage of the total volume of leg veins with an increase in skin venous volume. Compared with normothermic control, whole-body heating rapidly increases calf volume during the early phase of HUT, whereas whole-body cooling decreases the magnitude and the speed of change in calf volume 48) . Local heating to the legs in normothermia increases the blood flow in the warmed skin area and increases the speed of the change in calf volume the same nique, the effect of heat stress on the relationship between carotid distending pressure and HR has been examined in the supine position [50][51][52] .…”

Section: Increase In Leg Venous Compliancementioning

confidence: 99%

“…arterial pressure = HR × SV × total PVR), and the use of HR may be better for evaluating baroreflex sensitivity in the maintenance of arterial pressure. In a study as that during whole-body heating 48) . That is, the thermal modulation in leg venous distensibility is almost independent of whole-body or local heating.…”

Section: Increase In Leg Venous Compliancementioning

confidence: 99%

Heat stress and orthostatic tolerance

Yamazaki

2012

JPFSM

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In healthy individuals, exercise and nonexercise (i.e. passive body heating) heat stress induces vulnerability in the cardiovascular system, and is apt to cause hypotension during upright posture, resulting in a reduction of orthostatic tolerance. Reduced orthostatic tolerance is linked to multiple physiological mechanisms including 1) a redistribution of blood flow from central parts of the body to skin, 2) an increase in leg venous compliance, 3) altered baroreflex function, 4) an attenuated venoarterial response in the lower extremities, and 5) a decrease in plasma volume. A combination of countermeasures such as cooling of the body, rehydration, and heat acclimation, can improve orthostatic tolerance in a hot environment. The purpose of this review was to summarize findings investigating the causes of and preventive approaches to heat stress-induced orthostatic intolerance.

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“…In each thermal condition, we abruptly occluded the thigh at 20, 30, 50, 70, and 80 mmHg in this order in five subjects and in the opposite order in the remaining subjects. This enabled us to study the vascular response and swelling pattern of the calf over a wide range of transmural venous pressures, such as those that occur during changes in posture or tilt [17]. That is, we used this method to examine the isolated effect of local reflex in vasoconstriction in the lower extremities during HUT.…”

Section: Subjectsmentioning

confidence: 99%

“…Between each occlusion pressure, the thigh cuff pressure was abruptly released to zero by opening the inflation bulb. The criterion for deflating the cuff was either (i) when the increase of calf circumference reached a steady-state level or (ii) when its increase was less than 0.5 mm for 30 s [17,18]. The first was mainly used for the cuff pressures of 20, 30, and 50 mmHg, at which the calf circumference reached a steady state within 1-4 min.…”

Section: Subjectsmentioning

confidence: 99%

Whole-Body Heating Decreases Skin Vascular Response to Low Orthostatic Stress in the Lower Extremities

2006

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Abstract:To elucidate the influence of heat stress on cutaneous vascular response in the lower extremities during orthostatic stress, a head-up tilt (HUT) test at angles of 15°, 30°, 45°, and 60° for 4 min each was conducted under normothermic control conditions followed by whole-body heat stress produced by a hot water-perfused suit in healthy volunteers. Skin blood flows (SkBF) in the forearm, thigh, and calf were monitored using laser-Doppler flowmetry throughout the experiment. Furthermore, to elucidate the effects of increased core and local skin temperatures on the local vascular response in calf skin under increasing orthostatic stress, the thigh was occluded at 20, 30, 50, 70, and 80 mmHg with a cuff in both the normothermic condition and the whole-body or local heating condition. Significant decreases in forearm SkBF during HUT were observed at an angle of 60°d uring normothermia and at 30° or more during heating. SkBF in the thigh and calf was decreased significantly by HUT at 15° and above during normothermia, and there was no significant reduction of SkBF in these sites during HUT at the lower angles (15°-45°) during whole-body heating. Significant decreases of calf SkBF were observed at cuff pressures of 20 mmHg and above during normothermia and of 30 mmHg and above during wholebody and local heating, respectively. These results suggest that SkBF in the lower extremities shows a marked reduction compared with the upper extremities during low orthostatic stress in normothermia, and the enhanced skin vasoconstrictor response in the lower extremities is diminished by both whole-body and local heat stress.

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Effects of whole-body and local thermal stress on hydrostatic volume changes in the human calf

Cited by 10 publications

References 21 publications

Effect of skin surface cooling on central venous pressure during orthostatic challenge

Effect of skin surface cooling on central venous pressure during orthostatic challenge

Heat stress and orthostatic tolerance

Whole-Body Heating Decreases Skin Vascular Response to Low Orthostatic Stress in the Lower Extremities

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