Limitation of Heat Tolerance

Hales, J. R. S.; Hubbard, Richard W.; Gaffin, Stephen L.

doi:10.1002/cphy.cp040115

Cited by 49 publications

(73 citation statements)

References 409 publications

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“…It has previously been reported by Gonzalez-Alonso and colleagues (1999) that Q  reduces with dehydration and hyperthermia because of large decreases in S V (19-27%), compared with parallel increases in c f (5-10%). There is also a significant reduction in blood flow to the exercising muscle with dehydration during intense exercise in the heat, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction (Gonzalez-Alonso et al 1998 Sawka and colleagues (1996), S V augmentation has been attributed to heat-acclimationinduced PV expansion (Hales et al 1996). (Poliner et al 1980).…”

Section: Adaptation To Repeated Heat Stressmentioning

confidence: 99%

The Induction and Decay of Short-Term Heat Acclimation

Garrett

Goossens

Rehrer

et al. 2003

Medicine & Science in Sports & Exercise

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Abstract:Most advice for heat adaptation is to use long-term (>10 d) regimes, in which hydration status is maintained. We tested the hypothesis that short-term (5-day) heat acclimation would confer substantial improvements in physiological strain and exercise tolerance for exercise in the heat, and fluid regulatory strain provides a thermally-independent stimulus for such adaptations. Ten moderately-fit males were heat acclimated using controlled hyperthermia (rectal temperature 38.5°C) for 90 min on five consecutive days (T a = 40°C, 60% RH), on two occasions separated by a five-week washout, in a randomly assigned, cross-over design; one with euhydration (EUH) and one with dehydration (DEH) during acclimation bouts. One week before, then on the 2 nd day after each acclimation regime, a heat stress test (HST) was completed, comprising cycling at 40% peak power output for 90 min (T a = 35°C, 60% RH), before incrementing to exhaustion. Plasma volume (PV) at rest was measured using CO rebreathing. Acclimation exercise-induced response of In conclusion, short-term (5-day) heat acclimation was effective with several adaptations more pronounced after fluid-regulatory strain from a dehydration acclimation regime.

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Section: Adaptation To Repeated Heat Stressmentioning

confidence: 99%

The Induction and Decay of Short-Term Heat Acclimation

Garrett

Goossens

Rehrer

et al. 2003

Medicine & Science in Sports & Exercise

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“…With focus on the cerebrovasculature, we purposefully neglect the complete, multiorgan pathophysiology of heat stroke. The reader is referred to earlier elegant reviews in Comprehensive Physiology (182,385) for an overview on the integrated systems failure of heat stroke.…”

Section: Introductionmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…During the experiments the animals were submitted to two velocities, i.e., 21 and 24 m/min, always at 0% inclination, on a Modular Treadmill for rats (Columbus Instruments International Corporation, Columbus, OH, USA) until exhaustion, with exhaustion being defined as the time point when the animal was no longer able to maintain the preestablished velocity and needed to be stimulated with an electric shock (0.5 mV, 0.5 mA) (10). TET (in min) was defined as the time between the beginning of exercise and exhaustion.…”

mentioning

confidence: 99%

“…High tissue temperatures are known to induce structural and functional alterations in proteins involved in electrolyte transport through the cell membrane and sarcoplasmic reticulum, in actin-myosin interactions, and in mitochondrial respiration (14), changes that might lead to a reduction in physical performance, hyperthermia and/or even death (1,10). Within this context, both absolute T int and HSR represent important indicators for the continuous assessment of the risk of homeostatic disequilibrium, and thus play a role in the mechanisms involved in acute fatigue.…”

mentioning

confidence: 99%

Heat storage rate and acute fatigue in rats

Rodrigues

Oliveira

Lima

et al. 2003

Braz J Med Biol Res

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Thermal environmental stress can anticipate acute fatigue during exercise at a fixed intensity (%VO 2max ). Controversy exists about whether this anticipation is caused by the absolute internal temperature (T int , ºC), by the heat storage rate (HSR, cal/min) or by both mechanisms. The aim of the present study was to study acute fatigue (total exercise time, TET) during thermal stress by determining T int and HSR from abdominal temperature. Thermal environmental stress was controlled in an environmental chamber and determined as wet bulb globe temperature (ºC), with three environmental temperatures being studied: cold (18ºC), thermoneutral (23.1ºC) or hot (29.4ºC). Six untrained male Wistar rats weighing 260-360 g were used. The animals were submitted to exercise at the same time of day in the three environments and at two treadmill velocities (21 and 24 m/min) until exhaustion. After implantation of a temperature sensor and treadmill adaptation, the animals were submitted to a Latin square experimental design using a 2 x 3 factorial scheme (velocity and environment), with the level of significance set at P<0.05. The results showed that the higher the velocity and the ambient temperature, the lower was the TET, with these two factors being independent. This result indicated that fatigue was independently affected by both the increase in exercise intensity and the thermal environmental stress. Fatigue developed at different T int and HSR showed the best inverse relationship with TET. We conclude that HSR was the main anticipating factor of fatigue. Key wordsIt has been well documented that the total exercise time (TET) is reduced in warmer environments and internal body temperature (T int ) has been considered to be a limiting factor during prolonged physical exercise (1-5). This anticipation of fatigue seems to occur in order to prevent an increased T int from compromising homeostasis. The mechanisms responsible for exercise interruption due to an increase in T int are still not well understood; controversy exists about whether there is a critical absolute T int (in ºC) or whether the heat storage rate (HSR, in cal/min) is as important or even more important than T int in the origin of fatigue. Fuller et al. (6), studying the effect of warm environments on T int in rats during treadmill exercise, reported a shorter TET in animals exercising in warmer environments and similar abdominal and hypothalamic temperatures at the end of exercise at the time of fatigue, and suggested the existence of a critical absolute T int which may lead to the interruption of activity. Walters et al. (7),

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Limitation of Heat Tolerance

Cited by 49 publications

References 409 publications

The Induction and Decay of Short-Term Heat Acclimation

The Induction and Decay of Short-Term Heat Acclimation

Cerebral Vascular Control and Metabolism in Heat Stress

Heat storage rate and acute fatigue in rats

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