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Review
. 2018 Aug 2:2018:8306154.
doi: 10.1155/2018/8306154. eCollection 2018.

Aging and Thermoregulatory Control: The Clinical Implications of Exercising under Heat Stress in Older Individuals

Affiliations
Review

Aging and Thermoregulatory Control: The Clinical Implications of Exercising under Heat Stress in Older Individuals

Bryce N Balmain et al. Biomed Res Int. .

Abstract

Climate change is predicted to bring about a greater variability in weather patterns with an increase in extreme weather events such as sustained heat waves. This change may have a direct impact on population health since heat waves can exceed the physiological limit of compensability of vulnerable individuals. Indeed, many clinical reports suggest that individuals over the age of 60 years are consistently the most vulnerable, experiencing significantly greater adverse heat-related health outcomes than any other age cohort during environmental heat exposure. There is now evidence that aging is associated with an attenuated physiological ability to dissipate heat and that the risk of heat-related illness in these individuals is elevated, particularly when performing physical activity in the heat. The purpose of this review is to discuss mechanisms of thermoregulatory control and the factors that may increase the risk of heat-related illness in older individuals. An understanding of the mechanisms responsible for impaired thermoregulation in this population is of particular importance, given the current and projected increase in frequency and intensity of heat waves, as well as the promotion of regular exercise as a means of improving health-related quality of life and morbidity and mortality. As such, the clinical implications of this work in this population will be discussed.

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Figures

Figure 1
Figure 1
(a) At rest, the rate of Hprod (solid line) is balanced out by the rate of Hloss (dotted line), a combination of evaporative and dry heat exchange. At the onset of exercise, Hprod rapidly rises reaching a steady state within 5 min. Due to the delay in the onset of Hloss responses, Hloss does not immediately balance the rate of Hprod resulting in net heat storage. The additional heat energy stored inside the body initiates increases in sweating and skin blood flow to increase Hloss and achieve heat balance to prevent a continuing rise in core temperature (dashed line). (b) When heat balance cannot be achieved, core temperature will continue to rise to potentially dangerous limits and not plateau, due to limited Hloss capacity; the rate of Hloss required to achieve heat balance is greater than the maximum capacity for heat dissipation. Hprod: metabolic heat production; Hloss: net heat loss.
Figure 2
Figure 2
Trec (a), CVC (b), and LSR (c) values recorded at 10-min intervals during the submaximal cycling test. Hprod: metabolic heat production; Trec: rectal temperature; CVC: cutaneous vascular conductance; LSR: local sweat rate. Data are mean ± standard error of the mean. Significant group-time interaction, p < 0.05. Figure adapted from Balmain et al. [28].

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