Abstract
We tested the hypothesis that whole‐body passive heat stress reduces arterial stiffness in older adults. At preheat stress (baseline) and when core temperature was elevated by 0.6 ± 0.2°C (mild) and 1.2 ± 0.3°C (moderate), arterial stiffness was measured in eight healthy younger (26 ± 5 years) and eight healthy older (70 ± 4 years) adults in the supine position. Arterial stiffness was estimated from carotid‐to‐femoral pulse wave velocity (cfPWV, applanation tonometry). cfPWV was higher at baseline in older adults (8.8 ± 2.3 m/sec vs. 5.6 ± 0.9 m/sec, P < 0.01) and this difference was maintained throughout passive heat stress (P < 0.01). cfPWV did not change (P ≥ 0.49) with passive heat stress in either younger (at moderate heat stress: 6.0 ± 1.0 m/sec) or older (at moderate heat stress: 8.5 ± 1.6 m/sec) adults. However, the influence of baseline cfPWV on the change in cfPWV during mild (r = −0.66, P = 0.04) and moderate (r = −0.87, P < 0.01) heat stress were inversely related in older adults, and the strength of these relations was not statistically different (P = 0.08). In younger adults, the influence of baseline cfPWV on the change in cfPWV during mild heat stress was also inversely related (r = −0.79, P = 0.01), while the strength of this relation was attenuated at moderate heat stress (r = −0.24, P = 0.30). Changes in arterial stiffness during passive heat stress in adults aged ≥65 year are likely dependent on the magnitude of baseline arterial stiffness and not necessarily age.
Highlights
Whole-body passive heat stress reduces total peripheral resistance and elevates cardiac output (Wilson and Crandall 2011)
Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society
Skin blood flow and Cutaneous vascular conductance (CVC) increased with progressive whole-body passive heat stress (P < 0.01), but the magnitude of these increases was not different between groups (P ≥ 0.64, Table 2)
Summary
Whole-body passive (i.e., resting) heat stress reduces total peripheral resistance and elevates cardiac output (Wilson and Crandall 2011). These responses are caused primarily by cutaneous vasodilation, which occurs in proportion to increases in core and skin temperatures (Wilson and Crandall 2011). This increased skin blood flow results in an increased shear stress through large conduit arteries (Naylor et al 2011; Thomas et al.2016b).
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