As heart-rate variability (HRV) is under evaluation in clinical applications, the authors sought to better define the interdependent impact of age, maximal exercise, and diurnal variation under physiologic conditions. The authors evaluated the diurnal changes in HRV 24-h pre- and post-maximal aerobic exercise testing to exhaustion in young (19-25 yrs, n = 12) and middle-aged (40-55 yrs, n = 12) adults. Subjects wore a portable 5-lead electrocardiogram holter for 48 h (24 h prior to and following a maximal aerobic capacity test). Time-, frequency-, time-frequency-, and scale-invariant-domain measures of HRV were computed from RR-interval data analyzed using a 5-min window size and a 2.5-min step size, resulting in a different set of outputs every 2.5 min. Results were averaged (mean ± SE) over four prespecified time periods during the morning, afternoon, evening, and night on Day 1 and Day 2. Diurnal changes in HRV in young and middle-aged adults were compared using a two-way, repeated-measures analysis of variance (ANOVA). Young adults demonstrated higher HRV compared to middle-aged adults during periods of wakefulness and sleep prior to maximal exercise stress testing (i.e., high-frequency power during Day 1: young adults: morning 1862 ± 496 ms(2), afternoon 1797 ± 384 ms(2), evening 1908 ± 431 ms(2), and night 3202 ± 728 ms(2); middle-aged adults: morning 341 ± 53 ms(2), afternoon 405 ± 68 ms(2), evening 469 ± 80 ms(2), and night 836 ± 136 ms(2)) (p < .05). Exercise resulted in reductions in HRV such that multiple measures of HRV were not significantly different between age groups during the afternoon and evening periods. All measures of HRV demonstrated between-group differences overnight on Day 2 (p < .05). Young adults are associated with higher baseline HRV during the daytime. Sleep increases variability equally and proportionally to daytime variability. Given the higher baseline awake HRV and equal rise in HRV during sleep, the change in HRV from sleep to morning with exercise is greater in younger subjects. These physiologic results have clinical significance in understanding the pathophysiology of altered variability in ill patients.

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15 degrees head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T(body)) increased by 1.5 degrees C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T(re), CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T(body) > 0.6 degrees C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p < 0.001). CVC increased rapidly in the early stages of heating and achieved a stable elevated level in both HDT and URS at the mid-stage of heating (T(body) increase

We evaluated the effect of exercise-induced hyperthermia (EIH) on autonomic nervous system (ANS) function in the early (<80 min) and late (24 and 48 h) stages of recovery. Eight males underwent three repeated 6 min 70° head-up tilts (HUT1, HUT2 and HUT3), each separated by 10-min supine rest in a non-exercise/non-heat stress control state (NHS). On a separate day, three 6 min 70° HUT were performed following EIH (esophageal temperature ≥ 40°C) and repeated after 24 and 48 h of recovery. Heart rate, stroke volume (SV), mean arterial pressure and cardiac output ([Formula: see text]) were evaluated during the last min prior to a change in posture. Responses to 70° HUT were compared to the same challenge performed without prior exercise and under a NHS condition. Relative to NHS, [Formula: see text] was maintained during the repeated HUT's following EIH, despite significant reductions in SV and sustained elevations in esophageal temperature (p < 0.05). The preserved [Formula: see text] appears to be due to increased HR (HUT1: NRS = 76 ± 3 beats min(-1), EIH = 126 ± 6 beats min(-1)) stemming from modulation of the ANS toward sympathetic dominance. Parasympathetic withdrawal was evidenced by a reduction in root mean squared successive difference (i.e., HUT1: NHS = 66 ± 12 ms, EIH = 9 ± 1 ms) of heart rate variability and paralleled by a reduction in baroreceptor sensitivity for all HUT's following EIH (p < 0.05). Despite significant modulation in ANS activity, Q is maintained and participants do not become orthostatic intolerant/syncopal during the short-term recovery period following EIH. Normal ANS and cardiovascular function is restored following 24 h of recovery.

We conclude that the maintenance of MAP following exercise in the heat is mitigated by reductions in skin perfusion despite significant elevations in core temperature.

No abstract