Systemic Cardiovascular Adjustments during Recovery from Passive Heat Stress
Authors: Larson Emily A. , Kaiser Brendan W. , Reed Emma L. , Gibson Brandon M. , Atencio Jessica K. , Chapman Christopher L. , Kenney W. Larry , Halliwill John R. , Minson Christopher T. 
Published: May 2022

Much like exercise, heat stress elicits profound autonomic and hemodynamic responses which may persist in the post‐heating recovery period. In the same way that the post‐exercise recovery period contributes to vascular adaptation with exercise training, the post‐heating recovery period may potentiate beneficial vascular adaptation with chronic heat therapy. In contrast to the well‐studied post‐exercise recovery period, few studies have investigated the systemic cardiovascular adjustments accompanying recovery from whole‐body, passive heat stress. Hypothesis: We hypothesized that mean arterial pressure would be reduced in the post‐heating recovery period due to sustained post‐heating elevations in systemic vascular conductance and despite elevations in cardiac output.

Methods

Four subjects (1 F, 27±5 yrs, BMI 26±3 kg/m2) completed two experimental visits (randomized, crossover design) comprising either 60 min of passive heating (HT) or a time‐matched thermoneutral control intervention (TN). Rectal temperature, skin temperature (six sites), brachial blood pressure, cardiac output (open‐circuit acetylene washin method), and heart rate were assessed at baseline, at the end of HT or TN interventions, and for 2 hours of recovery in a 21.4±0.4°C room (REC‐HT/TN). Values are reported as the change in each variable from pre‐intervention baseline and presented as means ± SD. Paired t tests were used to compare responses between conditions.

Results

Heating increased mean body temperature (HT +1.26±0.23°C, TN ‐0.04±0.07°C) (P < 0.001). After 40 min of recovery, mean body temperature tended to remain elevated following heating (HT +0.48±0.18, TN +0.19±0.09°C, P = 0.06). There were no differences in mean body temperature between conditions at 80 min (P = 0.31) or 120 min of recovery (P = 0.37). Mean arterial pressure was reduced at the end of heating (HT ‐12±6, TN +5±4 mmHg, P < 0.01) as elevations in systemic vascular conductance (HT +55±18, TN ‐6±6 mL·min‐1·mmHg‐1, P < 0.01) were not offset by increases in cardiac output (HT +3.5±0.8, TN ‐0.2±0.6 L/min, P < 0.01) sustained by an increased heart rate (HT +40±8, TN ‐2±6 bpm, P < 0.01). Mean arterial pressure tended to remain reduced 40 min into the post‐heating recovery period (REC‐HT ‐6±6, REC‐TN +1±3 mmHg, P = 0.16) due to a tendency for elevations in systemic vascular conductance (REC‐HT +11±21, REC‐TN ‐6±15 mL·min‐1·mmHg‐1, P = 0.08). Cardiac output (REC‐HT +0.5±1.5, REC‐TN ‐0.5±1.1 L/min, P = 0.07) and heart rate (REC‐HT +6±9, REC‐TN ‐3±5 bpm, P = 0.07) also appeared to remain elevated 40 min into the post‐heating recovery period. Mean arterial pressure appeared similar between conditions from 80 minutes of recovery onward (P = 0.85) while systemic vascular conductance (P = 0.12) and cardiac output (P = 0.19) tended to remain elevated. These variables appeared similar between conditions after 120 min of recovery.

Conclusions

Recovery from heat stress is marked by sustained hypotension, vasodilation, and elevations in cardiac output and heart rate. These post‐heating recovery responses may facilitate vascular adaptation with heat therapy.