The acute effects of passive heating on endothelial function, muscle microvascular oxygen delivery, and expression of serum HSP90α.
Level 4 - case-series / case-control
Uncontrolled single-arm before-and-after physiological study with no concurrent control group.
PubMed 35276210 · doi:10.1016/j.mvr.2022.104356
What was done
Eight young, healthy subjects underwent a single bout of whole-body passive heating via immersion in a 40 °C hot tub, maintaining a 1 °C increase in rectal temperature for 60 minutes. Endothelium-dependent dilation (shear-rate corrected), serum heat shock protein 90α (HSP90α), resting muscle oxygen utilization, mean arterial pressure, and microvascular oxygenation kinetics were evaluated before and 24 hours after heating.
What was found
Twenty-four hours after heating, shear-rate corrected endothelium-dependent dilation increased (pre: 0.004 ± 0.002 %SR AUC vs. post: 0.006 ± 0.003 %SR AUC; p = 0.034). Serum HSP90α did not change (pre: 36.7 ± 10.3 ng/mL vs. post: 40.6 ± 15.9 ng/mL; p = 0.39). Resting muscle O2 utilization (pre: 0.17 ± 0.11 vs. post: 0.14 ± 0.09 mL O2 min^-1 [100 g]^-1; p = 0.28) and mean arterial pressure (pre: 74 ± 11 vs. post: 73 ± 11 mmHg; p = 0.79) remained unchanged. Time to peak after cuff release was significantly delayed for percentage O2 saturation (pre: 39 ± 8.9 s vs. post: 43.5 ± 8.2 s; p = 0.007) and deoxy-heme (pre: 41.3 ± 18.1 s vs. post: 51.4 ± 16.3 s; p = 0.018), with no change in oxy-heme (p = 0.19) or total-heme (p = 0.41).
Why it matters
A single 60-minute hot-water immersion session can produce measurable increases in conduit artery endothelial function that persist 24 hours later in healthy individuals.
Limits
The sample size was very small (n = 8) and there was no control or sham group. The study was conducted entirely in young, healthy volunteers, and outcomes were only measured at baseline and a single 24-hour post-intervention time point.
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