The acute effects of passive heating on endothelial function, muscle microvascular oxygen delivery, and expression of serum HSP90α

Abstract

Passive heating has been a therapeutic tool used to elevate core temperature and induce increases in cardiac output, blood flow, and shear stress. We aimed to determine the effects of a single bout of passive heating on endothelial function and serum heat shock protein 90α (HSP90α) levels in young, healthy subjects. 8 healthy subjects were recruited to participate in one bout of whole-body passive heating via immersion in a 40 °C hot tub to maintain a 1 °C increase in rectal temperature for 60 min. Twenty-four hours after heating, shear-rate corrected endothelium-dependent dilation increased (pre: 0.004 ± 0.002%SR_AUC; post: 0.006 ± 0.003%SR_AUC; p = 0.034) but serum [HSP90α] was not changed (pre: 36.7 ± 10.3 ng/mL; post: 40.6 ± 15.9 ng/mL; p = 0.39). Neither resting muscle O₂ utilization (pre: 0.17 ± 0.11 mL O₂ min^-1 (100 g)^-1; post: 0.14 ± 0.09 mL O₂ min^-1 (100 g)^-1); p = 0.28) nor mean arterial pressure (pre: 74 ± 11 mmHg; post: 73 ± 11 mmHg; p = 0.79) were influenced by the heating intervention. Finally, time to peak after cuff release was significantly delayed for % O₂ sat (TTP_pre = 39 ± 8.9 s and TTP_post = 43.5 ± 8.2 s; p = 0.007) and deoxy-[heme] (TTP_pre = 41.3 ± 18.1 s and TTP_post = 51.4 ± 16.3 s; p = 0.018), with no effect on oxy-[heme] (p = 0.19) and total-[heme] (p = 0.41). One bout of passive heating improved endothelium-dependent dilation 24 h later in young, healthy subjects. This data suggests that passive heat treatments may provide a simple intervention for improving vascular health.

Keywords: Heat shock protein; Passive heating; Vascular occlusion test.