Passive heat therapy improves cutaneous microvascular function in sedentary humans via improved nitric oxide-dependent dilation

Abstract

Passive heat therapy (repeated hot tub or sauna use) reduces cardiovascular risk, but its effects on the mechanisms underlying improvements in microvascular function have yet to be studied. We investigated the effects of heat therapy on microvascular function and whether improvements were related to changes in nitric oxide (NO) bioavailability using cutaneous microdialysis. Eighteen young, sedentary, otherwise healthy subjects participated in 8 wk of heat therapy (hot water immersion to maintain rectal temperature ≥38.5°C for 60 min/session; n = 9) or thermoneutral water immersion (sham, n = 9), and participated in experiments before and after the 8-wk intervention in which forearm cutaneous hyperemia to 39°C local heating was assessed at three microdialysis sites receiving 1) Lactated Ringer's (Control), 2) N(ω)-nitro-l-arginine (l-NNA; nonspecific NO synthase inhibitor), and 3) 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), a superoxide dismutase mimetic. The arm used for microdialysis experiments remained out of the water at all times. Data are means ± SE cutaneous vascular conductance (CVC = laser Doppler flux/mean arterial pressure), presented as percent maximal CVC (% CVCmax). Heat therapy increased local heating plateau from 42 ± 6 to 53 ± 6% CVCmax (P < 0.001) and increased NO-dependent dilation (difference in plateau between Control and l-NNA sites) from 26 ± 6 to 38 ± 4% CVCmax (P < 0.01), while no changes were observed in the sham group. When data were pooled across all subjects at 0 wk, Tempol had no effect on the local heating response (P = 0.53 vs. Control). There were no changes at the Tempol site across interventions (P = 0.58). Passive heat therapy improves cutaneous microvascular function by improving NO-dependent dilation, which may have clinical implications.

Keywords: hot water immersion; laser Doppler flowmetry; microdialysis; oxidative stress.

Copyright © 2016 the American Physiological Society.

Figures

Fig. 1.

Progression through the phases of the study.

Fig. 2.

Average normalized cutaneous vascular conductance across time into local heating in all subjects who completed 0 wk testing (n = 22) at three microdialysis sites receiving 1) Control (Lactated Ringer's solution), 2) 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), and 3) Nω-nitro-l-arginine (l-NNA). Data over time were averaged across subjects at 4 Hz (solid lines). Baseline, initial peak, nadir, and plateau were analyzed for each subject and presented as means ± SE. Note, for initial peak, the symbols do not line up exactly with the solid lines since they were analyzed at the subject's true peak cutaneous vascular conductance (CVC), rather than at a certain time point into local heating. *P < 0.05 vs. Control. †P < 0.05 vs. Tempol.

Fig. 3.

A: local heating plateau. B: nitric oxide (NO)-dependent dilation [difference in plateau between microdialysis sites receiving Lactated Ringer's (Control) and l-NNA] in subjects who participated in 8 wk of heat therapy or thermoneutral water immersion (sham). Heat therapy increased both plateau and NO-dependent dilation in every subject, as indicated by the individual data. Data are means ± SE. *P < 0.05 0 vs. 8 wk within group.