CHRONIC PASSIVE HEAT THERAPY IMPROVES MICROVASCULAR NITRIC OXIDE-DEPENDENT DILATION DURING SKIN LOCAL HEATING

1 in 4 deaths in the US are attributed to cardiovascular disease (CVD). Vascular dysfunction, often caused by deficient nitric oxide (NO) production, is present in the majority of CVD and is first detectible in the microcirculation. Heat stress can increase NO production via heat shock protein expression, and so chronic passive heat therapy (CHT) may help improve microvascular health and lower the risk for CVD across multiple patient populations. The cutaneous circulation is both easily accessible and represents overall microvascular health. PURPOSE: To observe the effect of 8 weeks of CHT on cutaneous NO-dependent dilation. METHODS: 6 healthy, sedentary subjects (age 22±1 yrs) were included in this study. Four subjects were immersed in 40.5°C hot water 4-5 times/week for 8 weeks to increase rectal temperature and maintain it at ≥38.5°C for 1 hour per session. Two subjects were immersed in 36.5°C water for the same duration (control). Prior to and immediately following the 8-week protocol, two intradermal microdialysis fibers were inserted into the forearm and infused with lactated Ringer’s solution (control) and L-NNA, to inhibit NO synthase. Local skin heaters were placed at each site over the fiber and heated to 39°C at a rate of 0.1C/sec, increasing skin blood flow, which was measured using laser-Doppler flowmetry. NO-dependent dilation was calculated as the difference between the control and the L-NNA sites in each individual and expressed as a percentage of maximal cutaneous vascular conductance (CVC; flow/mean arterial pressure). Data are presented as the change in NO-dependent dilation from 0 to 8 weeks. RESULTS: In our subjects, NO-dependent dilation increased by 104%CVCmax (p=0.04). No improvement was observed in the control subjects. CONCLUSION: In these subjects, our preliminary findings suggest that CHT increases cutaneous NO production and vasodilation. As such, heat therapy is capable of improving NO-dependent dilation in the human microcirculation, suggesting that continued exposure to passive heat may result in lower risk for CVD