Presenter: Taylor Eymann
Mentors: Christopher Minson and Vienna Brunt, Human Physiology
Poster: 21
Major: Human Physiology
Vascular dysfunction, often caused by deficient nitric oxide (NO) production, is present in the majority of cardiovascular disease and is first detectible in the microcirculation. Heat stress can increase NO production via
heat shock protein expression. Therefore chronic passive heat therapy (CHT) may improve microvascular health
and lower cardiovascular risk. The cutaneous circulation is easily accessible and represents overall microvascular health. PURPOSE: To observe the effects of 8wks of CHT on cutaneous NO-dependent dilation. METHODS: Seven healthy, sedentary subjects were immersed in either 40.5°C (N=5; CHT) or 36.5°C (N=2; sham group) water for 90min 4-5 times per week for 8 weeks. Before and after the 8wks, two intradermal microdialysis fibers were inserted into the forearm and infused with lactated Ringer’s solution (control) and a nitric oxide synthase competitive inhibitor (L-NNA), to inhibit NO synthase. Increased skin blood flow responding to local skin heating to 39°C, which is a test of microvascular health, was measured at each site using laser-Doppler flowmetry. NO-dependent dilation, calculated as the difference between control and L-NNA sites, was expressed as percent maximal cutaneous vascular conductance (%CVCmax; flow/mean arterial pressure). RESULTS: CHT increased NO-dependent dilation from 27±4 to 36±5%CVCmax (p<0.05). No improvement was observed in sham subjects. CONCLUSION: Our findings suggest heat therapy increases NO production and vasodilation in the human microcirculation. Continued exposure to passive heat may lower cardiovascular risk.