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PASSIVE HEAT THERAPY IMPROVES NITRIC OXIDE SIGNALING AND OXIDATVE STRESS

Abstract

T.M. Eymann, V.E. Brunt, K.M. Wiedenfeld-Needham, C.T. Minson, FACSM

University of Oregon, Eugene, OR

Cardiovascular disease is associated with vascular dysfunction, often mediated through impairments in nitric oxide signaling and increased oxidative stress. Heat shock proteins (HSP), expressed in response to heat exposure and exercise, upregulate proteins linked to improved vascular function, such as endothelial nitric oxide synthase (eNOS) and super oxide dismutase (SOD; an antioxidant). Heat therapy has recently been shown to improve vascular function in vivo. Thus, we sought to determine the cellular mechanisms behind these improvements by simulating heat therapy in cultured endothelial cells. PURPOSE: To investigate the effects of physiological levels of heat and circulating factors in human sera on eNOS, SOD, HSP70, and HSP90 expression in cultured endothelial cells. METHODS: Serum was collected from seven (23±2 yrs) sedentary human subjects before and after 8wks of heat therapy (hot water immersion 4-5x/wk to maintain rectal temperature ≥38.5°C for 60min). Post-heat therapy serum was collected at least 36h after the last session. Purchased human umbilical vein endothelial cells were cultured and exposed for 24h to either 37°C (control), direct heat at 39°C, or human sera collected at 0 and 8wks. eNOS, SOD, HSP70, and HSP90 protein expression was determined using Western blot normalized to vinculin loading control. Data are presented as mean ± S.E. fold change from 37°C (direct heat) or from 0wks (serum exposure). Changes in protein expression were compared using Student’s paired t-test. Significance was set to P<0.05. RESULTS: Direct heating increased SOD expression in endothelial cells by 1.35±0.12 fold (p=0.04), HSP70 expression by 1.32±0.03 fold (p<0.01), and HSP90 expression by 1.84±0.38 fold (p=0.04), but had no effect on eNOS (1.04±0.04 fold change, p=0.38). Serum exposure increased both eNOS (1.21±0.06 fold change, p<0.01) and SOD expression (1.47±0.19 fold change, p<0.05), with no change in HSP70 (1.07±0.16 fold change, p=0.69) or HSP90 (0.94±0.08 fold change, p=0.51). CONCLUSIONS: Heat therapy upregulates SOD via HSP-mediated mechanisms (i.e. direct heat) and upregulates both eNOS and SOD via HSP-independent mechanisms (i.e. circulating factors). Thus, our data suggest that heat therapy improves NO signaling and reduces oxidative stress; likely underlying previously observed improvements in vascular function. As exercise improves vascular function through similar cellular mechanisms, our data suggest that heat therapy could be a viable alternative to exercise for patient populations who cannot garner the full benefits of exercise.

Supported by AHA Grant #14PRE20380300 and the Eugene and Clarissa Evonuk Memorial Foundation.

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