To study the effects of prolonged kendo practice in a hot environment on cardiovascular function, certain hemodynamic parameters were measured in 5 male college kendo fencers before and after 1 hour of kendo practice performed at a dry bulb temperature of 30.4t and wet bulb temperature of 26.2°C After kendo practice, body weight was significantly decreased and both hematocrit and blood viscosity were significantly increased. The left ventricular end-diastolic dimension and the left atrial dimension, measured by echocardiography, were significantly reduced after kendo practice, and stroke volume, ejection fraction, and fractional shortening were also significantly decreased after practice. The same fencers were subjected to lower body negative pressure testing designed to reduce the left ventricular end-diastolic dimension to the same degree as kendo practice, and comparable decreases in stroke volume, ejection fraction, and fractional shortening were observed. The ratio of end-systolic wall stress to end-systolic volume index was significantly increased during both kendo practice and lower body negative pressure testing. We conclude that prolonged kendo practice in a hot environment impairs cardiac pump function by reducing preload in parallel with the decrease in venous return, that myocardial contractility may not deteriorate despite marked hemoconcentration, and that fluid intake during practice may prevent deterioration of cardiovascular function.

 Waon therapy uses a far infrared-ray dry sauna, which is evenly maintained at 60°C and differs from the traditional sauna. The patients were placed in a 60°C sauna system for 15 minutes, in which the deep-body temperature has increased by 1.0 to 1.2°C. Then, after leaving the sauna, they underwent bed rest with a blanket to keep them warm for an additional 30 minutes. All patients were weighed before and after the therapy, and they drank some water at the end of Waon therapy to compensate for weight lost due to perspiration and prevent the dehydration.  We have previously reported that Waon therapy improves the cardiac and vascular endothelial function in patients with chronic heart failure (CHF) and the limb ischemia and symptoms in patients with arteriosclerosis obliterans (ASO). As underlying molecular mechanisms, we demonstrated that Waon therapy upregulates nitric oxide (NO) and endothelial NO synthase (eNOS), which would improve vascular endothelial and cardiac function in TO-2 cardiomyopathic hamsters and augment ischemia-induced angiogenesis. In order to investigate the mechanism of Waon therapy, we examined the effect of Waon therapy on heat shock proteins (Hsp) in failed myocardium and ischemic limb. Hsp are stress response proteins that can be induced by stress signals, including thermal stimulation. Hsp function as chaperones to assist with protein folding in order to protect cells from protein denaturation or cell death under stress conditions.  In TO-2 cardiomyopathic hamsters, the cardiac expression of 4-hydroxy-2-nonenal (4HNE), a marker of oxidative stress, was decreased in the 4-week Waon therapy compared to untreated hamsters. Also, the cardiac expressions of Hsp 27, Hsp 32 and manganese superoxide dismutase (Mn-SOD), which reduce oxidative stress, were significantly upregulated by the 4-week Waon therapy compared to untreated hamsters. In addition, Waon therapy upregulated Hsp90, which contributes to the activation of the AkteNOSNO pathway, and induced angiogenesis in mice with hindlimb ischemia. However, Waon therapy did not increase the expression of Hsp70, Hsp60, Hsp32 and Hsp27 in the same model mice. The thermal stimulation with Waon therapy upregulated specific Hsp isoforms depending on different organs and diseases. The specific function of Hsp induced by Waon therapy is suggested to play an important role in improving cardiovascular diseases.

Introduction: Long-term cardiac hypertrophy causes heart failure. One of the mechanisms of this transition from hypertrophy to heart failure is collapse of hypoxic response and angiogenesis. Heat shock protein 27 (HSP27) was found to act as an anti-apoptotic protein and its phosphorylation is responsible for the protection of cells against heat stress. HSP27 has been reported to regulate p53 expression, which contributes to down-regulate angiogenic factors through hypoxia inducible factor-1α(HIF-1α). We have reported that thermal therapy, namely Waon therapy, improves cardiac and vascular function in patients with chronic heart failure. However, the effect of this therapy on cardiac hypertrophy due to pressure overload is unknown. The purpose of this study is to investigate the effects and mechanisms of thermal therapy (Waon therapy) on the transition from cardiac hypertrophy to heart failure after pressure overload. Methods: Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6 mice. At 2 weeks after TAC, all mice were examined by echocardiography and showed left ventricular hypertrophy. Then, mice were randomly divided into thermal therapy or untreated group. Thermal therapy group received thermal therapy using an experimental far infrared ray dry sauna, which elevates the core temperature by 1 degree Celsius for 30 minutes, daily for 4 weeks. Sham operated mice were used as control. At 6 weeks after TAC, we measured body weight, heart rate and blood pressure before sacrifice, and eviscerated heart and leg muscle. Western blot analysis of p53, phosphorylated HSP27, HIF-1α and vascular endothelial growth factor (VEGF) was performed using extracted protein form heart. Results: At 6 weeks after TAC, body weight, heart rate and blood pressure did not differ in three groups. Echocardiography showed that left ventricular fractional shortening of thermal therapy group was significantly larger than that of untreated group (Sham vs. Untreated vs. Thermal; 50.0±1.7 vs. 36.7±1.3 vs. 46.2±0.5, P<0.01, n=6 each). Heart weight/tibia length ratio of thermal therapy group was significantly smaller than that of untreated group (6.7±0.1 vs. 9.7±0.5 vs. 7.9±0.2, P<0.01, n=9 each). Western blot showed that thermal therapy increased phosphorylation of HSP27 and reduced p53. Thermal therapy also increased HIF-1α and VEGF at 6 weeks after TAC. Capillary/myofiber ratio was larger in thermal therapy group than that in untreated group (1.71±0.05 vs. 2.04±0.04 vs. 2.41±0.10, P<0.01, n=4 each). Conclusion: Thermal therapy, namely Waon therapy, prevented the transition from cardiac hypertrophy to heart failure induced by pressure overload in mice. As the mechanism, thermal therapy amplified the phosphorylation of HSP27 and inhibited p53, increased HIF-1α and VEGF, and then increased angiogenesis.