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Aims: It is controversial whether or not pulmonary nitric oxide (NO) production, reflected in the end-tidal alveolar NO concentration, is diminished in patients with heart failure. Since pulmonary perfusion is regulated by NO production, decreased NO production in the pulmonary vasculature is assumed to result in diminished lung perfusion and further increases in ventilationperfusion mismatch. The aim of this study is to investigate whether exhaled NO correlates with both exercise-induced hyperpnea and exercise tolerance in patients with heart disease. Methods and Results: Forty-two patients with heart disease were enrolled (history of prior myocardial infarction (ns19), dilated cardiomyopathy (ns2), hypertensive heart disease (ns5) and prior openheart surgery (ns16)). During cardiopulmonary exercise testing, exhaled air was collected and end-tidal NO (ETNO) was measured using a chemiluminescent method. Peak ETNO was found to correlate positively with both ventilatory anaerobic threshold (rs0.468) and peak VO (rs0.562). The VE-CO slope, which reflects the ventilatory response to exercise, correlated 2 2 negatively with peak ETNO (rsy0.588). Conclusion: These data indicate that NO exhalation correlates, inversely, with the ventilatory response to exercise and directly with exercise intolerance, although the weakness of the correlation coefficient suggests there may be other possible mechanisms.

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Blood viscosity (etaB) is low in athletes, but the effect of exercise training on etaB during endurance exercise at an anaerobic threshold (AT) intensity in non-athletes is not well known, although it is known that exercise training sometimes induces the hyperviscosity syndrome. Fourteen subjects were recruited and divided into 2 groups: those who trained at an AT intensity for 30 min/day, 3 times weekly for 1 year (Group T, n=8), and sedentary subjects (Group C, n=6). The test protocol consisted of a single 30-min treadmill exercise at each individual's AT intensity, which was determined in advance. The etaB, plasma viscosity (etaP), and hematocrit were measured just before and at the end of the treadmill exercise. The subjects were not allowed to drink any water before exercise. In the Group C subjects, the hematocrit and etaP increased significantly and the etaB tended to increase. However, in the Group T subjects, the hematocrit and etaP did not increase and the etaB decreased significantly. These data indicate that long-term exercise training attenuates the increase in blood viscosity during exercise.

Epicardial adipose tissue may affect hemodynamics and cardiorespiratory fitness as it is a metabolically active visceral adipose tissue and a source of inflammatory bioactive substances that can substantially modulate cardiovascular morphology and function. However, the associations between epicardial adipose tissue and hemodynamics and cardiorespiratory fitness remain unclear. This cross-sectional study aimed to examine the association between epicardial adipose tissue volume and hemodynamics, and cardiorespiratory fitness among Japanese individuals of various ages and of both sexes. Epicardial adipose tissue volume was measured in 120 participants (age, 21–85 years) by cardiac magnetic resonance imaging. To evaluate cardiorespiratory fitness, peak oxygen uptake was measured by cardiopulmonary exercise testing. Peak cardiac output and arteriovenous oxygen difference were calculated by impedance cardiography. The epicardial adipose tissue volume was significantly increased in middle-aged and older women. The epicardial adipose tissue volume was significantly and negatively correlated to peak cardiac output and peak oxygen uptake, regardless of age and sex; furthermore, epicardial adipose tissue showed a strong negative correlation with peak heart rate. Epicardial adipose tissue and peak cardiac output were significantly associated (β = -0.359, 95% confidence interval, -0.119 to -0.049, p < 0.001), even after multivariate adjustment (R2 = 0.778). However, in the multiple regression analysis with peak oxygen uptake as a dependent variable, the epicardial adipose tissue volume was not an independent predictor. These data suggest that increased epicardial adipose tissue volume may be correlated with decreased peak oxygen uptake, which might have mediated the abnormal hemodynamics among Japanese people of various ages and of both sexes. Interventions targeting epicardial adipose tissue could potentially improve hemodynamics and cardiorespiratory fitness.