Why the study?
Does moderate exercise modulate circulating adipokine levels differently in patients with hypertrophic cardiomyopathy compared to healthy controls?
Does moderate exercise modulate circulating adipokine levels differently in patients with hypertrophic cardiomyopathy compared to healthy controls?
Moderate exercise increases adiponectin and decreases leptin in patients with hypertrophic cardiomyopathy, suggesting a unique, potentially cardioprotective metabolic response to physical stress in this population.
Exercise may elicit beneficial adipokine shifts in HCM; leaves open differential effects versus controls and outcome implications.
INTRODUCTION: Studies conducted so far have shown that patients with left ventricular hypertrophy have increased adiponectin levels; however, these studies were performed only in resting condition. OBJECTIVES: The aim of the study was to compare adiponectin, resistin, and leptin levels (at rest and after exercise) between patients with hypertrophic cardiomyopathy (HCM) and healthy controls. Additionally, we examined potential relationships between the levels of the 3 adipokines and the left ventricular outflow tract (LVOT) gradient both at rest and at peak exercise. PATIENTS AND METHODS: We studied 29 patients with HCM (mean age 42.7 ±11.9 years, 16 men and 13 women). The control group included 19 healthy subjects matched for age-, sex-, and the body mass index. After echocardiographic examination in a supine position, all patients were placed in an upright position and treadmill exercise test was performed with simultaneous continuous echocardiographic monitoring of the LVOT gradient. Adiponectin, resistin, and leptin levels were measured immediately prior to exercise in a supine position and at peak exercise in an upright position. RESULTS: At baseline (at rest), adiponectin levels tended to be increased in patients with HCM (P = 0.09), while resistin and leptin levels were significantly higher in patients with HCM than in healthy controls. In HCM patients, exercise induced an increase in adiponectin (20.74 ±7.95 vs. 22.52 ±8.10 μg/ml, P <0.05), a decrease in leptin (22.78 ±6.08 vs. 20.63 ±5.57 ng/ml, P <0.05), and no significant effect on resistin. In the control group, all biomarkers mildly decreased at peak exercise (adiponectin 19.23 ±5.43 vs. 18.66 ±5.31 μg/ml P = 0.044), resistin 14.80 ±1.87 vs. 13.87 ±1.21 ng/ml, P = 0.030), (leptin 14.34 ±4.74 vs. 13.50 ±3.98 ng/ml, P = 0.045). In HCM patients, neither resting nor peak exercise values of the LVOT gradient correlated with any levels of adipokines. CONCLUSIONS: In patients with HCM, but not in healthy individuals, moderate exercise induced an increase in adiponectin levels and a decrease in leptin levels independent of a rise in the LVOT gradient. The potential cardioprotective role of adiponectin during exercise stress in HCM requires further studies.
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Dimitrow et al. (2011) studied this question.
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