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Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure
Hambrecht R, Fiehn E, Weigl C, Gielen S, Hamann C, Kaiser R, Yu J, Adams V, Niebauer J, Schuler G
Circulation 1998 Dec 15;98(24):2709-2715
clinical trial
5/10 [Eligibility criteria: No; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: No; Adequate follow-up: Yes; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

BACKGROUND: The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure (CHF). Endothelial dysfunction is a key feature of CHF, contributing to increased peripheral vasoconstriction and impaired exercise capacity. Local handgrip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF. METHODS AND RESULTS: Twenty patients were prospectively randomized to a training group (n = 10, left ventricular ejection fraction (LVEF) 24 +/- 4%) or a control group (n = 10, LVEF 23 +/- 3%). At baseline and after 6 months, peak flow velocity was measured in the left femoral artery using a Doppler wire; vessel diameter was determined by quantitative angiography. Peripheral blood flow was calculated from average peak velocity (APV) and arterial cross-sectional area. After exercise training, nitroglycerin-induced endothelium-independent vasodilation remained unaltered (271% versus 281%, p = NS). Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203% (from 152 +/- 79 to 461 +/- 104 mL/min, p < 0.05 versus control group) and the inhibiting effect of L-NMMA increased by 174% (from -46 +/- 25 to -126 +/- 19 mL/min, p < 0.05 versus control group). Peak oxygen uptake increased by 26% (p < 0.01 versus control group). The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow (r = 0.64, p < 0.005). CONCLUSIONS: Regular physical exercise improves both basal endothelial nitric oxide (NO) formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF. The correction of endothelium dysfunction is associated with a significant increase in exercise capacity.
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