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J Cardiovasc Nurs. 2011 May-Jun;26(3):218-23. doi: 10.1097/JCN.0b013e3181f29a46.

Resistance training improves vasoreactivity in end-stage heart failure patients on inotropic support.

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Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104-4217, USA.



Peripheral vascular abnormalities contribute to compromised functional status in heart failure (HF) patients. The purpose of the present study was to test whether the intervention of moderate-intensity, resistance training could improve peripheral vascular responsiveness, that is, flow-mediated dilation (FMD) in HF.


Baseline brachial artery FMD analysis (2 minutes of cuff occlusion and 5 minutes of reperfusion) was measured in HF patients on intravenous inotropic support (n = 9) awaiting cardiac transplantation. Unilateral, upper-body resistance exercises (moderate intensity, combination of isometric and isotonic exercises at 60%-80% of maximum) were performed 3 d/wk for 4 weeks. Follow-up FMD analysis was conducted after training. Central hemodynamics were defined via right-side-heart catheterization.


At baseline prior to training, HF patients elicited a significant hyperemic response 10 seconds following cuff occlusion (mean increase in blood flow: 194 ± 44 mL/min, P < .05). Despite this significant hyperemic response, HF patients demonstrated a mild, but paradoxical vasoconstriction of nearly 3% at 1-minute after cuff release. Four weeks of resistance training corrected the paradoxical vasoconstriction observed at baseline and resulted in vasodilatation (a positive increase in brachial artery diameter of 0.04 ± 0.04 mm, at 1 minute after cuff release; P < .05). Conversely, in a subset of 3 HF patients, studies in the untrained contralateral arm revealed no change in the FMD response.


Moderate-intensity upper-body resistance training improved brachial artery FMD in end-stage HF patients on inotropic support. The reversal of the paradoxical vasoconstrictive response to reactive hyperemia following 4 weeks of training may be secondary to local improvements in vascular endothelial function rather than a quantitative change in the reactive hyperemic stimulus.

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