Effect of endurance exercise training on endothelial function and arterial stiffness in older patients with heart failure and preserved ejection fraction: a randomized, controlled, single-blind trial

Dalane W Kitzman, Peter H Brubaker, David M Herrington, Timothy M Morgan, Kathryn P Stewart, W Gregory Hundley, Abdelhamed Abdelhamed, Mark J Haykowsky
Journal of the American College of Cardiology 2013 August 13, 62 (7): 584-92

OBJECTIVES: The study sought to evaluate the effects of endurance exercise training (ET) on endothelial-dependent flow-mediated arterial dilation (FMD) and carotid artery stiffness, and their potential contributions to the training-related increase in peak exercise oxygen consumption (Vo2) in older patients with heart failure with preserved ejection fraction (HFPEF).

BACKGROUND: Elderly HFPEF patients have severely reduced peak Vo2, which improves with ET, however, the mechanisms of this improvement are unclear. FMD and arterial distensibility are critical components of the exercise response and are reduced with aging. However, it is unknown whether these improve with ET in elderly HFPEF or contribute to the training-related improvement in peak Vo2.

METHODS: A total of 63 HFPEF patients (age 70 ± 7 years) were randomized to 16 weeks of ET (walking, arm and leg ergometry, n = 32) or attention control (CT) (n = 31). Peak Vo2, brachial artery FMD in response to cuff ischemia, carotid artery distensibility by high-resolution ultrasound, left ventricular function, and quality of life were measured at baseline and follow-up.

RESULTS: ET increased peak Vo2 (ET: 15.8 ± 3.3 ml/kg/min vs. CT: 13.8 ± 3.1 ml/kg/min, p = 0.0001) and quality of life. However, brachial artery FMD (ET: 3.8 ± 3.0% vs. CT: 4.3 ± 3.5%, p = 0.88), and carotid arterial distensibility (ET: 0.97 ± 0.56 vs. CT: 1.07 ± 0.34 × 10(-3) mm·mm Hg(-2); p = 0.65) were unchanged. Resting left ventricular systolic and diastolic function were unchanged by ET.

CONCLUSIONS: In elderly HFPEF patients, 16 weeks of ET improved peak Vo2 without altering endothelial function or arterial stiffness. This suggests that other mechanisms, such as enhanced skeletal muscle perfusion and/or oxygen utilization, may be responsible for the ET-mediated increase in peak Vo2 in older HFPEF patients. (Prospective Aerobic Reconditioning Intervention Study [PARIS]; NCT01113840).

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