Key result
Endurance exercise improves peak VO2 but fails to alter arterial stiffness or FMD in HFpEF.
Why the study?
Elderly HFPEF patients have severely reduced peak VO2 that improves with exercise training, but it was unknown whether improvements in FMD or arterial distensibility mediate this effect.
Does endurance exercise training improve brachial artery flow-mediated dilation and peak VO2 in older patients with HFPEF?
RCT (n=63)
Single-blind
randomized
No
Does endurance exercise training improve brachial artery flow-mediated dilation and peak VO2 in older patients with HFPEF?
Endurance exercise training improves peak exercise capacity in older HFpEF patients without altering large-vessel endothelial function or arterial stiffness, suggesting peripheral or skeletal muscle adaptations drive the benefit.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“The signals for improvement from exercise training, in symptoms and objective measures of exercise capacity, are considerably larger for HFpEF than for HFrEF.”
“Improvement in the cardiopulmonary reserve is what was observed across almost the whole subset of trials, so it looks like the type of exercise is not that important. It is important, however, that people use their muscles and expand their exercise capacity and do it in a safe, supervised environment.”
Endurance training improves peak VO2 in HFpEF without changing endothelial function or stiffness; challenges vascular mechanisms and directs research toward skeletal muscle adaptations.
Objectives 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 HFFEF 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's unknown whether these improve with ET in elderly HFPEF or contribute to the training-related improvement in peak VO2. Methods 63 HFPEF patients (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, LV function, and QOL were measured at baseline and follow-up. Results ET increased peak VO2 (ET: 15.8±3.3 vs. CT: 13.8±3.1 ml/kg/min, p=0.0001) and QOL. 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 × 10-3mm × mmHg-1 p=0.65) were unchanged. Resting LV 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.
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Kitzman et al. (2013) conducted an RCT in Heart failure with preserved ejection fraction (HFPEF) (n=63). Endurance exercise training vs. Attention control was evaluated on Brachial artery flow-mediated arterial dilation (FMD) (p=0.88). 16 weeks of endurance exercise training improved peak VO2 but did not alter brachial artery flow-mediated dilation or carotid arterial stiffness in older patients with HFPEF.
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