Key result
HFpEF is linked to greater intermuscular steatosis and impaired oxidative capacity, limiting exercise tolerance.
Why the study?
The study examined peripheral mechanisms of exercise intolerance, specifically skeletal muscle oxidative capacity and tissue composition, in HFpEF patients compared with healthy older adults.
How do skeletal muscle oxidative capacity and tissue composition differ between patients with HFpEF and healthy older adults in relation to exercise intolerance?
Case-Control
How do skeletal muscle oxidative capacity and tissue composition differ between patients with HFpEF and healthy older adults in relation to exercise intolerance?
In HFpEF patients, intermuscular steatosis and impaired skeletal muscle oxidative capacity both contribute to exercise intolerance through distinct physiological mechanisms.
Muscle steatosis and oxidative deficits may contribute to HFpEF exercise intolerance; leaves open whether these pathways are modifiable or causal.
We compared peripheral mechanisms of exercise intolerance in heart failure with preserved ejection fraction (HFpEF) patients and healthy older adults. HFpEF patients exhibited significantly greater intermuscular steatosis and impaired whole body and quadriceps oxidative capacity [i.e., peak O 2 uptake (V̇o 2peak ) and phosphocreatine recovery time constant (τPCr), respectively], all of which were associated with impaired exercise tolerance. However, increased intermuscular steatosis was not associated with impaired V̇o 2peak and τPCr, suggesting that steatosis and impaired oxidative capacity affect exercise tolerance through different physiological mechanisms.
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Bartlett et al. (2026) conducted a case-control in Heart failure with preserved ejection fraction (HFpEF). Heart failure with preserved ejection fraction (HFpEF) vs. Healthy older adults was evaluated on Intermuscular steatosis, whole body oxidative capacity (VO2peak), quadriceps oxidative capacity (phosphocreatine recovery time constant [τPCr]), and exercise tolerance.
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