Key result
Moderate aerobic exercise partially restores muscle performance and redox balance in a HFpEF mouse model.
Why the study?
The effects of aerobic exercise on skeletal muscle physiology, altered Ca2+ homeostasis, and oxidative stress in HFpEF remain unclear.
Does moderate-intensity aerobic exercise improve skeletal muscle function and oxidative stress in a mouse model of HFpEF?
Does moderate-intensity aerobic exercise improve skeletal muscle function and oxidative stress in a mouse model of HFpEF?
Aerobic exercise improves skeletal muscle function in a mouse model of HFpEF primarily by modulating redox homeostasis rather than normalizing calcium-handling gene expression.
Supports redox-targeted exercise for HFpEF muscle dysfunction; leaves open translation to humans and calcium mechanisms.
Heart failure with preserved ejection fraction ( HFpEF ) is associated with skeletal muscle dysfunction that contributes to exercise intolerance and disease progression. Altered Ca 2+ homeostasis and increased oxidative stress have been proposed as mechanisms underlying muscle weakness in HFpEF ; however, the effects of aerobic exercise on skeletal muscle physiology in this condition remain unclear. This study evaluated the impact of moderate‐intensity aerobic exercise on skeletal muscle contractile function, fatigue resistance, oxidative stress, and mRNA expression of key Ca 2+ ‐handling proteins in a model with features consistent with HFpEF . Male C57BL / 6J mice were assigned to Control, Exercise, HFpEF ( HFD + L‐ NAME ‐treated), and HFpEF +Exercise groups. HFpEF ‐like features were induced by an 8‐week high‐fat diet combined with L‐ NAME administration. During the final 4 weeks, mice underwent aerobic exercise training. Soleus muscles were analyzed using in vitro contractile recordings, oxidative stress markers, and RT ‐ qPCR for RyR1 , SERCA1 , and NCX3 mRNA expression. HFpEF ( HFD + L‐ NAME ‐treated mice) showed reduced contractile force and fatigue resistance, increased oxidative stress, and decreased SERCA1 and NCX3 expression. Aerobic exercise partially restored muscle performance and improved redox balance without normalizing Ca 2+ ‐handling gene expression. These findings suggest that aerobic exercise enhances skeletal muscle function in HFpEF ‐like models, primarily by modulating redox homeostasis.
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Martínez et al. (2026) studied Heart failure with preserved ejection fraction (HFpEF). Moderate-intensity aerobic exercise vs. No exercise (Control and HFpEF groups) was evaluated on Skeletal muscle contractile function, fatigue resistance, oxidative stress, and mRNA expression of key Ca2+-handling proteins. Moderate-intensity aerobic exercise partially restored muscle performance and improved redox balance in a mouse model of HFpEF, without normalizing Ca2+-handling gene expression.
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