Why the study?
Exercise intolerance and early fatigue are hallmarks of HFrEF and HFpEF driven in part by skeletal muscle alterations, warranting a summary of muscle abnormalities and therapeutic options.
What are the clinical and molecular alterations in skeletal muscles of HFrEF and HFpEF patients, and what are the effects of exercise training?
What are the clinical and molecular alterations in skeletal muscles of HFrEF and HFpEF patients, and what are the effects of exercise training?
This review highlights the role of skeletal muscle alterations in exercise intolerance among HF patients and discusses exercise training as a key therapeutic intervention.
Muscle alterations may underlie exercise intolerance in HF; leaves open exercise training benefits pending prospective trials.
Heart failure (HF) is a chronic and progressive syndrome affecting worldwide billions of patients. Exercise intolerance and early fatigue are hallmarks of HF patients either with a reduced (HFrEF) or a preserved (HFpEF) ejection fraction. Alterations of the skeletal muscle contribute to exercise intolerance in HF. This review will provide a contemporary summary of the clinical and molecular alterations currently known to occur in the skeletal muscles of both HFrEF and HFpEF, and thereby differentiate the effects on locomotor and respiratory muscles, in particular the diaphragm. Moreover, current and future therapeutic options to address skeletal muscle weakness will be discussed focusing mainly on the effects of exercise training.
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Mangner et al. (2023) studied this question.
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