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Skeletal muscle disorders in heart failure
P K Lunde1, I Sjaastad, H M Schiøtz Thorud
1Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Oslo, Norway.
Acta Physiologica Scandinavica
|June 20, 2001
Summary
Heart failure reduces exercise capacity due to skeletal muscle changes. While inactivity plays a role, impaired muscle contractility, potentially linked to altered calcium handling similar to the heart, is also implicated in heart failure.
Area of Science:
- Cardiology
- Exercise Physiology
- Skeletal Muscle Biology
Background:
- Heart failure (HF) is characterized by reduced exercise capacity, exceeding limitations solely from decreased maximal oxygen uptake (V̇O2max).
- Skeletal muscle alterations, including changes in morphology, metabolism, and function, are increasingly recognized as significant contributors to HF-related exercise intolerance.
- Factors like inactivity, malnutrition, hypoxia, and altered neurohumoral signaling contribute to skeletal muscle dysfunction in HF, though many are not HF-specific.
Purpose of the Study:
- To investigate whether the contractile deficit observed in the myocardium during congestive heart failure (CHF) is paralleled by a similar contractile deficit in skeletal muscles.
- To explore the potential mechanisms underlying skeletal muscle dysfunction in CHF, considering both phenotypic and functional changes.
Main Methods:
- Review of existing patient and experimental studies examining skeletal muscle characteristics in heart failure.
- Analysis of data on muscle phenotype, energy metabolism, atrophy, and contractile function.
- Consideration of intracellular mechanisms, including calcium (Ca2+) cycling and the role of cytokines.
Main Results:
- Studies indicate a shift towards a faster muscle phenotype and a more anaerobic energy metabolism in skeletal muscles of HF patients.
- Muscle atrophy is evident in patients but less pronounced in experimental models.
- Contrary to expectations of faster muscle function, both fast-twitch and slow-twitch muscles appear to slow down, potentially due to impaired intracellular Ca2+ cycling.
- Elevated cytokine levels in CHF patients suggest a potential neurohumoral link to these skeletal muscle changes.
Conclusions:
- Skeletal muscle dysfunction in CHF is multifactorial, with inactivity contributing significantly.
- A parallel contractile deficit in skeletal muscle, mirroring myocardial dysfunction, is a plausible but not yet fully elucidated aspect of CHF.
- Altered intracellular Ca2+ metabolism, a feature also seen in the failing myocardium, may underlie the impaired contractility of skeletal muscles in CHF.