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Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
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Musclin Counteracts Skeletal Muscle Dysfunction and Exercise Intolerance in Heart Failure With Preserved Ejection

Eng Leng Saw1, Louis Dominic Werner1, Hannah L Cooper1

  • 1Department of Medicine, Whitaker Cardiovascular Institute, Boston University Chobanian & Avedisian School of Medicine, MA (E.L.S., L.D.W., H.L.C., D.R.P., M.V.-M., F.S.).

Circulation. Heart Failure
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PubMed
Summary
This summary is machine-generated.

Musclin administration improves skeletal muscle function and exercise capacity in heart failure with preserved ejection fraction (HFpEF). This myokine enhances oxidative capacity, offering a potential therapeutic target for HFpEF-related exercise intolerance.

Keywords:
exercise toleranceheart failuremuscle, skeletalmyokinesnatriuretic peptides

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Area of Science:

  • Cardiovascular Research
  • Skeletal Muscle Physiology
  • Metabolic Disease

Background:

  • Exercise intolerance in heart failure with preserved ejection fraction (HFpEF) is linked to skeletal muscle (SkM) dysfunction and reduced oxidative capacity.
  • Myokines, such as musclin, are secreted by SkM to maintain oxidative capacity and influence natriuretic peptide (NP) and peroxisome proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α) signaling.

Purpose of the Study:

  • Investigate the role of musclin in skeletal muscle dysfunction within the context of HFpEF.
  • Evaluate the therapeutic potential of exogenous musclin in ameliorating HFpEF-related skeletal muscle impairments and exercise intolerance.

Main Methods:

  • Utilized a mouse model (SAUNA) for HFpEF induction, administering exogenous musclin during the intervention period.
  • Conducted molecular analyses on blood and skeletal muscle (soleus from mice, vastus lateralis from HFpEF patients) to assess signaling pathways and muscle fiber characteristics.

Main Results:

  • HFpEF was associated with increased musclin and decreased cyclic guanosine monophosphate and PGC-1α levels, indicating impaired NP signaling.
  • Exogenous musclin administration in HFpEF mice enhanced NP signaling, promoted a shift towards endurance-oriented muscle fibers (type-2A to type-1), and improved oxidative capacity markers.
  • Musclin treatment improved functional and exercise capacity in HFpEF mice and mitigated cardiac hypertrophy without adverse effects on blood pressure or diastolic function.

Conclusions:

  • Musclin exerts beneficial effects on skeletal muscle and cardiac function in HFpEF, likely by enhancing SkM oxidative capacity.
  • These findings suggest musclin as a potential therapeutic agent for improving exercise capacity in HFpEF patients, warranting further clinical investigation.