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Background <p>Statins are widely prescribed for dyslipidemia and cardiovascular prevention but may induce skeletal muscle alterations that remain undetected by conventional clinical markers.</p> Objectives <p>This study aimed to investigate morphological changes and their functional correlates in women undergoing chronic statin therapy.</p> Methods <p>Twenty-one women (50–80&#xa0;years) treated with simvastatin or atorvastatin were assessed through deltoid muscle biopsy, handgrip force–time analysis, and functional capacity testing. Histological examination revealed three phenotypes: normal morphology (<i>n</i> = 2), mitochondrial alterations (<i>n</i> = 12), and neurogenic alterations (<i>n</i> = 7). Despite preserved peak force across groups, force–time parameters discriminated functional profiles.</p> Results <p>The mitochondrial group achieved submaximal force more rapidly, sustained higher mean force, and demonstrated greater total work (<i>p</i> &lt; 0.05). In contrast, the neurogenic group exhibited delayed force development, lower mean force, and reduced work output (<i>p</i> &lt; 0.05). Functional testing showed better flexibility in the mitochondrial group and poorer coordination in the neurogenic group, while other domains remained similar between groups. Notably, histological abnormalities and functional impairments were identified in the absence of self-reported myalgia or elevated creatine kinase, highlighting the subclinical nature of these alterations.</p> Conclusions <p>These findings suggest that force–time curve analysis provides a sensitive tool for detecting neuromuscular changes associated with statin use, beyond maximal strength testing or biochemical markers. The integration of dynamometry and histopathology offers clinical potential for early identification and monitoring of statin-associated muscle dysfunction, supporting timely therapeutic adjustments and preventive strategies.</p>

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Force–time curve analysis and muscle histology in women aged 50–80 undergoing statin therapy: a pilot cross-sectional study

  • 期刊论文

  • 发表日期：

    2026年1月5日

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  • Gabriel de Souza Zanini,
  • Mariana Rotta Bonfim,
  • Elvis de Souza Malta,
  • Alexandre Daré de Almeida,
  • Danilo Alexandre Massini,
  • Dalton Muller Pessoa Filho,
  • Henrique Luiz Monteiro

摘要

Background

Statins are widely prescribed for dyslipidemia and cardiovascular prevention but may induce skeletal muscle alterations that remain undetected by conventional clinical markers.

Objectives

This study aimed to investigate morphological changes and their functional correlates in women undergoing chronic statin therapy.

Methods

Twenty-one women (50–80 years) treated with simvastatin or atorvastatin were assessed through deltoid muscle biopsy, handgrip force–time analysis, and functional capacity testing. Histological examination revealed three phenotypes: normal morphology (n = 2), mitochondrial alterations (n = 12), and neurogenic alterations (n = 7). Despite preserved peak force across groups, force–time parameters discriminated functional profiles.

Results

The mitochondrial group achieved submaximal force more rapidly, sustained higher mean force, and demonstrated greater total work (p < 0.05). In contrast, the neurogenic group exhibited delayed force development, lower mean force, and reduced work output (p < 0.05). Functional testing showed better flexibility in the mitochondrial group and poorer coordination in the neurogenic group, while other domains remained similar between groups. Notably, histological abnormalities and functional impairments were identified in the absence of self-reported myalgia or elevated creatine kinase, highlighting the subclinical nature of these alterations.

Conclusions

These findings suggest that force–time curve analysis provides a sensitive tool for detecting neuromuscular changes associated with statin use, beyond maximal strength testing or biochemical markers. The integration of dynamometry and histopathology offers clinical potential for early identification and monitoring of statin-associated muscle dysfunction, supporting timely therapeutic adjustments and preventive strategies.