Skeletal muscle changes in patients with obstructive sleep apnoea syndrome

Respir Med. 2003 Jul;97(7):804-10. doi: 10.1016/s0954-6111(03)00034-9.

Abstract

Previous studies have shown that chronic hypoxia leads to changes in skeletal muscle structure (fibre size and type) and activities of several bioenergetic enzymes. Whether this occurs also in conditions characterised by intermittent hypoxia, such as the obstructive sleep apnoea syndrome (OSAS), is unknown. To explore this possibility, we obtained a needle biopsy of the quadriceps femoris in 12 consecutive stable outpatients with severe OSAS (52 +/- 9 year, apnoea-hypopnoea index 70 +/- 14 h(-1)) (x +/- SD) and in six healthy volunteers (49 +/- 8 year), where we quantified fibre type, size and protein content, as well as phosphofructo-kinase (PFK) and cytochrome oxidase (CytOx) activities. We found that fibre-type distribution was similar in patients and controls. In contrast, the diameter of type II fibres (74 +/- 10 microm vs. 56 +/- 11 microm, P < 0.05) and protein content (100 +/- 14 vs. 88 +/- 8 microg/mg) was higher in patients with OSAS. Likewise, we observed upregulation of CytOx (0.93 +/- 0.38 vs. 0.40 +/- 0.22 microkat/mg protein, P < 0.01) and PFK activities (5.35 +/- 4.8 vs. 1.3 +/- 1.3 microkat/ mg protein, P < 0.05) in patients with OSAS. These results show that, paralleling which occurs in conditions characterised by continuous hypoxia, patients with OSAS (and intermittent hypoxia) also show structural and bioenergetic changes in their skeletal muscle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Electron Transport Complex IV / analysis
  • Humans
  • Middle Aged
  • Muscle Fibers, Skeletal / chemistry
  • Muscle Fibers, Skeletal / pathology
  • Muscle Proteins / analysis
  • Muscle, Skeletal / chemistry
  • Muscle, Skeletal / pathology*
  • Phosphofructokinases / analysis
  • Sleep Apnea Syndromes / pathology*
  • Statistics, Nonparametric

Substances

  • Muscle Proteins
  • Electron Transport Complex IV
  • Phosphofructokinases