Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Oliver Baum
  • Eleonora Torchetti
  • Corinna Malik
  • Birgitte Høier
  • Meegan Walker
  • Philip J Walker
  • Adolfo Odriozola
  • Franziska Graber
  • Stefan A Tschanz
  • Bangsbo, Jens
  • Hans H Hoppeler
  • Christopher D Askew
  • Hellsten, Ylva

Intermittent claudication (IC) is the most commonly reported symptom of peripheral arterial disease (PAD). Impaired limb blood flow is a major casual factor of lower exercise tolerance in PAD, but cannot entirely explain it. We hypothesized that IC is associated with structural changes of the capillary-mitochondria interface that could contribute to the reduction of exercise tolerance in IC-patients. Capillary and mitochondrial morphometry were performed after light and transmission electron microscopy using vastus lateralis muscle biopsies of 14 IC-patients and 10 age-matched controls and peak power output (PPO) was determined for all participants using an incremental single-leg knee-extension protocol. Capillary density was lower (411±90 mm(-2)versus 506±95 mm(-2); P≤0.05) in the biopsies of the IC patients than in those of the controls. The basement membrane (BM) around capillaries was thicker (543±82 nm versus 423±97 nm; P≤0.01) and the volume density of mitochondria was lower (3.51±0.56% versus 4.60±0.74; P≤0.01) in the IC-patients than the controls. In the IC-patients, a higher proportion of capillaries appeared with collapsed slit-like lumen and/or swollen endothelium. PPO was lower (18.5±9.9 W versus 33.5±9.4 W; P≤0.01) in the IC-patients than the controls. We suggest that several structural alterations in skeletal muscle, either collectively or separately, contribute to the reduction of exercise tolerance in IC-patients.

TidsskriftAmerican Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Udgave nummer10
Sider (fra-til)R943-R951
Antal sider9
StatusUdgivet - 2016

Bibliografisk note

CURIS 2016 NEXS 133

ID: 160055416