Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication
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Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication. / Baum, Oliver; Torchetti, Eleonora; Malik, Corinna; Høier, Birgitte; Walker, Meegan; Walker, Philip J; Odriozola, Adolfo; Graber, Franziska; Tschanz, Stefan A; Bangsbo, Jens; Hoppeler, Hans H; Askew, Christopher D; Hellsten, Ylva.
I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Bind 310, Nr. 10, 2016, s. R943-R951.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication
AU - Baum, Oliver
AU - Torchetti, Eleonora
AU - Malik, Corinna
AU - Høier, Birgitte
AU - Walker, Meegan
AU - Walker, Philip J
AU - Odriozola, Adolfo
AU - Graber, Franziska
AU - Tschanz, Stefan A
AU - Bangsbo, Jens
AU - Hoppeler, Hans H
AU - Askew, Christopher D
AU - Hellsten, Ylva
N1 - CURIS 2016 NEXS 133
PY - 2016
Y1 - 2016
N2 - 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.
AB - 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.
U2 - 10.1152/ajpregu.00480.2015
DO - 10.1152/ajpregu.00480.2015
M3 - Journal article
C2 - 27009051
VL - 310
SP - R943-R951
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 10
ER -
ID: 160055416