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1 Cumhuriyet University School of Medicine, 58140 Sivas, Turkey; and 2 Department of Physiology, University of Birmingham Medical School, Birmingham B15 2TT, United Kingdom
Whether chronic hypoxia
causes angiogenesis in skeletal muscle is controversial. Male Wistar
rats, 5-6 wk of age, were kept at constant 12% O2 for
3 wk, and frozen sections of their postural soleus (SOL), phasic
extensor digitorum longus (EDL), and tibialis anterior (TA) muscles
were compared with those of normoxic controls. Capillary supply
increased in SOL muscles [capillary-to-fiber ratio (C/F) = 2.55 ± 0.09 hypoxia vs. 2.17 ± 0.06 normoxia; capillary density (CD) = 942 ± 14 hypoxia vs. 832 ± 20 mm
2 normoxia, P < 0.01] but not in EDL
muscles (C/F = 1.44 ± 0.04 hypoxia vs. 1.42 ± 0.04 normoxia; CD = 876 ± 52 hypoxia vs. 896 ± 24 mm2 normoxia). The predominantly glycolytic cortex of TA
muscles showed higher C/F after hypoxia (1.79 ± 0.09 vs.
1.53 ± 0.05 normoxia, P < 0.05), whereas the
mainly oxidative TA core with smaller fibers showed no change in
capillarity. The region of the SOL muscle with large-sized (mean fiber
area 2,843 ± 128 µm2) oxidative fibers (90% type
I) had a higher C/F (by 30%) and CD (by 25%), whereas there was no
angiogenesis in the region with sparse (76%) and smaller-sized
(2,200 ± 85 µm2) type I fibers. Thus systemic
hypoxia differentially induces angiogenesis between and within hindlimb
skeletal muscles, with fiber size contributing either directly (via a
metabolic stimulus) or indirectly (via a mechanical stimulus) to the process.
capillary growth; histochemistry; hypoxemia; oxygen transport; rat
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