Capillary supply and mitochondrial content of different skeletal muscle fiber types in untrained and endurance-trained men. A histochemical and ultrastructural study

Abstract

The number of capillaries per fiber, per mm2, around each fiber type and relative to fiber area was determined in six untrained subjects (UT) and six elite cross-country skiers (ET). Average values for maximal oxygen uptake were 49.8 ml . kg-1 . min-1 (UT) and 77.9 ml . kg-1 . min-1 (ET). Type I fibers constituted 39.2% (UT) and 68.6% (ET), type II A fibers 39.6% (UT) and 19.2% (ET), while 12.8% (UT) and 6.6% (ET) of the fibers were type II B. The mean fiber area for the type II A fibers was significantly greater (p less than 0.01) than the areas for type I and II B in the untrained group. The average numbers of capillaries around each fiber type (CA) were 4.76-4.84-2.94 (UT) and 7.79-6.63-4.5 (ET) for type I, II A, and II B, respectively. There was a significant difference (p less than 0.01) in the CA values relative to fiber area for all fiber types in both groups, being highest for type I and lowest for type II B. The CA increased linearly with increasing size of the fibers for all fiber types in both groups. The mitochondrial content was determined semiquantitatively for each fiber type. The differences in capillary supply between the fiber types are accompanied by similar differences in mitochondrial content. The results indicate that endurance training increases the capillary supply of all fiber types in the human quadriceps muscle. The fact that light microscopical studies have given lower capillarization values than those obtained with the electron microscope is discussed.

Effects of endurance training on muscle fibre ATP‐ase activity, capillary supply and mitochondrial content in man.

“…The methods used have been published elsewhere (Brodal et al 1977;Gr0nner0d, Dahl & Vaage, 1977;Ingjer, 1977;Ingjer, 1978a) and these studies shoud be consulted for particulars and discussion of their validity.…”

“…Edstrom & Ekblom, 1972;Hoppeler, Luthi, Claassen, Weibel & Howard, 1973;Howald, 1975;Costill, Daniels, Evans, Fink, Krahenbuhl & Saltin, 1976;Brodal, Ingjer & Hermansen, 1977;Ingjer, 1978a). Although these studies indicate that training leads to an increase in the factors mentioned, it is impossible to decide with certainty whether the observed differences depend on the effect of training or on genetic differences.…”

Training for skeletal muscle capillarization: a Janus-faced role of exercise intensity?

“…Exercise is the most potent stimulator of angiogenesis in skeletal muscles, and few weeks of exercise training lead to measureable increases in muscle capillarization. Untrained subjects may enjoy 10-30 % increase in capillarization after 6-8 weeks of exercise training, whereas elite aerobic athletes with years of progressive exercise training express a capillary-to-muscle fiber ratio of more than 200 % of that of untrained individuals (Ingjer 1979). During exercise, vascular endothelial growth factor (VEGF) is secreted from the muscle fibres to the muscle interstitium.…”

Follistatin-like 1, a Secreted Muscle Protein, Promotes Endothelial Cell Function and Revascularization in Ischemic Tissue through a Nitric-oxide Synthase-dependent Mechanism

“…Skeletal muscle hypertrophy is associated with blood vessel recruitment, such that capillary density is either maintained or increased during muscle growth (1)(2)(3)(4). A number of studies have shown that the serine-threonine protein kinase Akt1 plays a key role in regulation of cellular hypertrophy and organ size (5).…”

“…The expression of constitutively active Akt1 in skeletal muscle stimulates muscle hypertrophy both in vitro and in vivo (6 -9). Adenovirus-mediated transduction of constitutively active Akt1 also promotes the induction of the vascular endothelial growth factor (VEGF), 3 and this is accompanied by an increase in limb perfusion and capillary density in muscles where Akt1 is overexpressed (6). Constitutive activation of Akt1 in the heart also promotes myocardial angiogenesis, which is partly mediated by the induction of VEGF (10,11).…”