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Title: Vascular growth in hypoxic skeletal muscle. Author: Hoppeler H. Journal: Adv Exp Med Biol; 1999; 474():277-86. PubMed ID: 10635007. Abstract: The critical role of skeletal muscle capillaries is the supply of oxygen to skeletal muscle fibers during conditions of maximal aerobic work. The supply of substrates under these conditions is not limited by the vascular bed but rather by the capacity of the sarcolemmal transporter systems. Because of this dominant role of oxygen supply in muscle tissue, hypoxia has generally been considered to be an important stimulus for capillary neo-formation in skeletal muscle. Early morphometric work seemed to indicate that animals exposed to permanent hypoxia had in fact a significantly improved vascular supply in muscle tissue. Later work questioned these early findings and it was concluded that hypoxia per se was not a sufficient stimulus for capillary neo-formation but that additional stimuli such as cold-exposure needed to be present. In humans exposed to severe hypoxia during simulated or real ascents to Mt. Everest an increase in capillary density was in fact found. However, this increase could be shown to result from a reduction of muscle fiber volume and not from capillary growth. Broadly compatible results were obtained in animal experiments in which changes in capillarity were assessed in muscles with limited blood supply which were exposed to chronic electrical stimulation. Recently we have shown that endurance exercise training in humans results in a rise in mRNA of vascular endothelial growth factor (VEGF) only when carried out vigorously and in hypoxia. These results indicate that molecular techniques will allow in the near future to delineate the role played by hypoxia in capillary neo-formation.[Abstract] [Full Text] [Related] [New Search]