Skeletal muscle capillarity and angiogenic mRNA levels after exercise training in
normoxia and chronic hypoxia.
Olfert, I. Mark, Ellen C. Breen, Odile Mathieu-Costello, and Peter D. Wagner.
1Department of Physiology and Pharmacology, Loma Linda University, Loma Linda
92350; and 2Division of Physiology, Department of Medicine, University of California,
San Diego, La Jolla, California 92093«hyphen»0623
APStracts 8:0298A, 2001.
Gene expression of vascular endothelial growth factor (VEGF) and to a lesser extent
transforming growth factor-ß1 (TGF-ß1) and basic fibroblast growth factor (bFGF) have
been found to increase in rat skeletal muscle after a single exercise bout. In addition,
acute hypoxia augments the VEGF mRNA response to exercise, which suggests that, if
VEGF is important in muscle angiogenesis, hypoxic training might produce greater
capillary growth than normoxic training. Therefore, we examined the effects of exercise
training (treadmill running at the same absolute intensity) in normoxia and hypoxia
(inspired O2 fraction = 0.12) on rat skeletal muscle capillarity and on resting and
postexercise gene expression of VEGF, its major receptors (flt-1 and flk-1), TGF-ß1, and
bFGF. Normoxic training did not alter basal or exercise-induced VEGF mRNA levels but
produced a modest approximately twofold increase in bFGF mRNA (P < 0.05). Rats
trained in hypoxia exhibited an attenuated VEGF mRNA response to exercise (1.8-fold
compared 3.4-fold with normoxic training, P < 0.05), absent TGF-ß1 and flt-1 mRNA
responses to exercise, and ~ threefold (P < 0.05) decrease in bFGF mRNA levels. Flk-1
mRNA levels were not significantly altered by either normoxic or hypoxic training. An
increase in skeletal muscle capillarity was observed only in hypoxically trained rats.
These data show that whereas training in hypoxia potentiates the adaptive angiogenic
response of skeletal muscle to a given absolute intensity of exercise, this was not evident
in the gene expression of VEGF or its receptors when assessed at the end of training.
Received 2 October 2000; accepted in final form 16 May 2001
APS Manuscript Number A987-0.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 18 June 2001