To dissect the independent effects of altitude-induced
hypoxemia and
anorexia on the capacity for cardiac
lactate metabolism, we examined the effects of 21 days of chronic hypobaric
hypoxia (CHH) and its associated decrease in food intake and right ventricle (RV)
hypertrophy on the monocarboxylate transporter 1 and 4 (MCT) expression, the rate of
lactate uptake into sarcolemmal vesicles, and the activity of
lactate dehydrogenase isoforms in rat muscles. In comparison with control rats (C), 1 mmol/L
lactate transport measured on skeletal muscle sarcolemmal vesicles increased by 33% and 58% in hypoxic (CHH, barometric pressure = 495 hPa) and rats pair-fed an equivalent quantity of food to that consumed by hypoxic animals, respectively. The increased
lactate transport was higher in PF than in CHH animals ( P < .05). No associated change in the expression of MCT1
protein was observed in skeletal muscles, whereas MCT1
mRNA decreased in CHH rats, in comparison with C animals (42%, P < .05), partly related to
caloric restriction (30%, P < .05). MCT4
mRNA and
protein increased during acclimatization to
hypoxia only in slow-oxidative muscles (68%, 72%, P < .05, respectively). The MCT4
protein content did not change in the plantaris muscle despite a decrease in transcript levels, related to
hypoxia and
caloric restriction. In both the left and right ventricles, the MCT1
protein content was unaffected by ambient
hypoxia or restricted food consumption. These results suggest that MCT1 and MCT4 gene expression in fast-glycolytic muscles is mainly regulated by posttranscriptional mechanisms. Moreover, the results emphasize the role played by
caloric restriction on the control of gene expression in response to chronic
hypoxia and suggest that
hypoxia-induced right ventricle
hypertrophy failed to alter
MCT proteins.