HIF-1α in endurance training: suppression of oxidative metabolism

• DOI: 10.1152/ajpregu.00335.2007
• Publication Date: 2007-09-14T00:43:34Z
• Authors: Steven D. Mason; Helene Rundqvist; Ioanna Papandreou; Roger Duh; Wayne J. McNulty; Richard A. Howlett; I. Mark Olfert; Carl Johan Sundberg; Nicholas C. Denko; Lorenz Poellinger; Randall S. Johnson
• Keywords: Endurance Training; Hypoxia

During endurance training, exercising skeletal muscle experiences severe and repetitive oxygen stress. The primary transcriptional response factor for acclimation to hypoxic stress is hypoxia-inducible factor-1alpha (HIF-1alpha), which upregulates glycolysis angiogenesis in low levels of tissue oxygenation. To examine the role HIF-1alpha we have created mice specifically lacking subjected them an training protocol. We found that only wild-type improve their oxidative capacity, as measured by respiratory exchange ratio; surprisingly, null already upregulated this parameter without training. Furthermore, untrained increased capillary fiber ratio elevated enzyme activities. These changes correlate with constitutively activated AMP-activated protein kinase muscles. Additionally, muscles decreased expression pyruvate dehydrogenase I, a target inhibits metabolism. data demonstrate removal causes adaptive akin provides evidence suppression mitochondrial biogenesis normal tissue.