Document Detail

A hypoxia complement differentiates the muscle response to endurance exercise.
MedLine Citation:
PMID:  20176680     Owner:  NLM     Status:  MEDLINE    
Metabolic stress is believed to constitute an important signal for training-induced adjustments of gene expression and oxidative capacity in skeletal muscle. We hypothesized that the effects of endurance training on expression of muscle-relevant transcripts and ultrastructure would be specifically modified by a hypoxia complement during exercise due to enhanced glycolytic strain. Endurance training of untrained male subjects in conditions of hypoxia increased subsarcolemmal mitochondrial density in the recruited vastus lateralis muscle and power output in hypoxia more than training in normoxia, i.e. 169 versus 91% and 10 versus 6%, respectively, and tended to differentially elevate sarcoplasmic volume density (42 versus 20%, P = 0.07). The hypoxia-specific ultrastructural adjustments with training corresponded to differential regulation of the muscle transcriptome by single and repeated exercise between both oxygenation conditions. Fine-tuning by exercise in hypoxia comprised gene ontologies connected to energy provision by glycolysis and fat metabolism in mitochondria, remodelling of capillaries and the extracellular matrix, and cell cycle regulation, but not fibre structure. In the untrained state, the transcriptome response during the first 24 h of recovery from a single exercise bout correlated positively with changes in arterial oxygen saturation during exercise and negatively with blood lactate. This correspondence was inverted in the trained state. The observations highlight that the expression response of myocellular energy pathways to endurance work is graded with regard to metabolic stress and the training state. The exposed mechanistic relationship implies that the altitude specificity of improvements in aerobic performance with a 'living low-training high' regime has a myocellular basis.
Silvia Schmutz; Christoph Däpp; Matthias Wittwer; Anne-Cécile Durieux; Matthias Mueller; Felix Weinstein; Michael Vogt; Hans Hoppeler; Martin Flück
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-22
Journal Detail:
Title:  Experimental physiology     Volume:  95     ISSN:  1469-445X     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-08-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  723-35     Citation Subset:  IM    
Institute for Biomedical Research into Human Movement and Health, Manchester Metropolitan University, Oxford Road, Manchester M1 5GD, UK.
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MeSH Terms
Anoxia / metabolism*
Energy Metabolism
Exercise / physiology*
Gene Expression Profiling
Lipid Metabolism
Muscle, Skeletal / ultrastructure*
Oxygen Consumption / physiology
Physical Endurance / physiology*
Comment In:
Exp Physiol. 2010 Jun;95(6):668   [PMID:  20484121 ]

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