Document Detail

Muscle intracellular oxygenation during exercise: optimization for oxygen transport, metabolism, and adaptive change.
MedLine Citation:
PMID:  21512800     Owner:  NLM     Status:  MEDLINE    
Exercise is the example par excellence of the body functioning as a physiological system. Conventionally we think of the O(2) transport process as a major manifestation of that system linking and integrating pulmonary, cardiovascular, hematological and skeletal muscular contributions to the task of getting O(2) from the air to the mitochondria, and this process has been well described. However, exercise invokes system responses at levels additional to those of macroscopic O(2) transport. One such set of responses appears to center on muscle intracellular PO(2), which falls dramatically from rest to exercise. At rest, it approximates 4 kPa, but during heavy endurance exercise it falls to about 0.4-0.5 kPa, an amazingly low value for a tissue absolutely dependent on the continual supply of O(2) to meet very high energy demands. One wonders why intracellular PO(2) is allowed to fall to such levels. The proposed answer, to be presented in the review, is that a low intramyocyte PO(2) is pivotal in: (a) optimizing oxygen's own physiological transport, and (b) stimulating adaptive gene expression that, after translation, enables greater exercise capacity-all the while maintaining PO(2) at levels sufficient to allow oxidative phosphorylation to operate sufficiently fast enough to support intense muscle contraction. Thus, during exercise, reductions of intracellular PO(2) to less than 1% of that in the atmosphere enables an integrated response that fundamentally and simultaneously optimizes physiological, biochemical and molecular events that support not only the exercise as it happens but the adaptive changes to increase exercise capacity over the longer term.
Peter D Wagner
Publication Detail:
Type:  Journal Article     Date:  2011-04-22
Journal Detail:
Title:  European journal of applied physiology     Volume:  112     ISSN:  1439-6327     ISO Abbreviation:  Eur. J. Appl. Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-09     Completed Date:  2012-05-15     Revised Date:  2012-12-12    
Medline Journal Info:
Nlm Unique ID:  100954790     Medline TA:  Eur J Appl Physiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1-8     Citation Subset:  IM    
University of California, San Diego, USA.
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MeSH Terms
Adaptation, Physiological / physiology
Biological Transport, Active / physiology
Models, Biological*
Muscle Contraction / physiology*
Muscle Fibers, Skeletal / physiology*
Muscle, Skeletal / physiology*
Oxygen / metabolism*
Oxygen Consumption / physiology*
Physical Exertion / physiology*
Reg. No./Substance:
Comment In:
Eur J Appl Physiol. 2012 Nov;112(11):3935-6; author reply 3937-8   [PMID:  22446957 ]

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