Document Detail


Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?
MedLine Citation:
PMID:  20007521     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study investigates the role of central vs. peripheral factors in the limitation of maximal oxygen uptake (Vo(2max)) with moderate hypoxia [inspired fraction (Fi(O(2))) =14.5%]. Fifteen endurance-trained athletes performed maximal cycle incremental tests to assess Vo(2max), maximal cardiac output (Q(max)), and maximal arteriovenous oxygen (a-vO(2)) difference in normoxia and hypoxia. Muscle biopsies of vastus lateralis were taken 1 wk before the cycling tests to evaluate maximal muscle oxidative capacity (V(max)) and sensitivity of mitochondrial respiration to ADP (K(m)) on permeabilized muscle fibers in situ. Those athletes exhibiting the largest reduction of Vo(2max) in moderate hypoxia (Severe Loss group: -18 +/- 2%) suffered from significant reductions in Q(max) (-4 +/- 1%) and maximal a-vO(2) difference (-14 +/- 2%). Athletes who well tolerated hypoxia, as attested by a significantly smaller drop of Vo(2max) with hypoxia (Moderate Loss group: -7 +/- 1%), also display a blunted Q(max) (-9 +/- 2%) but, conversely, were able to maintain maximal a-vO(2) difference (+1 +/- 2%). Though V(max) was similar in the two experimental groups, the smallest reduction of Vo(2max) with moderate hypoxia was observed in those athletes presenting the lowest apparent K(m) for ADP in the presence of creatine (K(m+Cr)). In already-trained athletes with high muscular oxidative capacities, the qualitative, rather than quantitative, aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising at low Fi(O(2)), presumably through the functional coupling between the mitochondrial creatine kinase and ATP production. This study suggests a potential role for peripheral factors, including the alteration of cellular homeostasis in active muscles, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.
Authors:
Elodie Ponsot; St?phane P Dufour; St?phane Doutreleau; Evelyne Lonsdorfer-Wolf; Eliane Lampert; Fran?ois Piquard; Bernard Geny; Bertrand Mettauer; Ren?e Ventura-Clapier; Ruddy Richard
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-09
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  298     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-01     Completed Date:  2010-03-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R558-66     Citation Subset:  IM    
Affiliation:
Service de Physiologie et d' Explorations Fonctionnelles, H?pital Civil and D?partement de Physiologie, UPRES E.A. 3072, Facult? de M?decine, Strasbourg, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adult
Anoxia / physiopathology*
Athletes*
Exercise / physiology*
Exercise Test
Heart Rate / physiology
Homeostasis / physiology
Humans
Male
Mitochondria / physiology*
Muscle, Skeletal / physiology*
Oxygen Consumption / physiology
Physical Endurance / physiology*
Pulmonary Gas Exchange / physiology
Stroke Volume / physiology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Mitochondrial content and distribution changes specific to mouse diaphragm after chronic normobaric ...
Next Document:  The antidiuretic neurohormone RhoprCAPA-2 down regulates fluid transport across the anterior midgut ...