Document Detail


Low intensity exercise in humans accelerates mitochondrial ATP production and pulmonary oxygen kinetics during subsequent more intense exercise.
MedLine Citation:
PMID:  11826176     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We undertook this study to determine whether low intensity exercise (55 % (O2,max) would significantly alter the metabolic and ventilatory responses observed during 10 min of subsequent moderate intensity exercise (75 % (O2,max). By executing this work, we hoped to further our understanding of the mechanisms that limit mitochondrial ATP production at the onset of exercise. Seven healthy human subjects performed 10 min of moderate intensity exercise in the presence and absence of 10 min of low intensity exercise, which preceded the moderate intensity exercise by 3 min. Muscle biopsy samples were obtained from the vastus lateralis at pre-determined time points and oxygen consumption kinetics were determined at rest and during low and moderate intensity exercise. Following low intensity exercise and 3 min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal levels, but (O2) had returned to the resting rate. When moderate intensity exercise was preceded by low intensity exercise, there was a significant sparing of phosphocreatine (PCr, approximately 25 %, P < 0.05) and reductions in glucose 6-phosphate (G-6-P, approximately 50 %, P < 0.05) and lactate (approximately 50 %, P < 0.05) accumulation during the first minute of moderate intensity exercise. No differences were observed after 10 min of moderate intensity exercise. The (O2) on-kinetic response over the first minute of moderate intensity exercise was accelerated when preceded by low intensity exercise. Collectively, our results suggest the lag in the oxidative ATP delivery at the onset of moderate intensity exercise can be overcome by prior low intensity exercise. Furthermore, our findings support the view that this lag is at least in part attributable to a limitation in acetyl group delivery/availability at the onset of exercise, rather than delayed oxygen supply.
Authors:
Síun P Campbell-O'Sullivan; Dumitru Constantin-Teodosiu; Nicholas Peirce; Paul L Greenhaff
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of physiology     Volume:  538     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2002 Feb 
Date Detail:
Created Date:  2002-02-04     Completed Date:  2002-04-25     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  931-9     Citation Subset:  IM    
Affiliation:
School of Biomedical Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham NG7 2UH, UK. siun@osullivan.net
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / biosynthesis*
Adult
Exercise / physiology*
Humans
Kinetics
Lung / metabolism*
Male
Mitochondria, Muscle / metabolism*
Muscle, Skeletal / metabolism
Oxygen Consumption*
Respiration
Time Factors
Chemical
Reg. No./Substance:
56-65-5/Adenosine Triphosphate
Comments/Corrections

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