Document Detail

Increased oxidative stress and anaerobic energy release, but blunted Thr172-AMPKα phosphorylation, in response to sprint exercise in severe acute hypoxia in humans.
MedLine Citation:
PMID:  22858621     Owner:  NLM     Status:  MEDLINE    
AMP-activated protein kinase (AMPK) is a major mediator of the exercise response and a molecular target to improve insulin sensitivity. To determine if the anaerobic component of the exercise response, which is exaggerated when sprint is performed in severe acute hypoxia, influences sprint exercise-elicited Thr(172)-AMPKα phosphorylation, 10 volunteers performed a single 30-s sprint (Wingate test) in normoxia and in severe acute hypoxia (inspired Po(2): 75 mmHg). Vastus lateralis muscle biopsies were obtained before and immediately after 30 and 120 min postsprint. Mean power output and O(2) consumption were 6% and 37%, respectively, lower in hypoxia than in normoxia. O(2) deficit and muscle lactate accumulation were greater in hypoxia than in normoxia. Carbonylated skeletal muscle and plasma proteins were increased after the sprint in hypoxia. Thr(172)-AMPKα phosphorylation was increased by 3.1-fold 30 min after the sprint in normoxia. This effect was prevented by hypoxia. The NAD(+)-to-NADH.H(+) ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia (P < 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia (P < 0.05). This could have led to lower liver kinase B1 (LKB1) activation by SIRT1 and, hence, blunted Thr(172)-AMPKα phosphorylation. Ser(485)-AMPKα(1)/Ser(491)-AMPKα(2) phosphorylation, a known negative regulating mechanism of Thr(172)-AMPKα phosphorylation, was increased by 60% immediately after the sprint in hypoxia, coincident with increased Thr(308)-Akt phosphorylation. Collectively, our results indicate that the signaling response to sprint exercise in human skeletal muscle is altered in severe acute hypoxia, which abrogated Thr(172)-AMPKα phosphorylation, likely due to lower LKB1 activation by SIRT1.
David Morales-Alamo; Jesús Gustavo Ponce-González; Amelia Guadalupe-Grau; Lorena Rodríguez-García; Alfredo Santana; Maria Roser Cusso; Mario Guerrero; Borja Guerra; Cecilia Dorado; José A L Calbet
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-08-02
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-17     Completed Date:  2013-02-05     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  917-28     Citation Subset:  IM    
Department of Physical Education, University of Las Palmas de Gran Canaria (Campus Universitario de Tafira Las Palmas de Gran Canaria, Spain.
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MeSH Terms
AMP-Activated Protein Kinases / metabolism*
Acute Disease
Anaerobic Threshold
Anoxia / enzymology*,  physiopathology
Blood Glucose / metabolism
Blood Proteins / metabolism
Energy Metabolism*
Exercise Test
GTPase-Activating Proteins / metabolism
Insulin / blood
Lactic Acid / metabolism
Muscle Contraction*
Muscle Strength
NAD / metabolism
Oxidative Stress*
Oxygen Consumption
Protein Carbonylation
Protein-Serine-Threonine Kinases / metabolism
Quadriceps Muscle / enzymology*,  physiopathology
Severity of Illness Index
Sirtuin 1 / metabolism
Time Factors
Young Adult
Reg. No./Substance:
0/Blood Glucose; 0/Blood Proteins; 0/GTPase-Activating Proteins; 0/Insulin; 0/TBC1D4 protein, human; 50-21-5/Lactic Acid; 53-84-9/NAD; 72-19-5/Threonine; EC 2.7.1.-/STK11 protein, human; EC Protein Kinases; EC protein, human; EC protein, human; EC Kinases; EC 3.5.1.-/SIRT1 protein, human; EC 3.5.1.-/Sirtuin 1

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