Document Detail


Intensive resistance exercise induces lymphocyte apoptosis via cortisol and glucocorticoid receptor-dependent pathways.
MedLine Citation:
PMID:  21393471     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intensive endurance exercise is known to induce lymphocyte apoptosis, which might affect immune function. Less is known about the effects of resistance exercise on apoptosis and its underlying mechanisms. In this study, subjects performed an intensive resistance test (IRT) and a moderate resistance test, and lymphocyte apoptosis, apoptosis-related parameters, and underlying mechanisms were investigated. IRT induced a significant increase of lymphocyte apoptosis 3 h after exercise, which was accompanied by a significant decrease of mitochondrial membrane potential, a reduction of Bcl-2, and an upregulation of the CD95 receptor. Blood lactate, IL-6, C-reactive protein, and cortisol increased significantly 3 h after IRT. A significant correlation was observed between the increase of apoptosis and cortisol levels 3 h after IRT. Incubation of freshly isolated lymphocytes in IRT serum indicated an important role of serum correlates for apoptosis induction. Selective incubation of lymphocytes in concentrations of selected serum parameters corresponding to levels found post in IRT serum demonstrated a major role for cortisol in apoptosis induction. This result was confirmed by attenutation of apoptosis after addition of mifepristone before incubation in IRT serum. In summary, resistance exercise induced lymphocyte apoptosis in an intensity-dependent way. Furthermore, cortisol signaling via glucocorticoid receptors might be an important mechanism for lymphocyte apoptosis after resistance exercise.
Authors:
K Krüger; S Agnischock; A Lechtermann; S Tiwari; M Mishra; C Pilat; A Wagner; C Tweddell; I Gramlich; F C Mooren
Publication Detail:
Type:  Journal Article     Date:  2011-03-10
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  110     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-12     Completed Date:  2011-09-30     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:  1226-32     Citation Subset:  IM    
Affiliation:
Department of Sports Medicine, Institute of Sports Sciences, Justus-Liebig-University Giessen, Giessen, Germany. karsten.krueger@sport.uni-giessen.de
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MeSH Terms
Descriptor/Qualifier:
Adult
Apoptosis / physiology*
Humans
Hydrocortisone / blood*
Lymphocytes / physiology*
Male
Physical Endurance / physiology*
Receptors, Glucocorticoid / blood*
Resistance Training / methods*
Signal Transduction / physiology*
Chemical
Reg. No./Substance:
0/Receptors, Glucocorticoid; 50-23-7/Hydrocortisone

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


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