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Mechanisms underlying exercise-induc...

Hubal, Monica J.

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Mechanisms underlying exercise-induced muscle damage.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Mechanisms underlying exercise-induced muscle damage./
Author:	Hubal, Monica J.
Description:	277 p.
Notes:	Adviser: Priscilla M. Clarkson.
Contained By:	Dissertation Abstracts International67-04B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3215766
ISBN:	9780542656705

Mechanisms underlying exercise-induced muscle damage.
Hubal, Monica J.

Mechanisms underlying exercise-induced muscle damage. - 277 p.

Adviser: Priscilla M. Clarkson.

Thesis (Ph.D.)--University of Massachusetts Amherst, 2006.

The goal of this dissertation was to identify and characterize underlying mechanisms of exercise-induced muscle damage (EIMD) and muscle adaptation to damage. Study I examined contributions of central and peripheral factors to EIMD. Forty-six subjects performed voluntary and stimulated contractions before and immediately following eccentric exercise of the elbow flexors. Subjects demonstrating greater strength loss (a hallmark of EIMD) after eccentric exercise also had greater impairment of peripheral function, but similar central function compared with lower strength loss subjects, suggesting that the mechanism(s) driving variation in strength loss are localized mainly within the periphery.

ISBN: 9780542656705Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Mechanisms underlying exercise-induced muscle damage.
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020 $a 9780542656705
035 $a (UMI)AAI3215766
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040 $a UMI $c UMI
100 1 $a Hubal, Monica J. $3 1293198
245 1 0 $a Mechanisms underlying exercise-induced muscle damage.
300 $a 277 p.
500 $a Adviser: Priscilla M. Clarkson.
500 $a Source: Dissertation Abstracts International, Volume: 67-04, Section: B, page: 1967.
502 $a Thesis (Ph.D.)--University of Massachusetts Amherst, 2006.
520 $a The goal of this dissertation was to identify and characterize underlying mechanisms of exercise-induced muscle damage (EIMD) and muscle adaptation to damage. Study I examined contributions of central and peripheral factors to EIMD. Forty-six subjects performed voluntary and stimulated contractions before and immediately following eccentric exercise of the elbow flexors. Subjects demonstrating greater strength loss (a hallmark of EIMD) after eccentric exercise also had greater impairment of peripheral function, but similar central function compared with lower strength loss subjects, suggesting that the mechanism(s) driving variation in strength loss are localized mainly within the periphery.
520 $a Study II further focused on peripheral factors, specifically molecular changes in gene expression within muscle tissue following eccentric exercise, to determine underlying molecular mechanisms of damage development. Three subjects performed an exercise in which one leg underwent concentric contractions, and the other leg performed both eccentric and concentric actions. Dependent variables included strength loss, soreness and serum creatine kinase activity. Muscle biopsy samples were taken 4-8h post-exercise. Microarray analysis of these samples identified upregulation of genes involved in inflammation, apoptosis (programmed cell death), structure and transcriptional regulation. These results provided the first global gene expression pattern of human muscle after eccentric exercise.
520 $a EIMD is attenuated naturally via the repeated bout effect, where an initial bout of exercise confers a protective effect on muscle that results in less damage induced by a second bout of exercise. Study III aimed to identify mechanisms driving this adaptation. Seven subjects performed two bouts of eccentric exercise of the leg spaced 4wk apart. Muscle strength and soreness were evaluated and biopsies were collected at 6h post-exercise. Muscle samples were tested for expression of a subset of inflammatory genes identified in Study II. Study III showed upregulation of monocyte chemoattractant protein-1 and the transcription factors CEBPD and ZFP36 following the repeated bout. Monocyte chemoattractant protein 1 (MCP-1) was co-localized to macrophages and satellite cells, which are vital to muscle regeneration. These data suggest that specific alterations in the inflammation response may drive the repeated bout effect, possibly by enhancing communication between macrophages and satellite cells, which may strengthen muscle regeneration following EIMD.
590 $a School code: 0118.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Health Sciences, Recreation. $3 1018003
650 4 $a Health Sciences, Rehabilitation and Therapy. $3 1017926
690 $a 0382
690 $a 0433
690 $a 0575
710 2 0 $a University of Massachusetts Amherst. $3 1019433
773 0 $t Dissertation Abstracts International $g 67-04B.
790 $a 0118
790 1 0 $a Clarkson, Priscilla M., $e advisor
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3215766