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Molecular regulation of the adaptive response to exercise in human skeletal muscle.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Molecular regulation of the adaptive response to exercise in human skeletal muscle./
Author:	Little, Jonathan Peter.
Description:	1 online resource (116 pages)
Notes:	Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: 4478.
Contained By:	Dissertation Abstracts International72-08B.
Subject:	Physiology. -
Online resource:	click for full text (PQDT)
ISBN:	9780494746417

Molecular regulation of the adaptive response to exercise in human skeletal muscle.
Little, Jonathan Peter.

Molecular regulation of the adaptive response to exercise in human skeletal muscle. - 1 online resource (116 pages)

Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: 4478.

Thesis (Ph.D.)--McMaster University (Canada), 2010.

Includes bibliographical references

This thesis examined the molecular regulation and metabolic consequences of human skeletal muscle mitochondrial adaptations to exercise. The transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator (PGC)-1alpha has emerged as a critical regulator of exercise-induced mitochondrial) biogenesis and has been implicated in the pathogenesis of metabolic-related diseases such as type 2 diabetes (T2D). The mechanisms of how PGC-1alpha might regulate the muscle adaptive response to exercise are not well defined. At rest, the majority of PGC-1alpha was detected in cytosolic fractions prepared from human skeletal muscle biopsy samples. In response to both acute endurance (90 min &sim;65% maximal oxygen uptake [VO2peak]) and high-intensity interval exercise (4 x 30-s "all-out" Wingate tests), there was an increase in nuclear PGC-1alpha abundance yet no change in total PGC-1alpha protein. Acute exercise increased the activation of cytosolic p38 mitogen activated protein kinase (p38 MAPK) and 5'-AMP activated protein kinase (AMPK), which are both proposed activators of PGC-1alpha. The increase in nuclear PGC-1alpha after interval exercise also coincided with increased mRNA expression of mitochondrial genes. Two weeks of low-volume high-intensity interval training (HIT), consisting of 6 sessions of 8-12 x 1-min &sim;100% VO2peak; increased nuclear PGC-1alpha, markers of skeletal muscle mitochondrial content, and exercise performance in young, healthy men. A similar low-volume HIT protocol (6 sessions of 10 x 1-min &sim;95% VO2peak) improved mitochondrial capacity, functional performance, and glycemic regulation in individuals with T2D and pre-diabetes but had no effect on nuclear or total PGC-1alpha protein content. These findings indicate that acute exercise may activate mitochondrial biogenesis by a mechanism involving increased nuclear PGC-1alpha abundance. Two weeks of practical low-volume HIT is an effective strategy to improve mitochondrial capacity and glycemic regulation in individuals with, and at risk for, T2D, but a sustained increase in PGC-1alpha did not appear to be required.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2018

Mode of access: World Wide Web

ISBN: 9780494746417Subjects--Topical Terms:

673386
Physiology.
Index Terms--Genre/Form:

554714
Electronic books.

Molecular regulation of the adaptive response to exercise in human skeletal muscle.
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520 $a This thesis examined the molecular regulation and metabolic consequences of human skeletal muscle mitochondrial adaptations to exercise. The transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator (PGC)-1alpha has emerged as a critical regulator of exercise-induced mitochondrial) biogenesis and has been implicated in the pathogenesis of metabolic-related diseases such as type 2 diabetes (T2D). The mechanisms of how PGC-1alpha might regulate the muscle adaptive response to exercise are not well defined. At rest, the majority of PGC-1alpha was detected in cytosolic fractions prepared from human skeletal muscle biopsy samples. In response to both acute endurance (90 min &sim;65% maximal oxygen uptake [VO2peak]) and high-intensity interval exercise (4 x 30-s "all-out" Wingate tests), there was an increase in nuclear PGC-1alpha abundance yet no change in total PGC-1alpha protein. Acute exercise increased the activation of cytosolic p38 mitogen activated protein kinase (p38 MAPK) and 5'-AMP activated protein kinase (AMPK), which are both proposed activators of PGC-1alpha. The increase in nuclear PGC-1alpha after interval exercise also coincided with increased mRNA expression of mitochondrial genes. Two weeks of low-volume high-intensity interval training (HIT), consisting of 6 sessions of 8-12 x 1-min &sim;100% VO2peak; increased nuclear PGC-1alpha, markers of skeletal muscle mitochondrial content, and exercise performance in young, healthy men. A similar low-volume HIT protocol (6 sessions of 10 x 1-min &sim;95% VO2peak) improved mitochondrial capacity, functional performance, and glycemic regulation in individuals with T2D and pre-diabetes but had no effect on nuclear or total PGC-1alpha protein content. These findings indicate that acute exercise may activate mitochondrial biogenesis by a mechanism involving increased nuclear PGC-1alpha abundance. Two weeks of practical low-volume HIT is an effective strategy to improve mitochondrial capacity and glycemic regulation in individuals with, and at risk for, T2D, but a sustained increase in PGC-1alpha did not appear to be required.
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