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Molecular regulation of the adaptive...
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Little, Jonathan Peter.
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Molecular regulation of the adaptive response to exercise in human skeletal muscle.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Molecular regulation of the adaptive response to exercise in human skeletal muscle./
作者:
Little, Jonathan Peter.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2010,
面頁冊數:
116 p.
附註:
Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: 4478.
Contained By:
Dissertation Abstracts International72-08B.
標題:
Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR74641
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.
- Ann Arbor : ProQuest Dissertations & Theses, 2010 - 116 p.
Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: 4478.
Thesis (Ph.D.)--McMaster University (Canada), 2010.
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 ∼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 ∼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 ∼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.
ISBN: 9780494746417Subjects--Topical Terms:
518431
Physiology.
Molecular regulation of the adaptive response to exercise in human skeletal muscle.
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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 ∼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 ∼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 ∼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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