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Exercise training prevents the infla...

Orth, Teresa A.

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Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules./
作者:	Orth, Teresa A.
面頁冊數:	174 p.
附註:	Adviser: Norberto C. Gonzalez.
Contained By:	Dissertation Abstracts International67-06B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3220361
ISBN:	9780542717352

Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules.
Orth, Teresa A.

Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules. - 174 p.

Adviser: Norberto C. Gonzalez.

Thesis (Ph.D.)--University of Kansas, 2006.

Systemic hypoxia produces a widespread inflammatory response characterized by an increased reactive oxygen species (ROS)/nitric oxide (NO) balance, mast cell degranulation (MCD), leukocyte adherence and emigration, and increased vascular permeability. Exercise training (ET) can have effects on NO synthases, antioxidants, circulating hormones, and immune system responses. The goals of this research were to determine the effects of ET on the inflammation of hypoxia, and to investigate the underlying mechanisms.

ISBN: 9780542717352Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules.
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245 1 0 $a Exercise training prevents the inflammatory response to hypoxia in locomotory and nonlocomotory skeletal muscle venules.
300 $a 174 p.
500 $a Adviser: Norberto C. Gonzalez.
500 $a Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 2909.
502 $a Thesis (Ph.D.)--University of Kansas, 2006.
520 $a Systemic hypoxia produces a widespread inflammatory response characterized by an increased reactive oxygen species (ROS)/nitric oxide (NO) balance, mast cell degranulation (MCD), leukocyte adherence and emigration, and increased vascular permeability. Exercise training (ET) can have effects on NO synthases, antioxidants, circulating hormones, and immune system responses. The goals of this research were to determine the effects of ET on the inflammation of hypoxia, and to investigate the underlying mechanisms.
520 $a ET prevented hypoxia-induced inflammation in the locomotory biceps femoris and the nonlocomotory cremaster indicating an effect independent of muscle contraction. Similar levels of tissue PO2, mechanical anti-adhesive forces, and blood leukocytes were seen in trained and untrained rats. No effect of ET on any of the NO synthase isoforms was detected. While ET led to increases in different antioxidants in each muscle, the nature of these changes suggests that increased antioxidant reserve may not be the only effect of ET. The inflammation induced by application of mast cell secretagogues was attenuated in exercise-trained rats; however, administration of mast cell-derived inflammatory mediators involved in the inflammation of hypoxia produced similar effects in ET and control rats. This suggests that ET acts at least in part at the mast cell level.
520 $a Recent data suggest that the inflammation of hypoxia may not be initiated by the local reduction in PO2 but by a circulating mediator released from a distant site that triggers inflammation independent of the local PO 2. This is supported by evidence of dissociation between local tissue PO2 and inflammation on one hand, and by the observation that topical application of plasma from hypoxic rats elicits inflammation in the normoxic cremaster on the other. Plasma obtained from hypoxic ET rats failed to produce inflammation in cremasters, suggesting that ET may modify the synthesis/release of the mediator, or alter the response of mast cells to the mediator.
520 $a In summary, ET prevents inflammation in locomotory and non locomotory muscles, suggesting a systemic mechanism of action. The effect of ET is not due to upregulation of NO synthases, or increase in antioxidant levels. On the other hand, the response of mast cells to hypoxia is attenuated by ET. A possible role of ET in the release/synthesis of a central mediator of inflammation is a future avenue of research.
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791 $a Ph.D.
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