The suppression of tumor necrosis factor-alpha production in response to pathogen stimulation by strenuous exercise and underlying mechanisms
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- Yano Hiromi
- Department of Health and Sports Science, Kawasaki University of Medical Welfare
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- Uchida Masataka
- Department of Health and Sports Science, Kawasaki University of Medical Welfare
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- Oyanagi Eri
- Department of Health Promotion and Exercise, National Institute of Health and Nutrition
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- Kawanishi Noriaki
- Graduate School of Sport Sciences, Waseda University
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- Shiva Daisuke
- Department of Health Science, Kurashiki University of Science and the Arts
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- Kitamura Hiromi
- Exercise Physiology Laboratory, Wayo Women's University
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In general, physical activity reduces the risk of cancer and infectious diseases. However, strenuous exercise has been shown to transiently increase the risk of infection, and this is referred to as the “open window.” Indeed, intense exercise reduces the concentrations of several cytokines in plasma in response to pathogens. The mechanisms responsible for this observation may depend on exercise-induced increased stress hormone secretion, especially that of catecholamines. Exercise-induced catecholamines, acting through β-adrenergic receptors, have been found to be responsible for exercise-induced suppression of plasma tumor necrosis factor-alpha (TNF-α) after lipopolysaccharide (LPS) administration. In the signaling mechanisms of cells, there are no changes in the surface expression of Toll-like receptor (TLR) 4. Although there are also no changes in the LPS-induced TNF-α mRNA expression in tissues after exercise, the TNF-α content in the tissues of exercised animals is lower than that in the tissues of non-exercised animals. Therefore, a strenuous exercise-induced reduction in plasma TNF-α concentration, despite pathogen stimulation, depends on the translation of TNF-α in tissues.
収録刊行物
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- The Journal of Physical Fitness and Sports Medicine
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The Journal of Physical Fitness and Sports Medicine 1 (4), 645-653, 2012
一般社団法人日本体力医学会
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詳細情報 詳細情報について
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- CRID
- 1390282680392255744
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- NII論文ID
- 10031159001
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- NII書誌ID
- AA12573156
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- ISSN
- 21868123
- 21868131
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- NDL書誌ID
- 024139941
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可