American Journal of Physiology

ArticleTHE POSSIBLE MECHANISMS OF CONTRACTING AND PAYING THE OXYGEN DEBT AND THE RÔLE OF LACTIC ACID IN MUSCULAR CONTRACTIONR. Margaria, H. T. Edwards, and D. B. DillR. MargariaFrom the Fatique Laboratory, Morgan Hall, Harvard University, BostonFrom the Fatigue Laboratory, Morgan Hall, Harvard University, Boston, H. T. EdwardsFrom the Fatique Laboratory, Morgan Hall, Harvard University, BostonFrom the Fatigue Laboratory, Morgan Hall, Harvard University, Boston, and D. B. DillFrom the Fatique Laboratory, Morgan Hall, Harvard University, BostonFrom the Fatigue Laboratory, Morgan Hall, Harvard University, BostonPublished Online:30 Nov 1933https://doi.org/10.1152/ajplegacy.1933.106.3.689MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByLactate as a myokine and exerkine: drivers and signals of physiology and metabolismGeorge A. Brooks, Adam D. Osmond, Jose A. Arevalo, Justin J. Duong, Casey C. Curl, Diana D. Moreno-Santillan, and Robert G. 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Robergs, Farzenah Ghiasvand, and Daryl Parker1 September 2004 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 287, No. 3High-speed running performance: a new approach to assessment and predictionMatthew W. Bundle, Reed W. Hoyt, and Peter G. Weyand1 November 2003 | Journal of Applied Physiology, Vol. 95, No. 5Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exerciseMichelle L. Parolin, Alan Chesley, Mark P. Matsos, Lawrence L. Spriet, Norman L. Jones, and George J. F. Heigenhauser1 November 1999 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 277, No. 5O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exerciseBarry W. Scheuermann, John M. Kowalchuk, Donald H. Paterson, and David A. Cunningham1 October 1998 | Journal of Applied Physiology, Vol. 85, No. 4Blood glucose turnover during high- and low-intensity exerciseD. M. Cooper, T. J. Barstow, A. Bergner, and W. N. Lee1 September 1989 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 257, No. 3 More from this issue > Volume 106Issue 3November 1933Pages 689-715 Copyright & PermissionsCopyright © 1933 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1933.106.3.689History Received 27 August 1933 Published online 30 November 1933 Published in print 30 November 1933 Metrics

R. Margaria

H. T. Edwards

D. B. Dill

American Journal of Physiology-Legacy Content

THE POSSIBLE MECHANISMS OF CONTRACTING AND PAYING THE OXYGEN DEBT AND THE RÔLE OF LACTIC ACID IN MUSCULAR CONTRACTION

氧债形成与偿还的可能机制及乳酸在肌肉收缩中的作用

Modgil Amit

Zhang Qi

Pingili Ajeeth

Singh Neha

Yao Fanrong

GE Jingyan

Guo Lirong

Xuan Chengluan

T O’Rourke Stephen

Sun Chengwen

アンジオテンシン-(1-7)は自然発症高血圧ラットニューロンにおけるPTENの刺激を介してアンジオテンシンIIに対する変時性反応を減弱する

血管紧张素-(1-7)通过刺激自发性高血压大鼠神经元中的PTEN减弱对血管紧张素II的变时性反应

Kim Sang Hyun

Asaka Meiko

Higashida Kazuhiko

Takahashi Yumiko

O Holloszy John

Han Dong-Ho

骨格筋においてβ-アドレナリン作動性刺激はp38 MAPキナーゼを活性化およびPGC-1αを誘発しない

在骨骼肌中，β-肾上腺素能刺激不会激活p38 MAP激酶并诱导PGC-1α。

Zhang Xi

Zhou Qiaoling

Chen Lihe

Berger Stefan

WU Hongyu

Xiao Zhou

Pearce David

Zhou Xiaodong

Zhang Wenzheng

鉱質コルチコイド受容体はDot1a-Af9複合体に拮抗して,αENaC転写を増加させる

矿物皮质激素受体通过拮抗Dot1a-Af9复合体，增加αENaC转录。

Lima Roberta

Yanes Licy L

Davis Deborah D

Reckelhoff Jane F

老齢の自発性高血圧雌ラットにおける高血圧の媒介に20-HETE,アンジオテンシンIIおよびエンドセリンが果たす役割

自发性高血压老年雌性大鼠中20-HETE、血管紧张素II和内皮素在高血压介导中的作用

公尊 渋江

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion

脂肪酸结合蛋白5通过调节肠内分泌K细胞在脂肪摄入后分泌的胃抑制多肽来调控饮食诱导的肥胖

脂肪酸结合蛋白5通过脂肪摄入引起的肠内分泌K细胞分泌GIP调控饮食诱导的肥胖

脂肪酸结合蛋白5通过调节脂肪摄入引起的肠内分泌K细胞分泌GIP来调控饮食诱导的肥胖

Publication Information	Publisher: American Physiological Society，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1945，Proportion of original research papers: 0.00%，Self Citation Rate:N.A.， Gold OA Rate: 0.00%
Average recruitment ratio	网友分享经验：容易

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THE POSSIBLE MECHANISMS OF CONTRACTING AND PAYING THE OXYGEN DEBT AND THE RÔLE OF LACTIC ACID IN MUSCULAR CONTRACTION

アンジオテンシン-(1-7)は自然発症高血圧ラットニューロンにおけるPTENの刺激を介してアンジオテンシンIIに対する変時性反応を減弱する

骨格筋においてβ-アドレナリン作動性刺激はp38 MAPキナーゼを活性化およびPGC-1αを誘発しない

鉱質コルチコイド受容体はDot1a-Af9複合体に拮抗して,αENaC転写を増加させる

老齢の自発性高血圧雌ラットにおける高血圧の媒介に20-HETE,アンジオテンシンIIおよびエンドセリンが果たす役割

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion

Fatty acid-binding protein 5 regulates diet-induced obesity via GIP secretion from enteroendocrine K cells in response to fat ingestion