期刊
SPORTS MEDICINE
卷 35, 期 7, 页码 575-583出版社
ADIS INTERNATIONAL LTD
DOI: 10.2165/00007256-200535070-00003
关键词
-
资金
- NIDDK NIH HHS [R01-DK-50277] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK050277] Funding Source: NIH RePORTER
Under normal healthy conditions, exercise initiates simultaneous elevations in hepatic glucose production (glucose R-a) and glucose utilisation. As a result, circulating glucose levels are maintained at a relatively constant level. This relatively simple and effective relationship between the liver and the skeletal muscle is maintained by a complex interplay of circulating and locally released neuroendocrine controllers. In large part, exercise-induced changes in the pancreatic secretion of glucagon and insulin are primarily responsible for the stimulation of glucose R-a during moderate exercise., However, exercise imposed on an additional metabolic stress (heavy exercise and poorly controlled diabetes mellitus) can increase sympathetic drive and has been suggested for decades to play a significant role in glucoregulation. In addition, blood-borne feedback and afferent reflex mechanisms may further modulate the glucose R-a response to exercise. This article discusses new findings from novel animal and human experiments specifically designed to examine the regulatory components of the neuroendocrine system and their influence on glucoregulation during exercise.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据