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运动和糖原耗竭对肌肉中糖异生的影响。

Effects of exercise and glycogen depletion on glyconeogenesis in muscle.

作者信息

Bonen A, Homonko D A

机构信息

Department of Kinesiology, University of Waterloo, Ontario, Canada.

出版信息

J Appl Physiol (1985). 1994 Apr;76(4):1753-8. doi: 10.1152/jappl.1994.76.4.1753.

Abstract

In the present study, we investigated the hypotheses that 1) skeletal muscle glyconeogenesis will increase after exercise, 2) greater changes in glyconeogenesis will be observed after exercise in fast-twitch muscles than in slow-twitch muscles, and 3) glycogen repletion will reduce the rates of glyconeogenesis. Mouse soleus and extensor digitorum longus (EDL) glycogen depots were reduced to the same levels by treadmill exercise (60 min) or epinephrine injection (75 micrograms/100 g body wt ip). Untreated animals were used as controls. We were able to prevent glycogen repletion by incubating muscles in vitro with sorbitol (75 mM) and to increase glycogen concentrations in vitro by incubating muscles with glucose (75 mM). The experimental results showed that glyconeogenesis was increased by exercise (EDL, +51%; soleus, +82%) when glycogen levels were kept low. When glycogen depots were increased, the rate of glyconeogenesis was lowered in the exercised EDL (P < 0.05) but not in the soleus (P > 0.05). Reductions in muscle glycogen by epinephrine did not change the rate of glyconeogenesis in EDL, either when glycogen depots were kept low or were repleted (P > 0.05). In contrast, in the soleus, epinephrine-induced reductions in glycogen did stimulate glyconeogenesis (P < 0.05). Analyses in EDL showed that in nonexercised muscles glycogen concentrations were minimally effective in altering the rates of glyconeogenesis. A 30% decrement in glycogen increased glyconeogenesis by 5% in resting muscles, whereas the same decrement increased glyconeogenesis by 51% in exercised muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在本研究中,我们探讨了以下假设:1)运动后骨骼肌糖异生作用会增强;2)快肌运动后糖异生作用的变化比慢肌更显著;3)糖原补充会降低糖异生作用的速率。通过跑步机运动(60分钟)或注射肾上腺素(75微克/100克体重,腹腔注射),将小鼠比目鱼肌和趾长伸肌(EDL)的糖原储备降至相同水平。未处理的动物作为对照。我们通过在体外将肌肉与山梨醇(75 mM)孵育来防止糖原补充,并通过在体外将肌肉与葡萄糖(75 mM)孵育来增加糖原浓度。实验结果表明,当糖原水平保持较低时,运动可增加糖异生作用(EDL增加51%;比目鱼肌增加82%)。当糖原储备增加时,运动的EDL中糖异生作用速率降低(P<0.05),但比目鱼肌中未降低(P>0.05)。无论是糖原储备保持较低还是补充时,肾上腺素引起的肌肉糖原减少均未改变EDL中的糖异生作用速率(P>0.05)。相反,在比目鱼肌中,肾上腺素引起的糖原减少确实刺激了糖异生作用(P<0.05)。对EDL的分析表明,在未运动的肌肉中,糖原浓度对改变糖异生作用速率的影响最小。在静息肌肉中,糖原减少30%可使糖异生作用增加5%,而在运动肌肉中相同程度的减少可使糖异生作用增加51%。(摘要截短至250字)

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