Department of Basic Medical Sciences, Gülhane Faculty of Dentistry, University of Health Sciences, Ankara, Turkey
Department of Physiology, Faculty of Medicine, Gazi University, Ankara, Turkey
Turk J Med Sci. 2021 Aug 30;51(4):2185-2192. doi: 10.3906/sag-2011-323.
BACKGROUND/AIM: Physical exercise is a state of physiological stress that requires adaptation of the organism to physical activity. Glycogen is an important and essential energy source for muscle contraction. Skeletal muscle and liver are two important glycogen stores, and the energy required to maintain exercise in rodents are provided by destruction of this glycogen depot. In this study, the effects of endogenous opioid peptide antagonism at the central nervous system level on tissue glycogen content after exhaustive exercise were investigated.
Rats had intracerebroventricularly (icv) received nonspecific opioid peptide receptor antagonist, naloxone (50 μg/10 μL in saline) and δ-opioid receptor-selective antagonist naltrindole (50 μg/10 μL in saline) and then exercised till exhaustion. After exhaustion, skeletal muscle, heart, and liver were excised immediately.
Both opioid peptide antagonists decreased glycogen levels in skeletal muscle. Although, in soleus muscle, this decrease was not statistically significant (p > 0.05), in gastrocnemius muscle, it was significant in the icv naloxone administered group compared with control (p < 0.05). Heart glycogen levels increased significantly in both naloxone and naltrindole groups compared to control and sham-operated groups (p < 0.05). Heart glycogen levels were higher in the naloxone group than naltrindole (p < 0.05). Liver glycogen levels were elevated significantly with icv naloxone administration compared with the control group (p < 0.05). Glycogen levels in the naloxone group was also significantly higher than the naltrindole group (p < 0.05).
Our findings indicate that icv administered opioid peptide antagonists may play a role in glycogen metabolism in peripheral tissues such as skeletal muscle, heart, and liver.
背景/目的：体育锻炼是一种生理应激状态，需要机体适应体力活动。糖原是肌肉收缩的重要和必需能量来源。骨骼肌和肝脏是两种重要的糖原储存库，啮齿动物维持运动所需的能量由破坏该糖原库提供。本研究探讨了中枢神经系统水平内源性阿片肽拮抗作用对剧烈运动后组织糖原含量的影响。
大鼠经侧脑室（icv）给予非特异性阿片肽受体拮抗剂纳洛酮（生理盐水 50μg/10μL）和δ-阿片受体选择性拮抗剂纳曲吲哚（生理盐水 50μg/10μL），然后进行力竭运动。力竭后，立即取出骨骼肌、心脏和肝脏。
两种阿片肽拮抗剂均降低了骨骼肌中的糖原水平。虽然在比目鱼肌中，这种降低没有统计学意义（p>0.05），但在腓肠肌中，与对照组相比，icv 纳洛酮给药组的降低有统计学意义（p<0.05）。与对照组和假手术组相比，纳洛酮和纳曲吲哚组的心脏糖原水平均显著升高（p<0.05）。纳洛酮组的心脏糖原水平高于纳曲吲哚组（p<0.05）。与对照组相比，icv 给予纳洛酮后肝糖原水平显著升高（p<0.05）。纳洛酮组的糖原水平也明显高于纳曲吲哚组（p<0.05）。
我们的发现表明，icv 给予的阿片肽拮抗剂可能在骨骼肌、心脏和肝脏等外周组织的糖原代谢中发挥作用。
