Exercise Physiology Research Center, Life Style Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Department of Physical Education and Sport Sciences, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Gene. 2023 Dec 15;887:147732. doi: 10.1016/j.gene.2023.147732. Epub 2023 Aug 23.
Sleep deprivation disrupt the circadian clock and exercise performance. Defective oxidative stress caused by sleep deprivation may affect the expression of genes involved in cell apoptosis. Since a number of studies have shown the anti-apoptotic effect of L-arginine, so the aim of this study was to evaluate the effect of eight weeks of L-arginine supplementation on the expression of brain and muscle ARNT-like protein 1 (BMAL1), cell cycle and apoptosis regulator 2 (CCAR2), and BAX and BCL2 genes during sleep deprivation and acute anaerobic exercise. Participants included 20 healthy men age 26-35 years, randomized into the L-arginine intervention group (n = 10) and a placebo control (n = 10). The running-based anaerobic sprint test (RAST) was used for anaerobic exercise. Intervention subjects took one 1000 mg L-arginine tablet daily for 8 weeks. The Real-Time PCR method was used to determine apoptosis gene expression in peripheral blood mononuclear cells (PBMCs). Acute anaerobic exercise and sleep deprivation both increased the expression of BAX and CCAR2 genes, and decreased the expression of BCL2 and BMAL1 genes (p < 0.05 for all). L-arginine supplementation increased the expression of BMAL1 and BCL2 genes and decreased the expression of BAX and CCAR2 genes relative to control (p < 0.05). L-Arginine controlled the increase in expression of BAX and CCAR2 genes and the decrease in expression of BCL2 and BMAL1 genes in response to sleep deprivation and acute anaerobic exercise (p < 0.05). Our results showed that 24-hour sleep deprivation and acute anaerobic exercise increased the expression of pro-apoptotic genes (BAX and CCAR2) and decreased the expression of anti-apoptotic genes (BCL2 and BMAL1), although the effect of sleep deprivation is greater. In this situation, L-arginine supplementation may balance the apoptotic state of peripheral blood mononuclear cells. However, any recommendation about this needs further research.
睡眠剥夺会破坏生物钟和运动表现。睡眠剥夺引起的氧化应激缺陷可能会影响细胞凋亡相关基因的表达。由于许多研究表明 L-精氨酸具有抗细胞凋亡作用，因此本研究旨在评估补充 L-精氨酸 8 周对睡眠剥夺和急性无氧运动期间脑和肌肉 ARNT 样蛋白 1 (BMAL1)、细胞周期和凋亡调节因子 2 (CCAR2)和 BAX 和 BCL2 基因表达的影响。参与者包括 26-35 岁的 20 名健康男性，随机分为 L-精氨酸干预组（n=10）和安慰剂对照组（n=10）。基于跑步的无氧冲刺测试（RAST）用于无氧运动。干预组每天服用一片 1000 毫克 L-精氨酸片，持续 8 周。实时 PCR 方法用于测定外周血单个核细胞（PBMCs）中凋亡基因的表达。急性无氧运动和睡眠剥夺均增加了 BAX 和 CCAR2 基因的表达，并降低了 BCL2 和 BMAL1 基因的表达（所有 p<0.05）。与对照组相比，L-精氨酸补充增加了 BMAL1 和 BCL2 基因的表达，并降低了 BAX 和 CCAR2 基因的表达（p<0.05）。L-精氨酸控制了睡眠剥夺和急性无氧运动引起的 BAX 和 CCAR2 基因表达增加以及 BCL2 和 BMAL1 基因表达降低（p<0.05）。我们的结果表明，24 小时睡眠剥夺和急性无氧运动增加了促凋亡基因（BAX 和 CCAR2）的表达，降低了抗凋亡基因（BCL2 和 BMAL1）的表达，尽管睡眠剥夺的影响更大。在这种情况下，L-精氨酸补充可能会平衡外周血单个核细胞的凋亡状态。然而，关于这一点的任何建议都需要进一步的研究。
