Lomonosova Yulia N, Shenkman Boris S, Kalamkarov Grigorii R, Kostrominova Tatiana Y, Nemirovskaya Tatyana L
Institute for Bio-Medical Problems, RAS, Moscow, Russia.
Emanuel Institute of Biochemical Physics, RAS, Moscow, Russia.
PLoS One. 2014 Apr 15;9(4):e94448. doi: 10.1371/journal.pone.0094448. eCollection 2014.
Eccentric exercise is known to disrupt sarcolemmal integrity and induce damage of skeletal muscle fibers. We hypothesized that L-arginine (L-Arg; nitric oxide synthase (NOS) substrate) supplementation prior to a single bout of eccentric exercise would diminish exercise-induced damage. In addition, we used N-nitro-L-arginine methyl ester hydrochloride (L-NAME; NOS inhibitor) to clarify the role of native NOS activity in the development of exercise-induced muscle damage. Rats were divided into four groups: non-treated control (C), downhill running with (RA) or without (R) L-Arg supplementation and downhill running with L-NAME supplementation (RN). Twenty four hours following eccentric exercise seven rats in each group were sacrificed and soleus muscles were dissected and frozen for further analysis. The remaining seven rats in each group were subjected to the exercise performance test. Our experiments showed that L-Arg supplementation prior to a single bout of eccentric exercise improved subsequent exercise performance capacity tests in RA rats when compared with R, RN and C rats by 37%, 27% and 13%, respectively. This outcome is mediated by L-Arg protection against post-exercise damage of sarcolemma (2.26- and 0.87-fold less than R and RN groups, respectively), reduced numbers of damaged muscle fibers indicated by the reduced loss of desmin content in the muscle (15% and 25% less than R and RN groups, respectively), and diminished µ-calpain mRNA up-regulation (42% and 30% less than R and RN groups, respectively). In conclusion, our study indicates that L-Arg supplementation prior to a single bout of eccentric exercise alleviates muscle fiber damage and preserves exercise performance capacity.
已知离心运动可破坏肌膜完整性并导致骨骼肌纤维损伤。我们推测,在单次离心运动前补充L-精氨酸(L-Arg;一氧化氮合酶(NOS)底物)可减轻运动诱导的损伤。此外,我们使用盐酸N-硝基-L-精氨酸甲酯(L-NAME;NOS抑制剂)来阐明内源性NOS活性在运动诱导的肌肉损伤发生过程中的作用。将大鼠分为四组:未处理的对照组(C)、补充L-Arg进行下坡跑的组(RA)、不补充L-Arg进行下坡跑的组(R)以及补充L-NAME进行下坡跑的组(RN)。离心运动24小时后,每组处死7只大鼠,解剖比目鱼肌并冷冻以备进一步分析。每组其余7只大鼠进行运动性能测试。我们的实验表明,与R组、RN组和C组相比,单次离心运动前补充L-Arg可使RA组大鼠随后的运动性能测试能力分别提高37%、27%和13%。这一结果是由L-Arg对运动后肌膜损伤的保护作用介导的(分别比R组和RN组少2.26倍和0.87倍),肌肉中结蛋白含量损失减少表明受损肌纤维数量减少(分别比R组和RN组少15%和25%),以及μ-钙蛋白酶原mRNA上调减少(分别比R组和RN组少42%和30%)。总之,我们的研究表明,单次离心运动前补充L-Arg可减轻肌纤维损伤并保持运动性能。