Mancinelli Rosa, Toniolo Luana, Di Filippo Ester Sara, Doria Christian, Marrone Mariangela, Maroni Camilla Reina, Verratti Vittore, Bondi Danilo, Maccatrozzo Lisa, Pietrangelo Tiziana, Fulle Stefania
Department of Neuroscience Imaging and Clinical Sciences, 'G. d'Annunzio' University of Chieti-Pescara, Chieti, Italy.
Interuniversity Institute of Myology, Rome, Italy.
Front Physiol. 2019 Nov 27;10:1459. doi: 10.3389/fphys.2019.01459. eCollection 2019.
Skeletal muscle aging is a multifactorial process strictly related to progressive weakness. One of the results that were focused on was the fiber phenotype modification and their loss. The physiological muscle recruitment to contraction, basically prosecuted under volitional control, can also be engaged by means of Neuromuscular Electrical Stimulation (NMES). Knowing that the NMES is effective in improving muscle strength in active healthy elderly, the aim was to investigate which physiological modifications were able to produce in the muscle and the pathways involved. It was found that NMES increased the cross sectional area and the isometric strength of type II myofibers together with the activated myogenic pathway in order to shift glycolytic toward the oxidative phenotype II myofibers, at a molecular level and with an increase of maximal voluntary contraction (MVC) at a functional level. Using the TaqMan low density array on 48 different genes, we found that NMES specific gene regulation highlighted: (i) increased protein synthesis with respect to protein degradation; (ii) the activation of an apoptotic pathway involved in the differentiation process; (iii) increased regeneration signals; (iv) oxidative enzyme regulation. These pathways were validated via confirmatory RT-PCR for genes involved in the regeneration process as well as Myosin isoforms. We also investigated the oxidative stress status analyzing superoxide anion levels, the protein expression of two different superoxide dismutase and the activity of both catalase and superoxide anion dismutase, being two main antioxidant enzymes. In conclusion, data demonstrates that NMES is effective in producing physiological adaptation on of active healthy elderly as well as providing new insights for further research on elderly who experienced muscle detriment for periodic or permanent immobility.
骨骼肌老化是一个与进行性肌无力密切相关的多因素过程。其中一个重点关注的结果是纤维表型改变及其丢失。生理状态下肌肉从募集到收缩,基本上受意志控制,也可通过神经肌肉电刺激(NMES)来实现。鉴于NMES能有效改善健康活跃老年人的肌肉力量,本研究旨在探究其在肌肉中能产生哪些生理改变以及涉及哪些途径。研究发现,NMES增加了II型肌纤维的横截面积和等长力量,并激活了生肌途径,从而在分子水平上使糖酵解型II型肌纤维向氧化型表型转变,在功能水平上增加了最大自主收缩(MVC)。通过TaqMan低密度芯片检测48个不同基因,我们发现NMES特异性基因调控表现为:(i)蛋白质合成相对于蛋白质降解增加;(ii)参与分化过程的凋亡途径激活;(iii)再生信号增加;(iv)氧化酶调控。这些途径通过对参与再生过程的基因以及肌球蛋白亚型进行验证性逆转录聚合酶链反应(RT-PCR)得以证实。我们还通过分析超氧阴离子水平、两种不同超氧化物歧化酶的蛋白表达以及过氧化氢酶和超氧阴离子歧化酶的活性(这两种是主要的抗氧化酶)来研究氧化应激状态。总之,数据表明NMES能有效促使健康活跃老年人产生生理适应性改变,同时为进一步研究因周期性或永久性活动受限而肌肉受损的老年人提供了新的见解。