Ganjayi Muni Swamy, Frank Samuel W, Krauss Thomas A, York Michael L, Bloch Robert J, Baumann Cory W
Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, United States.
Ohio Musculoskeletal and Neurological Institute, Ohio University, Athens, Ohio, United States.
J Appl Physiol (1985). 2024 Oct 1;137(4):903-909. doi: 10.1152/japplphysiol.00496.2024. Epub 2024 Aug 22.
The molecular mechanisms that drive muscle adaptations after eccentric exercise training are multifaceted and likely impacted by age. Previous studies have reported that many genes and proteins respond differently in young and older muscles following training. Keratin 18 (Krt18), a cytoskeletal protein involved in force transduction and organization, was found to be upregulated after muscles performed repeated bouts of eccentric contractions, with higher levels observed in young muscle compared with older muscle. Therefore, the purpose of this study was to determine if Krt18 mediates skeletal muscle adaptations following eccentric exercise training. The anterior crural muscles of Krt18 knockout (KO) and wild-type (WT) mice were subjected to either a single bout or repeated bouts of eccentric contractions, with isometric torque assessed across the initial and final bouts. Functionally, Krt18 KO and WT mice did not differ prior to performing any eccentric contractions ( ≥ 0.100). Muscle strength (tetanic isometric torques) and the ability to adapt to eccentric exercise training were also consistent across strains at all time points ( ≥ 0.169). Stated differently, immediate strength deficits and the recovery of strength following a single bout or multiple bouts of eccentric contractions were similar between Krt18 KO and WT mice. In summary, the absence of Krt18 does not impede the muscle's ability to adapt to repeated eccentric contractions, suggesting it is not essential for exercise-induced remodeling. The molecular processes that underlie the changes in skeletal muscle following eccentric exercise training are complex and involve multiple factors. Our findings indicate that Krt18 may not play a significant role in muscle adaptations following eccentric exercise training, likely due to its low expression in skeletal muscle. These results underscore the complexity of the molecular mechanisms that contribute to muscle plasticity and highlight the need for further research in this area.
离心运动训练后驱动肌肉适应性变化的分子机制是多方面的，并且可能受到年龄的影响。先前的研究报道，许多基因和蛋白质在训练后的年轻和老年肌肉中的反应有所不同。角蛋白18（Krt18）是一种参与力传导和组织的细胞骨架蛋白，发现在肌肉进行反复的离心收缩后会上调，与老年肌肉相比，在年轻肌肉中观察到的水平更高。因此，本研究的目的是确定Krt18是否介导离心运动训练后的骨骼肌适应性变化。对Krt18基因敲除（KO）小鼠和野生型（WT）小鼠的股前肌进行单次或反复的离心收缩，在最初和最后一次收缩过程中评估等长扭矩。在功能上，Krt18 KO小鼠和WT小鼠在进行任何离心收缩之前没有差异（≥0.100）。在所有时间点，各品系间的肌肉力量（强直等长扭矩）和适应离心运动训练的能力也一致（≥0.169）。换句话说，Krt18 KO小鼠和WT小鼠在单次或多次离心收缩后的即时力量缺陷和力量恢复情况相似。总之，Krt18的缺失并不妨碍肌肉适应反复离心收缩的能力，这表明它对于运动诱导的重塑并非必不可少。离心运动训练后骨骼肌变化背后的分子过程是复杂的，涉及多个因素。我们的研究结果表明，Krt18可能在离心运动训练后的肌肉适应中不发挥重要作用，这可能是由于其在骨骼肌中的低表达。这些结果强调了导致肌肉可塑性的分子机制的复杂性，并突出了该领域进一步研究的必要性。
