Effects of elevated H+ and Pi on the contractile mechanics of skeletal muscle fibres from young and old men: implications for muscle fatigue in humans.
Effects of elevated H+ and Pi on the contractile mechanics of skeletal muscle fibres from young and old men: implications for muscle fatigue in humans.
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H 和 Pi 升高对年轻和老年男性骨骼肌纤维收缩力学的影响：对人类肌肉疲劳的影响。
DOI：
10.1113/jp276018
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Fitts,RobertH
中科院分区：
文献类型：
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作者：
Sundberg,ChristopherW;Hunter,SandraK;Trappe,ScottW;Smith,CarolynS;Fitts,RobertH
随着年龄的增长，肌肉力量的损失和疲劳性的增加的机制还没有得到解决。我们表明，与年轻人相比，老年人股外侧肌纤维的收缩力学得到了很好的保护，但是，快速肌球蛋白重链II肌肉的选择性丢失与年龄相关的全肌肉力量和功率下降密切相关。和无机磷酸盐（Pi）是人体肌肉疲劳的重要介质，通过抑制跨桥循环和峰值功率的低到高力状态，但这些离子对跨桥功能的抑制作用在年轻人和老年人的纤维中相似。这些发现表明，与年龄相关的肌肉力量损失主要是由快纤维的萎缩决定的，但与年龄相关的疲劳性增加不能解释的交叉桥H+和Pi的敏感性增加。AbstractThe目前的研究旨在确定的机制，负责在肌肉力量的损失和疲劳性增加与老化的整体肌肉功能的措施与单纤维收缩力学。在调整老年人（73-89岁，n =6）的肌肉质量比年轻人（20-29岁，n =6）小22%之后，膝伸肌的等长扭矩和功率输出分别随年龄降低38%和53%。随着年龄的增长，可收缩性增加了2.7倍，并且与电诱发收缩特性的降低密切相关。为了测试跨桥机制是否可以解释膝关节伸肌功能的年龄相关性减退，我们将股外侧肌的肌纤维（n =254）暴露于模拟静止肌肉和酸中毒（H+）（pH 6.2）和无机磷酸盐（Pi）（30 mm）疲劳水平的条件下。模拟疲劳条件导致力显著降低，速度和功率缩短，并抑制跨桥循环的低到高力状态，证实了非人类研究的结果，即这些离子协同作用，损害跨桥功能。除了与年龄相关的快速纤维严重萎缩（-55%），收缩功能和疲劳模拟条件的抑郁作用在年轻人和老年人的纤维中没有差异。快速肌球蛋白重链II肌肉的选择性丢失与年龄相关的等长扭矩（r= 0.785）和功率（r= 0.861）降低密切相关。这些数据表明，与年龄相关的肌肉力量和力量损失主要是由快纤维的萎缩决定的，但与年龄相关的疲劳性增加不能用横桥对H+和Pi的敏感性增加来解释。
Key pointsThe mechanisms responsible for the loss in muscle power and increased fatigability with ageing are unresolved.We show that the contractile mechanics of fibres from the vastus lateralis of old men were well‐preserved compared to those of young men, but the selective loss of fast myosin heavy chain II muscle was strongly associated with age‐related decrements in whole‐muscle strength and power.We reveal that the combination of acidosis (H+) and inorganic phosphate (Pi) is an important mediator of muscle fatigue in humans by inhibiting the low‐ to high‐force state of the cross‐bridge cycle and peak power, but the depressive effects of these ions on cross‐bridge function were similar in fibres from young and old men.These findings suggest that the age‐related loss in muscle power is primarily determined by the atrophy of fast fibres, but the age‐related increased fatigability cannot be explained by an increased sensitivity of the cross‐bridge to H+and Pi.AbstractThe present study aimed to identify the mechanisms responsible for the loss in muscle power and increased fatigability with ageing by integrating measures of whole‐muscle function with single fibre contractile mechanics. After adjusting for the 22% smaller muscle mass in old (73–89 years,n =6) compared to young men (20–29 years,n =6), isometric torque and power output of the knee extensors were, respectively, 38% and 53% lower with age. Fatigability was ∼2.7‐fold greater with age and strongly associated with reductions in the electrically‐evoked contractile properties. To test whether cross‐bridge mechanisms could explain age‐related decrements in knee extensor function, we exposed myofibres (n =254) from the vastus lateralis to conditions mimicking quiescent muscle and fatiguing levels of acidosis (H+) (pH 6.2) and inorganic phosphate (Pi) (30 mm). The fatigue‐mimicking condition caused marked reductions in force, shortening velocity and power and inhibited the low‐ to high‐force state of the cross‐bridge cycle, confirming findings from non‐human studies that these ions act synergistically to impair cross‐bridge function. Other than severe age‐related atrophy of fast fibres (−55%), contractile function and the depressive effects of the fatigue‐mimicking condition did not differ in fibres from young and old men. The selective loss of fast myosin heavy chain II muscle was strongly associated with the age‐related decrease in isometric torque (r= 0.785) and power (r= 0.861). These data suggest that the age‐related loss in muscle strength and power are primarily determined by the atrophy of fast fibres, but the age‐related increased fatigability cannot be explained by an increased sensitivity of the cross‐bridge to H+and Pi.