Department of Biomedical Sciences, University of Padova, Padova, ITALY.
Med Sci Sports Exerc. 2024 Sep 1;56(9):1830-1839. doi: 10.1249/MSS.0000000000003473. Epub 2024 May 1.
Prior evidence has shown that neural factors contribute to the loss of muscle force after skeletal muscle disuse. However, little is known about the specific neural mechanisms altered by disuse. Persistent inward current (PIC) is an intrinsic property of motoneurons responsible for prolonging and amplifying the synaptic input, proportionally to the level of neuromodulation, thus influencing motoneuron discharge rate and force production. Here, we hypothesized that short-term unilateral lower limb suspension (ULLS) would reduce the neuromodulatory input associated with PIC, contributing to the reduction of force generation capacity. In addition, we tested whether physical exercise would restore the force generation capacity by reestablishing the initial level of neuromodulatory input.
In 12 young adults, we assessed maximal voluntary contraction pre- and post-10 d of ULLS and after 21 d of active recovery (AR) based on resistance exercise. PIC was estimated from high-density surface electromyograms of the vastus lateralis muscle as the delta frequency (Δ F ) of paired motor units calculated during isometric ramped contractions.
The values of Δ F were reduced after 10 d of ULLS (-33%, P < 0.001), but were fully reestablished after the AR (+29.4%, P < 0.001). The changes in estimated PIC values were correlated ( r = 0.63, P = 0.004) with the reduction in maximal voluntary contraction after ULLS (-29%, P = 0.002) and its recovery after the AR (+28.5%, P = 0.003).
Our findings suggest that PIC estimates are reduced by muscle disuse and may contribute to the loss of force production and its recovery with exercise. Overall, this is the first study demonstrating that, in addition to peripheral neuromuscular changes, central neuromodulation is a major contributor to the loss of force generation capacity after disuse, and can be recovered after resistance exercise.
先前的证据表明，神经因素会导致骨骼肌废用后肌肉力量的丧失。然而，对于废用引起的特定神经机制知之甚少。内向电流（PIC）是运动神经元的固有特性，负责延长和放大突触输入，与神经调制水平成正比，从而影响运动神经元的放电率和力的产生。在这里，我们假设短期单侧下肢悬吊（ULLS）会降低与 PIC 相关的神经调制输入，导致力产生能力下降。此外，我们还测试了运动是否可以通过重建初始神经调制输入来恢复力产生能力。
在 12 名年轻成年人中，我们在 10 天 ULLS 后和 21 天基于阻力运动的主动恢复（AR）后评估了最大自主收缩。通过对股外侧肌高密度表面肌电图的分析，我们将等长斜坡收缩期间计算的成对运动单位的频率差（Δ F）估计为 PIC。
ULLS 后 10 天，Δ F 值降低（-33%，P < 0.001），但 AR 后完全恢复（+29.4%，P < 0.001）。PIC 值的变化与 ULLS 后最大自主收缩的减少（-29%，P = 0.002）及其 AR 后的恢复（+28.5%，P = 0.003）相关（r = 0.63，P = 0.004）。
我们的研究结果表明，PIC 估计值因肌肉废用而降低，可能导致力产生减少及其在运动后的恢复。总体而言，这是第一项表明除了周围神经肌肉变化外，中枢神经调制也是废用后力产生能力丧失的主要原因，并可以通过阻力运动来恢复的研究。
