Movement-Interactions-Performance (MIP), UR-4334, Nantes Université, Nantes, UR-4334, France.
Toulouse NeuroImaging Center, Université de Toulouse, Inserm, UPS, Toulouse, France.
J Neurophysiol. 2024 Sep 1;132(3):890-905. doi: 10.1152/jn.00142.2024. Epub 2024 Jul 17.
The effectiveness of activated Ia afferents to discharge α-motoneurons is decreased during passive muscle lengthening compared with static and shortening muscle conditions. Evidence suggests that these regulations are explained by ) greater postactivation depression induced by homosynaptic postactivation depression (HPAD) and ) primary afferent depolarization (PAD). It remains uncertain whether muscle length impacts the muscle lengthening-related aspect of regulation of the effectiveness of activated Ia afferents to discharge α-motoneurons, HPAD, PAD, and heteronymous Ia facilitation (HF). We conducted a study involving 15 healthy young individuals. We recorded conditioned or nonconditioned soleus Hoffmann (H) reflex with electromyography (EMG) to estimate the effectiveness of activated Ia afferents to discharge α-motoneurons, HPAD, PAD, and HF during passive shortening, static, and lengthening muscle conditions at short, intermediate, and long lengths. Our results show that the decrease of effectiveness of activated Ia afferents to discharge α-motoneurons and increase of postactivation depression during passive muscle lengthening occur at all muscle lengths. For PAD and HF, we found that longer muscle length increases the magnitude of regulation related to muscle lengthening. To conclude, our findings support an inhibitory effect (resulting from increased postactivation depression) of muscle lengthening and longer muscle length on the effectiveness of activated Ia afferents to discharge α-motoneurons. The increase in postactivation depression associated with muscle lengthening can be attributed to the amplification of Ia afferents discharge. Original results are that in response to passive muscle lengthening and increased muscle length, inhibition of the effectiveness of activated Ia afferents to discharge α-motoneurons increases, with primary afferent depolarization and homosynaptic postactivation depression mechanisms playing central roles in this regulatory process. Our findings highlight for the first time a cumulative inhibitory effect of muscle lengthening and increased muscle length on the effectiveness of activated Ia afferents to discharge α-motoneurons.
在被动肌肉拉长时，与静态和缩短肌肉条件相比，激活 Ia 传入纤维对 α 运动神经元放电的有效性降低。有证据表明，这些调节可以通过 ) 由同源突触后激活抑制 (HPAD) 和 ) 初级传入纤维去极化 (PAD) 引起的更大的后激活抑制来解释。目前尚不清楚肌肉长度是否会影响激活 Ia 传入纤维对放电 α 运动神经元的有效性、HPAD、PAD 和异源性 Ia 易化 (HF) 的肌肉拉长相关调节方面。我们进行了一项涉及 15 名健康年轻人的研究。我们通过肌电图 (EMG) 记录条件反射或非条件反射的比目鱼肌 Hoffmann (H) 反射，以估计在被动缩短、静态和拉长肌肉条件下，在短、中和长长度时，激活 Ia 传入纤维对放电 α 运动神经元的有效性、HPAD、PAD 和 HF。我们的结果表明，在所有肌肉长度下，在被动肌肉拉长时，激活 Ia 传入纤维对放电 α 运动神经元的有效性降低和后激活抑制增加。对于 PAD 和 HF，我们发现更长的肌肉长度会增加与肌肉拉长相关的调节幅度。总之，我们的研究结果支持肌肉拉长和更长的肌肉长度对激活 Ia 传入纤维对放电 α 运动神经元的有效性的抑制作用（源自增加的后激活抑制）。与肌肉拉长相关的后激活抑制的增加可以归因于 Ia 传入纤维放电的放大。原始结果表明，响应于被动肌肉拉长和增加的肌肉长度，激活 Ia 传入纤维对放电 α 运动神经元的有效性的抑制增加，初级传入纤维去极化和同源突触后激活抑制机制在这个调节过程中起着核心作用。我们的研究结果首次强调了肌肉拉长和增加的肌肉长度对激活 Ia 传入纤维对放电 α 运动神经元的有效性的累积抑制作用。
