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Introduction: Motor recovery following nerve injury is dependent on time required for muscle reinnervation. This process is imperfect, however, and recovery is often incomplete. At the neuromuscular junction (NMJ), macrophage signaling aids muscle reinnervation.

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Sarcolemmal membrane excitability is often evaluated by considering the peak-to-peak amplitude of the compound muscle action potential (M wave). However, the first and second M-wave phases represent distinct properties of the muscle action potential, which are differentially affected by sarcolemma properties and other factors such as muscle architecture. Contrasting with previous studies in which voluntary contractions have been used to induce muscle fatigue, we used repeated electrically induced tetanic contractions of the adductor pollicis muscle and assessed the kinetics of M-wave properties during the course of the contractions.

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Muscle injuries often result in functional limitations due to insufficient healing. This study assessed the influence of calcitriol and vitamin D Receptor Modulator 2 (VDRM2) on muscle regeneration in male Wistar rats following open blunt muscle injury. The injured left soleus muscle of the rats was treated for the first four days after trauma with local injections of either calcitriol, VDRM2, or a 10% ethanol solution (control).

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Volumetric muscle loss (VML) is a composite loss of skeletal muscle, which heals with fibrosis, minimal muscle regeneration, and incomplete functional recovery. This study investigated whether collagen-glycosaminoglycan scaffolds (CGS) improve functional recovery following VML. 15 Sprague-Dawley rats underwent either sham injury or bilateral tibialis anterior (TA) VML injury, with or without CGS implantation.

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Skeletal muscle trauma is a common injury with a range of severity. Adenosine, lidocaine and Mg (ALM) is a protective solution and improves tissue perfusion and coagulopathy. Male Wistar rats were anesthetized and subjected to standardized skeletal muscle trauma of the left soleus muscle with the protection of the neurovascular structures.

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