Sex-Related Differences in Motor Unit Firing Rate and Pennation Angle.

Motor unit firing rate (MUFR) and pennation angle were measured concurrently in males and females from submaximal to maximal intensities. Thirty participants, (16F and 14M) performed isometric dorsiflexion contractions at 20%, 40%, 60%, 80% and 100% of maximal voluntary contraction (MVC). During each contraction, measures of MUFR were obtained via surface electromyography decomposition, and muscle fiber pennation angle and fascicle length were obtained via ultrasound.

How many motor units is enough? An assessment of the influence of the number of motor units on firing rate calculations.

The number of motor units included in calculations of mean firing rates varies widely in the literature. It is unknown how the number of decomposed motor units included in the calculation of firing rate per participant compares to the total number of active motor units in the muscle, and if this is different for males and females. Bootstrapped distributions and confidence intervals (CI) of mean motor unit firing rates decomposed from the tibialis anterior were used to represent the total number of active motor units for individual participants in trials from 20 to 100 % of maximal voluntary contraction.

Neuromuscular behaviour in the first dorsal interosseus following mental fatigue.

We examined sex-specific changes to neuromuscular function in response to mental fatigue. Twenty-five young, healthy adults (13 F, 12 M) performed a mentally fatiguing task and control condition for 30 min on two separate days. Neuromuscular function was assessed in the first dorsal interosseous before and after each condition.

Stathmin-2 loss leads to neurofilament-dependent axonal collapse driving motor and sensory denervation.

The mRNA transcript of the human STMN2 gene, encoding for stathmin-2 protein (also called SCG10), is profoundly impacted by TAR DNA-binding protein 43 (TDP-43) loss of function. The latter is a hallmark of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Using a combination of approaches, including transient antisense oligonucleotide-mediated suppression, sustained shRNA-induced depletion in aging mice, and germline deletion, we show that stathmin-2 has an important role in the establishment and maintenance of neurofilament-dependent axoplasmic organization that is critical for preserving the caliber and conduction velocity of myelinated large-diameter axons.