Motor unit discharge rate modulation during isometric contractions to failure is intensity‐and modality‐dependent

The physiological mechanisms determining the progressive decline in the maximal muscle torque production capacity during isometric contractions to task failure are known to depend on task demands. Task-specificity of the associated adjustments in motor unit discharge rate (MUDR), however, remains unclear. This study examined MUDR adjustments during different submaximal isometric knee extension tasks to failure. Participants performed a sustained and an intermittent task at 20% and 50% of maximal voluntary torque (MVT), respectively (Experiment 1). High-density surface EMG signals were recorded from vastus lateralis (VL) and medialis (VM) and decomposed into individual MU discharge timings, with the identified MUs tracked from recruitment to task failure. MUDR was quantified and normalised to intervals of 10% of contraction time (CT). MUDR of both muscles exhibited distinct modulation patterns in each task. During the 20% MVT sustained task, MUDR decreased until ∼50% CT, after which it gradually returned to baseline. Conversely, during the 50% MVT intermittent task, MUDR remained stable until ∼40–50% CT, after which it started to continually increase until task failure. To explore the effect of contraction intensity on the observed patterns, VL and VM MUDR was quantified during sustained contractions at 30% and 50% MVT (Experiment 2). During the 30% MVT sustained task, MUDR remained stable until ∼80–90% CT in both muscles, after which it continually increased until task failure. During the 50% MVT sustained task the increase in MUDR occurred earlier, after ∼70–80% CT. Our results suggest that adjustments in MUDR during submaximal isometric contractions to failure are contraction modality- and intensity-dependent

Reductions in motoneuron excitability during sustained isometric contractions are dependent on stimulus and contraction intensity

Cervicomedullary stimulation provides a means of assessing motoneuron excitability. Previous studies demonstrated that during low-intensity sustained contractions, small cervicomedullary evoked potentials (CMEPs) conditioned using transcranial magnetic stimulation (TMS-CMEPs) are reduced, whereas large TMS-CMEPs are less affected. As small TMS-CMEPs recruit motoneurons most active during low-intensity contractions whereas large TMS-CMEPs recruit a high proportion of motoneurons inactive during the task, these results suggest that reductions in motoneuron excitability could be dependent on repetitive activation. To further test this hypothesis, this study assessed changes in small and large TMS-CMEPs across low- and high-intensity contractions. Twelve participants performed a sustained isometric contraction of the elbow flexor for 4.5 min at the electromyography (EMG) level associated with 20% maximal voluntary contraction force (MVC; low intensity) and 70% MVC (high intensity). Small and large TMS-CMEPs with amplitudes of ∼15% and ∼50% Mmax at baseline, respectively, were delivered every minute throughout the tasks. Recovery measures were taken at 1-, 2.5- and 4-min postexercise. During the low-intensity trial, small TMS-CMEPs were reduced at 2-4 min (P ≤ 0.049) by up to -10% Mmax, whereas large TMS-CMEPs remained unchanged (P ≥ 0.16). During the high-intensity trial, small and large TMS-CMEPs were reduced at all time points (P < 0.01) by up to -14% and -33% Mmax, respectively, and remained below baseline during all recovery measures (P ≤ 0.02). TMS-CMEPs were unchanged relative to baseline during recovery following the low-intensity trial (P ≥ 0.24). These results provide novel insight into motoneuron excitability during and following sustained contractions at different intensities and suggest that contraction-induced reductions in motoneuron excitability depend on repetitive activation

Monitoring of post-match fatigue in professional soccer: Welcome to the real world

Participation in soccer match-play leads to acute and transient subjective, biochemical, metabolic and physical disturbances in players over subsequent hours and days. Inadequate time for rest and regeneration between matches can expose players to the risk of training and competing whilst not entirely recovered. In professional soccer, contemporary competitive schedules can require teams to compete in-excess of 60 matches over the course of the season while periods of fixture congestion occur prompting much attention from researchers and practitioners to the monitoring of fatigue and readiness to play. A comprehensive body of research has investigated post-match acute and residual fatigue responses. Yet the relevance of the research for professional soccer contexts is debatable notably in relation to the study populations and designs employed. Monitoring can indeed be invasive, expensive, time-inefficient and difficult to perform routinely and simultaneously in a large squad of regularly competing players. Uncertainty also exists regarding the meaningfulness and interpretation of changes in fatigue response values and their functional relevance, and practical applicability in the field. The real-world need and cost-benefit of monitoring must be carefully weighed up. In relation to professional soccer contexts, this opinion paper intends to: 1) debate the need for PMF monitoring, 2) critique the real-world relevance of the current research literature, 3) discuss the practical burden relating to measurement tools and protocols and the collection, interpretation and application of data in the field, and, 4) propose future research perspectives

Surviving Mousepox Infection Requires the Complement System

Poxviruses subvert the host immune response by producing immunomodulatory proteins, including a complement regulatory protein. Ectromelia virus provides a mouse model for smallpox where the virus and the host's immune response have co-evolved. Using this model, our study investigated the role of the complement system during a poxvirus infection. By multiple inoculation routes, ectromelia virus caused increased mortality by 7 to 10 days post-infection in C57BL/6 mice that lack C3, the central component of the complement cascade. In C3−/− mice, ectromelia virus disseminated earlier to target organs and generated higher peak titers compared to the congenic controls. Also, increased hepatic inflammation and necrosis correlated with these higher tissue titers and likely contributed to the morbidity in the C3−/− mice. In vitro, the complement system in naïve C57BL/6 mouse sera neutralized ectromelia virus, primarily through the recognition of the virion by natural antibody and activation of the classical and alternative pathways. Sera deficient in classical or alternative pathway components or antibody had reduced ability to neutralize viral particles, which likely contributed to increased viral dissemination and disease severity in vivo. The increased mortality of C4−/− or Factor B−/− mice also indicates that these two pathways of complement activation are required for survival. In summary, the complement system acts in the first few minutes, hours, and days to control this poxviral infection until the adaptive immune response can react, and loss of this system results in lethal infection