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Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation.

ABSTRACT: Maximal-rate rhythmic repetitive movements cannot be sustained for very long, even if unresisted. Peripheral and central mechanisms of fatigue, such as the slowing of muscle relaxation and an increase in M1-GABA_b inhibition, act alongside the reduction of maximal execution rates. However, maximal muscle force appears unaffected, and it is unknown whether the increased excitability of M1 GABAergic interneurons is an adaptation to the waning of muscle contractility in these movements. Here, we observed increased M1 GABA_b inhibition at the end of 30 s of a maximal-rate finger-tapping (FT) task that caused fatigue and muscle slowdown in a sample of 19 healthy participants. The former recovered a few seconds after FT ended, regardless of whether muscle ischaemia was used to keep the muscle slowed down. Therefore, the increased excitability of M1-GABA_b circuits does not appear to be mediated by afferent feedback from the muscle. In the same subjects, continuous (inhibitory) and intermittent (excitatory) theta-burst stimulation (TBS) was used to modulate M1 excitability and to understand the underlying central mechanisms within the motor cortex. The effect produced by TBS on M1 excitability did not affect FT performance. We conclude that fatigue during brief, maximal-rate unresisted repetitive movements has supraspinal components, with origins upstream of the motor cortex.

SUBMITTER: Madinabeitia-Mancebo E

PROVIDER: S-EPMC7822864 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation.

Madinabeitia-Mancebo Elena E Madrid Antonio A Oliviero Antonio A Cudeiro Javier J Arias Pablo P

Scientific reports 20210122 1

Maximal-rate rhythmic repetitive movements cannot be sustained for very long, even if unresisted. Peripheral and central mechanisms of fatigue, such as the slowing of muscle relaxation and an increase in M1-GABA<sub>b</sub> inhibition, act alongside the reduction of maximal execution rates. However, maximal muscle force appears unaffected, and it is unknown whether the increased excitability of M1 GABAergic interneurons is an adaptation to the waning of muscle contractility in these movements. H ...[more]

PMID: 33483562

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Project description:BACKGROUND:Musculoskeletal disorders are more prevalent among women than among men, which may be explained by aspects of motor control, including neuromuscular requirements and motor variability. Using an exploratory approach, this study aimed to evaluate sex differences in neuromuscular responses and motor variability during a repetitive task performed on 3 days. METHODS:Thirty women and 27 men performed the non-fatiguing, repetitive, 1-h screwing task. For neuromuscular responses, the mean and difference values of static, median, and peak percentile muscle activity levels (normalized to a reference voluntary contraction force) and, for motor variability, the mean and difference values of relative and absolute cycle-to-cycle variability across days were compared between both sexes for each muscle. A mixed-design analysis of variance was used to assess differences between both sexes. RESULTS:The non-fatiguing character of the screwing task was confirmed by the absence of decreased force levels in maximal voluntary contractions performed before and after the task and by absence of electromyographic signs of muscle fatigue. The static and median muscle activity levels tended to be higher among women (on average 7.86 and 27.23 %RVE) than men (on average 6.04 and 26.66 %RVE). Relative motor variability of the flexor and biceps muscles and absolute motor variability of both upper arm muscles were lower in women (on average 0.79 and 29.70 %RVE) than in men (on average 0.89 and 37.55 %RVE). The median activity level of both upper arms muscles tended to decrease within days among women (on average - 2.63 %RVE) but increase among men (on average + 1.19 %RVE). Absolute motor variability decreased within days among women (on average - 5.32 to - 0.34%RVE), whereas it tended to decrease less or increase within days among men (on average - 1.21 to + 0.25 %RVE). CONCLUSION:Women showed higher levels of muscle activity and lower initial relative and absolute motor variability than males when performing the same occupational task, implying women may have a higher risk for developing disorders and point to both sexes using different intrinsic motor control strategies in task performance. Clearly, biological aspects alone cannot explain why women would be at higher risk for developing disorders than men. Therefore, a wider range of individual and environmental factors should be taken into account for optimizing work station designs and organizations by taking into account sex differences.

Project description:BACKGROUND:Peripheral nerve injury causes limb muscle/bone atrophy, leading to chronic pain. However, the mechanisms underlying muscle/bone atrophy after peripheral nerve injury remain unknown. It was recently reported that M1 macrophages are the main factors responsible for neurogenic inflammation after peripheral nerve injury. We hypothesized that M1 macrophages are important in muscle/bone atrophy after nerve injury. Therefore, we investigated the influence of M1 macrophages on muscle/bone atrophy after nerve injury in mice to prevent muscle/bone atrophy by suppressing M1 macrophages. METHODS:Hindlimb muscle weight and total bone density were measured in a chronic constriction injury (CCI) mouse model. Immunohistochemical analysis and intravital microscopy were performed to visualize hindlimb muscles/bones, and cells were quantified using flow cytometry. We compared M1 macrophage infiltration into muscles/bones and muscle/bone atrophy between macrophage depletion and untreated groups. We also investigated muscle/bone atrophy using administration models for anti-inflammatory and neuropathic pain drugs. RESULTS:Peripheral nerve injury caused significant reduction in muscle weight and total bone density at 1 and 3 weeks after CCI, respectively, compared with that in controls. Osteoclast numbers were significantly higher at 1 week after CCI in the CCI group than in the control group. M1 macrophage infiltration into muscles was observed from 2 h after CCI via intravital microscopy and 1 week after CCI, and it was significantly higher 1 week after CCI than in the control group. In the macrophage depletion group, dexamethasone, pregabalin, and loxoprofen groups, M1 macrophage infiltration into muscles/bones was significantly lower and muscle weight and total bone density were significantly higher than in the untreated group. CONCLUSIONS:M1 macrophage infiltration exacerbates muscle/bone atrophy after peripheral nerve injury. By suppressing M1 macrophages at the neural injury local site, muscle/bone atrophy could be avoided.

Project description:BACKGROUND:Muscle fatigue induced by repetitive movements contributes to the development of musculoskeletal disorders. Men and women respond differently to muscle fatigue during isometric single-joint efforts, but sex differences during dynamic multi-joint tasks have not been clearly identified. Moreover, most studies comparing men and women during fatigue development assessed endurance time. However, none evaluated sex differences in kinematic adaptations to fatigue during multi-joint dynamic tasks. The objective of the study was to compare how men and women adapt their upper body kinematics during a fatiguing repetitive pointing task. METHODS:Forty men and 41 women performed repetitive pointing movements (one per second) between two targets while maintaining their elbow elevated at shoulder height. The task ended when participants rated a perceived level of fatigue of 8/10. Trunk, humerothoracic, and elbow angles were compared between the first and last 30 s of the experiment and between men and women. Linear positions of the index finger (distance from the target) and the elbow (arm elevation) as well as movement timing were documented as task performance measures. RESULTS:Men (7.4?±?3.2 min) and women (8.3?±?4.5 min) performed the repetitive pointing task for a similar duration. For both sex groups, trunk range of motion increased with fatigue while shoulder's and elbow's decreased. Moreover, participants modified their trunk posture to compensate for the decreased humerothoracic elevation. Movements at all joints also became more variable with fatigue. However, of the 24 joint angle variables assessed, only two Sex × Fatigue interactions were observed. Although average humerothoracic elevation angle decreased in both subgroups, this decrease was greater in men (standardized response mean [SRM] -?1.63) than in women (SRM -?1.44). Moreover, the movement-to-movement variability of humerothoracic elevation angle increased only in women (SRM 0.42). CONCLUSION:Despite many similarities between men's and women's response to fatigue induced by repetitive pointing movements, some sex differences were observed. Those subtle differences may indicate that men's shoulder muscles were more fatigued than women's despite a similar level of perceived exertion. They may also indicate that men and women do not adapt the exact same way to a similar fatigue.

Project description:Protein S-glutathionylation is an important reversible post-translational modification implicated in redox signaling. Oxidative modifications to protein thiols can alter the activity of metabolic enzymes, transcription factors, kinases, phosphatases, and the function of contractile proteins. However, the extent to which muscle contraction induces oxidative modifications in redox sensitive thiols is not known. The purpose of this study was to determine the targets of S-glutathionylation redox signaling following fatiguing contractions. Anesthetized adult male CB6F1 (BALB/cBy × C57BL/6) mice were subjected to acute fatiguing contractions for 15 min using in vivo stimulations. The right (stimulated) and left (unstimulated) gastrocnemius muscleswere collected 60 min after the last stimulation and processed for redox proteomics assay of S-glutathionylation. Using selective reduction with a glutaredoxin enzyme cocktail and resin-assisted enrichment technique, we quantified the levels of site-specific protein S-glutathionylation at rest and following fatiguing contractions. Redox proteomics revealed over 2200 sites of S-glutathionylation modifications, of which 1290 were significantly increased after fatiguing contractions. Muscle contraction leads to the greatest increase in S-glutathionylation in the mitochondria (1.03%) and the smallest increase in the nucleus (0.47%). Regulatory cysteines were significantly S-glutathionylated on mitochondrial complex I and II, GAPDH, MDH1, ACO2, and mitochondrial complex V among others. Similarly, S-glutathionylation of RYR1, SERCA1, titin, and troponin I2 are known to regulate muscle contractility and were significantly S-glutathionylated after just 15 min of fatiguing contractions. The largest fold changes (> 1.6) in the S-glutathionylated proteome after fatigue occurred on signaling proteins such as 14-3-3 protein gamma and MAP2K4, as well as proteins like SERCA1, and NDUV2 of mitochondrial complex I, at previously unknown glutathionylation sites. These findings highlight the important role of redox control over muscle physiology, metabolism, and the exercise adaptive response. This study lays the groundwork for future investigation into the altered exercise adaptation associated with chronic conditions, such as sarcopenia.

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Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation.

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Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation.

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