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Exercise-induced fatigue causes changes within the central nervous system that decrease force production capacity in fatigued muscles. The impact on unrelated, non-exercised muscle performance is still unclear. The primary aim of this study was to examine the impact of a bilateral forearm muscle contraction on the motor function of the distal and unrelated ankle plantar-flexor muscles. The secondary aim was to compare the impact of maximal and submaximal forearm contractions on the non-fatigued ankle plantar-flexor muscles. Maximal voluntary contractions (MVC) of the forearm and ankle plantar-flexor muscles as well as voluntary activation (VA) and twitch torque of the ankle plantar-flexor muscles were assessed pre-fatigue and throughout a 10-min recovery period. Maximal (100 % MVC) and submaximal (30 % MVC) sustained isometric handgrip contractions caused a decreased handgrip MVC (to 49.3 ± 15.4 and 45.4 ± 11.4 % of the initial MVC for maximal and submaximal contraction, respectively) that remained throughout the 10-min recovery period. The fatigue protocols also caused a decreased ankle plantar-flexor MVC (to 77 ± 8.3 and 92.4 ± 6.2 % of pre-fatigue MVC for maximal and submaximal contraction, respectively) and VA (to 84.3 ± 15.7 and 97.7 ± 16.1 % of pre-fatigue VA for maximal and submaximal contraction, respectively). These results suggest central fatigue created by the fatiguing handgrip contraction translated to the performance of the non-exercised ankle muscles. Our results also show that the maximal fatigue protocol affected ankle plantar-flexor MVC and VA more severely than the submaximal protocol, highlighting the task-specificity of neuromuscular fatigue.

Abstract Muscle stiffness estimated using shear wave elastography can provide an index of individual muscle force during isometric contraction and may therefore be a promising method for quantifying co-contraction. We estimated the shear modulus of the lateral gastrocnemius (LG) muscle using supersonic shear wave imaging and measured its myoelectrical activity using surface electromyography (sEMG) during graded isometric contractions of plantar flexion and dorsiflexion ( n =7). During dorsiflexion, the average shear modulus was 26±6 kPa at peak sEMG amplitude, which was significantly less ( P =0.02) than that measured at the same sEMG level during plantar flexion (42±10 kPa). The passive tension during contraction was estimated using the passive LG muscle shear modulus during a passive ankle rotation measured at an equivalent ankle angle to that measured during contraction. The passive shear modulus increased significantly ( P <0.01) from the plantar flexed position (16±5 kPa) to the dorsiflexed position (26±9 kPa). Once this change in passive tension from joint rotation was accounted for, the average LG muscle shear modulus due to active contraction was significantly greater ( P <0.01) during plantar flexion (26±8 kPa) than at sEMG-matched levels of dorsiflexion (0±4 kPa). The negligible shear modulus estimated during isometric dorsiflexion indicates negligible active force contribution by the LG muscle, despite measured sEMG activity of 19% of maximal voluntary plantar flexion contraction. This strongly suggests that the sEMG activity recorded from the LG muscle during isometric dorsiflexion was primarily due to cross-talk. However, it is clear that passive muscle tension changes can contribute to joint torque during isometric dorsiflexion.

Abstract Satellite cells are the myogenic stem and progenitor population found in skeletal muscle. These cells typically reside in a quiescent state until called upon to support repair, regeneration, or muscle growth. The activities of satellite cells are orchestrated by systemic hormones, autocrine and paracrine growth factors, and the composition of the basal lamina of the muscle fiber. Several key intracellular signaling events are initiated in response to changes in the local environment causing exit from quiescence, proliferation, and differentiation. Signals emanating from Notch, wingless-type mouse mammary tumor virus integration site family members, and transforming growth factor-β proteins mediate the reversible exit from growth 0 phase while those initiated by members of the fibroblast growth factor and insulin-like growth factor families direct proliferation and differentiation. Many of these pathways impinge upon the myogenic regulatory factors (MRF), myogenic factor 5, myogenic differentiation factor D, myogenin and MRF4, and the lineage determinate, Paired box 7, to alter transcription and subsequent satellite cell decisions. In the recent past, insight into mouse transgenic models has led to a firm understanding of regulatory events that control satellite cell metabolism and myogenesis. Many of these niche-regulated functions offer subtle differences from their counterparts in livestock pointing to the existence of species-specific controls. The purpose of this review is to examine the mechanisms that mediate large animal satellite cell activity and their relationship to those present in rodents.

The aim of this study was to determine how unilateral pain, induced in two knee extensor muscles, affects muscle coordination during a bilateral pedaling task. Fifteen participants performed a 4-min pedaling task at 130 W in two conditions (Baseline and Pain). Pain was induced by injection of hypertonic saline into the vastus medialis (VM) and vastus lateralis (VL) muscles of one leg. Force applied throughout the pedaling cycle was measured using an instrumented pedal and used to calculate pedal power. Surface electromyography (EMG) was recorded bilaterally from eight muscles to assess changes in muscle activation strategies. Compared to Baseline, during the Pain condition, EMG amplitude of muscles of the painful leg (VL and VM—the painful muscles, and RF—another quadriceps muscle with no pain) was lower during the extension phase [(mean ± SD): VL: −22.5 ± 18.9%; P  < 0.001; VM: −28.8 ± 19.9%; P  < 0.001, RF: −20.2 ± 13.9%; P  < 0.001]. Consistent with this, pedal power applied by the painful leg was also lower during the extension phase (−16.8 ± 14.2 W, P  = 0.001) during Pain compared to Baseline. This decrease was compensated for by an 11.3 ± 8.1 W increase in pedal power applied by the non-painful leg during its extension phase ( P  = 0.04). These results support pain adaptation theories, which suggest that when there is a clear opportunity to compensate, motor adaptations to pain occur to decrease load within the painful tissue. Although the pedaling task offered numerous possibilities for compensation, only between-leg compensations were systematically observed. This finding is discussed in relation to the mechanical and neural constraints of the pedaling task.

Skeletal muscle satellite cells (SC) play a critical role in the hypertrophic growth of postnatal muscle. Increases in breast meat yield have been consistently observed in broiler chickens fed 25-hydroxycholecalciferol (25OHD3), but it is unclear whether this effect is mediated by SC. Thus, our objective was to determine the effect of vitamin D status improvement by replacing the majority of dietary vitamin D3 (D3) with 25OHD3 on SC activity and muscle growth characteristics in the pectoralis major (PM) and the biceps femoris (BF) muscles. Day-old, male Ross 708 broiler chickens (n = 150) were fed 1 of 2 corn and soybean meal-based diets for 49 d. The control diet (CTL) contained 5,000 IU D3 per kg of diet and the experimental diet (25OHD3) contained 2,240 IU D3 per kg of diet + 2,760 IU 25OHD3 per kg of diet. Ten birds per treatment were harvested every 7 d. Two hours before harvest, birds were injected intraperitoneally with 5'-bromo-2'deoxyuridine (BrdU) to label mitotically active cells. Blood was collected from each bird at harvest to measure circulating concentrations of 25OHD3, a marker of vitamin D status. The PM and BF muscles were weighed and processed for cryohistological determination of skeletal muscle fiber cross-sectional area, enumeration of Myf-5+ and Pax7+ SC, and mitotically active (BrdU+) SC using immunofluorescence microscopy. Circulating 25OHD3 concentrations were greater in 25OHD3-fed birds on d 7, 14, 21, 28, 35, 42, and 49 when compared with CTL (P < 0.001). Growth performance and feed efficiency did not differ among dietary treatments (P > 0.10). Improved vitamin D status as a result of feeding 25OHD3 increased the number of mitotically active (Pax7+;BrdU+) SC (P = 0.01) and tended to increase the density of Pax7+ SC (P = 0.07) in the PM muscles of broilers on d 21 and 35, respectively. Broiler chickens fed 25OHD3 also tended to have greater Myf-5+ SC density (P = 0.09) on d 14, greater total nuclear density (P = 0.05) on d 28, and a greater muscle fiber cross-sectional area (P = 0.09) on d 49 in their PM muscles compared with CTL birds. Collectively, these results suggest that improvement of vitamin D status by replacing the majority of D3 in the diet with 25OHD3 can stimulate SC activity in the predominantly fast-twitch PM muscle and provide evidence toward understanding the mechanism behind previously observed increases in breast meat yield in 25OHD3-fed commercial broiler chickens.

A longstanding goal in regenerative medicine is to reconstitute functional tissues or organs after injury or disease. Attention has focused on the identification and relative contribution of tissue specific stem cells to the regeneration process. Relatively little is known about how the physiological process is regulated by other tissue constituents. Numerous injury models are used to investigate tissue regeneration, however, these models are often poorly understood. Specifically, for skeletal muscle regeneration several models are reported in the literature, yet the relative impact on muscle physiology and the distinct cells types have not been extensively characterised. We have used transgenic Tg:Pax7nGFP and Flk1GFP/+ mouse models to respectively count the number of muscle stem (satellite) cells (SC) and number/shape of vessels by confocal microscopy. We performed histological and immunostainings to assess the differences in the key regeneration steps. Infiltration of immune cells, chemokines and cytokines production was assessed in vivo by Luminex®. We compared the 4 most commonly used injury models i.e. freeze injury (FI), barium chloride (BaCl2), notexin (NTX) and cardiotoxin (CTX). The FI was the most damaging. In this model, up to 96% of the SCs are destroyed with their surrounding environment (basal lamina and vasculature) leaving a \"dead zone\" devoid of viable cells. The regeneration process itself is fulfilled in all 4 models with virtually no fibrosis 28 days post-injury, except in the FI model. Inflammatory cells return to basal levels in the CTX, BaCl2 but still significantly high 1-month post-injury in the FI and NTX models. Interestingly the number of SC returned to normal only in the FI, 1-month post-injury, with SCs that are still cycling up to 3-months after the induction of the injury in the other models. Our studies show that the nature of the injury model should be chosen carefully depending on the experimental design and desired outcome. Although in all models the muscle regenerates completely, the trajectories of the regenerative process vary considerably. Furthermore, we show that histological parameters are not wholly sufficient to declare that regeneration is complete as molecular alterations (e.g. cycling SCs, cytokines) could have a major persistent impact.

Extensive analyses of mice carrying null mutations in paired box 7 (Pax7) have confirmed the progressive loss of the satellite cell lineage in skeletal muscle, resulting in severe muscle atrophy and death. A recent study using floxed alleles and tamoxifen-induced inactivation concluded that after 3 wk of age, Pax7 was entirely dispensable for satellite cell function. Here, we demonstrate that Pax7 is an absolute requirement for satellite cell function in adult skeletal muscle. Following Pax7 deletion, satellite cells and myoblasts exhibit cell-cycle arrest and dysregulation of myogenic regulatory factors. Maintenance of Pax7 deletion through continuous tamoxifen administration prevented regrowth of Pax7-expressing satellite cells and a profound muscle regeneration deficit that resembles the phenotype of skeletal muscle following genetically engineered ablation of satellite cells. Therefore, we conclude that Pax7 is essential for regulating the expansion and differentiation of satellite cells during both neonatal and adult myogenesis.

Electromechanical delay is the time lag between onsets of muscle activation and muscle force production and reflects both electro-chemical processes and mechanical processes. The aims of the present study were two-fold: to experimentally determine the slack length of each head of the biceps brachii using elastography and to determine the influence of the length of biceps brachii on electromechanical delay and its electro-chemical/mechanical processes using very high frame rate ultrasound. First, 12 participants performed two passive stretches to evaluate the change in passive tension for each head of the biceps brachii. Then, they underwent two electrically evoked contractions from 120 to 20° of elbow flexion (0°: full extension), with the echographic probe maintained over the muscle belly and the myotendinous junction of biceps brachii. The slack length was found to occur at 95.5 ± 6.3° and 95.3 ± 8.2° of the elbow joint angle for the long and short heads of the biceps brachii, respectively. The electromechanical delay was significantly longer at 120° (16.9 ± 3.1 ms; p<0.001), 110° (15.0 ± 3.1 ms; p<0.001) and 100° (12.7 ± 2.5 ms; p = 0.01) of elbow joint angle compared to 90° (11.1 ± 1.7 ms). However, the delay between the onset of electrical stimulation and the onset of both muscle fascicles (3.9 ± 0.2 ms) and myotendinous junction (3.7 ± 0.3 ms) motion was not significantly affected by the joint angle (p>0.95). In contrast to previous observations on gastrocnemius medialis, the onset of muscle motion and the onset of myotendinous junction motion occurred simultaneously regardless of the length of the biceps brachii. That suggests that the between-muscles differences reported in the literature cannot be explained by different muscle passive tension but instead may be attributable to muscle architectural differences.

A central tenet of skeletal muscle biology is the existence of an inverse relationship between the oxidative fibre capacity and its size. However, robustness of this relationship is unknown. We show that superimposition of Estrogen-related receptor gamma (Errγ) on the myostatin (Mtn) mouse null background (Mtn(-/-)/Errγ(Tg/+)) results in hypertrophic muscle with a high oxidative capacity thus violating the inverse relationship between fibre size and oxidative capacity. We also examined the canonical view that oxidative muscle phenotype positively correlate with Satellite cell number, the resident stem cells of skeletal muscle. Surprisingly, hypertrophic fibres from Mtn(-/-)/Errγ(Tg/+) mouse showed satellite cell deficit which unexpectedly did not affect muscle regeneration. These observations 1) challenge the concept of a constraint between fibre size and oxidative capacity and 2) indicate the important role of the microcirculation in the regenerative capacity of a muscle even when satellite cell numbers are reduced.