Muscles, Volume 1, Issue 1 (June 2022) – 8 articles

A recent study describing unique effects of myostatin inhibition on a severely dystrophic (mdx) muscle, and independent experiments showing that branched fibers are uniquely sensitive to activity-induced membrane rupture, have led to a new hypothesis of dystrophic pathogenesis. This hypothesis states that the absence of dystrophin directly results in some degree of unrestrained satellite cell activation that is not dependent upon prior fiber injury. The hypothesis further states that dystrophin promotes satellite cell quiescence, and that its absence directly results in a lack of control over the mechanism(s) by which muscle activity regulates satellite cell activation and fiber growth during passive stretch and concentric and eccentric exercise. The ultimate consequence of this lack of control is to produce branched, weak, and fragile fibers that accumulate at a rate dependent upon the history of activation for each dystrophic muscle. The purpose of this opinion paper is to summarize the results in support of this new hypothesis in an attempt to stimulate further research on the regulation of satellite cell activity in dystrophic muscle. Full article

We investigated genetic and clinical features in two siblings with an unreported frameshift mutation in the GJB1 gene, encoding connexin 32, to study CMTX-1 and its intrafamilial phenotypic variability. Connexin 32 is a gap junction protein that is located in paranodal regions and Schmidt–Lanterman incisures. Clinical features, family history, and genetic and microRNA information were collected. Genetic analysis determination was performed on genomic DNA from the two cases. Muscle-specific miR-206 was also investigated in serum. A muscle biopsy was conducted in one case, and EMG with conduction velocities was performed in both patients. In the first genetic analysis, no duplication of the PMP22 gene was found. A second genetic analysis of a panel of genes associated with inherited peripheral neuropathies was performed. We found a frameshift mutation in the connexin 32 (GJB1) gene, c.281_287del in hemizygosity, not previously reported, that segregated with the clinical phenotype. An X-linked hereditary sensory motor neuropathy was caused by the mutation in the connexin 32 gene. We found overexpression of miR-206 that was 4-fold up-regulated in the older brother and over 10-fold in the younger brother versus the controls; this might be correlated with a different muscle mass and regeneration. The two siblings presented differently evolving neuropathies due to environmental factors and lifestyles that caused nerve degeneration. We hypothesized that in this X-linked CMT, there is no expression of a truncated connexin 32 (Cx32) protein, with loss of function markedly reduced in the gap junction. In the peripheral nervous system (PNS), this might be mitigated by the presence of another connexin, Cx43. Such a reduction might affect not only gap junction formation but also myelination and muscle trophism, resulting in variable miR-206 expressivity. Full article

The load scenario within the shoulder joint among its muscle–tendon complexes during fast motions is of interest, as it would allow an evaluation of critical, accident-like motions. To enhance knowledge, a modelling approach was carried out and compared to experimental data. Nine subjects were investigated while performing tasks that ranged from easy to demanding. Motions were (1) an easy lift of a small weight, (2) a push against a force measurement device, and (3) a gentle side fall against the immovable force measurement device. Extracted data were the kinematics of the right arm and the contact force on the elbow. A simple direct dynamics shoulder model actuated by Hill-type muscle models was arranged to simulate the three experimental motions. The Hatze-based activation of the muscle models was used without any further simulation of neural regulation. For fast motions, the simple shoulder model predicts well the shoulder angle or contact force values, and data fit well into the variability of the data measured experimentally. Because there was no implementation of more complex neural regulation, slow motions, as performed by the subjects, were, in part, not predicted by the shoulder model. Simple mechanisms can be described by the simple model: When activated, the larger deltoid muscle is able to protect the smaller supraspinatus muscle. Furthermore, in awkward conditions, the gentle side fall against an immovable device alone has enough momentum to damage small muscles. Full article

Efficacy of obesity treatments varies between individuals, highlighting the presence of responders and non-responders. Whilst exercise alone or exercise combined with diet leads to underwhelming weight loss for most, there exist super responders losing significant weight. Furthermore, in response to weight loss, the majority but not all patients tend to regain weight. Within the biopsychosocial model, biology as a determinant of response has been underappreciated. The understanding of the role that organs beyond adipose tissue and the gastrointestinal tract play in appetite control and body weight regulation has developed in recent years. The aim of this review is to highlight potential myokines that may be important in appetite physiology and overall energy balance. A number of attractive targets are described that warrant further investigation. A deeper understanding of how these myokines may drive feeding behaviours has the potential to improve measures to prevent and treat obesity through a precision medicine approach. Full article

Background: Skeletal muscle adaptations are affected by resistance training (RT)-induced acute and chronic transcriptional responses. An under-explored gene target involved in mechanotransduction is the expression of the G protein-coupled receptor 56 (GPR56). However, studies investigating the acute and chronic effects of RT manipulations on GPR56 mRNA are scarce. Methods: Twenty subjects had each leg randomly assigned to a standard ((CON) no specific manipulation) or a variable RT (manipulations in load, volume, muscle action, and pause in a session-by-session fashion (VAR)). GPR56 mRNA expression was assessed before and after 16 training sessions (chronic effect) and 24 h after a 17th session (acute effect). Results: Acute GPR56 mRNA expression increased at 24 h (p < 0.01) without differences between CON and VAR (p > 0.05). No differences were found in GPR56 mRNA expression when comparing each VAR condition (load vs. sets vs. eccentric actions vs. pause) nor with CON at 24 h (p > 0.05). Chronic GPR56 mRNA expression increased at Post compared with Pre (p < 0.02) for VAR only, with a tendency (p = 0.058) toward higher expression for VAR as compared with CON. Conclusion: GPR56 mRNA expression is acutely and chronically modulated by RT. Additionally, chronic GPR56 mRNA expression is modulated by RT variable manipulations. Full article

A detraining period after resistance training causes a significant decrease in trained-induced muscular adaptations. However, it is unclear how long muscle strength and hypertrophy gains last after different detraining periods. Thus, the present systematic review with meta-analysis aimed to evaluate the chronic effects of detraining on muscle strength and hypertrophy induced by resistance training. Searches were conducted on PubMed, Scopus, EBSCO, CINAHL, CENTRAL, and Web of Science. The difference in means and pooled standard deviations of outcomes were converted into Hedges’ g effect sizes (g). Twenty randomized and non-randomized trials (high and moderate risks of bias, respectively, and fair quality) were included for qualitative analysis of muscle strength and hypertrophy, while only two studies were included in the meta-analysis for maximum muscle strength. The resistance training group presented a significant increase in one-repetition maximum (1RM) chest press (g: 4.43 [3.65; 5.22], p < 0.001) and 1RM leg press strength (g: 4.47 [2.12; 6.82], p < 0.001) after training. The strength gains observed in the resistance training group were also maintained after 16–24 weeks of detraining (g: 1.99 [0.62; 3.36], p = 0.004; and g: 3.16 [0.82; 5.50], p = 0.008; respectively), when compared to the non-exercise control group. However, 1RM chest press and leg press strength level was similar between groups after 32 (g: 1.81 [−0.59; 4.21], p = 0.139; and g: 2.34 [−0.48; 5.16], p = 0.104; respectively) and 48 weeks of detraining (g: 1.01 [−0.76; 2.79], p = 0.263; and g: 1.16 [−1.09; 3.42], p = 0.311; respectively). There was not enough data to conduct a meta-analysis on muscular hypertrophy. In conclusion, the present systematic review and meta-analysis demonstrated that, when taking random error into account, there is no sufficient high-quality evidence to make any unbiased claim about how long changes in muscle strength induced by RT last after a DT period. Moreover, the effect of different DT periods on muscle hypertrophy induced by RT remains unknown since there was not enough data to conduct a meta-analysis with this variable. Full article