Muscles

Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder caused by loss-of-function mutations in the dystrophin gene, leading to progressive muscle degeneration, motor decline, respiratory compromise, and cardiomyopathy. Diagnosis typically occurs in early childhood following recognition of motor delays, markedly elevated creatine kinase, and confirmatory genetic testing. Over the past decade, the therapeutic landscape for DMD has expanded substantially, evolving from exclusively supportive care to patient-centric multifaceted treatment paradigms, including corticosteroids, mutation-specific therapies, small molecule disease-modifying approaches, and gene replacement strategies. Despite these advances, no currently available therapy restores full-length dystrophin or completely halts disease progression. This review provides a clinically oriented comprehensive overview of currently Food and Drug Administration (FDA)-approved medications for DMD, with particular emphasis on corticosteroids, exon-skipping therapies, nonsense mutation readthrough agents, recently approved gene therapy, and select ongoing gene therapy trials. We summarize mechanisms of action, clinical efficacy, safety considerations, regulatory status, and highlight the challenges of integrating these therapies into longitudinal care. Through illustrative clinical vignettes, we highlight the real-world complexity of treatment selection, shared decision-making, and longitudinal care planning in contemporary DMD management.

Peripheral arterial disease is a leading cause of amputation and/or death worldwide. Phosphodiesterase 4 (PDE 4) inhibitors demonstrated beneficial effects in ischemia–reperfusion (IR) settings, but whether PDE 4 inhibition protects skeletal muscle against IR deleterious effects is unknown. We therefore performed limb IR (two hours each) in twenty-one male Swiss mice (12–16-week-old) treated or not with Rolipram (1 mg/kg i.p. 30 min before ischemia and 5 min before reperfusion). The muscles were analyzed 4 h after the onset of ischemia. IR significantly increased leucocyte infiltration (93.13 ± 6.886 vs. 150.1 ± 18.38 cells/mg of muscle, p < 0.05) and apoptosis (Bax/Bcl2 ratio, +239%, p < 0.05), together with enhanced mitochondrial fission transcripts (+224% for Drp1, p < 0.01 and +368%, p < 0.0001 for Fis1), and decreased mitochondrial respiration and antioxidant defense. PDE 4 inhibition reduced leucocyte infiltration (150.1 ± 18.38 vs. 55.58 ± 13.83; p < 0.01) and apoptosis (+67%, NS) in association with reduced fission markers (+91% for Drp 1 and +111%, p < 0.05, for Fis 1). Muscle mitochondrial respiration did not improve. In conclusion, PDE 4 inhibition using Rolipram partly protected skeletal muscles against IR-induced deleterious effects. These data support further studies investigating the usefulness of leucocytes modulation in lower-limb IR and a potential beneficial effect of PDE 4 inhibition in peripheral arterial disease.

Studies examining the electromyographic activation of pectoralis major (PM) and triceps brachii (TB) muscles during push-ups of varied hand positions are limited, and findings are inconsistent. The aim was to investigate the electromyographic activation of PM and TB during standard, diamond, and wide hand position push-ups. Twenty young males performed six repetitions of each push-up variation while the electrical activity of PM and TB was recorded, averaged, and normalized to the peak root mean square (RMS) across repetitions for each push-up. RMS (mV) and normalized RMS (%) were calculated for each muscle, push-up variation, and contraction phase (eccentric/concentric). Two separate three-way ANOVAs with Bonferroni post hoc correction were used (α = 0.05). TB demonstrated statistically significantly higher RMS (mV) and normalized RMS (%) than PM (p < 0.05), in diamond, followed by standard and wide push-ups. A statistically significant higher activation of RMS (mV) was observed in concentric compared to eccentric (p < 0.05); however, after normalizing RMS (%), contraction phase had no effect (p > 0.05) and there was no significant three-way interaction (p > 0.05). Diamond push-ups elicited the highest relative activation for both the PM and TB. Normalized RMS revealed the consistency of muscle effort in both contraction phases, sustaining near-maximal activation regardless of hand position. These findings support adaptable training strategies, with potential applications in rehabilitation and strength training contexts.