Assessing the Effects of Aging on Muscle Stiffness Using Shear Wave Elastography and Myotonometer

The current study investigated the differences in muscle stiffness between older and young adults at rest and during contraction. We also evaluated the differences in muscle stiffness assessments using a myotonometer (MyotonPRO) and shear wave elastography (SWE). Twenty-two older adults (mean age, 66.6 ± 1.6 years) and 23 young adults (mean age, 66.6 ± 1.6 years) participated in this study. Muscle stiffness of the tibialis anterior (TA) and medial gastrocnemius (MG) muscles at rest and during contraction were measured using SWE and the MyotonPRO. The stiffness increase rate (SIR) was also calculated to determine the absolute stiffness difference. The mean muscle stiffness of the TA and MG muscles was significantly lower in older adults than in young adults at rest and during contraction (p < 0.05). Similarly, the SIR values of the TA and MG were significantly lower in older adults than in young adults (p < 0.05). Our results indicate that both instruments could be used to quantify muscle stiffness changes and serve as a cornerstone for assessing aging-related losses in muscle function. Stiffness measures may help exercise professionals to develop an in-depth understanding of muscle impairment at the tissue level.

Chronic Systemic Curcumin Administration Antagonizes Murine Sarcopenia and Presarcopenia

Curcumin administration attenuates muscle disuse atrophy, but its effectiveness against aging-induced, selective loss of mass or force (presarcopenia or asthenia/dynopenia), or combined loss (sarcopenia), remains controversial. A new systemic curcumin treatment was developed and tested in 18-month-old C57BL6J and C57BL10ScSn male mice. The effects on survival, liver toxicity, loss of muscle mass and force, and satellite cell responsivity and commitment were evaluated after 6-month treatment. Although only 24-month-old C57BL10ScSn mice displayed age-related muscle impairment, curcumin significantly increased survival of both strains (+20–35%), without signs of liver toxicity. Treatment prevented sarcopenia in soleus and presarcopenia in EDL of C57BL10ScSn mice, whereas it did not affect healthy-aged muscles of C57BL6J. Curcumin-treated old C57BL10ScSn soleus preserved type-1 myofiber size and increased type-2A one, whereas EDL maintained adult values of total myofiber number and fiber-type composition. Mechanistically, curcumin only partially prevented the age-related changes in protein level and subcellular distribution of major costamere components and regulators. Conversely, it affected satellite cells, by maintaining adult levels of myofiber maturation in old regenerating soleus and increasing percentage of isolated, MyoD-positive satellite cells from old hindlimb muscles. Therefore, curcumin treatment successfully prevents presarcopenia and sarcopenia development by improving satellite cell commitment and recruitment.

Respiratory Muscle Dysfunction in COVID-19 Patients with Persistent Symptoms

In a cross-sectional analysis, we have identified a high prevalence of respiratory muscle dysfunction in persistently symptomatic patients after COVID-19 (‘Long COVID’). Respiratory muscle impairment in these patients was associated with exercise-induced deoxygenation, impaired exercise tolerance, activity and functional outcomes after COVID-19.

Sarcopenic Obesity in Chronic Kidney Disease: Challenges in Diagnosis using Different Diagnostic Criteria

Obesity and muscle impairment (low muscle mass or strength) are present in chronic kidney disease (CKD) and associated to worse prognosis. However, the various existing definitions for these conditions make the diagnosis variable. The aim of the study was to evaluate the agreement between diagnostic criteria for sarcopenic obesity and its components in CKD. Two hundred and sixty seven patients with CKD were included in the study. We assessed body composition by dual energy X-ray absorptiometry (DXA) and muscle function by handgrip strength (HGS); adiposity by BMI, waist circumference (WC), fat mass index (FMI), and percentage of fat mass (%FM). Diagnosis of muscle impairment was made by HGS, appendicular lean mass (ALM) and index (ALMI); obesity by BMI, WC, FMI and %FM, and sarcopenic obesity was diagnosed by concomitant presence of muscle impairment and obesity. Prevalence of muscle impairment varied from 11 to 50%, higher when low muscle mass criteria was used. Prevalence of obesity varied from 26 to 62%, higher when WC and %FM criteria was used. Prevalence of sarcopenic obesity varied from 2 to 23%. Women were more affected by sarcopenic obesity. Muscle impairment and sarcopenic obesity were more prevalent among patients on hemodialysis and obesity among non-dialysis-dependent and kidney transplant patients. The agreement was poor between muscle mass and strength criteria; substantial between FMI, BMI, and %FM and only fair between WC and the others measures; for sarcopenic obesity, varied from poor to almost perfect. Significant differences were found among the various diagnostic criteria that are used in the diagnosis of sarcopenic obesity.

Dysregulation of Muscle-Specific MicroRNAs as Common Pathogenic Feature Associated with Muscle Atrophy in ALS, SMA and SBMA: Evidence from Animal Models and Human Patients

Motor neuron diseases (MNDs) are neurodegenerative disorders characterized by upper and/or lower MN loss. MNDs include amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA), and spinal and bulbar muscular atrophy (SBMA). Despite variability in onset, progression, and genetics, they share a common skeletal muscle involvement, suggesting that it could be a primary site for MND pathogenesis. Due to the key role of muscle-specific microRNAs (myomiRs) in skeletal muscle development, by real-time PCR we investigated the expression of miR-206, miR-133a, miR-133b, and miR-1, and their target genes, in G93A-SOD1 ALS, Δ7SMA, and KI-SBMA mouse muscle during disease progression. Further, we analyzed their expression in serum of SOD1-mutated ALS, SMA, and SBMA patients, to demonstrate myomiR role as noninvasive biomarkers. Our data showed a dysregulation of myomiRs and their targets, in ALS, SMA, and SBMA mice, revealing a common pathogenic feature associated with muscle impairment. A similar myomiR signature was observed in patients’ sera. In particular, an up-regulation of miR-206 was identified in both mouse muscle and serum of human patients. Our overall findings highlight the role of myomiRs as promising biomarkers in ALS, SMA, and SBMA. Further investigations are needed to explore the potential of myomiRs as therapeutic targets for MND treatment.

Clinical Classification and Scales for Myasthenia Gravis

The variable predominance of the affected muscle groups and the fluctuating severity and extent of myasthenia gravis (MG) makes it difficult to assess and classify these patients. With new treatments being developed and applied, it has become more important to properly classify MG patients and objectively evaluate the results of treatment. So far, a number of clinical classification and assessment systems have been proposed and used individually. However, for the comparative analysis, a uniform set of classifications and reliable measurement methods of muscle impairment are necessary. In this article, MG-clinical classification and several MG-specific assessment tools that are widely used are mentioned.

Digenic Variants in the TTN and TRAPPC11 Genes Co-segregating With a Limb-Girdle Muscular Dystrophy in a Han Chinese Family

Limb-girdle muscular dystrophies (LGMD) are hereditary genetic disorders characterized by progressive muscle impairment which predominantly include proximal muscle weaknesses in the pelvic and shoulder girdles. This article describes an attempt to identify genetic cause(s) for a LGMD pedigree via a combination of whole exome sequencing and Sanger sequencing. Digenic variants, the titin gene (TTN) c.19481T&gt;G (p.Leu6494Arg) and the trafficking protein particle complex 11 gene (TRAPPC11) c.3092C&gt;G (p.Pro1031Arg), co-segregated with the disease phenotype in the family, suggesting their possible pathogenicity.

Quantitative assessment of left ventricular longitudinal function and myocardial deformation in Duchenne muscular dystrophy patients

Background Duchenne muscular dystrophy (DMD) manifests in males mainly by skeletal muscle impairment, but also by cardiac dysfunction. The assessment of the early phases of cardiac involvement using echocardiography is often very difficult to perform in these patients. The aim of the study was to use cardiac magnetic resonance (CMR) strain analysis and mitral annular plane systolic excursion (MAPSE) in the detection of early left ventricular (LV) dysfunction in DMD patients. Methods and results In total, 51 male DMD patients and 18 matched controls were examined by CMR. MAPSE measurement and functional analysis using feature tracking (FT) were performed. Three groups of patients were evaluated: A/ patients with LGE and LV EF < 50% (n = 8), B/ patients with LGE and LVEF ≥ 50% (n = 13), and C/ patients without LGE and LVEF ≥ 50% (n = 30). MAPSE and global LV strains of the 3 DMD groups were compared to controls (n = 18). Groups A and B had significantly reduced values of MAPSE, global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS) in comparison to controls (p < 0.05). The values of MAPSE (11.6 ± 1.9 v 13.7 ± 2.7 mm) and GCS (− 26.2 ± 4.2 v − 30.0 ± 5.1%) were significantly reduced in group C compared to the controls (p < 0.05). Conclusion DMD patients had decreased LV systolic function measured by MAPSE and global LV strain even in the case of normal LV EF and the absence of LGE. FT and MAPSE measurement provide sensitive assessment of early cardiac involvement in DMD patients.

GH/IGF-1 Abnormalities and Muscle Impairment: From Basic Research to Clinical Practice

The impairment of skeletal muscle function is one of the most debilitating least understood co-morbidity that accompanies acromegaly (ACRO). Despite being one of the major determinants of these patients’ poor quality of life, there is limited evidence related to the underlying mechanisms and treatment options. Although growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels are associated, albeit not indisputable, with the presence and severity of ACRO myopathies the precise effects attributed to increased GH or IGF-1 levels are still unclear. Yet, cell lines and animal models can help us bridge these gaps. This review aims to describe the evidence regarding the role of GH and IGF-1 in muscle anabolism, from the basic to the clinical setting with special emphasis on ACRO. We also pinpoint future perspectives and research lines that should be considered for improving our knowledge in the field.