Sarcopenia refers to a condition of progressive loss of skeletal muscle mass and function associated with a higher risk of falls and fractures in older adults. Musculoskeletal aging leads to reduced muscle mass and strength, affecting the quality of life in elderly people. In recent years, several studies contributed to improve the knowledge of the pathophysiological alterations that lead to skeletal muscle dysfunction; however, the molecular mechanisms underlying sarcopenia are still not fully understood. Muscle development and homeostasis require a fine gene expression modulation by mechanisms in which microRNAs (miRNAs) play a crucial role. miRNAs modulate key steps of skeletal myogenesis including satellite cells renewal, skeletal muscle plasticity, and regeneration. Here, we provide an overview of the general aspects of muscle regeneration and miRNAs role in skeletal mass homeostasis and plasticity with a special interest in their expression in sarcopenia and skeletal muscle adaptation to exercise in the elderly.

Fatigue is one of the most disabling symptoms of multiple sclerosis (MS); it influences patients’ quality of life. The etiology of fatigue is complex, and its pathogenesis is still unclear and debated. The objective of this review was to describe potential brain structural and functional dysfunctions underlying fatigue symptoms in patients with MS. To reach this purpose, a systematic review was conducted of published studies comparing functional brain activation and structural brain in MS patients with and without fatigue. Electronic databases were searched until 24 February 2021. The structural and functional outcomes were extracted from eligible studies and tabulated. Fifty studies were included: 32 reported structural brain differences between patients with and without fatigue; 14 studies described functional alterations in patients with fatigue compared to patients without it; and four studies showed structural and functional brain alterations in patients. The results revealed structural and functional abnormalities that could correlate to the symptom of fatigue in patients with MS. Several studies reported the differences between patients with fatigue and patients without fatigue in terms of conventional magnetic resonance imaging (MRI) outcomes and brain atrophy, specifically in the thalamus. Functional studies showed abnormal activation in the thalamus and in some regions of the sensorimotor network in patients with fatigue compared to patients without it. Patients with fatigue present more structural and functional alterations compared to patients without fatigue. Specifically, abnormal activation and atrophy of the thalamus and some regions of the sensorimotor network seem linked to fatigue.

Aim: Force expression is characterized by an interplay of biological and molecular determinants that are expected to differentiate males and females in terms of maximal performance. These include muscle characteristics (muscle size, fiber type, contractility), neuromuscular regulation (central and peripheral factors of force expression), and individual genetic factors (miRNAs and gene/protein expression). This research aims to comprehensively assess these physiological variables and their role as determinants of maximal force difference between sexes.Methods: Experimental evaluations include neuromuscular components of isometric contraction, intrinsic muscle characteristics (proteins and fiber type), and some biomarkers associated with muscle function (circulating miRNAs and gut microbiome) in 12 young and healthy males and 12 females.Results: Male strength superiority appears to stem primarily from muscle size while muscle fiber‐type distribution plays a crucial role in contractile properties. Moderate‐to‐strong pooled correlations between these muscle parameters were established with specific circulating miRNAs, as well as muscle and plasma proteins.Conclusion: Muscle size is crucial in explaining the differences in maximal voluntary isometric force generation between males and females with similar fiber type distribution. Potential physiological mechanisms are seen from associations between maximal force, skeletal muscle contractile properties, and biological markers.

This study aims to test the separated and combined effects of mechanoreflex activation and nociception through exercise-induced muscle damage (EIMD) on central and peripheral hemodynamics before and during single passive leg movement (sPLM). Eight healthy young males undertook four experimental sessions, in which a sPLM was performed on the dominant limb while in each specific session the contralateral was: 1) in a resting condition (CTRL), 2) stretched (ST), 3) resting after EIMD called delayed onset muscle soreness (DOMS) condition, or 4) stretched after EIMD (DOMS + ST). EIMD was used to induce DOMS in the following 24–48 h. Femoral blood flow (FBF) was assessed using Doppler ultrasound whereas central hemodynamics were assessed via finger photoplethysmography. Leg vascular conductance (LVC) was calculated as FBF/mean arterial pressure (MAP). RR-intervals were analyzed in the time (root mean squared of successive intervals; RMSSD) and frequency domain [low frequency (LF)/high frequency (HF)]. Blood samples were collected before each condition and gene expression analysis showed increased fold changes for P2X4 and IL1β in DOMS and DOMS + ST compared with baseline. Resting FBF and LVC were decreased only in the DOMS + ST condition (−26 mL/min and −50 mL/mmHg/min respectively) with decreased RMSSD and increased LF/HF ratio. MAP, HR, CO, and SV were increased in ST and DOMS + ST compared with CTRL. Marked decreases of Δpeaks and AUC were observed for FBF (Δ: −146 mL/min and −265 mL respectively) and LVC (Δ: −8.66 mL/mmHg/min and ±1.7 mL/mmHg/min respectively) all P < 0.05. These results suggest that the combination of mechanoreflex and nociception resulted in decreased vagal tone and concomitant rise in sympathetic drive that led to increases in resting central hemodynamics with reduced limb blood flow before and during sPLM. NEW & NOTEWORTHY Exercise-induced muscle damage (EIMD) is a well-known model to study mechanical hyperalgesia and muscle peripheral nerve sensitizations. The combination of static stretching protocol on the damaged limb extensively increases resting central hemodynamics with reduction in resting limb blood flow and passive leg movement-induced hyperemia. The mechanism underlining these results may be linked to reduction of vagal tone with concomitant increase in sympathetic activity following mechano- and nociceptive activation.