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  • 1.6
    Impact Factor
  • 1.7
    CiteScore
  • 36 days
    Submission to First Decision
  • 6 days
    Acceptance to Publication

Muscles

Muscles is an international, peer-reviewed, open access journal on muscle biology and physiology published quarterly online by MDPI. The Korean Society of Physical Medicine (KSPM) is affiliated with Muscles and its members receive discounts on the article processing charges.
  • Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
  • High Visibility: indexed within ESCI (Web of Science), Scopus, PubMed, PMC, Embase, and other databases.
  • Journal Rank: CiteScore - Q2 (General Medicine)
  • Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 35.8 days after submission; acceptance to publication is undertaken in 5.6 days (median values for papers published in this journal in the first half of 2026).
  • Recognition of Reviewers: Reviewers whose reports are timely and of high quality receive an APC discount voucher for a future publication in an MDPI journal. Become a reviewer.

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All Articles (221)

  • Review
  • Open Access

Cisplatin causes skeletal muscle wasting in tumor-free rodents, reducing muscle mass, myofiber size and, where measured, strength. This critical narrative review appraises that phenotype and its mechanistic basis. Tumor-bearing models show that the loss also occurs under tumor burden, but most cannot separate drug from tumor effects. Melatonin influences mitochondrial, redox, regenerative, and structural outcomes in skeletal muscle under non-cisplatin conditions. Direct melatonin–cisplatin evidence is limited to pretreatment studies in C2C12 cells from one research group. No in vivo melatonin-plus-cisplatin skeletal-muscle study and no clinical study of melatonin against cisplatin-associated muscle loss were identified in searches through 22 September 2026. Biological plausibility is supported, but protection has not been demonstrated. A controlled tumor-free study would provide a more interpretable test of whether melatonin protects skeletal muscle during cisplatin exposure. Translational validation would then require a separate tumor-bearing study testing whether protection persists under tumor burden and whether cisplatin’s antitumor activity is preserved.

Muscles

16 October 2026

Cisplatin-associated skeletal muscle wasting: phenotype and mechanistic convergence. In tumor-free rodents, cisplatin exposure reduces food intake and body weight and perturbs six overlapping mechanistic domains in skeletal muscle: proteostasis and anabolic suppression, endoplasmic-reticulum stress and translational suppression, mitochondrial dysfunction, redox imbalance, regulated cell death and autophagy-related signaling, and inflammatory/immune contribution. Solid module borders mark domains for which endpoint-specific pharmacological or genetic intervention provides partial supporting evidence; dashed borders mark domains that remain association-level in vivo. The autophagy-related node is explicitly qualified because steady-state marker changes do not establish autophagic flux. The resulting phenotype comprises reduced whole-muscle mass, an organ-level endpoint; reduced myofiber size, reported only where morphometry was quantified; and impaired strength, force, or endurance, reported only where function was directly assessed. No single domain is depicted as sufficient to explain the phenotype, and no melatonin content is included in this figure.
  • Review
  • Open Access

Background: Fatigue in high-intensity exercise is often attributed to a defended ceiling of peripheral fatigue; evidence is mixed. Objectives: We aimed to assess whether the end-exercise potentiated-twitch decrement behaves as a regulated variable across candidate mechanisms. Methods: PubMed/MEDLINE, Scopus, and Web of Science were searched to 12 August 2026. Evidence came from controlled studies in adults, with permeabilized-fiber, rodent, and isolated-actomyosin experiments only where human measurement is impossible. Results: Nine mechanisms met the criteria. Inorganic phosphate and hydrogen ions impair the cross-bridge cycle; reduced sarcolemmal excitability (K+) and reduced sarcoplasmic reticulum Ca2+ release reverse over minutes and days, respectively. Only the cross-bridge effects are driven by metabolites (protons, ATP, lactate) that are agonists of group III/IV afferents; the afferents do not sense contractile impairment itself. Oxygen delivery, respiratory-muscle work, substrate availability, and perceptual load altered fatigue rate more than the end-exercise value, which varied with duration, prior exercise, muscle mass, and mode. Conclusions: Evidence fits a threshold in the phosphate–force relationship, though this does not demonstrate a defended limit. The decrement is not constant across tasks; we propose, as a testable hypothesis, that the regulated quantity is the summed afferent and effort signal. Selection was purposive, without formal risk-of-bias appraisal.

Muscles

9 October 2026

Proposed integrative model (hypothetical) of the relationship between the afferent signal, its laboratory estimate, and the systems that set the rate of accumulation. Group III/IV muscle afferents respond to protons, ATP, and lactate via acid-sensing ion channels, P2X, and TRPV1 receptors, and their central projection reduces motor output. Blocking that projection with lumbar intrathecal fentanyl raises motor output and accelerates the decline in contractile force. We propose that exercise ends when this feedback, summed with afferent traffic from the respiratory muscles and the corollary discharge accompanying the motor command, becomes intolerable; this termination rule is inferred from converging observations and has not been demonstrated directly. The quantity proposed to be regulated is that summed signal; the potentiated-twitch decrement estimates it only in proportion to the metabolite-driven share of contractile impairment, because the afferents sense the metabolites and not the impairment itself. The afferent agonists [2] and the effects of fentanyl blockade [15,31,32] rest on direct experiments; the summation across sources and the termination rule are inferences. The diagram is schematic: no values are plotted, and no fixed end-exercise threshold of contractile impairment is depicted or implied, consistent with the argument developed in Section 3.1, Section 3.2, Section 3.3, Section 3.4, Section 3.5, Section 3.6, Section 3.7 and Section 3.8. In the studies reviewed, arterial oxygen delivery, respiratory muscle work, substrate availability, and perceived effort changed the rate at which the signal accumulates more than its end-exercise value.
  • Article
  • Open Access

The Impact of Aging on the Tongue Proteome

  • Kay Ohlendieck,
  • Margit Zweyer and
  • Paul Dowling
  • + 2 authors

The tongue is a highly important, multifunctional, and complex organ in human physiology. It is critical for digestion, speech, immune surveillance, and sensory perception, playing a dynamic role in daily life. Abnormalities in the innervation and/or myofiber integrity of the tongue can have severe pathophysiological effects on swallowing, speaking, chewing and bodily balance. The age-related decrease in skeletal muscle mass and contractile strength, a recognized risk factor for sarcopenia and frailty, also impacts the tongue muscles. This report has examined the tongue proteome and evaluated changes in protein abundance associated with the aging phenotype. Interestingly, the proteomic cataloging of the contractile apparatus of tongue muscle identified myosin heavy chain isoform MyHC-13, which is the superfast type of myosin that is restricted to specialized skeletal muscles such as extraocular and laryngeal muscles. Proteomics revealed that tongue aging is associated with considerable changes in the protein expression pattern. Decreases were identified in membrane repair-associated annexin A isoforms, luminal calcium-binding proteins, contractile proteins, and cytoskeletal elements. Lower levels of fast myosin isoform MyHC-2B suggests potential age-associated fiber type shifting towards slower twitch properties. Elevated levels of the fibrosis marker collagen COL-VI, which increased deposition in aged tongue muscle was verified by immunofluorescence microscopy, agrees with the idea of a higher degree of susceptibility to reactive myofibrosis in sarcopenia of old age.

Muscles

9 October 2026

Overview of the bioanalytical strategy to determine the tongue proteome. The experimental workflow and the findings from the bioinformatic PANTHER (http://pantherdb.org) [62] analysis of protein classes in the tongue proteome are shown.
  • Article
  • Open Access

Performance fatigability is characterized by a decline in the capacity to maintain force or power during sustained or repeated activity. This exploratory study quantified knee-extensor mechanical performance and rectus femoris surface electromyographic (sEMG) changes during repeated maximal isokinetic knee extensions and explored sex-related differences. Twenty-nine healthy adults (20 men, 9 women; 20–31 years) performed 30 maximal concentric knee extensions at 180°·s−1. Mechanical outcomes were analyzed in all 29 participants, whereas rectus femoris sEMG outcomes were analyzed in 23 participants. Peak torque (PT) decreased by 32.75 ± 11.66% (adjusted p = 6.08 × 10−11), work per repetition by 33.35 ± 11.97% (adjusted p = 2.12 × 10−11), and mean frequency (MNF) by 23.44 ± 8.33% (adjusted p = 6.08 × 10−11). RMS increased significantly from Start to End (adjusted p = 0.000639), with a mean FI-RMS of −17.12 ± 23.11%. FI-PT and FI-work were very strongly associated (ρ = 0.938, adjusted p = 3.71 × 10−13), whereas no association involving rectus femoris MNF or RMS remained statistically significant after Holm–Bonferroni correction. No statistically significant sex-related differences were detected. Repeated maximal knee extensions reduced mechanical performance and rectus femoris MNF while increasing RMS. FI summarizes Start-to-End change across the measured outcomes; its reliability and validity require further investigation.

Muscles

4 October 2026

Individual Start-to-End changes in mechanical and rectus femoris sEMG outcomes. (A) work per repetition (J·rep−1), (B) peak torque (PT, N·m), (C) mean frequency (MNF, Hz), and (D) root mean square (RMS, mV). Blue—Start, Orange—End. Paired points represent individual participants; boxplots summarize group distributions, with whiskers indicating the observed range. Mechanical outcomes include 29 participants; sEMG outcomes include 23 participants.

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Muscles - ISSN 2813-0413