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Molecular Mechanisms Related to Exercise
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Molecular Mechanisms Related to Exercise

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 January 2026) | Viewed by 3596

Special Issue Editor

Dr. Giorgia Scarfò

E-Mail Website
Guest Editor
Division of General Medicine, Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: polycystic ovarian syndrome; diet; physical exercise; epigenetic modifications

Special Issue Information

Dear Colleagues,

Regular exercise induces long-term systemic adaptations with positive effects on the musculoskeletal, respiratory, cardiovascular, and nervous systems as well as on metabolism and redox balance. These changes are mediated by molecular and intracellular mechanisms, including the regulation of gene expression and the activation of signaling pathways that primarily account for mitochondrial biogenesis, increased glucose uptake, angiogenesis, muscle hypertrophy, bone formation, the release of neurotrophic factors, and molecules with antioxidant capabilities and anti-inflammatory effects.

Therefore, this Special Issue aims to provide a platform for original research and review articles to understand the physiological, molecular, and intracellular mechanisms associated with physical activity, which are the foundation of the primary adaptations induced by regular exercise.

Dr. Giorgia Scarfò
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • exercise
  • mitochondrial biogenesis
  • intracellular pathways
  • inflammation
  • oxidative stress
  • hypertrophy
  • metabolism angiogenesis

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Published Papers (3 papers)

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Research

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13 pages, 1129 KB  
Article
Transcriptomic Analysis of High-Intensity Interval Training in High-Fat-Diet-Induced Spontaneous Hypertensive Rats’ Brains
by Arslan Sadiq, Iqbal Ali Shah, Bor-Tsang Wu, Yi-Yuan Lin, Yi-An Su, Ai-Lun Yang and Shin-Da Lee
Int. J. Mol. Sci. 2026, 27(1), 304; https://doi.org/10.3390/ijms27010304 - 27 Dec 2025
Viewed by 943
Abstract
Hypertension contributes to brain dysfunction through apoptosis, oxidative stress, reduced neuronal connectivity, and neurotransmitter imbalance. Exercise training is a non-pharmacological strategy known to modulate these molecular alterations. This study investigated the effects of high-intensity interval training (HIIT) on transcriptomic changes in the cerebral [...] Read more.
Hypertension contributes to brain dysfunction through apoptosis, oxidative stress, reduced neuronal connectivity, and neurotransmitter imbalance. Exercise training is a non-pharmacological strategy known to modulate these molecular alterations. This study investigated the effects of high-intensity interval training (HIIT) on transcriptomic changes in the cerebral cortex of spontaneously hypertensive rats (SHR) fed a high-fat diet (HFD). Rats were assigned to either a HIIT intervention group (HIIT-HFD-SHR) or a sedentary control group (HFD-SHR). Cortical RNA was extracted, sequenced using the Illumina NovaSeq 6000 platform, and analyzed with DESeq2. Functional enrichment was conducted using Metascape. RNA-seq identified 1223 differentially expressed genes (DEGs) (adjusted p < 0.05), with 51 remaining significant under stringent criteria (adjusted p < 0.001, |log2FC| > 0.5). Among these, eight key genes were closely associated with the regulation of apoptosis and autophagy, including seven downregulated (Egr1, Atf3, Tgm2, Lgals1, Nr4a1, Plekhf1, Nupr1) and one upregulated (Trim39). This transcriptomic analysis following HIIT also modulated circadian rhythm, long-term memory processes, and hypoxia response in the hypertensive brain. These findings indicate that HIIT decreases apoptosis and autophagy and improves circadian rhythm, long-term memory, and hypoxia in hypertensive rats’ brains. Full article
(This article belongs to the Special Issue Molecular Mechanisms Related to Exercise)
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Review

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33 pages, 2243 KB  
Review
Systemic Integrative Mechanisms and Intervention Strategies in Exercise-Induced Skeletal Muscle Damage: Evidence from Animal, Clinical, and Multi-Omics Studies
by Tianhang Peng, Zike Zhang, Ju Wei, Ni Ding, Wanyuan Liang and Xiuqi Tang
Int. J. Mol. Sci. 2026, 27(5), 2451; https://doi.org/10.3390/ijms27052451 - 6 Mar 2026
Viewed by 675
Abstract
Exercise-induced muscle damage (EIMD) has classically been attributed to localized mechanical disruption following eccentric contractions. Emerging evidence, however, indicates that EIMD represents a systems-level failure of stress integration within skeletal muscle rather than a purely mechanical lesion. Mechanical loading initiates disturbances in intracellular [...] Read more.
Exercise-induced muscle damage (EIMD) has classically been attributed to localized mechanical disruption following eccentric contractions. Emerging evidence, however, indicates that EIMD represents a systems-level failure of stress integration within skeletal muscle rather than a purely mechanical lesion. Mechanical loading initiates disturbances in intracellular Ca2+ homeostasis, which interact with metabolic stress, redox imbalance, and immune activation to form self-reinforcing feedback loops. When compensatory capacity is exceeded, transient injury may shift toward maladaptive remodeling marked by mitochondrial dysfunction, ferroptosis, chronic inflammation, and impaired regeneration. Recent studies identify reactive oxygen species accumulation, iron-dependent lipid peroxidation, dysregulated energy sensing, and aberrant immune polarization as key molecular tipping points governing injury reversibility. Beyond their regenerative role, satellite cells act as integrators of metabolic history and epigenetic memory, linking repetitive injury to reduced muscle adaptability, age-related sarcopenia, and heightened metabolic disease risk. Here, we synthesize evidence from animal models, clinical studies, and multi-omics analyses to establish a systems biology framework for EIMD. We delineate the spatiotemporal interactions among mechanical, metabolic, oxidative, immune, and regenerative modules; identify regulatory nodes that determine adaptive repair versus pathological outcomes; and critically evaluate current nutritional, physical, pharmacological, and regenerative interventions from a mechanism-oriented perspective. Finally, we discuss how multi-omics, digital monitoring, and individualized rehabilitation may enable precision management of EIMD and advance understanding of muscle stress resilience and adaptive limits. Full article
(This article belongs to the Special Issue Molecular Mechanisms Related to Exercise)
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25 pages, 1480 KB  
Review
Effects of Rapid Weight Loss on the Immune System in Combat Sports Athletes: A Systematic Review
by Hae Sung Lee
Int. J. Mol. Sci. 2026, 27(1), 508; https://doi.org/10.3390/ijms27010508 - 3 Jan 2026
Viewed by 1653
Abstract
Rapid weight loss (RWL) is a common strategy among combat sports athletes aiming for a competitive advantage. However, it imposes significant immunological stress that compromises both innate and adaptive immune defenses. This systematic review synthesizes current experimental and mechanistic evidence on the effects [...] Read more.
Rapid weight loss (RWL) is a common strategy among combat sports athletes aiming for a competitive advantage. However, it imposes significant immunological stress that compromises both innate and adaptive immune defenses. This systematic review synthesizes current experimental and mechanistic evidence on the effects of RWL in combat sports, focusing on cellular immunity, neuroendocrine regulation, and inflammatory pathways. Acute RWL activates the hypothalamic–pituitary–adrenal axis, elevating plasma cortisol and suppressing lymphocyte proliferation, T-cell function, and natural killer cell cytotoxicity. Although neutrophil counts increase, their phagocytic and oxidative burst capacities decline, reflecting impaired host defense. Monocyte and macrophage systems shift toward proinflammatory phenotypes, while mucosal immunity is weakened by reductions in secretory immunoglobulin A, leading to increased upper respiratory tract infection risk. The magnitude and speed of weight loss are critical determinants of immune dysfunction, with reductions exceeding 5% of body mass producing particularly severe consequences. Evidence-based intervention strategies—including gradual weight management, nutritional optimization, and biomarker monitoring—are essential to mitigate immunosuppression and safeguard athlete health. This review highlights key gaps in combat sports-specific protocols and proposes integrated approaches to preserve immune competence and optimize performance. Full article
(This article belongs to the Special Issue Molecular Mechanisms Related to Exercise)
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