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Molecular Mechanisms Associated with Exercise for Health and Performance
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Molecular Mechanisms Associated with Exercise for Health and Performance

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: 20 June 2026 | Viewed by 5733

Special Issue Editor

Dr. Ciro José Brito

E-Mail Website
Guest Editor
Department of Physical Education, Federal University of Juiz de Fora, Juiz de Fora 36036-900, Brazil
Interests: concussion diagnosis; sports-related concussion; traumatic brain injury; epidemiology; contact sports injuries; return-to-play protocols; neuroimaging in sports; biomarkers for concussion; athlete brain health; concussion prevention; sports neurology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Physical exercise is a pillar for health promotion and disease prevention, as well as for optimizing athletic performance. This Special Issue aims to explore the molecular nexus that connects these dimensions. The aim is to present research that elucidates the cellular and molecular mechanisms triggered by acute and chronic exercise, explaining how they mediate beneficial physiological adaptations for healthy populations and athletes.

Lines of investigation:

  1. Cellular Signaling and Adaptation Pathways:
    (a) Roles of AMPK, mTOR, PGC-1α, Sirtuins, FOXO, MAPKs, CaMK, and NF-κB in response to exercise.
    (b) Cellular sensors (energy, stress, damage) activated by exercise.
    (c) Specific signaling pathways for mitochondrial adaptations (biogenesis, function).
    (d) Regulation of muscle protein synthesis (hypertrophy) and degradation (proteolysis) post-exercise.
  2. Oxidative Stress, Inflammation, and Immune Response:
    (a) Molecular mechanisms of exercise-induced redox balance (endogenous antioxidants, production of ROS as signaling molecules).
    (b) Roles of myokines and adipokines in inter-organ communication and immunomodulation.
    (c) Exercise as a modulator of chronic low-grade inflammation: molecular mechanisms (e.g., via the NLRP3 inflammasome).
    (d) Effects of exercise on cellular and humoral immune function (acute vs. chronic).
  3. Energy Metabolism and Homeostasis:
    (a) Molecular regulation of glucose and lipid metabolism (uptake, utilization, storage) in response to exercise.
    (b) Role of transporters (GLUT4), key enzymes, and metabolic transcription factors.
    (c) Mechanisms of action of exercise on insulin sensitivity and the prevention of insulin resistance.
    (d) Metabolic adaptations in adipose tissue (white, brown, beige).

Dr. Ciro José Brito
Guest Editor

Manuscript Submission Information

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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 science
  • sports medicine
  • aging
  • genetic and exercise
  • endocrinology
  • immunology

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Published Papers (4 papers)

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Research

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14 pages, 919 KB  
Article
Genome-Wide Association Study of Vertical Jump Performance Among Elite Badminton Players
by Fevzi Coşkun Sökmen, Anıl Kasakolu, Celal Bulgay, Naoki Kikuchi, Hasan Hüseyin Kazan, Seyrani Koncagul, Yeliz Ay Yildiz, Attila Szabo, Nicola Luigi Bragazzi and Mehmet Ali Ergün
Int. J. Mol. Sci. 2026, 27(6), 2533; https://doi.org/10.3390/ijms27062533 - 10 Mar 2026
Viewed by 764
Abstract
Vertical jump performance is known to be a moderately heritable trait. However, previous studies on sport genetics have largely relied on candidate-gene approaches, which do not adequately reflect the polygenic nature of explosive performance, particularly among elite badminton players. Therefore, the aim of [...] Read more.
Vertical jump performance is known to be a moderately heritable trait. However, previous studies on sport genetics have largely relied on candidate-gene approaches, which do not adequately reflect the polygenic nature of explosive performance, particularly among elite badminton players. Therefore, the aim of the present study was to identify genetic variants associated with lower-limb explosive performance, assessed via vertical jump measures, among elite Turkish badminton players using a genome-wide association study (GWAS) approach. The present study included 90 elite male (n = 47) and female (n = 43) badminton players, and 557 non-athletic controls sourced from a public database. Performance-related traits were evaluated through countermovement jump (CMJ), squat jump (SJ), and their differential. Genome-wide genotyping was performed using DNA microarrays, and associations were examined using linear mixed models fixed for sex/gender, body mass index, and sport experience. Although no variants reached genome-wide significance (p < 1.00 × 10−7), 13 single-nucleotide polymorphisms (SNPs) exceeded the suggestive threshold (p < 1.00 × 10−5). CMJ-associated variants were rs4905767, rs2911702, rs10246591, and rs9842454; SJ-associated variants were rs55817650, rs62318127, rs115197840, rs78317172, and rs35930589; and CMJ–SJ-associated variants were rs34638064, rs6679342, rs4931233, and rs9442615. The present study provides preliminary evidence that lower-limb explosive performance among elite badminton players is polygenic, involving regulatory and signaling pathways rather than single performance genes. Full article
(This article belongs to the Special Issue Molecular Mechanisms Associated with Exercise for Health and Performance)
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17 pages, 3575 KB  
Article
Role of Exercise in Visceral Adipose Tissue Inflammation and Macrophage Polarization in Hypertensive Mice
by Venkata Polaki, Harshal Sawant, Brody Pinson, Cindy Zhu, Shuzhen Chen and Ji Chen Bihl
Int. J. Mol. Sci. 2026, 27(1), 251; https://doi.org/10.3390/ijms27010251 - 25 Dec 2025
Viewed by 788
Abstract
Macrophages accumulate in visceral adipose tissue (VAT) during hypertension and may contribute to hypertension-associated inflammation. Exercise has shown beneficial effects on hypertension; however, the exact mechanisms by which the activated immune cells lead to the protective effects remain unclear. Our study aimed to [...] Read more.
Macrophages accumulate in visceral adipose tissue (VAT) during hypertension and may contribute to hypertension-associated inflammation. Exercise has shown beneficial effects on hypertension; however, the exact mechanisms by which the activated immune cells lead to the protective effects remain unclear. Our study aimed to determine how exercise influences VAT inflammation by modulating the macrophage polarization in hypertensive mice. Renin transgenic (R+) mice were used as a hypertensive mouse model and subjected to exercise (8 weeks). The body weight and blood pressure were monitored, VAT morphology was assessed by H&E and Masson Trichrome staining, macrophage polarization was determined by immunostaining and flow cytometry, and macrophage phenotype-related proteins were analyzed within the VAT via Western Blots. Results showed that exercise reduced the adipocyte size and collagen content of VAT and increased cell infiltration in R+ mice. Immunostaining and flow cytometry data showed that the ratio of pro-inflammatory macrophages (M1) to anti-inflammatory macrophages (M2) was increased in the VAT of R+ mice, while exercise corrected the macrophage polarization, which was consistent with protein level changes in VAT. Together, our data suggest that exercise improves vascular remodeling and VAT function (reduced adipocyte size, loss of collagen) by modulating VAT inflammation (polarization of macrophages) in hypertensive mice. Full article
(This article belongs to the Special Issue Molecular Mechanisms Associated with Exercise for Health and Performance)
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Review

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31 pages, 1761 KB  
Review
Metabolic Overdrive in Elite Sport: A Systems Model of AMPK–mTOR Oscillation, NAD+ Economy, and Epigenetic Drift
by Dan Cristian Mănescu, Camelia Daniela Plăstoi, Răzvan Liviu Petre, Iulius Radulian Mărgărit, Andreea Maria Mănescu and Ancuța Pîrvan
Int. J. Mol. Sci. 2026, 27(4), 1817; https://doi.org/10.3390/ijms27041817 - 13 Feb 2026
Cited by 8 | Viewed by 1354
Abstract
Exercise adaptation depends on a dynamic alternation between catabolic and anabolic states coordinated primarily by AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR). While transient activation of these pathways underpins beneficial molecular remodeling, the system-level consequences of sustained anabolic drive remain [...] Read more.
Exercise adaptation depends on a dynamic alternation between catabolic and anabolic states coordinated primarily by AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR). While transient activation of these pathways underpins beneficial molecular remodeling, the system-level consequences of sustained anabolic drive remain insufficiently conceptualized in exercise biology. This article presents a conceptual mechanistic narrative review integrating evidence from molecular nutrition, exercise physiology, redox biology, and epigenetic regulation to define limits of adaptive signaling. We propose the Metabolic Overdrive Model, a systems-level framework describing the transition from adaptive AMPK–mTOR oscillation to a high-anabolic lock-in state characterized by persistent mTORC1 activation, suppressed AMPK signaling, altered NAD+ economy (SIRT1–PARP imbalance), redox dysregulation, and progressive epigenetic drift. Using exercise and training as models of sustained metabolic stress, we synthesize mechanistic parallels across energy sensing, oxidative signaling, and chromatin regulation without implying pathological causality. The framework generates testable predictions linking prolonged post-exercise anabolic signaling (>24 h) to specific molecular signatures, including AMPK phosphorylation status, NAD+ availability, PARylation, histone acetylation, and DNA methylation dynamics. By reframing exercise adaptation as a loss-of-oscillation phenomenon rather than a linear continuum, this model provides a mechanistic language for hypothesis generation, biomarker-guided periodization, and future experimental validation. Full article
(This article belongs to the Special Issue Molecular Mechanisms Associated with Exercise for Health and Performance)
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18 pages, 1109 KB  
Review
Exercise-Based Mechanotherapy: From Biomechanical Principles and Mechanotransduction to Precision Regenerative Rehabilitation
by Guang-Zhen Jin
Int. J. Mol. Sci. 2026, 27(2), 694; https://doi.org/10.3390/ijms27020694 - 9 Jan 2026
Cited by 1 | Viewed by 2236
Abstract
Mechanical loading generated during physical activity and exercise is a fundamental determinant of musculoskeletal development, adaptation, and regeneration. Exercise-based mechanotherapy, encompassing structured movement, resistance training, stretching, and device-assisted loading, has evolved from empirical rehabilitation toward mechanism-driven and precision-oriented therapeutic strategies. At the macroscopic [...] Read more.
Mechanical loading generated during physical activity and exercise is a fundamental determinant of musculoskeletal development, adaptation, and regeneration. Exercise-based mechanotherapy, encompassing structured movement, resistance training, stretching, and device-assisted loading, has evolved from empirical rehabilitation toward mechanism-driven and precision-oriented therapeutic strategies. At the macroscopic level, biomechanical principles governing load distribution, stress–strain relationships, and tissue-specific adaptation provide the physiological basis for exercise-induced tissue remodeling. At the molecular level, mechanical cues are transduced into biochemical signals through conserved mechanotransduction pathways, including integrin–FAK–RhoA/ROCK signaling, mechanosensitive ion channels such as Piezo, YAP/TAZ-mediated transcriptional regulation, and cytoskeleton–nucleoskeleton coupling. These mechanisms orchestrate extracellular matrix (ECM) remodeling, cellular metabolism, and regenerative responses across bone, cartilage, muscle, and tendon. Recent advances in mechanotherapy leverage these biological insights to promote musculoskeletal tissue repair and regeneration, while emerging engineering innovations, including mechanoresponsive biomaterials, 4D-printed dynamic scaffolds, and artificial intelligence-enabled wearable systems, enable mechanical loading to be quantified, programmable, and increasingly standardized for individualized application. Together, these developments position exercise-informed precision mechanotherapy as a central strategy for prescription-based regenerative rehabilitation and long-term musculoskeletal health. Full article
(This article belongs to the Special Issue Molecular Mechanisms Associated with Exercise for Health and Performance)
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