Chronic pain is a significant and complex health condition characterized by persistent or recurrent pain lasting more than three months. Exercise-based rehabilitation is an effective non-pharmacological intervention, yet its underlying mechanisms have not been fully elucidated. This review systematically maps the molecular pathways of exercise-induced analgesia onto the pathophysiological cascades of chronic pain, aiming to fill a key gap in the current literature. It explores the molecular and cellular mechanisms underpinning the pathophysiology of chronic pain, indicating that the persistence of chronic pain stems from peripheral sensitization driven by inflammatory mediators and central sensitization involving glial cell activation and N-methyl-D-aspartate (NMDA) receptor-mediated neuroplasticity. Exercise can interrupt these pathological cascades through multi-system adaptations, including activation of the endogenous opioid and serotonergic systems activation and anti-inflammation. However, a significant gap remains in translating this mechanistic understanding of chronic pain into optimized, personalized exercise prescriptions, requiring future research into different exercise modalities, sex-specific responses, and the impact of comorbidities.

Depression is a prevalent and complex neuropsychiatric disorder that substantially impairs quality of life worldwide. Current pharmacological and psychotherapeutic interventions are often limited by inadequate efficacy and restricted accessibility. Exercise has emerged as a potent non-pharmacological alternative, exhibiting antidepressant effects comparable to conventional treatments, with the microbiota–gut–brain (MGB) axis increasingly recognized as a key mediator. Despite growing interest, existing research articles largely describe associations without mapping the molecular pathways from exercise-altered microbes to neurobiological changes in depression. This review addresses these gaps by comprehensively dissecting the molecular cascades from microbial remodeling to synaptic and systemic adaptations, thereby providing a mechanistic roadmap absent in current syntheses. We first delineate how gut dysbiosis contributes to depression via endocrine, neural, and immune pathways. Subsequently, we highlight the ability of exercise to reverse these pathological states by restoring microbial diversity, reinforcing intestinal barrier function, and modulating the production of microbial metabolites. These exercise-driven changes collectively attenuate systemic and neuroinflammation, enhance brain-derived neurotrophic factor signaling, augment serotonin synthesis, and dampen hypothalamic–pituitary–adrenal axis hyperactivity. By reinstating intestinal homeostasis, exercise acts as a central regulator of the MGB axis and represents a promising therapeutic strategy. This integrative framework offers novel insights into depression pathogenesis and opens avenues for multifaceted intervention.

Patellar tendinopathy affects approximately 18% of athletes and up to 45% of volleyball players, representing a common cause of load-related anterior knee pain and functional limitation in jumping and landing sports. Clinical diagnosis relies primarily on history and physical examination. However, no consensus has yet been established on standardized diagnostic criteria, particularly for imaging-based assessment, and no definitive clinical practice guideline currently exists; imaging abnormalities frequently coexist with symptoms but are also common in asymptomatic athletes, and incidental findings may carry a risk of overdiagnosis and unnecessary imaging-guided management. This narrative review synthesizes the current evidence on the clinical management of patellar tendinopathy in athletes, spanning diagnosis, treatment, long-term prognosis, and return to sport; the literature was identified through structured searches of PubMed, Web of Science, and Google Scholar, with the final search conducted on 1 July 2026. Exercise therapy represents the most extensively studied conservative approach and may be considered a reasonable first-line option, although no single loading mode has demonstrated clear superiority and the underlying evidence is of low to very low certainty; injection strategies differ in mechanisms and evidence strength, but most data come from short-term studies. These studies commonly combine injections with exercise, making the injection’s isolated effect unclear. Additionally, shockwave therapy is not supported by current evidence as a first-line or stand-alone option. Because structural imaging changes and clinical symptoms frequently diverge, functional outcomes rather than imaging endpoints should guide load progression and return-to-sport decisions. This review provides clinicians with a practical synthesis of the currently available evidence for treatment selection and patient management, and identifies remaining uncertainties, particularly in adolescent populations and long-term outcome prediction.

Seasonal affective disorder (SAD) is a recurrent mood disorder associated with reduced photoperiod exposure and circadian disruption during autumn and winter. Emerging evidence links SAD to alterations in serotonergic signaling, neuroimmune activity, metabolism, and the microbiota–gut–brain axis; however, the causal relationships among these systems remain incompletely understood. A structured search of PubMed, Web of Science, and Scopus identified relevant publications from 2000 to 2025, with clinical and preclinical evidence evaluated separately. Proposed links between circadian misalignment, inflammatory signaling, and tryptophan metabolism toward the kynurenine pathway are based largely on associative and preclinical findings rather than confirmed mechanisms in SAD. The microbiota–gut–brain axis in SAD is likely bidirectional, as seasonal changes in feeding behavior, physical activity, and circadian phase may themselves influence gut microbial composition and function. Accordingly, microbiome alterations in affective disorders may reflect both potential upstream modulators and downstream consequences of disease-related behavior. Psychobiotics have been proposed as modulators of gut–brain communication in affective disorders. Among candidate strains, Lacticaseibacillus rhamnosus GG (formerly Lactobacillus rhamnosus GG; LGG) has shown effects on intestinal barrier function, immune signaling, and host tryptophan metabolism in preclinical studies. However, evidence derives largely from animal or non-seasonal depression models, and direct evidence in SAD is lacking. Thus, LGG should be considered a mechanistically plausible candidate for future investigation rather than an established therapy. This review synthesizes evidence on circadian regulation, serotonergic and tryptophan metabolism, and microbiota–gut–brain interactions in SAD, and highlights mechanistic gaps for future studies.