Journal of Exercise & Organ Cross Talk

Abstract Movement disorders such as Parkinson’s disease frequently present with comorbid sleep disturbances, which exacerbate motor symptoms and reduce patients’ quality of life. The striatum, a critical basal ganglia structure, is implicated in both motor control and sleep regulation and represents the key anatomical locus affected in these disorders. While nutritional and exercise interventions have shown promise independently, a significant gap remains in understanding the synergistic molecular crosstalk between these lifestyle modifications and how they collectively target the striatal mechanisms disrupted by sleep deprivation. This review synthesizes evidence to elucidate the integrated, neurobiological effects of combined nutritional and exercise interventions on sleep deprivation-associated movement disorders, emphasizing the striatum’s pivotal role. We establish that exercise, through the induction of neurotrophic factors (like BDNF/GDNF) and enhanced dopaminergic signaling (DAT), provides a critical foundation for synaptic repair. This foundation is synergistically amplified by targeted nutritional strategies, such as polyphenols and omega-3s, which augment antioxidant capacity, dampen neuroinflammation (NRF2/NFκB axis), and modulate key receptors (like A2AR) within the striatum. These combined, non-pharmacological approaches more effectively restore striatal homeostasis and redox balance than either intervention alone, resulting in superior improvement in both motor function and sleep quality. Further longitudinal and mechanistic studies (e.g., RCTs with multimodal endpoints) are warranted to refine optimal intervention protocols and personalize therapeutic strategies. Incorporating these findings into clinical guidelines could promote holistic, synergistic management strategies that improve patient outcomes and reduce healthcare costs.

Abstract Hepatic steatosis is increasingly being recognized as an important pathological feature of disease that commonly reported in patients with inflammatory bowel disease. This study aimed to investigate the effects of High-Intensity Interval Training (HIIT) on the expression of interleukin-10 and Signal transducer and activator of transcription 3 (STAT3) genes in intestinal tissue in an animal model of fatty liver. In this experimental study, 24 rats (weighing 200-250 gr) were selected and randomly divided into 3 groups including healthy control, fatty liver, and fatty liver + HIIT, groups. In order to induce fatty liver, oral tetracycline 140 mg/kg/day in 2 mL of water in form of a solution was given to the rats by gavage for 7 days. HIIT exercise program performed on treadmill five sessions per week for 5 weeks. Data were analyzed by one-way ANOVA and Tukey post hoc tests. P<0.05 was considered significant. The results showed that IL10 gene expression in HIIT groups was significantly lower than in the fatty liver group (p<0.0001). Also, the expression of the STAT3 gene in intestinal tissue was significantly upper in HIIT groups than that in the fatty liver group (p<0.0001). Regulation of IL-10 and STAT3 gene expression in fatty liver-induced adipose tissue can be modulated by HIIT exercise. Therefore, intense interval training can be considered as a non-pharmacological strategy in the treatment of fatty liver.