Journal of Exercise & Organ Cross Talk

Abstract Sedentary obesity is associated with chronic inflammation, oxidative stress, and impaired angiogenesis, leading to endothelial dysfunction. Interval training and CoQ10 each improve redox balance and vascular health, possibly via inter-organ crosstalk, but their combined effects in sedentary obese men are unclear. Sixty sedentary obese men (30–45 years) were randomized into four groups (n=15): control, CoQ10 (100 mg/day), moderate-intensity intermittent training (3×/week, 8 weeks), and training + CoQ10. Serum VEGF, TAC, and H₂O₂ were measured pre/post-n via ELISA and colorimetric assays. Data were analyzed with repeated-measures ANOVA (α=0.05). Effect sizes (partial η²) were reported. Training significantly raised VEGF (p < 0.001, η² = 0.363) and TAC (p < 0.001, η² = 0.290), while strongly reducing H₂O₂ (p < 0.001, η² = 0.520). CoQ10 showed no significant main or interactive effects on TAC or H₂O₂; however, a significant three-way interaction (time × exercise × supplement) was observed for VEGF (p = 0.001, η² = 0.187). Post-hoc analysis revealed that the exercise-only group showed a greater increase in VEGF compared to the combined group, though the direct comparison between TR and TR+SUP at post-intervention did not reach statistical significance (p > 0.05). Eight weeks of interval training robustly improves VEGF and redox homeostasis in sedentary obese men, possibly through myokines/exerkines enhancing muscle–adipose–endothelial crosstalk and HIF-1α/VEGF signaling. CoQ10 provides no added benefit for most outcomes and may be associated with a modest attenuation of the exercise-induced VEGF response.

Abstract Obesity is associated with chronic low-grade inflammation and elevated oxidative stress. This study investigated the independent and combined effects of an 8-week aerobic interval-style continuous training program and CoQ10 supplementation on serum TGF-β and MDA concentrations in inactive obese men. Sixty inactive obese men (aged 30–45 years) were randomly assigned to four groups (n=15 each): control (CONT), CoQ10 supplementation (SUP; 100 mg/day), training (TR), and combined training + supplementation (TR+SUP). The supervised training protocol was performed three sessions per week for 8 weeks with progressive intensity. Fasting venous blood samples were collected before and after the intervention. Serum MDA was measured using colorimetric assay, and TGF-β was quantified via ELISA. Data was analyzed using two-way repeated-measures ANOVA. Significant time × exercise interactions were observed for both MDA (F(1,56) = 28.793, p < 0.001) and TGF-β (F(1,56) = 30.617, p < 0.001), with reductions in the exercise groups (MDA: exercise groups from 210 nmol/L to 156 nmol/L; TGF-β: from 35 nmol/L to 30 pg/mL). Time × supplementation interactions were also significant but smaller (MDA: η_p² = 0.082; TGF-β: η_p² = 0.068). No significant three-way interaction was detected for either marker. These findings highlight aerobic interval-style continuous training as a cornerstone intervention for mitigating obesity-related oxidative stress and fibrotic signaling. CoQ10 supplementation produced a small independent reduction in both markers, but no synergistic or additive interaction with exercise was observed.

Abstract Programmed cell death is a critical element of the body’s defense system. Exercise represents a physiological stressor that triggers an adaptive response within the body. It has been suggested that various forms of programmed cell death are essential for the adaptation process associated with exercise. During physical activity, mechanisms such as apoptosis and autophagy are activated to mitigate tissue damage, restore cellular integrity, resolve inflammatory responses, and facilitate direct signals that promote adaptation. The induction of programmed cell death is mediated by specific factors, including reactive oxygen species, cytokines, and hormones. These cell death pathways are initiated by the presence of altered proteins and organelles, with the objective of conserving and recycling cellular resources. In scenarios where cells accumulate damaged molecules and repair mechanisms become overwhelmed, programmed cell death is triggered. In this review article, we have examined the types of programmed death and the effect of aerobic training on these deaths.