بهزاد حاجی زاده ملکی

Aging is influenced by a wide range of biological processes, with increasing attention focused on physical exercise as an effective, non-pharmacological intervention to support healthy aging and extend lifespan. This review examines how exercise influences aging mechanisms by activating Forkhead Box O (FOXO) proteins—especially FOXO3, a critical regulator of oxidative stress resistance, metabolism, and cellular repair. By integrating evidence from both animal models and human studies, we explore how different types of physical activity, including endurance and resistance training, enhance FOXO signaling pathways that govern mitochondrial health, autophagy, and inflammation control. FOXO activation appears to play a central role in mitigating age-related diseases such as sarcopenia, cardiovascular disease, neurodegeneration, and cancer. While preclinical studies consistently demonstrate these protective effects, human data are more variable, highlighting the influence of age, sex, and intervention type. Understanding the molecular connection between exercise and FOXO activity can help develop targeted exercise recommendations to promote longevity and delay age-associated functional decline.

Purpose: Vigorous physical exercise causes notable alterations in the circulatory system, affecting stress hormones and plasma proteins. Cortisol serves as a primary glucocorticoid hormone, while albumin, globulin, and hemoglobin function as important carrier proteins. However, how cortisol levels after exercise interact with these proteins is not well understood. This research aimed to explore the association between serum cortisol and the levels of albumin, globulin, and hemoglobin following a single session of intense aerobic exercise in young male runners. Method: Twelve healthy young male runners (average age 21.38 ± 0.95 years; VO₂max 50.81 ± 2.35 ml/kg/min) completed a 15-minute Balke treadmill test. Blood samples were collected before exercise, immediately after, and three hours post-exercise (recovery) to assess serum cortisol, albumin, globulin, and hemoglobin concentrations. Hematocrit measurements were used to adjust for changes in plasma volume. Statistical analysis involved one-way repeated measures ANOVA with Tukey’s post hoc test and Pearson correlation. Results: Immediately after exercise, there were significant increases in cortisol (61.4%), albumin (7.5%), globulin (10.5%), and hemoglobin (10.5%) (p<0.05). After three hours of recovery, cortisol, albumin, and hemoglobin levels returned to baseline, whereas globulin remained significantly elevated (p<0.05). No significant correlations were detected between cortisol changes and any of the carrier proteins at any time point (p>0.05). Conclusion: A single session of intense aerobic exercise markedly raises serum cortisol and key carrier proteins in young runners. The absence of correlation between cortisol and these proteins suggests that their immediate post-exercise increases are likely driven by factors other than cortisol fluctuations, such as hemoconcentration and changes in hydrostatic pressure, rather than direct hormonal stimulation.