Exercise is increasingly recognized as a complementary therapy for numerous diseases, including cardiovascular, metabolic, urologic, and psychiatric conditions. This special issue of the International Neurourology Journal focuses on the multifaceted protective effects of exercise on brain, muscle, and vascular health. The articles herein explore the mechanisms through which exercise beneficially impacts neurological, metabolic, and vascular function using a variety of experimental models. Collectively, this issue provides new insights into the physiological mechanisms underlying the benefits of exercise and demonstrates the translational potential of these findings in clinical practice.
Hwang et al. [1] investigated how psychiatric disorders such as autism spectrum disorder and depression suppress voluntary physical activity and metabolic energy. Their results highlight the importance of interventions targeting both behavioral and metabolic dysfunctions, and underscore that exercise can restore motivation for physical activity while ameliorating energy imbalance in neuropsychiatric disorders. Lee et al. [2] demonstrated that treadmill exercise prevents age-related cognitive decline in mice. They further showed that regular aerobic exercise preserves the functional integrity of the blood-brain barrier, thereby reducing neuroinflammation and enhancing cognitive function, which suggests a neurovascular protective role for exercise during aging. Kim et al. [3] examined whether treadmill exercise and vitamin D have synergistic protective effects in healthy mice. Their findings revealed improvements in spatial memory, reductions in pro-inflammatory cytokines, prevention of blood-brain barrier breakdown, and enhanced mitochondrial function. These results suggest that non-pharmacological interventions like exercise may confer neuroprotective benefits even in the absence of disease. Li et al. [4] discussed the impact of a high-fat diet on obesity-related vascular dysfunction and showed that aerobic exercise can reverse perivascular adipose tissue (PVAT) dysfunction. Exercise reduced PVAT inflammation, restored adipokine levels, and improved endothelial signaling, highlighting its potential to counteract metabolic disease-induced cardiovascular dysfunction. Won et al. [5] investigated the effects of high-intensity aerobic exercise against angiotensin II-induced skeletal muscle atrophy, a key mechanism in the development of hypertension. They found that high-intensity aerobic exercise stimulates protein synthesis and autophagy pathways, both of which are essential for muscle preservation, and provided evidence for the molecular mechanisms underlying exercise’s protective effects.
Collectively, the studies featured in this issue compellingly demonstrate that exercise exerts beneficial effects on brain function, metabolic regulation, vascular homeostasis, and muscle maintenance. These findings offer valuable insights into a wide range of urological dysfunctions, including bladder dysfunction, pelvic floor weakness, and age-related decline in urological function. Further research expanding on these observations may clarify how exercise-based interventions influence neuroimmune and metabolic targets relevant to lower urinary tract physiology. Such efforts could ultimately lead to the development of effective non-pharmacological treatments for challenging urological disorders.







