Catechins and cocoa flavanols combined with exercise in brain aging and neurodegeneration: a comparative neurobiological framework

Aging is associated with progressive alterations in mitochondrial function, metabolic regulation, vascular integrity, neuromuscular performance, and cognitive function, contributing to increased vulnerability to frailty, cardiometabolic disorders, and neurodegenerative diseases. Lifestyle interventions combining regular physical activity with targeted nutritional strategies have attracted increasing attention as potential approaches to support healthy aging. Among dietary polyphenols, green tea catechins and cocoa flavanols have been extensively investigated because of their antioxidant, neuroprotective, and vasculoprotective properties. This narrative review provides a comparative neurobiological framework to examine the available evidence regarding the combined effects of catechins or cocoa flavanols with exercise on brain aging and neurodegeneration, with particular emphasis on mitochondrial bioenergetics, apoptosis and cell survival, neuromuscular function and sarcopenia, and cardiovascular regulation. Current evidence suggests that catechins may exert more direct intracellular effects by supporting mitochondrial function, reducing oxidative stress, modulating apoptotic signaling, and influencing neuroinflammatory pathways, whereas cocoa flavanols appear to predominantly improve vascular function through enhanced nitric oxide bioavailability, endothelial function, and tissue perfusion. Existing studies also suggest that both compounds may interact with exercise-induced adaptations, although catechins have been more consistently associated with mitochondrial biogenesis and muscle regeneration, while cocoa flavanols have shown greater effects on vascular and cardiorespiratory function. Nevertheless, much of the available evidence is derived from preclinical studies, and further well-designed clinical trials are needed to clarify comparative efficacy, long-term safety, and underlying mechanisms. Overall, the available evidence supports the potential complementary roles of these interventions in healthy brain aging; however, additional high-quality clinical and mechanistic studies are required before definitive conclusions can be drawn.