ReviewFrontiers in nutrition2026
Skeletal muscle mitochondrial-methylation-neurotransmitter crosstalk: a novel synergistic model of betaine, tyrosine, and Cordyceps for exercise performance in older adults, individuals with metabolic disorders, and healthy populations.
Review in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Athletic performance and exercise adaptation are influenced by intricately coordinated interactions among mitochondrial bioenergetics, methylation-dependent metabolic pathways, and the regulation of central neurotransmitters. The potential of Cordyceps-based supplementation to enhance mitochondrial ATP production, optimize oxygen utilization, and improve fatigue resistance has been extensively studied. Nevertheless, the exploration of its integration with complementary metabolic modulators remains inadequately addressed. This review introduces an innovative systems-level model that synthesizes Cordyceps with betaine and tyrosine, aiming to target both peripheral and central determinants of athletic performance. Betaine acts as a methyl donor and osmolyte, facilitating creatine synthesis, enhancing cellular hydration, and promoting metabolic resilience, thereby improving muscle power output and fostering adaptations in body composition. Tyrosine, serving as a precursor for catecholamines, significantly influences dopaminergic and noradrenergic signaling, with the potential to mitigate central fatigue and enhance cognitive endurance in the presence of physiological stress. We propose a comprehensive integrative framework of mitochondrial-methylation-neurotransmitter interactions to elucidate how these agents may collectively augment ATP efficiency, redox equilibrium, neuromuscular performance, and recovery processes. Notably, this model may possess translational implications not solely for healthy athletes but also for elderly populations and individuals experiencing metabolic dysfunction, wherein compromised mitochondrial activity and neurotransmitter signaling play a pivotal role in diminished exercise capacity. Subsequent mechanistic and clinical investigations are essential to substantiate this multi-faceted supplementation approach aimed at precision performance enhancement.
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