Caffeine as an Ergogenic Aid for Neuromuscular Performance: Mechanisms of Action from Brain to Motor Units.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and neurophysiological evidence without systematic search methodology.
PubMed 41599866 · doi:10.3390/nu18020252
What was done
This narrative review synthesized existing neurophysiological literature on the mechanisms underlying caffeine's ergogenic effects on neuromuscular performance. The authors evaluated central pathways (adenosine receptor antagonism, arousal, corticospinal excitability, and motor unit recruitment and firing behavior) versus direct peripheral mechanisms on skeletal muscle excitation-contraction coupling (ryanodine receptors).
What was found
The abstract provides no quantitative data or numerical effect sizes. It reports that caffeine's ergogenic actions at physiological doses are driven primarily by central adenosine receptor antagonism, which reduces inhibitory neuromodulation and alters motor unit firing dynamics. The authors note that the concentrations required to directly affect muscle ryanodine receptors exceed safe human levels, making direct peripheral contractile augmentation unlikely in vivo.
Why it matters
This review clarifies that caffeine enhances neuromuscular performance predominantly by tuning central nervous system motor gain rather than directly augmenting muscle contractility. It helps direct future research toward central neural mechanisms rather than peripheral muscle targets.
Limits
This is a narrative review with no empirical data, sample size, or systematic search methodology presented in the abstract. Key unresolved areas noted include persistent inward currents, sex-dependent effects (such as estrogen-related receptor expression), and neural adaptations from repeated caffeine use.
Cited by
- supports Caffeine exerts its physiological effects by acting on adenosine receptors.