Visceral signals, such as cardiac oscillations, are considered a significant source influencing ongoing cortical activity. Research has shown that perceptual and cognitive functions fluctuate with the heart cycle. Seminal studies proposed that upstream signals tied to cardiac contraction (i.e., systole) inhibit brain activity. However, a clear relationship between cardiac phases and cortical excitability, measured by motor-evoked potentials (MEPs) via transcranial magnetic stimulation (TMS), is not yet established. To examine the link between cardiac signals and corticospinal excitability (CSE), we combined electrophysiological measures with TMS targeting the left motor cortex (lM1) in healthy individuals. Input-output (I/O) curves of MEPs were modelled relative to cardiac phases, assessing CSE variations between systole and diastole. We also investigated how different cardiac output affect MEP amplitudes on a trial-by-trial basis. Overall, I/O curves highlighted a greater inhibition of CSE during systoles, characterized by decreased MEP amplitudes at maximal stimulation intensities and a diminished corticomotor gain. Trial-by-trial assessment also indicated that MEPs amplitude may be negatively affected by the strength of cardiac output, indexed by the length of interbeat-intervals (IBIs). These findings suggest that cardiac signals actively modulate brain excitability, which holds significant implications. Accounting for the cardiac cycle can reduce variability in TMS and electrophysiological studies, improving reproducibility. Clinically, aligning non-invasive brain stimulation or neurorehabilitation protocols with phases of higher excitability (e.g., diastole) may enhance treatment efficacy and motor recovery. More broadly, the results contribute to models of brain-body interaction and may provide a physiological marker of altered heart-brain coupling in clinical populations.
Luzio et al. (Fri,) studied this question.