- Corticospinal excitability is influenced by cardiac phase; insights come from TMS input-output curves.1
- The relationship informs brain–body timing and core electrophysiology (NeuroImage, Volume 328).1 1
Gardner updates
- Input-output curves show influence of cardiac phases on cortico-spinal excitability (Di Luzio et al., NeuroImage). 1
Weekly enrichment (2026-07-20)
- The study (Di Luzio, Perrucci, Ferri & Costantini, NeuroImage vol. 328, 2026) tested whether the cardiac cycle modulates corticospinal excitability by combining electrophysiology with TMS over the left primary motor cortex (lM1) in healthy participants.2 3
- Rather than single-intensity probes, the authors modelled full motor-evoked-potential (MEP) input-output (I/O) curves separately for systole and diastole to characterize excitability across stimulation intensities.2 3
- The I/O curves showed greater inhibition of corticospinal excitability during systole, with decreased MEP amplitudes at maximal stimulation intensities and a diminished corticomotor gain.2 3
- A trial-by-trial analysis linked MEP amplitude negatively to cardiac output strength, indexed by interbeat-interval (IBI) length, indicating heartbeat-to-heartbeat modulation of excitability.2 3
- The authors argue accounting for cardiac phase can reduce variability in TMS and electrophysiology experiments, improving reproducibility of excitability measures.2 3
- Clinically, they suggest timing non-invasive brain stimulation or neurorehabilitation to higher-excitability phases (e.g., diastole) could enhance treatment efficacy and motor recovery, relevant to stroke rehabilitation.2 3
- The systolic-inhibition result aligns with seminal proposals that cardiac-contraction signals dampen brain activity, but contrasts with other TMS work (e.g., a PLOS Biology study) reporting corticospinal excitability is highest during systole, underscoring that the direction of the effect remains debated.2 4
- Prior TMS studies also diverge, with at least one real-time EKG-EMG study finding no significant effect of cardiac phase on MEP amplitude or variability, so the field has not converged on a consistent heart-brain excitability relationship.4 5