Sport-related concussion alters cerebral hemodynamic activity during controlled respiration.

Sport-related concussion (SRC) is known to disrupt neurohemodynamic activity, cardiac function, and blood pressure (BP) autoregulation. This study aims to observe changes in cerebrovascular and cardiovascular responses during controlled respiration after sustaining an SRC. University varsity athletes ( = 81) completed a preseason physiological assessment and were followed up within 5 days of sustaining an SRC. During preseason and follow-up assessments, participants' continuous beat-to-beat BP was collected by finger photoplethysmography, and right prefrontal cortex oxygenation was collected using near-infrared spectroscopy (NIRS). Participants completed 5 min of seated rest and 5 min of a 6-breaths per minute controlled breathing protocol (5 s inhale and 5 s exhale; 0.10 Hz). Wavelet transformation was applied to the NIRS and BP signals, separating them into respiratory (0.10-0.6 Hz) and cardiac (0.6-2 Hz) frequency intervals. Of the 81 participants, 74 had a usable BP signal, 43 had usable NIRS signals, and 28 had both usable BP and NIRS signals. Wavelet amplitudes were calculated and coherence between NIRS and BP on the 28 participants were assessed. There was a significant ( < 0.05) decrease in oxygenated hemoglobin amplitude from 0.062 to 0.054 Hz and hemoglobin difference amplitude from 0.059 to 0.051 Hz, both at the respiratory (0.10-0.6 Hz) frequency interval, from preseason to acute SRC, respectively. Therefore, during controlled respiration, there was a reduction in intensity at the respiratory band, suggesting a protective, reduced respiratory contribution to cerebral hemodynamic activity following acute SRC. This study investigated cerebral hemodynamic activity following sport-related concussion. Prefrontal cortex oxygenation was assessed by near-infrared spectroscopy (NIRS) during a controlled breathing protocol. Wavelet transformation of the NIRS signals showed significant decreases in HbO and HbD amplitude at the respiratory frequency interval (0.10-0.6 HZ) from preseason baseline to acute concussion. These results suggest a decreased respiratory contribution to cerebral hemodynamic activity following acute concussion.