The Effects of an Acute Bout of Subconcussive Head Impacts on Sympathetic Reactivity

Abstract

Symptomatic concussed athletes (tested within ~7 d of injury) exhibit an attenuated rise in blood pressure and heart rate during the cold pressor test (CPT), which is indicative of sympathetic hyporeactivity. However, resting blood pressure is elevated following a sports season that has a high incidence of repetitive subconcussive head impacts (SHI) which suggests autonomic or vascular dysfunction. A single session of experimentally induced repetitive SHI increases circulating biomarkers of neuronal injury. In this context, it is unknown if a session of repetitive SHI alters autonomic function.PURPOSEWe tested the hypothesis that the sympathetically‐mediated rise in heart rate and blood pressure during the CPT would be attenuated following a session of repetitive SHI in healthy young adults.METHODSTen healthy participants (age: 20±2 y; 6 females) with ≥3 years of soccer heading experience completed three separate study visits. The CPT (left hand submerged up to the wrist in agitated 0°C water for 120 s) was conducted before soccer heading (0h) and at 2 h (2h), 24 h (24h), and 72 h (72h) after soccer heading. 20 SHI were completed using a soccer heading protocol (ball projected at ~11.2 m/s from 12.2 m every 30 s). Heart rate (HR; 5‐lead electrocardiogram) and beat‐to‐beat blood pressure (MAP; finger photoplethysmography) were continuously recorded at 1 kHz. Mean HR and MAP were extracted during the final minute of the CPT baseline (BL) and every 30 s throughout the CPT. We used mixed‐effects ANOVAs to compare the change (∆) from BL between and within experimental visits. Values are reported as ∆ BL (mean ± SD).RESULTSThere were no differences across timepoints at BL for HR (0h: 58±9 vs. 2h: 60±7, 24h: 59±8, 72h: 62±9 bpm; P=0.19) or MAP (0h: 98±15 vs. 2h: 99±9, 24h: 89±8, 72h: 95±8 mmHg; P=0.09). There was a main effect of time post SHI for ∆ HR (P<0.01) but multiple comparisons did not reveal where differences occurred between 0h (8±6 bpm) vs. 2h (9±7 bpm; P>0.99), 24h (10±7 bpm; P=0.19), and 72h (8±6 bpm; P<0.99). The mean ∆MAP throughout the CPT was lower at 0h (17±13 mmHg) vs. 2h (21±15 mmHg; P<0.01), 24h (23±17 mmHg; P<0.01), and 72h (20±16 mmHg; P<0.01). The ∆MAP during the CPT was lower at 60 s of 0h vs. 24h (24±12 vs. 31±13 mmHg; P<0.01), at 90 s of 0h vs, all post‐SHI (0h: 28±14 vs. 2h: 34±12, 24h: 38±12, 72h: 33±13 mmHg; P<0.01), and at 120 s of 0h vs. all post‐SHI (0h: 27±15 vs. 2h: 33±12, 24h: 37±10, 72h: 34±13 mmHg; P<0.01).CONCLUSIONContrary to our hypothesis, these preliminary data indicate that a single session of repetitive SHI does not attenuate sympathetically‐mediated cardiovascular responses to the CPT. The increase in HR was similar before and after soccer heading; however, the increase in MAP was exacerbated during the CPT at all post‐SHI time points. Thus, there appears to be sympathetic hyperreactivity following a single session of repetitive SHI. This sympathetic hyperreactivity might explain the increase in blood pressure following a sports season associated with a high incidence of repetitive SHI.