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

Poster Board Number: E421

Morgan Worley (University at Buffalo, University at Buffalo), Devin Rettke (Indiana University), Isabella Alexander (Indiana University), Rachel Kalbfell (Indiana University), Keisuke Kawata (Indiana University), Blair Johnson (Indiana University)

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. 

Purpose:  We 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. 

Methods:  Ten 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). 

Results:  There 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 (Plt;0.01) but multiple comparisons did not reveal where differences occurred between 0h (8±6 bpm) vs. 2h (9±7 bpm; Pgt;0.99), 24h (10±7 bpm; P=0.19), and 72h (8±6 bpm; Plt;0.99). The mean ∆MAP throughout the CPT was lower at 0h (17±13 mmHg) vs. 2h (21±15 mmHg; Plt;0.01), 24h (23±17 mmHg; Plt;0.01), and 72h (20±16 mmHg; Plt;0.01). The ∆MAP during the CPT was lower at 60 s of 0h vs. 24h (24±12 vs. 31±13 mmHg; Plt;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; Plt;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; Plt;0.01). 

Conclusion:  Contrary 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.

Supported by NINDS R21NS116548.