Concussed Athletes Exhibit Impaired Tolerance to a Central Hypovolemic Challenge

Abstract

Concussed patients exhibit autonomic dysfunction that likely contributes to abnormal cardiovascular responses to head‐up tilt and sit‐to‐stand tests. However, these tests also activate the vestibular system, whereas lower body negative pressure (LBNP) induces central hypovolemia without vestibular activation. It is unknown if concussed patients exhibit abnormal cardiovascular responses to LBNP.PURPOSEWe tested the hypothesis that symptomatic concussed athletes (CA) have a greater reduction in blood pressure during LBNP vs. healthy controls (HC).METHODSTen CA (age: 19±2 y, 7 females) and ten HC (age: 21±2 y, 6 females) completed one study visit. After 5 min of resting baseline, 40 mmHg of LBNP was applied for up to 5 min to induce central hypovolemia. Heart rate (HR; ECG), mean arterial pressure (MAP; photoplethysmography), stroke volume (SV; Modelflow), middle cerebral artery blood velocity (MCAv; transcranial Doppler), and end tidal partial pressure of carbon dioxide (ETCO2) were recorded continuously. Cerebral vascular resistance (CVR) was calculated as MAP/MCAv. The change in HR divided by the change in MAP was calculated as an indicator of cardiac baroreflex sensitivity. CA completed a visual analogue concussion symptom scale (VAS) pre and post‐LBNP. Mean values across every min of LBNP were recorded for analyses. Outcome variables are reported and analyzed as a change from baseline for the first 60 s (stage 1) and the final stage because LBNP was terminated early due to some participants exhibiting signs of pre‐syncope (CA: n = 6; HC: n = 2).RESULTSHR (CA: 60±10 vs HC: 63±10 bpm; P=0.22), MAP (CA: 93±10 vs HC: 95±6 mmHg; P=0.31), SV (CA: 88±10 vs HC: 96±32 mL; P=0.24), MCAv (CA: 63±17 vs HC: 64±11 cm/s; P=0.41), ETCO2 (CA: 45±2 vs HC: 45±3 mmHg; P=0.37), and CVR (CA: 1.57±0.37 vs HC: 1.55±0.27 mmHg/cm/s; P=0.37) were not different at baseline. At stage 1, the change in HR (CA: 27±9 vs HC: 21±8 bpm; P=0.39), MAP (CA: −13±4 vs HC: −10±4 mmHg; P=0.57), SV (CA: −40±11 vs HC: −30±15 mL; P=0.31), MCAv (CA: −11±5 vs HC: −15±20 cm/s; P=0.69), ETCO2 (CA: −5±2 vs HC: −3±2 mmHg; P=0.16), CVR (CA: 0.09±0.11 vs HC: 0.09±0.22 mmHg/cm/s; P=0.97), and the HR/MAP ratio (CA: −2.28±1.59 vs HC: −2.52±1.77 bpm/mmHg; P=0.82) were not different between CA and HC. At the final stage, the change in HR (CA: 31±19 vs HC: 40±21 bpm; P=0.20), MAP (CA: −28±17 vs HC: −23±17 mmHg; P=0.39), SV (CA: −39±18 vs HC: −45±27 mL; P=0.54), MCAv (CA: −16±7 vs HC: −19±8 cm/s; P=0.35), and ETCO2 (CA: −6±3 vs HC: 7±5 mmHg; P=0.62) were not different between CA and HC. The change in CVR (CA: −0.09±0.28 vs HC: 0.15±0.26 mmHg/cm/s; P=0.05) and the HR/MAP ratio (CA: −0.43±4.07 vs HC: −2.90±2.38; P=0.02) were different between CA and HC at the final stage. Total LBNP time was lower in CA (201±95 s) vs HC (270±64 s; P=0.04). The VAS score increased in CA from pre‐LBNP (2±2) to post‐LBNP (4±2; P=0.02).CONCLUSIONCA had an impaired tolerance to LBNP likely due to a reduction in cardiac baroreflex sensitivity. CA also had a reduction in CVR during LBNP, which may be indicative of abnormal cerebral autoregulation during a decrease in MAP.Support or Funding InformationNIH Grant UL1TR001412This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.