Circulating Mitochondrial DNA Levels in Collegiate Football Players: A Pilot Study

Abstract

Traumatic injury causes the release of circulating mitochondrial alarmins or damage‐associated molecular patterns (DAMPs) including mitochondrial DNA (mtDNA), peptides, and lipids from intracellular molecules into the extracellular space. Here, we sought to investigate whether circulating mtDNA concentration is a valuable hallmark of the sports‐related subconcussive brain injuries in collegiate football players.MethodsBlood samples were collected in K2EDTA vacutainers from male, collegiate football players (n = 13, aged 20.0 ± 1.0, BMI 32.1 ± 5.3 kg/m2) at 4 different time points: pre‐full‐contact practice, post‐full‐contact practice, pre‐season, and post‐season. These subjects include 8 defensive and 5 offensive line players. Samples are analyzed to determine the absolute amount of circulating mtDNA markers (COX3 and ND1, ng/ml) using a RT‐PCR method. Analysis of Bac16s levels was included in each run as a negative control to ensure reliability. The absolute mtDNA/ml of plasma sample was determined using a standard curve constructed using Lambda DNA of known concentration. Head impact kinematics data were collected during a full‐contact practice session using the Vector mouth guard (Biometrics Inc) which measures linear and angular head kinematics during impact. Data used in this study include number of hits, sum of peak linear acceleration, sum of peak angular acceleration, and sum and average of head injury criterion. A p‐value less than 0.05 was deemed significant for all comparisons.ResultsThere were no significant changes in the level of circulating mtDNA between pre‐full‐contact‐practice and post‐full‐contact practice in both offensive and defensive players. There were no statistically significant correlations of the changes in the value of circulating mtDNA the pre‐ vs. post‐practice with head impact kinematics data recorded during the practice sessions. Kinematics data in conjunction with mtDNA data indicated that circulating mtDNA levels are more indicative of activity level, rather than the degree of subconcussive head impacts. For the Pre‐ vs. Post‐season comparisons, the levels of circulating mtDNA were not significantly increased post‐season. However, the offensive group exhibited higher levels of COX 3 and ND1 levels in post‐season, as compared to those of the defensive group. Specifically, COX3 concentrations were 0.012 ± 0.004 ng/ml (pre‐season, defensive), 0.011 ± 0.004 (post‐season, defensive), 0.022 ± 0.009 (pre‐season, offensive) and 0.022 ± 0.002 (post‐season, offensive). ND1 concentrations were 0.007 ± 0.002 (pre‐season, defensive), 0.006 ± 0.002 (post‐season, defensive), 0.013 ± 0.006 (pre‐season, offensive) and 0.013 ± 0.001 (post‐season, offensive).ConclusionHigher circulating mtDNA level was observed in offensive line payers who sustains less frequent, but greater magnitude of head and body impacts during play. Our preliminary results warrant further study in a larger group of collegiate athletes engaged in contact sports.Support or Funding InformationSupported by NIH Grant R01NS102157This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.