TY - JOUR
T1 - Neurobiomarker and body temperature responses to recreational marathon running
AU - Stacey, M.J.
AU - Leckie, T.
AU - Fitzpatrick, D.
AU - Hodgson, L.
AU - Barden, A.
AU - Jenkins, R.
AU - Galloway, R.
AU - Weller, C.
AU - Grivas, G.V.
AU - Pitsiladis, Y.
AU - Richardson, A.J.
AU - Woods, D.R.
N1 - Funding information:
The study was funded internally by the UK Surgeon General and practical support was given by Human Telemetrics (London, UK). The authors retained the right to collect, analyse and interpret data independently to approve or disapprove publication of the finished manuscript.
UK Defence Medical Services (Research & Clinical Innovation) provided Surgeon General Funding via its Research Steering Group. Borja Muniz-Pardos, Fergus Guppy, Asimina Pitsiladis, Ross Bundy and Mike Miller contributed to core temperature elements of the manuscript (data collection and analysis). Volunteers from the University of Brighton and Brighton and Sussex medical schools, the race organisers, St John's Ambulance volunteers and the Brighton Marathon Medical Team are warmly thanked, as are the race participants who volunteered for the study.
Publisher Copyright:
Crown Copyright © 2023 Published by Elsevier Ltd on behalf of Sports Medicine Australia.
PY - 2023/11
Y1 - 2023/11
N2 - Objectives: To assess how biomarkers indicating central nervous system insult (neurobiomarkers) vary in peripheral blood with exertional-heat stress from prolonged endurance exercise.Design: Observational study of changes in neuron specific enolase (NSE), S100 calcium-binding protein B (S100β), Glial Fibrillary Acid Protein (GFAP) and Ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) at Brighton Marathon 2022.Methods: In 38 marathoners with in-race core temperature (Tc) monitoring, exposure (High, Intermediate or Low) was classified by cumulative hyperthermia – calculated as area under curve of Time × Tc > 38 °C – and also by running duration (finishing time). Blood was sampled for neurobiomarkers, cortisol and fluid-regulatory stress surrogates, including copeptin and creatinine (at rested baseline; within 30 min of finishing; and at 24 h).Results: Finishing in 236 ± 40 min, runners showed stable GFAP and UCH-L1 across the marathon and next-day. Significant (P < 0.05) increases from baseline were shown post-marathon and at 24 h for S100β (8.52 [3.65, 22.95] vs 39.0 [26.48, 52.33] vs 80.3 [49.1, 99.7] ng·L−1) and post-marathon only for NSE (3.73 [3.30, 4.32] vs 4.85 [4.45, 5.80] μg·L−1, P < 0.0001). Whilst differential response to hyperthermia was observed for cortisol, copeptin and creatinine, neurobiomarker responses did not vary. Post-marathon, only NSE differed by exercise duration (High vs Low, 5.81 ± 1.77 vs. 4.69 ± 0.73 μg·L−1, adjusted P = 0.0358).Conclusions: Successful marathon performance did not associate with evidence for substantial neuronal insult. To account for variation in neurobiomarkers with prolonged endurance exercise, factors additional to hyperthermia, such as exercise duration and intensity, should be further investigated.
AB - Objectives: To assess how biomarkers indicating central nervous system insult (neurobiomarkers) vary in peripheral blood with exertional-heat stress from prolonged endurance exercise.Design: Observational study of changes in neuron specific enolase (NSE), S100 calcium-binding protein B (S100β), Glial Fibrillary Acid Protein (GFAP) and Ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) at Brighton Marathon 2022.Methods: In 38 marathoners with in-race core temperature (Tc) monitoring, exposure (High, Intermediate or Low) was classified by cumulative hyperthermia – calculated as area under curve of Time × Tc > 38 °C – and also by running duration (finishing time). Blood was sampled for neurobiomarkers, cortisol and fluid-regulatory stress surrogates, including copeptin and creatinine (at rested baseline; within 30 min of finishing; and at 24 h).Results: Finishing in 236 ± 40 min, runners showed stable GFAP and UCH-L1 across the marathon and next-day. Significant (P < 0.05) increases from baseline were shown post-marathon and at 24 h for S100β (8.52 [3.65, 22.95] vs 39.0 [26.48, 52.33] vs 80.3 [49.1, 99.7] ng·L−1) and post-marathon only for NSE (3.73 [3.30, 4.32] vs 4.85 [4.45, 5.80] μg·L−1, P < 0.0001). Whilst differential response to hyperthermia was observed for cortisol, copeptin and creatinine, neurobiomarker responses did not vary. Post-marathon, only NSE differed by exercise duration (High vs Low, 5.81 ± 1.77 vs. 4.69 ± 0.73 μg·L−1, adjusted P = 0.0358).Conclusions: Successful marathon performance did not associate with evidence for substantial neuronal insult. To account for variation in neurobiomarkers with prolonged endurance exercise, factors additional to hyperthermia, such as exercise duration and intensity, should be further investigated.
KW - Brain injuries, traumatic
KW - Copeptin
KW - GFAP protein, human
KW - Heat illness
KW - Heat stroke
KW - Ubiquitin carboxyl-terminal hydrolase L-1, human
UR - http://www.scopus.com/inward/record.url?scp=85172922275&partnerID=8YFLogxK
U2 - 10.1016/j.jsams.2023.09.011
DO - 10.1016/j.jsams.2023.09.011
M3 - Journal article
C2 - 37777396
AN - SCOPUS:85172922275
SN - 1440-2440
VL - 26
SP - 566
EP - 573
JO - Journal of Science and Medicine in Sport
JF - Journal of Science and Medicine in Sport
IS - 11
ER -
