Exercise and Nutritional Supplements' Role in Reducing Traumatic Brain Injury in American Football
Keywords:
Exercise, Traumatic brain injury, Concussion, Vitamin D, Caffeine, Omega-3 fatty acid, American footballAbstract
Given the prevalence of traumatic brain injuries (TBI) in contact sports such as American Football, the need for increased research in TBI has been dramatically increased over the last 20-years. TBI has two main mechanisms that cause neuronal cell death following an incident: direct axonal death and neuronal inflammation, with the latter being the most common because it persists more than a decade and chronically affects neighboring neurons. Therefore, proper management that reduces inflammation post-TBI should be stressed in order to facilitate propitious recovery. While sideline concussion protocols have been implemented in sports fields, it is important immediately to initiate recovery protocols in order to minimize the degree of progressive neuronal death caused by TBI. While difficult to individualize symptoms for each occurrence, it is essential to incorporate a pretest of cognition, memory, and balance as a means of determining the severity of TBI. Although the sports concussion assessment tool 2 has been used by collegiate and professional teams, this tool is just based on observation and comparison. Thus, more precise and advanced diagnosis using biological methods are needed to accurately assess individual symptoms, which should save lives. One example is to use serum creatine kinase (CK) levels because CK released from damaged brain tissues enters the bloodstream and thus TBI can be quickly assessed and identified. While the immediate diagnosis of TBI is one part of management, efficacious treatments of post-TBI is also critical. Regarding this, exercise and nutritional supplementation have been reported to be effective. While specific pathways of neuroprotective mechanisms remain to be elucidated, endurance exercise along with supplementation of fish oil, caffeine, and vitamin D seems to elicit neuroprotective effects. This review provides potential mechanisms responsible for exercise and nutritional supplementation-mediated neuroprotection against TBI. Since human subjects are limited to mechanistic studies requiring invasive surgical procedures, research involving animals (e.g., mouse and rat) are also introduced in this review.
References
Faul MXL, Wald MM, Coronado V, Dellinger AM. Traumatic brain injury in the United States: National estimates of prevalence and incidence, 2002-2006. Injury Prevention. 2010; 16(1): 1. doi: 10.1136/ip.2010.029215.951
Thurman DJ, Alverson C, Dunn KA, Guerrero J, Sniezek JE. Traumatic brain injury in the United States: A public health per-spective. J Head Trauma Rehabil. 1999; 14(6): 602-615.
Corrigan JD, Hammond FM. Traumatic brain injury as a chronic health condition. Arch Phys Med Rehabil. 2013; 94(6): 1199-1201. doi: 10.1016/j.apmr.2013.01.023
Gardner RC, Langa KM, Yaffe K. Subjective and objective cog-nitive function among older adults with a history of traumatic brain injury: A population-based cohort study. PLoS Med. 2017; 14(3): e1002246. doi: 10.1371/journal.pmed.1002246
Cope EC, Morris DR, Scrimgeour AG, VanLandingham JW, Levenson CW. Zinc supplementation provides behavioral resil-iency in a rat model of traumatic brain injury. Physiol Behav. 2011; 104(5): 942-947. doi: 10.1016/j.physbeh.2011.06.007
Mills JD, Bailes JE, Sedney CL, Hutchins H, Sears B. Omega-3 fatty acid supplementation and reduction of traumatic axonal in-jury in a rodent head injury model. J Neurosurg. 2011; 114(1): 77-84. doi: 10.3171/2010.5.JNS08914
Mills JD, Hadley K, Bailes JE. Dietary supplementation with the omega-3 fatty acid docosahexaenoic acid in traumatic brain injury. Neurosurgery. 2011; 68(2): 474-481. doi: 10.1227/ NEU.0b013e3181ff692b
Moro N, Katayama Y, Igarashi T, Mori T, Kawamata T, Kojima J. Hyponatremia in patients with traumatic brain injury: Incidence, mechanism, and response to sodium supplementation or retention therapy with hydrocortisone. Surg Neurol. 2007; 68(4): 387-393. doi: 10.1016/j.surneu.2006.11.052
Wu A, Ying Z, Gomez-Pinilla F. Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats. J Neurotrauma. 2004; 21(10): 1457-1467. doi: 10.1089/neu.2004.21.1457
National Football League (NFL). Diagnosis and Management of Concussion. 2016.
NCAA. Concussion Diagnosis and Management Best Practices. NCAA Sports Science. 2016.
Putukian M. The acute symptoms of sport-related concussion: diagnosis and on-field management. Clin Sports Med. 2011; 30(1): 49-61. doi: 10.1016/j.csm.2010.09.005
Schmid KE, Tortella FC. The diagnosis of traumatic brain in-jury on the battlefield. Front Neurol. 2012; 3: 90. doi: 10.3389%2Ff-neur.2012.00090
Toman E, Harrisson S, Belli T. Biomarkers in traumatic brain injury: A review. J R Army Med Corps. 2016; 162(2): 103-108. doi: 10.1136/jramc-2015-000517
Sharma R, Rosenberg A, Bennett ER, Laskowitz DT, Acheson SK. A blood-based biomarker panel to risk-stratify mild traumatic brain injury. PloS One. 2017; 12(3): e0173798. doi: 10.1371/journal. pone.0173798
Boeck CR, Carbonera LS, Milioli ME, et al. Mitochondrial re-spiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-Daspartate. Mol Cell Biochem. 2013; 384(1-2): 129-137. doi: 10.1007/s11010- 013-1790-8
Somer H, Kaste M, Troupp H, Konttinen A. Brain creatine kinase in blood after acute brain injury. J Neurol Neurosurg Psychiatry. 1975 Jun; 38(6): 572-576.
Karkela J, Bock E, Kaukinen S. CSF and serum brain-specif-ic creatine kinase isoenzyme (CK-BB), neuron-specific enolase (NSE) and neural cell adhesion molecule (NCAM) as prognostic markers for hypoxic brain injury after cardiac arrest in man. J Neu-rol Sci. 1993; 116(1): 100-109.
Cherry JD, Stein TD, Tripodis Y, et al. CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheim-er's disease. PLoS One. 2017; 12(9): e0185541. doi: 10.1371/journal. pone.0185541
Piao CS, Stoica BA, Wu J, et al. Late exercise reduces neuroin-flammation and cognitive dysfunction after traumatic brain injury. Neurobiol Dis. 2013; 54: 252-63. doi: 10.1016/j.nbd.2012.12.017
Glushakov AO, Glushakova OY, Korol TY, et al. Chronic up-regulation of cleaved-caspase-3 associated with chronic myelin pathology and microvascular reorganization in the thalamus af-ter traumatic brain injury in rats. Int J Mol Sci. 2018; 19(10). doi: 10.3390/ijms19103151
Itoh T, Imano M, Nishida S, et al. Exercise increases neural stem cell proliferation surrounding the area of damage following rat traumatic brain injury. J Neural Transm (Vienna). 2011; 118(2): 193-202. doi: 10.1007/s00702-010-0495-3
Kim H, Heo HI, Kim DH, et al. Treadmill exercise and methyl-phenidate ameliorate symptoms of attention deficit/hyperactivity disorder through enhancing dopamine synthesis and brain-derived neurotrophic factor expression in spontaneous hypertensive rats. Neurosci Lett. 2011; 504(1): 35-39. doi: 10.1016/j.neulet.2011.08.052
Griesbach GS, Gomez-Pinilla F, Hovda DA. Time window for voluntary exercise-induced increases in hippocampal neuroplasti-city molecules after traumatic brain injury is severity dependent. J Neurotrauma. 2007; 24(7): 1161-7111. doi: 10.1089/neu.2006.0255
Weightman MM, Bolgla R, McCulloch KL, Peterson MD. Physical therapy recommendations for service members with mild traumatic brain injury. J Head Trauma Rehabil. 2010; 25(3): 206-218. doi: 10.1097/HTR.0b013e3181dc82d3
Yoon KJ, Kim DY. Immediate Effects of a single exercise on behavior and memory in the early period of traumatic brain in-jury in rats. Ann Rehabil Med. 2018; 42(5): 643-651. doi: 10.5535/ Lee Y, et al arm.2018.42.5.643
Saraiva AL, Ferreira AP, Silva LF, et al. Creatine reduces oxida-tive stress markers but does not protect against seizure susceptibil-ity after severe traumatic brain injury. Brain Res Bull. 2012; 87(2-3): 180-186. doi: 10.1016/j.brainresbull.2011.10.010
Ainsley Dean PJ, Arikan G, Opitz B, Sterr A. Potential for use of creatine supplementation following mild traumatic brain injury. Concussion. 2017; 2(2): Cnc34. doi: 10.2217/cnc-2016-0016
Freire Royes LF, Cassol G. The effects of creatine supplemen-tation and physical exercise on traumatic brain injury. Mini Rev Med Chem. 2016; 16(1): 29-39.
Sakellaris G, Kotsiou M, Tamiolaki M, et al. Prevention of complications related to traumatic brain injury in children and ado-lescents with creatine administration: An open label randomized pilot study. J Trauma. 2006; 61(2): 322-329. doi: 10.1097/01. ta.0000230269.46108.d5
Wu A, Ying Z, Gomez-Pinilla F. Oxidative stress modulates Sir2alpha in rat hippocampus and cerebral cortex. Eur J Neurosci. 2006; 23(10): 2573-2580. doi: 10.1111/j.1460-9568.2006.04807.x
Wang T, Van KC, Gavitt BJ, et al. Effect of fish oil supplemen-tation in a rat model of multiple mild traumatic brain injuries. Restor Neurol Neurosci. 2013; 31(5): 647-659. doi: 10.3233/RNN-130316
Sun GY, Simonyi A, Fritsche KL, et al. Docosahexaenoic acid (DHA): An essential nutrient and a nutraceutical for brain health and diseases. Prostaglandins Leukot Essent Fatty Acids. 2018; 136: 3-13. doi: 10.1016/j.plefa.2017.03.006
Suzuki K, Koike T. Mammalian Sir2-related protein (SIRT) 2-mediated modulation of resistance to axonal degeneration in slow wallerian degeneration mice: A crucial role of tubulin deacet-ylation. Neuroscience. 2007; 147(3): 599-612. doi: 10.1016/j.neuro-science.2007.04.059
Wu A, Ying Z, Gomez-Pinilla F. Omega-3 fatty acids supple-mentation restores mechanisms that maintain brain homeostasis in traumatic brain injury. J Neurotrauma. 2007; 24(10): 1587-1595. doi: 10.1089/neu.2007.0313
Fisone G, Borgkvist A, Usiello A. Caffeine as a psychomotor stimulant: mechanism of action. Cell Mol Life Sci. 2004; 61(7-8): 857-872. doi: 10.1007/s00018-003-3269-3
Cuenca L, Gil-Martinez AL, Cano-Fernandez L, et al. Parkin-son's disease: A short story of 200-years. Histol Histopathol. 2018; 18073. doi: 10.14670/HH-18-073
Lusardi TA, Lytle NK, Szybala C, Boison D. Caffeine prevents acute mortality after TBI in rats without increased morbidity. Exp Neurol. 2012; 234(1): 161-168. doi: 10.1016/j.expneurol.2011
Ning YL, Yang N, Chen X, et al. Chronic caffeine exposure attenuates blast-induced memory deficit in mice. Chin J Traumatol. 2015; 18(4): 204-211.
Kuzmin A, Johansson B, Gimenez L, Ogren SO, Fredholm BB. Combination of adenosine A1 and A2A receptor blocking agents induces caffeine-like locomotor stimulation in mice. Eur Neuropsychopharmacol. 2006; 16(2): 129-136. doi: 10.1016/j.euro-neuro.2005.07.001
Astorino TA, Rohmann RL, Firth K. Effect of caffeine inges-tion on one-repetition maximum muscular strength. Eur J Appl Physiol. 2008; 102(2): 127-132. doi: 10.1007/s00421-007-0557-x
Sachse KT, Jackson EK, Wisniewski SR, et al. Increases in cerebrospinal fluid caffeine concentration are associated with fa-vorable outcome after severe traumatic brain injury in humans. J Cereb Blood Flow Metab. 2008; 28(2): 395-401. doi: 10.1038/ sj.jcbfm.9600539
Adams JW, Alvarez VE, Mez J, et al. Lewy body pathology and chronic traumatic encephalopathy associated with contact sports. J Neuropathol Exp Neurol. 2018; 77(9): 757-768. doi: 10.1093/jnen/ nly065
Pearce N, Gallo V, McElvenny D. Head trauma in sport and neurodegenerative disease: An issue whose time has come? Neu-robiol Aging. 2015; 36(3): 1383-1389. doi: 10.1016/j.neurobiolag-ing.2014.12.024
Young JS, Hobbs JG, Bailes JE. The impact of traumatic brain injury on the aging brain. Curr Psychiatry Rep. 2016; 18(9): 81. doi: 10.1007/s11920-016-0719-9
Owolabi JO, Olatunji SY, Olanrewaju AJ. Caffeine and can-Submit your article to this journal | https://openventio.org/submit-manuscript/ nabis effects on vital neurotransmitters and enzymes in the brain tissue of juvenile experimental rats. Ann Neurosci. 2017; 24(2): 65- 73. doi: 10.1159%2F000475895
Essawy SS, Tawfik MK, Korayem HE. Effects of adenosine receptor antagonists in MPTP mouse model of parkinson's dis-ease: Mitochondrial DNA integrity. Arch Med Sci. 2017; 13(3): 659- 669. doi: 10.5114/aoms.2017.67284
Fleet JC. What have genomic and proteomic approaches told us about vitamin D and cancer? Nutrition Reviews. 2007; 65(8 Pt 2): S127-S130.
Tripkovic L, Lambert H, Hart K, et al. Comparison of vita-min D2 and vitamin D3 supplementation in raising serum 25-hy-droxyvitamin D status: A systematic review and meta-analysis. Am J Clin Nutr. 2012; 95(6): 1357-1364. doi: 10.3945/ajcn.111.031070
Jamall OA, Feeney C, Zaw-Linn J, et al. Prevalence and corre-lates of vitamin D deficiency in adults after traumatic brain injury. Clin Endocrinol (Oxf). 2016; 85(4): 636-644. doi: 10.1111/cen.13045
Cui C, Cui J, Jin F, et al. Induction of the vitamin D receptor attenuates autophagy dysfunction-mediated cell death following traumatic brain injury. Cell Physiol Biochem. 2017; 42(5): 1888-1896. doi: 10.1159/000479571
Hua F, Reiss JI, Tang H, et al. Progesterone and low-dose vita-min D hormone treatment enhances sparing of memory follow-ing traumatic brain injury. Horm Behav. 2012; 61(4): 642-651.
Stein DG, Cekic MM. Progesterone and vitamin d hormone as a biologic treatment of traumatic brain injury in the aged. PM R. 2011; 3(6 Suppl 1): S100-S110. doi: 10.1016/j.pmrj.2011.03.010
Downloads
Published
How to Cite
Issue
Section
License

This work is licensed under a Creative Commons Attribution 4.0 International License.
All content published in Sports and Exercise Medicine (SEM) is licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0). This license allows anyone to copy, distribute, transmit, and adapt the work — including for commercial purposes — provided appropriate credit is given to the original author(s) and source.