Is over-exercise driving your depression?

Elite athletes are susceptible to anxiety, depression and substance abuse.

More than 1 in 4 footballers have depression or anxiety.  According to the Professional Footballers’ Association the number of players seeking mental health support is soaring.   The Rugby Players’ Association have described mental health problems in the professional game as “a major issue”, other elite sports have been experiencing similar challenges.

There is no evidence or consensus based guidelines for diagnosis and management of mental health symptoms and disorders in elite athletes (International Olympic Committee, 2019).  In this article I highlight the biological implications of regular high intensity exercise, over-training and inflammation in regards to serotonin production. I propose potential nutritional interventions in an over-looked area in the management of mental health disorders in elite performers.

It is understood that anxiety, depression, stress and issues around anger are centred around, politics, moving teams, insecurity over contracts, pressure surrounding performance and anger and isolation after retirement.  These elite athletes are also living in a fiercely competitive environment where performance can be an indicator of self-worth resulting in players feeling vulnerable and open to self-criticism and poor-self esteem.  Psychological support for mental health is as important as physiotherapy and nutritional support for an elite athlete, as a preventative and as a therapy. 

Once the emotional components are accounted for, an understated area of mental health in athletes is that of inflammation and cortisol.  An elite athlete’s training schedule places high demands on the body.  Athletes are regularly breaking down and re-building muscle tissue resulting in acute inflammation, a necessary response for body to rebuild and grow.  In sporadic and contained periods of time this can be beneficial to the immune system. Ensuring rest days are included during the week is necessary for the muscles to repair, rebuild and strengthen.  However, prolonged high intensity exercise with little rest, can suppress the immune system, causing chronic inflammation.  Post exercise immune function depression is most prominent when exercise is continuous, prolonged, of moderate to high intensity and performed without adequate food intake.  Periods of intensified training that results in over-reaching have demonstrated to chronically suppress immune function, with leukocyte* functions measured at rest still suppressed 24 hours after exercise.   Meaning your immune system is not doing what it needs to ensure efficient recovery.  Although it is contested that intense exercise does not decrease immune function, it is generally understood that over training can have a significant detrimental effect on the immune system.

*Leukocytes are part of the body’s immune system helping to fight infection and diseases.

How does this relate to mental health?

An increasing amount of research is confirming that depression is accompanied by immune system deregulation and inflammation.  Like an allergic reaction, inflammation can trigger depression.  It does this by preventing tryptophan (an amino acid we get from our diet) converting to serotonin (the neurotransmitter involved in regulating mood and sleep).  Instead, the tryptophan is metabolised down the kynurenine pathway (see previous blog post on depression and inflammation) creating neuro-toxic molecules instead.  These neuro-toxic molecules (e.g quinolinic acid) function as NMDA antagonists making anxiety reactions more sensitive.

To make matters worse some inflammatory proteins can pass over to the brain producing neuro-inflammation.  When neuro-inflammation occurs, the likelihood of depression and anxiety symptoms increase.  Managing inflammation (when it’s become problematic) by ensuring an adequate intake of anti-oxidants should be considered.  Furthermore, ensuring proper rest is taken and not returning to training before injuries are properly healed is imperative.    

Competing Amino Acids

In order to recover and rebuild muscle we need protein.  Protein is made up of amino acids.  Branch chain amino acids (BCAA) are the set of amino acids involved in muscle growth.  Different amino acids are needed to building our feel good neuro-transmitters such as tryptophan, tyrosine, and phenylalanine amongst others.   It is important to be aware that amino acids compete for absorption.  In regards to tryptophan absorption the carrier protein it uses prefers leucine, so in it’s presence tryptophan fails to be absorbed, leaving the athlete susceptible to symptoms of low serotonin.  If the athlete has a genetic susceptibility or previous experience with depression they are at an even higher risk of experiencing tryptophan-depleted depression and may experience increased aggression.  For further reading on competing amino acids head to ( 


Cortisol (the stress hormone) switches off what we don’t need when we’re running away from a tiger or facing a 6 ft 6 muscle-bound human on the rugby pitch.  In these moments it isn’t necessary to digest food, metabolise fat amongst a host of other things.  In these moments it is advantageous to have blood pumping to the muscles, pupils to dilate and the lungs to expand taking in more oxygen.  The body is perfectly fine at using cortisol and adrenaline for a short amount of time then switching back when the threat is gone and we enter our normal state of rest and digest (also known as the parasympathetic nervous system), this is when healing takes place.  It becomes problematic however, when cortisol is heightened day-in-day-out several times a day.  Cortisol can be heightened due to a number of reasons: stress beyond the pitch, unresolved psychological issues, over consumption of caffeine, inflammation, over-training, or any of the matters discussed at the start of this article. 

In depression, the hippocampus and prefrontal cortex have shown to be smaller than average, which is synonymous with the damage that cortisol (and adrenaline) causes to these parts of the brain.  Hyper secretion of cortisol and adrenocorticotropic hormone (ACTH), owing to excessive HPA activity (hypothalamic pituitary adrenal axis), may also alter carrier proteins that maintain serotonin receptor integrity, reducing serotonin uptake.  Mentioned earlier in this article is the kynurenine pathway, tryptophan can be metabolised down this pathway, failing to convert to serotonin, as a result of cortisol. 

Above describes how inflammation and cortisol can prevent serotonin production, how neuro-inflammation from over training and cortisol can lead to lowered mood and how competing amino acids lowers serotonin production.

Here are a few scientifically researched areas that can aid in these areas.  More research is needed to target these specific areas in elite performers alongside psychological support. 


A randomised, double-blinded, placebo-controlled trial using trained athletes during 3 months of winter training, demonstrated that daily probiotic supplementation reduced exercise-induced tryptophan degradation rates as well as reducing the rates of upper respiratory tract infections.  This is likely due to the importance of the composition of gut bacteria in its ability to regulate tryptophan.  Further research demonstrates the role of the microbiome in modulating tryptophan thus having control over serotonin levels in the host.  This didn’t affect athletic performance however this is a significant finding in the way of preventing tryptophan depletion depression. 

Tryptophan supplementation

Tryptophan availability for serotonin production can be enhanced by increasing carbohydrate intake and by reducing protein intake.  Carbohydrates do not change the levels of circulating tryptophan but they do aid in decreasing circulating competing amino acids by activating insulin.  This in turn increases the availability of carrier proteins to transport tryptophan to the brain.

Protein contains relatively low concentrations of tryptophan but high levels of other competing amino acids in comparison.  As we mentioned earlier, a high protein meal increases the competition for absorption, lowering the availability of tryptophan for the brain.  Carbohydrate: protein ratios have the potential to modulate the availability of tryptophan synthesis for brain serotonin, however as little as 4% protein in a carbohydrate heavy meal can prevent the increase in tryptophan availability.

Because protein consumption is of significant importance to any athlete and each meal is an opportunity to repair muscle damage whilst providing protein for the immune system minimising protein is unconventional.  Supplementation of tryptophan is currently the most reliable way of improving tryptophan levels in the brain because the high concentration is able to compete with the other large amino acids.  Furthering this supplementation is able to take place away from meals.


Sleep is integral.  Scientists have confirmed that during sleep, cerebrospinal fluid pulsates through the brain draining it of toxins.  Simply put, the brain takes out the trash at night.  Without adequate sleep this process is unable to take place and the build up of toxins can result in brain fog, lower moods, and lower memory recall.

Good quality rest.  Physical exertion, consuming too much caffeine, playing intense video games or challenging personal relationships can raise the heart rate and encourage cortisol production.  If cortisol levels are raised, your body’s ability to recover efficiently decreases.

Anti-inflammatory diet

Ensuring each meal contains anti-oxidants in the form of food will help reduce inflammation.  By reducing inflammation markers tryptophan is more likely to convert to serotonin rather than quinolinic acid.  The Mediterranean diet has shown to have promising effects on neuro-inflammatory pathologies such as Alzheimer’s disease. Certain foods have also shown to increase inflammatory markers. 

The competitive nature of sports means that individuals are pushing themselves past their limits to be noticed or even to maintain their position.  All to often you see players returning from injury too soon, or become un-motivated due to burn-out or simply can’t shake an infection or cold.  All of which, affect the mood of the individual.

Management of mental health symptoms and disorders in athletes should take a comprehensive, integrative approach that puts the athlete at the centre and addresses the full range of emotional, mental, physical, social and environmental influences that effects an individuals mental health.  Drop me a message and we can discuss how a personalised nutrition and lifestyle plan can protect you from inflammation driven mental health issues.


“A 12-Month Prospective Cohort Study Of Symptoms Of Common Mental Disorders Among Professional Rugby Players.” European Journal of Sport Science (2020).

A, Neumeister. “Tryptophan Depletion, Serotonin, And Depression: Where Do We Stand? – Pubmed – NCBI .” N. p., 2020.

Akbaraly T, Kerlau C, Wyart M, Chevallier N, Ndiaye L, Shivappa N, et al. Dietary inflammatory index and recurrence of depressive symptoms: results from the Whitehall II Study. Clin Psychol Sci 2016;4:1125e34. 10.1177/2167702616645777.

Bachero-Mena, Beatriz, Fernando Pareja-Blanco, and Juan J. González-Badillo. “Enhanced Strength And Sprint Levels, And Changes In Blood Parameters During A Complete Athletics Season In 800 M High-Level Athletes.” Frontiers in Physiology 8 (2017): n. pag.

D’Mello, C. and Swain, M. (2016). Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression. Inflammation-Associated Depression: Evidence, Mechanisms and Implications, pp.73-94.

Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008). From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci 9, 46−56.

Detopoulou P, Panagiotakos DB, Antonopoulou S, Pitsavos C, Stefanadis C. Dietary choline and betaine intakes in relation to concentrations of inflammatory markers in healthy adults: the ATTICA study. Am J Clin Nutr 2008;87: 424e30

Dowlati, Y., Herrmann, N., Swardfager, W., Liu, H., Sham, L., Reim, E. K., et al. (2010). A meta-analysis of cytokines in major depression. Biol Psychiatry 67, 446−457.

Evans, D. L., Charney, D. S., Lewis, L., Golden, R. N., Gorman, J. M., Krishnan, K. R., et al. (2005). Mood disorders in the medically ill: scientific review and recommendations. Biol Psychiatry 58, 175−189.

Evans, J.M.; Morris, L.S.; Marchesi, J.R. The gut microbiome: The role of a virtual organ in the endocrinology of the host. J. Endocrinol. 2013, 218, R37–R47.

Evrensel, Alper, Barış Önen Ünsalver, and Mehmet Emin Ceylan. “Neuroinflammation, Gut-Brain Axis And Depression.” Psychiatry Investigation 17.1 (2020): 2-8.

Fried, E. (2017). The 52 symptoms of major depression: Lack of content overlap among seven common depression scales. Journal of Affective Disorders, 208, pp.191-197.

Gouttebarge, Vincent et al. “Symptoms Of Common Mental Disorders In Professional Rugby: An International Observational Descriptive Study.” International Journal of Sports Medicine 38.11 (2017): 864-870.

Gouttebarge, Vincent, and Gino M. M. J. Kerkhoffs. “Mental Health In Professional Football Players.” Return to Play in Football (2018): 851-859.

Hajihashemi P, Azadbakht L, Hashemipor M, Kelishadi R, Esmaillzadeh A. Whole-grain intake favorably affects markers of systemic inflammation in obese children: a randomized controlled crossover clinical trial. Mol Nutr Food Res 2014;58:1301e8

Hammen, C. (2015). Stress and depression: old questions, new approaches. Current Opinion in Psychology, 4, pp.80-85.

Holth, Jerrah K. et al. “The Sleep-Wake Cycle Regulates Brain Interstitial Fluid Tau In Mice And CSF Tau In Humans.” Science 363.6429 (2019): 880-884.

Horn, Peggy & Pyne, David & Hopkins, W & Barnes, Chris. (2010). Lower white blood cell counts in elite athletes training for highly aerobic sports. European journal of applied physiology. 110. 925-32.

Hughes, Lynette, and Gerard Leavey. “Setting The Bar: Athletes And Vulnerability To Mental Illness.” British Journal of Psychiatry 200.2 (2012): 95-96.

Jacka FN, O’Neil A, Opie R, Itsiopoulos C, Cotton S, Mohebbi M, et al. A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial). BMC Med 2017;15. s12916-017-0791-y.

JD, Fernstrom. “Large Neutral Amino Acids: Dietary Effects On Brain Neurochemistry And Function. – Pubmed – NCBI .” N. p., 2020.

Kim, Yong-Ku, and Sang Won Jeon. “Neuroinflammation And The Immune-Kynurenine Pathway In Anxiety Disorders.” Current Neuropharmacology 16.5 (2018): 574-582.

Lin PY and Su KP. ‘A meta-analytic review of double-blind, placebo-controlled trials of antidepressant efficacy of omega-3 fatty acids’  J Clin Psychiatry, 2007 Jul;68(7):1056-61

Mackinnon, L. “Immunity In Athletes.” International Journal of Sports Medicine 18.S 1 (1997): S62-S68.

McGrattan, Andrea M. et al. “Diet And Inflammation In Cognitive Ageing And Alzheimer’S Disease.” Current Nutrition Reports 8.2 (2019): 53-65.

Milano, W. Pizza, V. Capasso, A. (2018). Benefical effects of mediterranean diet in neuroinflammation and related diseases. Integrative Food, Nutrition and Metabolism. 5 (1), 1 – 10.

Miller, A. and Raison, C. (2015). The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nature Reviews Immunology, 16(1), pp.22-34.

Miller, A. H., Maletic, V., & Raison, C. L. (2009). Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biol Psychiatry 65, 732−741.

Pierozan, P., Colín-González, A., Biasibetti, H., da Silva, J., Wyse, A., Wajner, M. and Santamaria, A. (2017). Toxic Synergism Between Quinolinic Acid and Glutaric Acid in Neuronal Cells Is Mediated by Oxidative Stress: Insights to a New Toxic Model. Molecular Neurobiology, 55(6), pp.5362-5376.

Reardon, Claudia L et al. “Mental Health In Elite Athletes: International Olympic Committee Consensus Statement (2019).” British Journal of Sports Medicine 53.11 (2019): 667-699.

Richard, Dawn M et al. “L-Tryptophan: Basic Metabolic Functions, Behavioral Research And Therapeutic Indications.” International Journal of Tryptophan Research 2 (2009): IJTR.S2129.

Schwarcz, R., & Pellicciari, R. (2002). Manipulation of brain kynurenines: glial targets, neuronal effects, and clinical opportunities. J Pharmacol Exp Ther 303, 1−10.

Strasser, Barbara et al. “Probiotic Supplements Beneficially Affect Tryptophan–Kynurenine Metabolism And Reduce The Incidence Of Upper Respiratory Tract Infections In Trained Athletes: A Randomized, Double-Blinded, Placebo-Controlled Trial.” Nutrients 8.11 (2016): 752.

Tolkien, K. Bradburn, S. Murgatroyd, C. (2018). An anti-inflammatory diet as a potential intervention for depressive disorders: A systematic review and meta-analysis.. Clinical Nutrition. 18 (20), 32540-32548.

Leave a Reply

%d bloggers like this: