Testosterone replacement for the retired mixed martial artist

by | Apr 21, 2022 | Uncategorized | 0 comments

This article is especially relevant for previous generations, the modern-day mixed martial arts (MMA) athlete hopefully will have a better education on the topics related to in this article and some of the risk factors can be mitigated (extreme weight cuts, brain trauma, anabolic androgenic steroid usage etc).

USADA (United States Anti-Doping Association) officially started testing UFC (Ultimate Fighting Championship) athletes in 2015. USADA is recognised by state congress as the official anti-doping organisation for all Olympic sport in the United States. Prior to USADA and the UFC’s partnership in 2015, drug testing was very much commission mandated drugs testing, often seen as an IQ rather than a drugs test and out of competition drug testing was non-existent. This is still very much the case in all other top tier MMA organisations around the world.

Anabolic androgenic steroids (AAS) have been used in the sport from the infancy of the sport to modern day, particularly currently in organisations outside of the USADA testing program. The ethical dilemma of using anabolic steroids to gain an unfair advantage over opposition is another discussion. AAS use become prevalent in the 1950s when Olympic athletes used them to improve sports performance. One of the unfavourable side effects of AAS is anabolic steroid induced hypogonadism (ASIH), ASIH is a secondary cause of hypogonadism in young men who use AAS (Park, 2018). The concerning symptoms of ASIH are low endogenous testosterone levels, testicular atrophy, sexual dysfunction and hepatic dysfunction (Park, 2018). Management strategies include transient testosterone replacement therapy (TRT), selective estrogen receptor modulators (SERMS) and human chorionic gonadotropin (hCG) (Rahnema et al, 2014). This should be diagnosed and administered through a medical professional (Park, 2018).

Relative energy deficiency in sports (RED-S) is terminology used to describe male/female reproductive health disruptions associated with exercise (Hackney, 2020). There are varying forms of reproductive disruptions to athletic men, displaying a relative hypogonadism condition. These conditions may be driven acutely due to RED-S or overtraining/excessive training load and can be transient in nature (Hackney, 2020).

Excessive training loads found in MMA combined with calorie restriction, both of which are heavily associated with training camps for athletes have been shown to be associated with low serum testosterone and low total free testosterone (Cangemi et al, 2010). There are manifestations of a more chronic hypogonadism, that can persist for years, the exercise hypogonadal male condition (Hackney, 2020).

Several theories surround the physiological cascades that lead to low testosterone, the theories are driven by disruption of the HPG axis resulting in hypogonadism. Disruptions proposed to be caused by stress hormone interference or calorie deficiency/relative energy deficit (Hackney. 2020). Despite these theories it is important to note that low testosterone can exist in athletes due to TBI (traumatic brain injury) and prior AAS usage.

Traumatic brain injury (TBI) is defined as neuropathologic damage and dysfunction to the brain resulting from external mechanical force to the head or body (Mckee & Daneshvar, 2015). A concussion is a traumatically induced transient disturbance of brain function (Harmon et al, 2013). Concussions are a subset of TBI’s and their acute symptoms often resolve completely over time.

Hormone disruption is a known consequence of moderate and sever TBI (Wagner et al, 2010). In TBI patients, levels of growth hormone (GH), insulin like growth factor (IGF-1), luteinizing hormone (LH) and follicle stimulating hormone (FSH) and testosterone all decrease transiently during the acute post injury period (Wagner et al, 2010). Testosterone may be neuroprotective in men (Chisu et al, 2006), the suppression and absence of such in the acute post injury window may be unfavourable (Wagner et al, 2010).

Schlegel et al, (2021) noted that head trauma in mixed martial arts accounted for 58%-78% of all injuries. That possible medical interventions should be made during a career but also post career due to the consequences of TBI’s and the risks of chronic traumatic encephalopathy (CTE) and other associated affects.

Testosterone replacement therapy (TRT), currently illegal in professional mixed martial arts (it was however legal for a period of time in mixed martial arts) another topic of discussion. Post career is a now an option for men with hypogonadism, which has shown improvements in libido, sexual function, bone density, muscle mass, body composition, mood, cognition, quality of life and cardiovascular disease (Bassil et al, 2009).

The triad of failures of a past generation of mixed martial artists serves as a warning to upcoming athletes in the sport, to not follow in their footsteps and look at better practice from the start, including not using AAS, not doing extreme weight cuts and reducing the number of TBI’s and head impacts one takes through training. Many of these changes will only take place when there are sanctions regarding AAS usage and weight cutting and there is a cultural shift regarding head trauma.

Quality of life may be the most important thing for a fighter from the previous generation and TRT may be at the very least a consideration.

The easiest to identify clinical signs of hypogonadism is a decrease in muscle mass and strength, a decrease in bone mass and osteoporosis and an increase in central bodyfat (Bassil et al, 2009). Other more subjective symptoms may occur which may include, a decrease in libido, forgetfulness, loss of memory, difficulty in concentration, insomnia and a decreased sense of wellbeing (Basil et al, 2009). With the subjective measures it become difficult to identify the root cause, with many of the symptoms being similar to those of chronic traumatic encephalopathy (CTE), a progressive neurological deterioration caused by repetitive TBIs (Mckee et al, 2015).

Due to many symptoms having commonalties with CTE and other conditions that come with aging its essential to test serum testosterone levels and well as symptoms prior to any treatment modality (Bassil et al, 2009). Unfortunately, there are a limited number of randomised controlled trials and studies in general on the long-term health complications of TRT therapy. There does appear to be contraindications to therapy based on the available literature including, prostatic cancer, previous heart conditions and elevated haematocrit levels (Bassil et al, 2009).

Underlying health conditions seem to play a major factor in determining effective TRT usage, however a major consideration of usage is elevated haematocrit, TRT has been shown to elevate levels by as much a 7-10% (Bachman et al, 2014). Whether considering starting treatment or being undertreatment its essential to work with a healthcare professional.

Practical application for retired fighters’ pharma logical treatments such as TRT or clomiphene citrate have been shown to be effective in treating hypogonadism and improving athlete quality of life and performance. Athletes currently competing who may be experiences similar symptoms, are unable to use TRT under USADA and WADA guidelines, therefore a honest look at nutritional interventions, weight cutting and modification of training may be able to optimise a males health and sports performance (Hooper et al, 2018).

References

  • Bachman, E., Travison, T. G., Basaria, S., Davda, M. N., Guo, W., Li, M., Connor Westfall, J., Bae, H., Gordeuk, V., & Bhasin, S. (2014). Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point. The journals of gerontology. Series A, Biological sciences and medical sciences69(6), 725–735.
  • Bassil, N., Alkaade, S., & Morley, J. E. (2009). The benefits and risks of testosterone replacement therapy: a review. Therapeutics and clinical risk management5(3), 427–448.
  • Bassil, N., Alkaade, S., & Morley, J. E. (2009). The benefits and risks of testosterone replacement therapy: a review. Therapeutics and clinical risk management5(3), 427–448.
  • Cangemi, R., Friedmann, A. J., Holloszy, J. O., & Fontana, L. (2010). Long-term effects of calorie restriction on serum sex-hormone concentrations in men. Aging cell9(2), 236–242.
  • Chisu, V., Manca, P., Lepore, G., Gadau, S., Zedda, M., & Farina, V. (2006). Testosterone induces neuroprotection from oxidative stress. Effects on catalase activity and 3-nitro-L-tyrosine incorporation into alpha-tubulin in a mouse neuroblastoma cell line. Archives italiennes de biologie144(2), 63–73.
  • Hackney A. C. (2020). Hypogonadism in Exercising Males: Dysfunction or Adaptive-Regulatory Adjustment?. Frontiers in endocrinology11, 11.
  • Harmon, K. G., Drezner, J. A., Gammons, M., Guskiewicz, K. M., Halstead, M., Herring, S. A., Kutcher, J. S., Pana, A., Putukian, M., & Roberts, W. O. (2013). American Medical Society for Sports Medicine position statement: concussion in sport. British journal of sports medicine47(1), 15–26.
  • Hooper, D. R., Tenforde, A. S., & Hackney, A. C. (2018). Treating exercise-associated low testosterone and its related symptoms. The Physician and sportsmedicine46(4), 427–434.
  • Mckee, A. C., & Daneshvar, D. H. (2015). The neuropathology of traumatic brain injury. Handbook of clinical neurology127, 45–66.
  • McKee, A. C., Stein, T. D., Kiernan, P. T., & Alvarez, V. E. (2015). The neuropathology of chronic traumatic encephalopathy. Brain pathology (Zurich, Switzerland)25(3), 350–364.
  • Park H. J. (2018). Anabolic steroid-induced hypogonadism: a challenge for clinicians. Journal of exercise rehabilitation14(1), 2–3.
  • Rahnema, C. D., Lipshultz, L. I., Crosnoe, L. E., Kovac, J. R., & Kim, E. D. (2014). Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertility and sterility101(5), 1271–1279.
  • Schlegel, P., Novotny, M., Valis, M., & Klimova, B. (2021). Head injury in mixed martial arts: a review of epidemiology, affected brain structures and risks of cognitive decline. The Physician and sportsmedicine49(4), 371–380.
  • Wagner, J., Dusick, J. R., McArthur, D. L., Cohan, P., Wang, C., Swerdloff, R., Boscardin, W. J., & Kelly, D. F. (2010). Acute gonadotroph and somatotroph hormonal suppression after traumatic brain injury. Journal of neurotrauma27(6), 1007–1019.

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