Testosterone, TRT, and Competitive Sport

Testosterone itself and every esterified form: testosterone cypionate, enanthate, propionate, undecanoate (Nebido), decanoate, isocaproate, and phenylpropionate. Sustanon 250 — a blend of four esters — is prohibited. The newer oral testosterone undecanoate (Kyzatrex) is equally prohibited despite its novel absorption pathway.

Intramuscular injections, subcutaneous injections, transdermal gels (Testogel, Tostran, AndroGel), transdermal patches, oral preparations, buccal tablets, nasal gels (Natesto), implantable pellets. There is no "safer" route from an anti-doping perspective. If it delivers exogenous testosterone into your system, it is prohibited.

Human chorionic gonadotropin (hCG) is prohibited under S2.2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics — in males only. This is significant because hCG is a cornerstone of fertility-preserving protocols during TRT. An athlete on a TUE for testosterone who also needs hCG for fertility will need separate TUE documentation for both substances.

Selective oestrogen receptor modulators (SERMs) including clomiphene citrate and enclomiphene are prohibited under S4 — Hormone and Metabolic Modulators. Aromatase inhibitors (anastrozole, letrozole) are also prohibited under S4. Even compounds used to manage TRT side effects or preserve fertility during treatment fall under the ban — the clinical justification does not remove the anti-doping obligation. If you need any of these substances alongside testosterone, each one requires its own TUE documentation.

Dehydroepiandrosterone (DHEA), androstenedione, androstenediol, and all other prohormones that convert to testosterone in the body are prohibited under S1.1b — Endogenous Anabolic Androgenic Steroids when exogenously administered. Many "natural testosterone boosters" sold online contain these compounds. Taking them is a doping violation regardless of what the label says.

Primary organic hypogonadism: Klinefelter syndrome and variants (47,XXY), congenital anorchia, bilateral orchiectomy, testicular torsion with subsequent atrophy, severe bilateral orchitis (typically post-mumps) with testicular atrophy, radiation therapy or chemotherapy affecting the testes, 46,XY disorders of sex development.

Secondary organic hypogonadism: Congenital pituitary defects causing multiple pituitary hormone deficiency (MPHD), pituitary tumours (prolactinomas, non-functioning adenomas), pituitary surgery or irradiation, Kallmann syndrome, traumatic brain injury with documented pituitary damage, infiltrative diseases (haemochromatosis, sarcoidosis) affecting the hypothalamus or pituitary.

The common thread: there must be a demonstrable structural or genetic cause. The condition must be organic — not functional.

Minimum two morning samples: Total testosterone measured between 07:00 and 11:00 on at least two separate occasions, both below the laboratory's lower reference limit. A single low result is insufficient.

Gonadotropin levels: LH and FSH — to distinguish primary from secondary hypogonadism and confirm the pattern is consistent with the claimed aetiology.

Complete pituitary function panel: For secondary hypogonadism — prolactin, morning cortisol, ACTH stimulation test, TSH, free T4. This excludes other pituitary pathology and confirms the specific deficiency pattern.

Karyotype: For suspected Klinefelter syndrome.

Pituitary MRI with and without contrast: For secondary hypogonadism — to visualise tumours, structural abnormalities, or post-surgical changes.

Chronological documentation: All laboratory results must be submitted in chronological order (most recent first). All clinical notes in chronological order. Surgical reports if the condition is iatrogenic (post-orchiectomy, post-radiation). The TUEC expects to be able to independently verify the diagnosis from the documentation alone — as if they had never seen the patient.

The committee evaluates whether:

• • The diagnosis is organic, not functional
• • The biochemistry is unambiguously abnormal (not borderline)
• • The clinical picture is consistent with the claimed pathology
• • Non-prohibited alternatives have been considered and ruled out
• • The proposed treatment dose is physiological, not supraphysiological
• • There is no history of prior prohibited substance use without a TUE

Any gap, inconsistency, or ambiguity in the documentation is grounds for denial. Incomplete or disorganised applications are returned without review. This is not a process where "close enough" works.

The TUEC specifies the maximum permissible dose. This is always physiological — the goal is restoration to low-normal, not optimisation. You must be able to produce prescription records, pharmacy dispensing records, and injection logs (with dates, doses, and batch numbers) at any time. Any dose above the approved amount is a violation.

Anti-doping laboratories can distinguish exogenous from endogenous testosterone using carbon isotope ratio analysis (IRMS). If your urine sample shows a T/E ratio outside the reference range or other anomalies, IRMS testing will be triggered. Athletes on a TUE should expect this to happen — it's routine, not suspicious. Your TUE documentation should demonstrate that any exogenous testosterone detected is consistent with your approved prescription.

Some TUECs and NADOs may impose conditions requiring periodic serum testosterone measurements to verify that your levels remain within the physiological range. Results above the reference range — suggesting supraphysiological dosing — can result in TUE revocation. Keep all blood test results and share them proactively with your NADO if requested.

TUEs for testosterone are typically granted for 12 months. Re-application requires updated blood work, clinical notes, and evidence of ongoing clinical need. If the underlying condition is permanent (Klinefelter, bilateral orchiectomy), re-approval is usually straightforward. For conditions that could theoretically resolve, the TUEC may request more extensive re-evaluation.

Use Informed Sport or Informed Choice certified products. These are batch-tested for prohibited substances. No certification system eliminates risk entirely, but these are the gold standard.

Check GlobalDRO (Global Drug Reference Online). This database — available for UK, US, Australian, Canadian, Swiss, Japanese, and New Zealand medications — lets you verify the anti-doping status of specific medications and ingredients. It does not cover supplements, but it's essential for prescription and over-the-counter medications.

Be sceptical of "testosterone boosters." Any supplement that genuinely raises testosterone to a meaningful degree is, by definition, likely to contain a prohibited substance. Products that work through legitimate mechanisms (zinc, vitamin D, sleep optimisation) don't raise testosterone enough to matter — or to trigger a positive test. If it seems too good to be true, it probably contains something you don't want in your system.

Keep a detailed supplement log. Record every supplement you take: brand, batch number, purchase date, and the Informed Sport/Choice certification number if available. If you test positive, this documentation is critical for demonstrating the contamination source and potentially reducing your sanction.

Presentation: A 42-year-old competitive masters cyclist with known 47,XXY karyotype diagnosed in adolescence. Never started TRT previously. Progressive fatigue, loss of performance, confirmed testosterone of 5.2 nmol/L on two morning samples. Elevated LH and FSH. No history of AAS use.

Outcome: Clear organic primary hypogonadism with genetic documentation. Strong TUE application. Prescribed physiological-dose testosterone gel. TUE granted by UKAD. Annual re-application with updated bloods — straightforward because the condition is permanent and genetically confirmed.

Presentation: A 53-year-old club-level runner. Fatigue, reduced libido, difficulty recovering between sessions. Total testosterone 9.4 nmol/L — in the BSSM grey zone. Normal LH and FSH. BMI 28. No organic pathology identified.

Outcome: This is functional hypogonadism in the context of age and mild obesity. Under WADA rules, this does not qualify for a TUE — regardless of the man's symptoms. The honest conversation: optimise weight, sleep, and training load. If symptoms persist and testosterone remains low, treatment is available — but it means stepping back from competition. I present both options clearly and let the patient decide.

Presentation: A 38-year-old triathlete with a history of anabolic steroid use in his mid-twenties (roughly 5 years of use, ceased at 30). Now consistently low testosterone (6.1 nmol/L on two samples). Low LH, low FSH. No pituitary pathology on MRI. Symptomatic.

Outcome: The most difficult scenario. This man has genuine biochemical hypogonadism — likely AAS-induced suppression of the HPG axis that hasn't recovered. But WADA criterion 4 states: "The necessity for the use of the prohibited substance or method is not a consequence, wholly or in part, of the prior use of a substance or method which was prohibited at the time of use." A TUE application will almost certainly be denied. The man needs treatment, but he cannot compete while receiving it. This is a consequence — unfair as it may feel — of historical choices.

Presentation: A 29-year-old county cricketer who underwent unilateral orchiectomy for testicular cancer two years ago, followed by surveillance (no chemotherapy). Remaining testis functioning but with borderline compensation — total testosterone 7.8 nmol/L, mildly elevated LH. Symptomatic fatigue.

Outcome: Organic aetiology (surgical loss of testicular tissue). Documented pathology. The remaining testis may not provide adequate compensation long-term. A TUE application is appropriate — though the TUEC may first ask whether the remaining testis can be supported with hCG (which would also need a separate TUE) rather than exogenous testosterone. This requires careful specialist navigation and comprehensive documentation of the cancer treatment, surgical reports, and longitudinal biochemistry.