Hyperthyroidism in Athletes: Causes and the Link with Training Load and Pharmacology
Effortless weight loss, a high resting pulse, and “endless” energy may seem like a desirable state to an athlete. Yet behind them sometimes hides an excess of thyroid hormones — a condition that destroys muscles and bones and raises the risk of arrhythmias. The editorial team examines why hyperthyroidism develops, how it differs from factitious thyrotoxicosis caused by taking hormones, and what athletic load changes.
Hyperthyroidism and thyrotoxicosis: what is the difference
Thyrotoxicosis is the general name for the state in which the body's tissues are exposed to an excess of thyroid hormones, regardless of the cause. Hyperthyroidism is a narrower concept: it is the term for the situation in which the excess of hormones is produced by the thyroid gland itself, working in overdrive (Ross et al., 2016).
This difference has practical significance. Thyrotoxicosis can also arise without hyperfunction of the gland: with inflammation, when stores of hormones are released from damaged cells, or with the intake of hormones from outside — in the form of tablets. Treatment in these cases is fundamentally different, so the doctor's first task is to establish the source of the excess.
Thyroid hormones enhance metabolism in all tissues. Hence the typical manifestations: rapid heartbeat, trembling hands, sweating, heat intolerance, weight loss with a preserved or increased appetite, irritability, insomnia, frequent bowel movements, and in women — menstrual cycle disturbances. At the same time, the breakdown of protein, in particular muscle protein, increases.
According to reviews, overt hyperthyroidism occurs in about 0.2–1.3% of the population in regions with adequate iodine supply, more often in women (De Leo et al., 2016). The subclinical form — with suppressed TSH and normal hormones — is more widespread.
The main causes
The most frequent cause of hyperthyroidism in young people is Graves' disease (diffuse toxic goiter). This is an autoimmune condition in which the body produces antibodies that stimulate the TSH receptors, and the gland works without control from the pituitary. The disease may be accompanied by eye involvement — endocrine ophthalmopathy, one of the proven risk factors for which is smoking.
In older people and in regions with a historical iodine deficiency, to which Ukraine belongs, toxic multinodular goiter and toxic adenoma often occur — nodules that produce hormones on their own. A sudden intake of large amounts of iodine (contrast agents, amiodarone, supplements with seaweed) is able to “awaken” such nodules.
A separate group is thyroiditis: subacute (often after a viral infection, with neck pain), painless, and postpartum. In these cases thyrotoxicosis is usually short-lived and may later be replaced by temporary hypothyroidism, since the hormone stores in the destroyed cells run out.
| Cause | Mechanism | Characteristic clues |
|---|---|---|
| Graves' disease | Antibodies stimulate the TSH receptor | Diffuse enlargement of the gland, eye symptoms, antibodies to the TSH receptor |
| Toxic nodules | Autonomous work of the nodules | Nodules on ultrasound, more often older age |
| Thyroiditis | Release of hormones from destroyed cells | Neck pain or a painless course, a transient phase |
| Iodine excess | Excessive substrate for synthesis | Contrast, amiodarone, seaweed in the history |
| Exogenous hormones | Taking T4/T3 from outside | Low thyroglobulin, a history of intake |
Factitious thyrotoxicosis and pharmacology
Especially characteristic of the sports environment is factitious (exogenous) thyrotoxicosis — a consequence of taking levothyroxine or liothyronine (T3) preparations to accelerate weight loss. Such drugs are common among bodybuilders during the preparation period, and they are also part of illegal “fat burners,” where their presence is not always indicated on the label.
Exogenous hormones suppress TSH, and the person's own gland “falls asleep.” A laboratory sign that helps distinguish this state from Graves' disease is a low level of thyroglobulin in the blood, whereas with enhanced work of the gland it is usually elevated. Ultrasound and scintigraphy show reduced activity of the gland.
An excess of T3 accelerates the breakdown not only of fat but also of muscle proteins, raises the heart rate, and increases the excitability of the myocardium. Combination with other stimulants — caffeine in large doses, synephrine, clenbuterol — sums up the sympathomimetic effects and raises the risk of arrhythmias. An Endocrine Society review (Pope et al., 2014) mentions thyroid hormones among the agents used together with other drugs to improve “shape.”
Another scenario is false thyrotoxicosis on the form. High doses of biotin in supplements for hair and skin distort immunochemical tests, giving a falsely low TSH and falsely high T4 and T3, which can mimic Graves' disease. The FDA has specifically warned about such interference. Biotin intake must be reported to the doctor.
Load: masking and risks
Physical loads do not cause hyperthyroidism, but they can substantially complicate its recognition. A trained athlete is used to an elevated pulse, sweating, and a high appetite, and often perceives weight loss as a success of a diet. Resting tachycardia is written off as being due to coffee or overwork.
At the same time, thyrotoxicosis reduces tolerance to loads: the heart rate rises at the same work, fatigue sets in faster, and muscle weakness appears, primarily in the proximal muscles of the thighs and shoulders. An athlete may notice that squats or climbing stairs come harder, despite the “vigor.”
An excess of hormones enhances heat production, so training in the heat and in warm gyms increases the risk of heat overload. The most serious risk is atrial fibrillation and other arrhythmias, the likelihood of which rises with a combination of intense load, stimulants, and dehydration.
- resting pulse noticeably higher than usual for you over several days;
- weight loss without a change in diet or with an increased appetite;
- trembling hands, sweating, heat intolerance;
- insomnia, anxiety, irritability;
- weakness of the thigh and shoulder muscles, a drop in strength performance.
Consequences for an athlete's body
Prolonged thyrotoxicosis accelerates bone metabolism and reduces bone mineral density. For athletes, especially women and those who already have energy deficiency, this raises the risk of stress fractures. Even subclinical hyperthyroidism in older people is associated with an increased risk of osteoporosis and atrial fibrillation.
Enhanced protein catabolism leads to a loss of muscle mass and strength, which negates the results of training. Carbohydrate metabolism is disrupted, and glucose tolerance may decrease. The negative changes also affect the psyche: anxiety, irritability, and sleep disturbances worsen recovery.
A rare but life-threatening complication is a thyrotoxic crisis: a sharp exacerbation with a high temperature, pronounced tachycardia, confusion, and heart failure. It can be provoked by an infection, surgery, or an abrupt cessation of antithyroid treatment and requires emergency care in a hospital.
Most of these consequences are partly or fully reversible after the hormone level normalizes, but lost bone mass recovers slowly. That is why early diagnosis has direct practical value for an athlete.
Editorial conclusions
Hyperthyroidism in athletes is most often associated with Graves' disease, toxic nodules, or thyroiditis, and the sports-specific aspect lies mainly in the fact that the symptoms are long masked as fitness and “good shape.”
A scenario separate and characteristic of sport is factitious thyrotoxicosis from taking thyroid hormones for the purpose of weight loss, often in combination with stimulants. It threatens arrhythmias and loss of muscle and bone mass. Another source of confusion is biotin, which distorts test results.
Persistent resting tachycardia, weight loss, tremor, and heat intolerance are a reason to take TSH and see an endocrinologist, honestly telling them about all drugs and supplements.
We also recommend reading our articles on the diagnosis of hyperthyroidism, on hypothyroidism in athletes, and on the risks of fat burners for the heart.
References
- Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343–1421.
- De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet. 2016;388(10047):906–918.
- Kahaly GJ, Bartalena L, Hegedüs L, et al. 2018 European Thyroid Association guideline for the management of Graves' hyperthyroidism. Eur Thyroid J. 2018;7(4):167–186.
- Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
- U.S. Food and Drug Administration. Biotin (Vitamin B7): Safety Communication — may interfere with lab tests. FDA; 2017 (updated 2019).
Andriy Melnyk
A strength-sports coach and author of programs for beginner and intermediate levels. Writes about training planning.
