In August of 2012, I watched two scintillating performances by British hero, Mo Farrah, as he strode to victory in the 5000 and 10 000m track races. It was the first long-distance Olympic victory by a Brit for decades, and he swept aside the best that Africa had to offer, including Ethiopian world record-holder, Kenenisa Bekele. However, not to diminish the enormity of this achievements, within athletic circles, there has since been some controversy over the medication that he had been taking; in particular, issues that have been raised by Bekele’s Dutch agent Jos Hermens, pertaining to thyroid medication.
The Silver medalist in the 10 000m was white American athlete Galen Rupp – both he and Farrah were being coached by legend Alberto Salazar. According to a Wall Street Journal article (1), Salazar referred athletes to endocrinologist Dr Jeffrey Brown, and referred to him as the best endocrinologist in the world. During his medical career, Brown claimed to have treated 15 Olympic Gold medallists, including the great Carl Lewis. Galen Rupp was publicly diagnosed with hypothyroidism by Dr Brown in 2006, although online information about Farrah appears to be less conclusive. Other top endocrinologists, including Ian Hay from the Mayo Clinic (1), have gone on record to say that it is very unusual to see large numbers of young athletic males with thyroid deficiency problems. But Dr Brown believes that large amounts of training can suppress the body’s ability to produce sufficient levels of thyroid hormones – a belief apparently shared by increasing numbers of athletes.
Thyroid – the physiology
The thyroid gland is often considered as the seat of metabolism. It weighs around 15 to 20 grams and, as seen in Diagram 1, is located over the first part of the trachea and under the larynx. Under influence of Thyrotropin Releasing Factor (TRH) from the hypothalamus and Thyroid Stimulating Hormone (TSH) from the anterior pituitary gland, the thyroid secretes the major metabolic hormones, thyroxine (T4) and triiodothyronine (T3). As illustrated in Diagram 1, these hormones should then feedback to the anterior pituitary to modulate the further outflow of TSH. Typically, in a blood test, if you see a high T4 value, TSH will be low, and if you see a low T4 value, TSH will be high, as the pituitary gland tries in vain to stimulate a reluctant thyroid gland. If TSH and T4 levels are both low, it may indicate pituitary dysfunction – this is much less common, but very possible in a case of what I call ‘whole body metabolic fatigue’.
More T4 than T3 is secreted from the thyroid gland, but T3 is the more metabolically-active hormone. Most T3 in circulation is produced by the conversion from T4, principally in the liver and kidneys, via a process called deiodination. Thyroxine-binding globulin serves as the main transporter of thyroid hormones in the bloodstream.
According to exercise physiologists McCardle, Katch and Katch (2), T4 secretion raises the metabolism of all cells in the body, except in the brain, spleen, testes, uterus and thyroid. Additionally, they note that high T4 secretion rates can raise basal metabolic rate (BMR) up to four-fold, often meaning rapid weight loss in hyperthyroid individuals. Conversely, the more frequently seen hypothyroid situation tends to suppress BMR, and can be a primary physiological reason for fatigue and weight gain. Additionally, primary roles of thyroid hormones are for protein synthesis, regulation of macronutrient metabolism and increasing the body’s responses to catecholamines (adrenaline, noradrenaline and dopamine) (3).
McCardle, Katch and Katch (2) note that free T4 levels may increase by 35 per cent during exercise, potentially due to the increase in core temperature diminishing the protein binding of thyroid hormones. However, our endocrinology specialist Dr Des Gilmore, who wrote in the last edition of FSN (4), acknowledged that experimental evidence with regards to thyroid output and exercise is conflicting, and the observed changes in T3 and T4 during and after exercise may be minor….