In our consulting practice and community work, we occasionally see somewhat elevated levels of thyroid-stimulating hormone (TSH) in athletes. Slightly elevated TSH seems to correlate with recent intensive exercise. But does this observation has a confirmation in literature? We set out to check and took several notes along the way.

Our observations of slightly elevated TSH in athletes do not seem to find a satisfactory confirmation in the published literature. Notably, in a study (1), 22 hours after a marathon, TSH levels in runners were lower than before the race.

Further investigations and analysis are needed to explain elevated TSH that we occasionally see in athletic individuals.

A side note: help is available.

If you need help with selecting the correct laboratory tests, understanding, interpreting and improving your thyroid hormone levels, do not hesitate to get in contact with us.

Notes on thyroid hormones and TSH.

Thyroid hormone levels and exercise.

Mennitti, 2020 (4):

Thyroid hormone levels can increase, decrease or remain unchanged depending on the type of exercise, intensity and duration. These ambiguous results could be due to various elements such as the athlete’s nutritional status, environmental factors and the blood sampling procedure.

TSH was markedly decreased 22 h after a marathon race.

Sander and Rocker, 1988 (1):

Thyroid hormones were studied in 16 well-trained male amateur runners (mean age 31.8 years) before, immediately after, and 60 mm and 22 h after marathon running. Thyroid-stimulating hormone (TSH) was significantly increased immediately after the race, returned to the control value 1 h later, and was markedly decreased 22 h after a marathon race.

Thyroid-stimulating hormone (TSH) was significantly increased immediately after the race, returned to the control value 1 h later, and was markedly decreased 22 h after a marathon race. Source: Sander, 1988.

Sander and Rocker, 1999 (1), further list a number of factoids on thyroid hormone levels in different condition of diet and exercise. The information is useful as a quick reminder.

Sander and Rocker, 1988 (1):

Subjects with carbohydrates’ restriction were found to have low T3 concentrations under resting conditions and during physical exercise.

Similar changes with an increase in plasma rT3 and a decrease
in plasma T3 (low T3 syndrome) were found in fasting subjects
or in subjects with a carbohydrate-restricted diet.

Short-term exercise changes thyroid hormone conversion in favor of the active hormone T3.

The following may be used as a “hack” to increase active T3 hormone.

Sander and Rocker, 1988 (1):

Contrary to the results found in prolonged exercises, a change in conversion in favor of the active hormone T3 was observed in short-term exercises (k < 20 mm).

Thyroid hormones and rheumatoid arthritis.

Patients with rheumatoid arthritis are at a higher risk of autoimmune thyroid disease and regular assessment of thyroid hormones may be useful for RA screening.

Thyroid dysfunction is common in rheumatoid arthritis (RA).

Hannawi et al., 2016 (2):

Thyroid dysfunction is common in rheumatoid arthritis (RA). Subclinical hypothyroidism is the first most common, followed by clinical hypothyroidism. Thyroid dysfunction in RA had been found to increase the risk of cardiovascular disease.

Definition of subclinical hypothyroidism.

Hannawi et al., 2016 (2):

Subclinical hypothyroidism is defined as increased serum thyroid stimulating hormone (TSH) concentration with normal serum free thyroxine (T4) level.

Elevated TSH in established rheumatoid arthritis and early rheumatoid arthritis.

Hannawi et al., 2016 (2):

While the mean TSH, T3 and T4 were within normal range in both groups, there were significant differences in the mean values between ERA and established RA. TSH was 2.12±1.52 in ERA vs. 5.8±8.3 in established RA (NR:0.27-4.2 mlU/L), p=0.04.

Low thyroid and atherosclerosis: rheumatoid arthritis, low carb diets, animal experiments.

Do we see a common pattern when we look at the following facts?

1. Hypothyroidism in rheumatoid arthritis increases the risk of cardiovascular disease.

2. People on low carb diets often have low T3 levels.

3. In animal experiments, damage to thyroid in dogs is necessaray to produce atherosclerosis.

Keys, 1952 (3):

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding. The nearest approach to metabolic comparability is the dog which requires extensive thyroid damage as well as tremendous amounts of dietary cholesterol before positive effects can be elicited.

TSH and leptin.

Some illustrations on the link between TSH and leptin from a study in anorexic, normal weidht and obese female adolescents.

Reinehr et al., 2008 (6):

In a partial regression adjusted to changes in weight, the changes in leptin correlated significantly to changes in TSH (r = 0.40, p = 0.040) and fT3 (r = 0.57, p !0.001), but not to changes in fT4 (r = 0.09, p = 0.309).

BMI, thyroid hormones and leptin in anorexic, normal-weight and obese adolescent girls. Source: Reinehr, 2008.

Reinehr et al., 2008 (6):

Conclusions:Thyroid function seems to be reversibly related to weight status with increased TSH and fT3 concentrations in obesity and decreased TSH and fT3 levels in AN. We hypothesize that leptin may be the link between weight status and TSH.

Table 1.Age, gender, pubertal stage, weight status, leptin, insulin, glucose and insulin resistance index HOMA in adolescent females with AN, obesity, and in healthy controls. Source: Reinehr, 2008

Kok et al., 2005 (8):

Spontaneous diurnal thyrotropin secretion is enhanced in proportion to circulating leptin in obese premenopausal women.

Thyroid hormone regulation.

“Negative feedback by T4 and T3” on TSH.

Roelfsema, Veldhuis, 2013 (6):

Precise regulation of circulating and intracellular concentrations of thyroid hormones (T 4and T3 ) is essential for the control of many metabolic processes, heat production, physical development, weight maintenance, cell differentiation, and growth (9). The prime stimulatory hormone for the thyroid is TSH, with numerous secondary modulators, including IGF-I, inflammatory cytokines (IL-1, IL-6, and TNF-), and iodide availability (10). TSH in turn is under the stimulatory control of bilaterally represented paraventricular TRH neurons, the inhibitory neurotransmitters dopamine and SST, and negative feedback by T4 and T3 (11–13).

Simplified ensemble regulation of TSH secretion. Schematic drawing of the regulation of the HPT axis. Abbreviations: aMSH,melanocyte-stimulating hormone; ARC, arcuate nucleus; CART, cocaine and amphetamine-related transcript; NPY, neuropeptide Y; AGRP, agouti-related protein; E2 , estradiol; PVN, paraventricular nucleus; SS, somatostatin;, inhibition;, stimulation. Source: Roelfsema, Veldhuis, 2013.

Stimulating impact of catecholamines on TRH and TSH would explain why TSH rises during a marathon race and returns to baseline one hour after the race.

Sander and Rocker, 1988 (1):

Thyroid-stimulating hormone (TSH) was significantly increased immediately after the race, returned to the control value 1 h later, and was markedly decreased 22 h after a marathon race.

TSH Secretion in the Healthy Human.

The 24-hour serum TSH concentration profile in a healthy male volunteer aged 34 years with a BMI of 23 kg/m 2 (data of Ferdinand Roelfsema). The black bar indicates the period with lights off. Source: Roelfsema, Veldhuis, 2013.

Roelfsema, Veldhuis, 2013 (6):

Collectively, these studies suggest that the TSH “pulse generator,” of which the anatomical and functional details are not known, is a robust and stable system under different conditions, in contrast to LH pulsing.

Influence of gender and age.

Twenty-four-hour serum TSH concentration time series in 24 healthy men and 22 healthy women. Blood samples were taken every 10 minutes for 24 hours. Blood sampling started at 9AM. Lights were off between 11PMand 7:30AM. Data are shown as the group mean and SEM. [Reproduced from F. Roelfsema et al: Thyrotropin secretion profiles are not different in men and women.J Clin Endocrinol Metab. 2009.

Changes in thyroid hormones and TSH in human physiology.

Thyroid Hormone and TSH Levels in Human Physiology. Roelfsema, Veldhuis, 2013.

Roelfsema, Veldhuis, 2013 (6):

Literature inferences in epidemiological studies on thyroid function in humans in relation to age are also not unanimous.

One hundred subjects or more with a body mass index (BMI) in the relevant range and ages from 20 – 80 years may be required to establish firmly the impact of age, gender, and BMI on TSH secretion, as was done in comparable studies on ACTH-cortisol secretion and GH secretion in healthy subjects (105, 106).

Roelfsema, Veldhuis, 2013 (6):s

Prolonged fasting also diminishes TSH secretion by reducing burst amplitude and blunts the nocturnal increase (132–136) (Figure 6). These changes may be mediated by the concomitant decrease in circulating leptin because the fasting-associated decrease in TSH is prevented by leptin administration (137, 138).

Plasma TSH concentrations during normal food intake and during the last 24 hours of a 60-hour fast. Each curve represents the mean of 8 subjects. [Reproduced from J. A. Romijn et al: Pulsatile secretion of thyrotropin during fasting: a decrease of thyrotropin pulse amplitude.J Clin Endocrinol Metab. 1990;70:1631– 1636

The circadien spike in TSH may be important for bone health. Can it be abolished by some restrictive diets?

Ma et al., 2011 (9):

We have shown that thyroid-stimulating hormone (TSH) has a direct inhibitory effect on osteoclastic bone resorption.

TSH has a bone protective action by negatively regulating osteoclastogenesis.

Evidence for direct effects of TSH on both components of skeletal remodeling.

Abe et al., 2003 (10):

The osteoporosis associated with hyperthyroidism is traditionally viewed as a secondary consequence of altered thyroid function. We provide evidence for direct effects of TSH on both components of skeletal remodeling, osteoblastic bone formation, and osteoclastic bone resorption, mediated via the TSH receptor (TSHR) found on osteoblast and osteoclast precursors. Even a 50% reduction in TSHR expression produces profound osteoporosis (bone loss) together with focal osteosclerosis (localized bone formation). TSH inhibits osteoclast formation and survival by attenuating JNK/c-jun and NFkappaB signaling triggered in response to RANK-L and TNFalpha. TSH also inhibits osteoblast differentiation and type 1 collagen expression.

These studies define a role for TSH as a single molecular switch in the independent control of both bone formation and resorption.

Sampath et al., 2007 (11):

TSH’s actions are mediated by its inhibitory effects on RANKL-induced osteoclast formation and bone resorption coupled with stimulatory effects on osteoblast differentiation and bone formation.
Systemically administered TSH prevents bone loss and restores bone mass in aged ovariectomized rats through both antiresorptive and anabolic effects on bone remodeling.

We need to note that elevated TSH does not protect bones of patients with rheumatoid arthritis.

Cross-talk of brain and bones: an interesting subject to explore.

There is an interesting figure on brain and bone cross-talk from a 2020 study by Otto et al., 2020 (12), that we reproduce below. Note, however, that leptin is depicted as being a negative mediator for bone. This contradicts the fact that leptin is stimulating for TSH. And since TSH is a positive mediator for bone, leptin should be too. Is this a complexity or just an error of the authors?

Molecular bases of brain and bone crosstalk. Summary of the predominant mediator effect of (a) brain-derived on bone, (b) bone-derived on brain, (c) adipocyte-derived on bone via central modulation and (d) locally synthesized mediators affecting brain and bone concurrently. The mediator effect on brain function and bone mass previously reported was summarized as positive (+) and negative (−). Abbreviations: ACh = acetylcholine, ACTH = adrenocorticotrophic hormone, AgRP = agouti-related peptide, AVP = arginine-vasopressin, BDNF = brain-derived neurotrophic factor, BMPs = bone morphogenic proteins, CART = cocaine amphetamine regulated transcript, CGRP = calcitonin gene related peptide, DA = dopamine, FSH = follicular stimulating hormone, DKK1 = dickkopf-related protein 1, GH = growth hormone, GLU = glutamate, IGF-1 = insulin-like growth factor 1, LCN2 = lipocalin 2, NE = norepinephrine, NMU = neuromedin U, NPY = neuropeptide Y, OCN = osteocalcin, OPN = osteopontin, OT = oxytocin, PRL = prolactin, POMC = proopiomelanocortin, RANKL = receptor activator of nuclear factor-κB ligand, TSH = thyroid-stimulating hormone, VIP = vasoactive intestinal peptide. Source: Otto, 2020.

TSH in primary hypothyroidism and nonthyroidal illness.

Twenty-four-hour serum TSH concentration time series in 8 patients with severe hypothyroidism, 8 patients with mild hypothyroidism, and 38 healthy control subjects. Data are shown as mean and SEM on a logarithmic scale. [Reproduced from F. Roelfsema et al: Thyrotropin secretion in mild and severe primary hypothyroidism is distinguished by amplified burst mass and basal secretion with increased spikiness and approximate entropy. J Clin Endocrinol Metab. 2010;95:928 –934 (62)

Nonthyroidal illness:

Roelfsema, Veldhuis, 20134 (6):

The current available data indicate that critical illness leads to diminished TSH secretion, especially of the pulsatile component, with loss of the nocturnal increase and unchanged pulse frequency. In the very ill patient, T4 levels decrease, and the magnitude of decrease is related to the chance of death (229). Although undernutrition, high glucocorticoids, and inflammatory cytokines likely play major roles, the precise pathophysiological mechanisms are not fully known yet

Conclusions by Roelfsema and Veldhuis, 2013 (6).

Roelfsema and Veldhuis, 2013 (6):

Basal, pulsatile, and entropic features of TSH secretion are regulated by feedforward and feedback signals acting on the hypothalamic-thyrotrope unit in healthy volunteers, obese premenopausal women, and patients with pituitary disorders and primary hypothyroidism. Inhibitory effects of dopamine, SST, and glucocorticoids operate in healthy subjects. There is also a negative impact of calorie deprivation and NTI. Although T4and T3both feedback negatively on TSH secretion, comparable to cortisol on ACTH, the long half-lives of total T3and T4 have precluded precise analyses of feedback kinetics and endogenous dose-responsive inhibition. Dynamics of the HPT axis remain largely unexplored in common clinical and social conditions, such as overweight, chronic stress, puberty, diabetes mellitus, and aging. Such potentially important, but expensive and time-consuming, investigations should ultimately include other neuroendocrine systems in order to dissect multihormone interactive physiology.

A Test: Do we need to add TSH to the list of laboratory tests?

1. Do you think TSH is an informative biomarker?

2. Who should do tests of their TSH levels and how often?

Summary statements and help with thyroid hormones.

Thyroid hormone replacement in athletes with subclinical hypothyroidism.

We do not recommend thyroid hormone replacement in athletes with subclinical hypothyroidism. A thorough analysis of biomarkers, adjustments in diet and exercise regiment, improve thyroid hormone profile in most of the cases.

Low T3 and/or free T3 during dietary restriction or carbohydrate restriction.

Low T3 and/or low free T3 are often observed in people who practice dietary restriction or carbohydrate restriction. We recommend against a metabolic state with chronically low T3 and/or free T3. We recommend against low normal TSH in aging individuals.

Suppression of nocturnal increase in leptin.

We warn about possible suppression of nocturnal leptin increase and the negative impact of such suppression.

Tests of thyroid hormones.

Follow the link below to read our Summary Statement on laboratory tests for thyroid hormones.

Tests of thyroid hormones. A summary statement.

Help is available.

If you need help with understanding, interpreting and improving your thyroid hormones, do not hesitate to get in contact with us.

Selected references:

1. Sander M, Röcker L. Int J Sports Med. 1988 Apr;9(2):123-6.

2. Hannawi S, Al Salmi I, Hannawi H. Thyroid Function in Early Versus Established Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/thyroid-function-in-early-versus-established-rheumatoid-arthritis/. Accessed September 22, 2020.

3. Ancel Keys. Human Atherosclerosis and the Diet. Circulation, Volume V, January, 1952.

4. Mennitti et al. J Clin Med. 2020 Aug 6;9(8):2540.

5. Lombardo et al. Clin Chem Lab Med. 2019 Sep 25;57(10):1450-1473.

6. Reinehr et al. Horm Res 2008;70:51–57 55

7. Roelfsema, Veldhuis. Endocrine Reviews, October 2013, 34(5):619 – 657.

8. Kok P. et al. J Clin Endocrinol Metab. 2005;90:6185– 6191.

9. Ma et al Thyroid. 2011;21(8):897-906.

10. Abe et al. Cell. 2003 Oct 17;115(2):151-62.

1 Comment

Pingback: Tests of thyroid hormones. - The New Neander's Medical

Comments are closed.