Thyroid Hormone & GH in Bodybuilding: Why T3/T4 Incinerate Muscle Tissue
The T3 Trap: How Thyroid Hormones Destroy Your Hard-Earned Muscle
Author
Cormac Mannion (Type-IIx)
Date
Friday, October 03 2025
Introduction
Key Takeaways
Key Takeaways
Exogenous T3 significantly breaks down muscle protein
T3 selectively destroys growth-responsive type IIA muscle fibers
GH naturally increases peripheral conversion of T4 to T3, which is beneficial
The reduction in serum T4 from GH use is typically not problematic for healthy individuals
Thyroid hormone supplementation is irrational for bodybuilders as it accelerates muscle loss
Exogenous GH cannot cause central hypothyroidism but may reveal pre-existing conditions
Thyroid hormone misuse carries serious health risks including cardiac arrhythmias
Common bodybuilding practices of using T3 deep into competition prep can be extremely destructive to muscle mass
Introduction
Here’s another Q&A format article that was asked by a user in the Type-IIx & Team Ampouletude Telegram group and led to a fruitful discussion… and fleeting references to still widespread bad practices among bodybuilders with respect to thyroid hormone use… something so destructive to muscle mass deep into prep when it’s typically applied… commonly with a hand-wave to the effect that “he’s on Halo, he won’t notice any muscle loss…“
Thyroid hormone is potently muscle catabolic. It chews through muscle aggressively and selectively, especially the growth-responsive type II fibers.
Question
Since exogenous growth hormone (exogenous GH) reduces serum T4, should a healthy bodybuilder supplement exogenous T4 (Levothyroxine; Synthroid; Tiromel) or T3 (Liothyronine; Cytomel) as a rule with exogenous GH?
Definitions
T3: Triiodothyronine
T3 (exogenous) [Cytomel, LT3]: Liothyronine
T4: Thyroxine
T4 (exogenous) [Tiromel, Synthroid, LT4]: Levothyroxine
T3 in its endogenous (triiodothyronine) and exogenous (liothyronine) form is the actively catabolic hormone among the thyroid hormones (e.g., T2, T3, T4). T4, despite some endogenous effects, for enhanced bodybuilding discussion is effectively the prodrug to the active T3.
fT3; FT3: free T3, the bioactive fraction in blood
RMR: resting metabolic rate
REE: resting energy expenditure
UCP: uncoupling protein
LBM: lean body mass
Dose-Response
Metabolic Rate
Given a seventy-five microgram (75 µg) Cytomel dose (daily for 14 days):
fT3 increased by 1.7-fold
RMR increased by 15% (adjusted for LBM)
UCP2 increased 1.7-fold and UCP3 increased 2.4-fold. [1]
A trend was also seen for a direct correlation between REE/LBM and increases in fT3 levels, with an average 0.11 kcal/kg/d increase in REE/LBM for each 10 pg/dL increase in fT3.
This is the average time-course for fT3 in healthy euthyroid adults given a single fifty microgram (50 µg) oral dose of Cytomel (Liothyronine). [2] There is, however, substantial interindividual heterogeneity or variation in dose/response. [3]
Muscle Catabolism
Seventy-five micrograms (75 µg) of exogenous T3 increases RMR by 15% and 100 µg exogenous T3 for 2 weeks reduced type IIA fiber cross-sectional area (CSA) in line with this increased RMR though there may be some compensatory mechanism that antagonizes the protein catabolic effects over longer periods. [4] [5]
These findings provide evidence that [75 mcg daily] accelerates the rates of protein breakdown (+ 12%) and amino acid oxidation (+24%) in excess of a small increase in the rate of protein synthesis (+9%), thereby resulting in net protein loss. [5-1]
That, to most, should be a stark message about the utility of thyroid hormones for recomping, not to mind bulking. [4-1]
Thyroid hormone strips muscle!
Simply dieting – eating in a caloric deficit – suppresses thyroid function and thyroid hormone blood levels and explains why energy is sapped and brain fog permeates during hard dieting, lowering sympathetic drive, thyroid output, T3, etc.
Indeed, it is the prevailing evolutionarily conserved theory that the body’s suppression of thyroid function is an adaptation to stave off muscle loss, since T3 is so catabolic.
Mechanism of Action
The primary mechanism by which T4 (exogenous, Tiromel) increases RMR in humans is through conversion to T3.
The primary mechanism by which T3 increases RMR in humans is not through transcriptional control of the genes encoding mitochondrial proteins, unlike in rats. [1-1]
While in rats, T3 works by uncoupling electron transport from ATP synthesis via increased mRNA expression and mitochondrial protein levels of the endogenous uncoupling protein (like “natty DNP”), UCP-3, in humans, T3 increases RMR/REE without altering the respiratory chain transcription program [1-1] [6]
Other Projects
Bolus
A Practical and Reference Guide for the Use of Human Growth Hormone and GH Secretagogues
For those interested in growth hormone and related pathways, my book, Bolus, covers the deeper science behind these anabolic mechanisms.
Risks and Complications
Hypothyroidism is not a foreseeable risk of exogenous GH use: while recombinant human GH use cannot cause central hypothyroidism, it may reveal its pre-existence. [7]
Thyrotoxicosis
Toxic levels of thyroid hormone
Liothyronine (Cytomel) and Levothyroxine (Tiromel) are associated with increased cardiac arrhythmia events; and may lead to (drug-induced) thyrotoxicosis.
Overt thyrotoxicosis is defined as elevated serum free thyroxine (FT4) and free triiodothyronine (FT3), and suppressed thyrotropin (TSH) concentrations. Thyrotoxicosis with TSH suppression only (TTSO), and normal thyroid hormone concentrations, is also defined as mild thyrotoxicosis. Both overt thyrotoxicosis and TTSO may be caused by the same thyroid disorders. The most common cause of thyrotoxicosis is the use of excessive doses of L-thyroxine for the treatment of hypothyroidism.
Classic symptoms of thyrotoxicosis include:
Heat intolerance
Palpitations
Anxiety
Fatigue
Weight loss, and
Tremor
In euthyroid persons (non-hypothyroid), higher fT4 levels are associated with higher risk of atrial fibrillation. [8]
Hypothyroidism
Low levels of thyroid function
Symptoms of Hypothyroidism
Though therapeutic use of exogenous GH does not cause central hypothyroidism, it may reveal it. A primary mechanism in exogenous GH’s lipolysis is the peripheral conversion of T4 to T3.
The following symptoms categorically arise out of frank hypothyroidism:
Dry and scaly skin
Sensitivity to cold
Brittle hair and nails
Slow movements and thoughts
Depression
Only if not using clenbuterol, muscle cramps may be considered as an additional symptom
There are other symptoms of hypothyroidism; however, they are easily confused with primary effects of exogenous GH and/or AAS use.
Conclusion
Answer
No, a healthy bodybuilder should not supplement exogenous T4 (Levothyroxine; Synthroid; Tiromel) or T3 (Liothyronine; Cytomel) as a rule while using exogenous GH.
One of two things (A or B) might occur after initiating a course of exogenous GH:
(A) T4 is reduced but within the normal/healthy range, T3 is elevated perhaps (well) out of the normal/healthy range. This normal direct GH effect is of benefit for RMR and tissue-level thyroid hormone action since the decrement to T4 is a result of enhanced peripheral T3 activity, doing more with less, and “pulling” on the ‘reserve’ pool of T4.
In this case, since thyroid hormone is potently and selectively *muscle* catabolic, its use is irrational in bodybuilding.
(B) If T4 is reduced below the normal/healthy range and/or you have several Symptoms of Hypothyroidism, then you need to be tested (e.g., by an endocrinologist or thyroid specialist) for pre-existing central hypothyroidism since exogenous GH can reveal but not cause it.
In this case, since you are ill, you are not a healthy bodybuilder; you should not be using any hormones that aren’t prescribed until you get yourself a diagnosis and treatment plan.
Summary
Summary
This article examines the relationship between exogenous growth hormone (GH) and thyroid function in bodybuilders. It debunks the common misconception that bodybuilders using GH should supplement with thyroid hormones (T3/T4). The research presented demonstrates that T3 is highly catabolic to muscle tissue, particularly type IIA fibers which have the greatest growth potential. While GH does reduce serum T4 levels, this occurs because GH enhances peripheral conversion of T4 to T3, effectively “doing more with less.” For healthy bodybuilders, this natural adaptation is beneficial and doesn’t require intervention with thyroid medications. The article also addresses the risks of thyroid hormone supplementation, including thyrotoxicosis and cardiac complications, while acknowledging that GH may reveal pre-existing central hypothyroidism that requires medical attention.
About the Author
Type-IIx is an expert on all methods used in enhanced bodybuilding and the author of Bolus: A Practical and Reference Guide for the Use of Human Growth Hormone and GH Secretagogues. His articles can be found on Meso-Rx and his Team Ampouletude website along with his other projects like the Gear, Growth, and Gains Podcast on the web [www] – [telegram] – [spotify] – and everywhere podcasts stream!
References
Barbe, Pierre, et al. “Triiodothyronine-Mediated Upregulation of UCP2 and UCP3 mRNA Expression in Human Skeletal Muscle Without Coordinated Induction of Mitochondrial Respiratory Chain Genes.” FASEB Journal, vol. 15, no. 1, 2001, pp. 13–15.↩︎↩︎
Jonklaas, Jacqueline, et al. “Single-Dose T3 Administration: Kinetics and Effects on Biochemical and Physiological Parameters.” Therapeutic Drug Monitoring, vol. 37, no. 1, 2015, pp. 110–18.↩︎
Goede, Simon L, et al. “High Resolution Free Triiodothyronine-Thyrotropin (FT3-TSH) Responses to a Single Oral Dose of Liothyronine in Humans: Evidence of Distinct Inter-Individual Differences Unraveled Using an Electrical Network Model.” Journal of Biological Systems, vol. 25, no. 1, 2017, pp. 119–43.↩︎
Bond, Peter. “Thyroid Hormone Effects on Energy Metabolism and Protein Turnover at a Glance.” Meso-Rx, 24 Dec. 2021, https://thinksteroids.com/articles/thyroid-hormone-effects-energy-metabolism-protein-turnover/.↩︎↩︎
Martin, WH 3rd, et al. “Mechanisms of Impaired Exercise Capacity in Short Duration Experimental Hyperthyroidism.” Journal of Clinical Investigation, vol. 88, no. 6, 1991, pp. 2047–53.↩︎↩︎
de Lange, Pieter, et al. “Uncoupling Protein-3 Is a Molecular Determinant for the Regulation of Resting Metabolic Rate by Thyroid Hormone.” Endocrinology, vol. 142, no. 8, 2001, pp. 3414–20.↩︎
Wong, Kara, et al. Predictors and Growth Consequences of Central Hypothyroidism in Pediatric Patients Receiving Recombinant Human Growth Hormone. 2010.↩︎
Baumgartner, Christine, et al. “Thyroid Function Within the Normal Range, Subclinical Hypothyroidism, and the Risk of Atrial Fibrillation.” Circulation, vol. 136, no. 22, 2017, pp. 2100–16.↩︎