The Complete Guide to Blood Work for Bodybuilders

Regular blood work is the single most important harm-reduction tool available to enhanced athletes. Yet most bodybuilders either skip it entirely or panic over results that are completely normal for someone with their muscle mass and protocol.

This guide covers every major blood marker, explains what it means in a PED context, and helps you understand what actually matters versus what you can safely ignore.

Why Standard Reference Ranges Don't Apply to You

Lab reference ranges are built from sedentary, non-enhanced populations. When you're carrying significantly more muscle mass and running performance-enhancing compounds, several markers will naturally sit outside those ranges.

A high creatinine in a 120 kg bodybuilder isn't kidney failure: it's a byproduct of high muscle mass. Research confirms that serum creatinine is significantly influenced by muscle mass and physical activity, making it an unreliable marker of renal function in muscular populations (Baxmann et al., 2008). Elevated AST after a heavy leg session isn't liver damage: it's muscle breakdown. A study in the British Journal of Clinical Pharmacology showed that a single bout of muscular exercise can produce "highly pathological" liver function test results in otherwise healthy men (Pettersson et al., 2008). Understanding the difference between genuinely concerning results and expected variations is what separates informed athletes from anxious ones.

When to Get Blood Work Done

Pre-cycle baseline: 4-6 weeks before starting any protocol, with no compounds in your system. This is your personal reference point.

Mid-cycle check: 6-8 weeks into a cycle to catch problems early. This is especially important for your first cycle with any new compound.

Post-cycle / PCT check: 4-6 weeks after your last dose (or mid-PCT) to assess recovery.

Routine maintenance: Every 3-4 months if you're on TRT or blast-and-cruise. At minimum, twice per year.

Liver Markers

Your liver processes everything you put into your body, including oral AAS. These markers tell you how it's coping.

ALT and AST

ALT (Alanine Aminotransferase) is the most liver-specific of the two. Elevations above 2-3x the upper reference limit during an oral cycle warrant attention.

AST (Aspartate Aminotransferase) is found in both liver and muscle tissue. It will spike after intense training, particularly leg day. If AST is elevated but ALT is normal, it's almost certainly from training rather than liver damage (Pettersson et al., 2008).

GGT

GGT (Gamma-Glutamyl Transferase) is a more sensitive marker for liver stress from oral AAS and alcohol. If GGT is climbing alongside ALT, your liver is genuinely under stress.

Bilirubin

Bilirubin can be mildly elevated in people with Gilbert's syndrome (around 5-10% of the population) without any clinical significance. However, rising bilirubin alongside elevated liver enzymes can indicate cholestasis.

Kidney Markers

Creatinine and eGFR

Creatinine is a byproduct of creatine metabolism in muscle tissue. More muscle = more creatinine = higher baseline. A reading of 120 µmol/L in a 100 kg bodybuilder is not the same as 120 µmol/L in a sedentary 70 kg adult. This has been confirmed in testosterone-treated populations where muscle hypertrophy elevates creatinine independently of kidney function (Ashouri et al., 2024).

eGFR is calculated from creatinine and will therefore appear falsely low in muscular individuals. If your eGFR looks concerning, ask your doctor about a cystatin C-based eGFR instead; cystatin C isn't affected by muscle mass and provides a more accurate estimate of true kidney function (Baxmann et al., 2008).

Urea (BUN)

Urea rises with high protein intake, perfectly normal for athletes eating 2-3g/kg protein. Only concerning if it's climbing alongside creatinine.

Hormones

Testosterone

Total testosterone is obviously suppressed on cycle (exogenous AAS replaces endogenous production) and should be assessed post-cycle to gauge recovery. On TRT, you're monitoring to stay within your target range.

Free testosterone is the bioavailable fraction and arguably more clinically relevant than total. It's affected by SHBG levels.

Oestradiol (E2)

Oestradiol management is one of the most debated topics in the enhanced community. The key points:

• E2 is essential for cardiovascular health, bone density, libido, and joint health. Research shows oestrogens are critical regulators of bone health in men (Vandenput & Ohlsson, 2009)
• Crashing E2 with excessive AI use causes more problems than mildly elevated E2. A landmark NEJM study demonstrated that both testosterone and oestradiol deficiency independently contribute to adverse changes in body composition, strength, and sexual function in men (Finkelstein et al., 2013)
• The sensitive LC/MS assay is more accurate than standard immunoassay for males
• Symptoms matter more than numbers: treat symptoms, not lab values

LH and FSH

LH and FSH will be suppressed to near-zero on any exogenous androgen. Post-cycle, you're watching for these to recover as a sign of HPTA restart.

Prolactin

Prolactin can be elevated by 19-nor compounds like Nandrolone and Trenbolone. Research has shown that nandrolone decanoate affects dopaminergic receptor expression in the brain, which can disrupt the dopamine-prolactin axis (Birgner et al., 2008). Significantly elevated prolactin can cause sexual dysfunction and gynecomastia (Patanè et al., 2020).

Lipids

Anabolic steroids, particularly oral compounds and Trenbolone, have a significant negative impact on lipid profiles. A literature review in Archives of Internal Medicine documented the atherogenic effects of AAS on serum lipid levels (Glazer, 1991).

HDL and LDL

HDL (the "good" cholesterol) will drop on cycle. Research has shown AAS use significantly reduces HDL and alters apolipoprotein profiles (Hartgens et al., 2004). This is expected but still represents genuine cardiovascular risk if sustained.

LDL often rises on cycle. The combination of suppressed HDL and elevated LDL is the primary cardiovascular concern for long-term AAS users.

Triglycerides

Triglycerides are heavily influenced by diet. Fasted readings above 1.7 mmol/L deserve dietary attention regardless of PED use.

Haematology

Haematocrit and Haemoglobin

Haematocrit and haemoglobin are two of the most important markers for enhanced athletes. Testosterone and other androgens stimulate erythropoiesis (red blood cell production) via increased erythropoietin and suppressed hepcidin (Bachman et al., 2014), which can push haematocrit dangerously high. This testosterone-induced erythrocytosis is one of the most common adverse effects of TRT (Jones et al., 2015).

Haematocrit above 54% increases the risk of blood clots, stroke, and cardiovascular events. The CYTO-PV trial demonstrated that maintaining a lower haematocrit target significantly reduced thrombotic events (Marchioli et al., 2013), and elevated haematocrit is increasingly recognized as an independent determinant of thrombotic risk (Gordeuk et al., 2019). This is one marker where you should take action rather than dismiss it.

Management options include regular blood donation, therapeutic phlebotomy, naringin supplementation, or dose reduction.

RBC and Platelets

Red blood cell count tracks alongside haematocrit. Platelets can be affected by certain compounds and are worth monitoring as part of the full blood count.

Other Important Markers

Fasting Glucose and HbA1c

Fasting glucose and HbA1c are particularly important if you're using insulin or growth hormone. GH use can induce insulin resistance through multiple mechanisms including impaired post-receptor insulin signalling (Kim & Park, 2017). A comprehensive review in Endocrine Reviews confirmed that GH has profound effects on glucose, lipid, and protein metabolism in human subjects (Møller & Jørgensen, 2009). Monitoring these markers catches insulin resistance early.

Thyroid (TSH, T3, T4)

TSH, Free T3, and Free T4 should be checked at least annually. Some compounds can affect thyroid function, and symptoms of hypothyroidism (fatigue, weight gain, cold intolerance) overlap with other issues.

Ferritin and Iron

Ferritin is your iron storage marker. Regular blood donation to manage haematocrit can deplete iron stores over time, leading to fatigue despite normal haemoglobin. The REDS-II Donor Iron Status Evaluation (RISE) study found significant iron deficiency among regular blood donors (Cable et al., 2012), and further research confirmed that frequent whole-blood donation measurably reduces body iron stores (Reddy et al., 2020). Monitor ferritin if you're donating regularly.

CRP

C-Reactive Protein is a general inflammation marker. Chronically elevated CRP alongside poor lipids compounds cardiovascular risk. Note that it will spike after intense training or illness, so interpret in context.

Building Your Testing Protocol

For most enhanced athletes, this is the minimum panel to request:

Every blood draw:

• Full blood count (FBC): includes haematocrit, haemoglobin, RBC, WBC, platelets
• Liver panel: ALT, AST, GGT, bilirubin
• Kidney panel: creatinine, eGFR, urea
• Lipid panel: total cholesterol, HDL, LDL, triglycerides
• Hormones: testosterone (total + free), oestradiol (sensitive), SHBG

Every 6-12 months (or if symptomatic):

• Thyroid panel: TSH, free T3, free T4
• Iron studies: ferritin, iron, transferrin saturation
• Metabolic: fasting glucose, HbA1c, fasting insulin
• Inflammation: CRP
• Prolactin (if running 19-nors)
• LH/FSH (post-cycle recovery assessment)

How to Read Your Results

1. Compare to your own baseline, not just the reference range
2. Look at trends over time, not single snapshots
3. Consider context: training intensity, diet, hydration, time of draw
4. Don't panic over one elevated value: retest in 2-4 weeks before making protocol changes
5. Act on genuinely concerning patterns: particularly haematocrit, liver enzymes trending up, or lipids that aren't recovering

Key Takeaways

• Blood work is non-negotiable for harm reduction
• Standard lab ranges don't account for muscle mass or PED use
• Most "flagged" results are normal for enhanced athletes, but some genuinely matter
• Haematocrit, liver enzymes, and lipids are your highest-priority markers
• Track trends over time, not just individual results
• Morning fasted draws give the most consistent results
• Get a baseline before every new protocol

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References

1. Ashouri, R., Lertkitcharoenpon, A., Maidaa, M., et al. (2024). Creatinine and cystatin C: A measure of renal function in men with testosterone-induced muscle hypertrophy. American Journal of Men's Health, 18(5). PubMed

2. Bachman, E., Travison, T. G., Basaria, S., et al. (2014). Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin. The Journals of Gerontology Series A, 69(6), 725-735. PubMed

3. Baxmann, A. C., Ahmed, M. S., Marques, N. C., et al. (2008). Influence of muscle mass and physical activity on serum and urinary creatinine and serum cystatin C. Clinical Journal of the American Society of Nephrology, 3(2), 348-354. PubMed

4. Bhasin, S., Brito, J. P., Cunningham, G. R., et al. (2018). Testosterone therapy in men with hypogonadism: An Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 103(5), 1715-1744. PubMed

5. Birgner, C., Kindlundh-Högberg, A. M., Alsiö, J., et al. (2008). The anabolic androgenic steroid nandrolone decanoate affects mRNA expression of dopaminergic but not serotonergic receptors. Brain Research, 1240, 221-228. PubMed

6. Bond, P., Llewellyn, W., & Van Mol, P. (2016). Anabolic androgenic steroid-induced hepatotoxicity. Medical Hypotheses, 93, 150-153. PubMed

7. Brambilla, D. J., Matsumoto, A. M., Araujo, A. B., & McKinlay, J. B. (2009). The effect of diurnal variation on clinical measurement of serum testosterone and other sex hormone levels in men. Journal of Clinical Endocrinology & Metabolism, 94(3), 907-913. PubMed

8. Cable, R. G., Glynn, S. A., Kiss, J. E., et al. (2012). Iron deficiency in blood donors: The REDS-II Donor Iron Status Evaluation (RISE) study. Transfusion, 52(4), 702-711. PubMed

9. Finkelstein, J. S., Lee, H., Burnett-Bowie, S. A., et al. (2013). Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine, 369(11), 1011-1022. PubMed

10. Glazer, G. (1991). Atherogenic effects of anabolic steroids on serum lipid levels: A literature review. Archives of Internal Medicine, 151(10), 1925-1933. PubMed

11. Gordeuk, V. R., Key, N. S., & Prchal, J. T. (2019). Re-evaluation of hematocrit as a determinant of thrombotic risk in erythrocytosis. Haematologica, 104(4), 653-658. PubMed

12. Hartgens, F., Rietjens, G., Keizer, H. A., Kuipers, H., & Wolffenbuttel, B. H. (2004). Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein(a). British Journal of Sports Medicine, 38(3), 253-259. PubMed

13. Jones, S. D. Jr., Dukovac, T., Sangkum, P., Yafi, F. A., & Hellstrom, W. J. (2015). Erythrocytosis and polycythemia secondary to testosterone replacement therapy in the aging male. Sexual Medicine Reviews, 3(2), 101-112. PubMed

14. Kim, S. H. & Park, M. J. (2017). Effects of growth hormone on glucose metabolism and insulin resistance in human. Annals of Pediatric Endocrinology & Metabolism, 22(3), 145-152. PubMed

15. Marchioli, R., Finazzi, G., Specchia, G., et al. (2013). Cardiovascular events and intensity of treatment in polycythemia vera. New England Journal of Medicine, 368(1), 22-33. PubMed

16. Møller, N. & Jørgensen, J. O. (2009). Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects. Endocrine Reviews, 30(2), 152-177. PubMed

17. Patanè, F. G., Liberto, A., Maglitto, A. N. M., et al. (2020). Nandrolone decanoate: Use, abuse and side effects. Medicina, 56(11), 606. PubMed

18. Pettersson, J., Hindorf, U., Persson, P., et al. (2008). Muscular exercise can cause highly pathological liver function tests in healthy men. British Journal of Clinical Pharmacology, 65(2), 253-259. PubMed

19. Reddy, K. V., Shastry, S., Raturi, M., & Baliga, B. P. (2020). Impact of regular whole-blood donation on body iron stores. Transfusion Medicine and Hemotherapy, 47(1), 75-79. PubMed

20. Vandenput, L. & Ohlsson, C. (2009). Estrogens as regulators of bone health in men. Nature Reviews Endocrinology, 5(8), 437-443. PubMed