ALT (GPT)
ALT is a liver-specific marker, but it is not organ-specific. Reference ranges depend on the population and the measurement method; a single value does not constitute a direct liver function test and should be interpreted in the context of other liver function tests.
Auch bekannt als: Alanin-Aminotransferase
What ALT actually measures
ALT stands for alanine aminotransferase. A basic chapter on tissue distribution describes the highest ALT activity in the liver, followed by kidney, myocardium and skeletal muscle. ALT is therefore liver-specific, but not exclusively liver-born. A clinical guideline classifies ALT, AST, ALP and bilirubin as “liver chemistries” and “liver tests” respectively. They are not direct measurements of liver function; the pattern of elevation guides further clarification.
The standard ALT activity test does not distinguish the organ of origin or the ALT isoforms measured. In a molecular biological study, ALT2 was localized in the mitochondrial fraction and endoplasmic reticulum in cultured human skeletal muscle cells and ALT1 was localized in the cytosol and endoplasmic reticulum in hepatocytes. This is a cellular and molecular finding, but not a clinically validated assignment of an individual serum value.
The scheme summarizes tissue ranking, molecular localization and clinical pattern recognition. It is not proof of a specific organ source in a single person.
Which reference intervals apply
A multicenter IFCC reference interval study of 765 adults, including 411 women and 354 men aged 18 to 85 years, found 8 to 41 U/L for women and 9 to 59 U/L for men. These numbers belong to the reference population examined and the standardized measurement method. They are not universal diagnostic or treatment thresholds; the training status of these reference persons was not examined.
The reference range of the specific laboratory should therefore be taken into account when reading the results. A single value cannot be meaningfully separated from population, method and clinical pattern.
How an increased value is classified
The ACG professional guideline distinguishes a hepatocellular pattern, when AST and ALT are disproportionately elevated relative to ALP, from a cholestatic pattern. The pattern of liver chemistry guides further workup; The isolated term “ALT increased” does not provide the entire classification.
If conjugated bilirubin is elevated along with abnormal liver chemistry, this suggests possible hepatocellular disease or cholestasis in most settings. The total bilirubin should then be divided into direct and indirect fractions. The finding is an indication for further investigation, but not proof of a single cause.
Neither the tissue distribution nor the activity test can reliably determine which organ an elevated ALT value comes from in a person. A muscle or liver assignment from ALT alone is therefore not reliable.
What can be derived from strength training
A direct human study of 15 healthy men accustomed to moderate physical activity without weightlifting examined a one-hour weightlifting program. ALT, AST, lactate dehydrogenase, creatine kinase and myoglobin increased significantly and remained elevated for at least seven days. Bilirubin, GGT and ALP remained within normal limits.
The finding shows that a single intense force load can influence ALT and AST over several days. However, it neither proves that a specific ALT value comes from the muscle, nor that a specific training break is sufficient for every person.
The data therefore does not provide a universal hourly or daily indication for a fixed training break before a blood test. The direct study describes a course over at least seven days, but does not validate a general 48-hour or three-day rule, no specific two- or three-fold increase and no strength sport-specific threshold of permanently more than three times the laboratory-dependent upper limit.
What role 17α-alkylated AAS play
A mechanistic review comes to the qualitative conclusion that 17α-alkylated anabolic-androgenic steroids appear hepatotoxic. The 17α-alkylation therefore delays hepatic degradation and makes the substances orally bioavailable; the mechanism is not fully understood.
This review contains a risk classification for this class of substances, but no frequency, no standardized dose-response relationship and no specific size of an ALT elevation. This does not mean that any statement can be made about every oral product.
Which is practically justifiable
- Use the reference range of your own laboratory because the population and measurement method influence the intervals.
- Classify ALT together with AST, ALP and bilirubin as patterns of liver chemistry rather than reading ALT as a direct test of function.
- If conjugated bilirubin is elevated, have the total bilirubin fractionated and further clarify the situation with a doctor.
- If you have recently performed intensive weight lifting, indicate the time of blood draw in the clinical assessment. No reliable organ source can be derived from ALT alone, even together with CK or GGT. A fixed training-related break or the “triple upper limit” threshold is not validated for strength athletes.
Sources
- Kwo PY et al. ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. Am J Gastroenterol. 2017. PubMed
- Ceriotti F et al. Common reference intervals for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and γ-glutamyl transferase (GGT) in serum: results from an IFCC multicenter study. Clin Chem Lab Med. 2010. PubMed
- Glinghammar B et al. Detection of the mitochondrial and catalytically active alanine aminotransferase in human tissues and plasma. Int J Mol Med. 2009. PubMed
- Vroon DH et al. Aminotransferases. . 1990. PubMed
- Bond P et al. Anabolic androgenic steroid-induced hepatotoxicity. Med Hypotheses. 2016. PubMed
- Pettersson J et al. Muscular exercise can cause highly pathological liver function tests in healthy men. Br J Clin Pharmacol. 2008. PubMed
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