Gamma-GT (GGT)

What is being measured

Gamma-glutamyltransferase is located in the membranes of the bile duct cells and liver cells. Its task lies in glutathione metabolism: it breaks down glutathione outside the cell and makes its building blocks available again, especially cysteine, from which the cell builds new glutathione.

For strength training, the most important thing is how it behaves when the muscle is suffering: it doesn't move while the transaminases are working. The obvious reason is that it is rarely present in skeletal muscle; What is measured below is the behavior, not the distribution in the tissue.

Reference range

• Men around 10 to 60 U/l
• Women around 8 to 40 U/l

Conventions of laboratory medicine, not study findings. They differ depending on the measurement method, the area depends on your own findings.

Why it is useful when training

Fifteen healthy men accustomed to moderate exercise without resistance training completed a one-hour weight lifting program. Thereafter, AST, ALT, LD, CK, and myoglobin increased significantly and remained elevated for at least seven days. Bilirubin, gamma-GT and alkaline phosphatase remained within normal limits.

The fact that the participants were inexperienced speaks more for rather than against the finding: experience has shown that unusual stress causes more damage to the muscle than usual stress, and yet the GGT did not budge. However, there is no comparison between usual and unusual stress in the work; that is a consideration and not a result.

So it belongs together Bilirubin and the alkaline phosphatase to the values that remained unaffected by the load in this experiment OLD and AST rose. This is not an investigation that tests the accuracy of this distinction. More on this below Liver.

A second observation is important and is usually overlooked. In one study, exercisers had higher baseline levels of CK, CK-MB, ALT and LDH than sedentary comparison subjects. This was a group difference in the resting value, not the difference after one session. It is not a historical measurement that shows how an individual's resting value shifts under training; However, the direction fits with the caution not to immediately attribute increased transaminases in exercisers to the liver.

Together with alkaline phosphatase

The second task of the GGT is the allocation of an increase in alkaline phosphatase. This also comes from the bone, the GGT does not. In a study of AP subtypes in liver disease, a high degree of agreement was found between the biliary tract subtype and total GGT. If both rise together, this indicates the bile ducts; If AP alone increases, a source outside the liver becomes more likely. The paper did not examine how accurate this rule is in individual cases.

What increases the value

• Alcohol. The classic trigger and the reason why an elevated level is often misunderstood as a drinking level.
• Cholestasis. Anabolic androgenic steroids can cause cholestatic liver injury. In a series of 44 young men following bodybuilding supplements, all had clinical signs of such damage, the median time to damage was 73 days, and 71 percent were hospitalized. A disruption of antioxidant factors, increased bile acid synthesis and an increase in liver cells are discussed as mechanisms.
• Fat distribution, not fat quantity. In a study of 62 people, there was no connection between GGT and total fat mass. However, it increased with belly fat (β = 0.35) and decreased with hip fat (β = −0.48).
• Enzyme-inducing drugs, such as some anti-epileptic drugs.

The amount differs between causes. In a comparison of four liver diseases, the GGT in fatty liver was the lowest of the four at around 200 U/l. This does not result in a limit value for individual cases: which value requires clarification depends on the laboratory, the cause and the person.

Which lowers him

Coffee, and measurable. In a study of 12,687 health screening people, higher coffee consumption was independently associated with lower GGT in men, particularly among those who drank more alcohol. This association was absent among men who did not drink alcohol; it was weak among women.

A cross-sectional study, i.e. no assignment of causes. What it suggests is a connection with alcohol and not a liver drug: no effect was seen without alcohol.

The value says more than just something about the liver

This is where things get interesting, in both directions. In population studies, high GGT levels are associated with a surprising number of things that have little to do with the liver. This means a connection across groups and not a prediction for an individual person. Across 7,458 men, followed for an average of almost 13 years, the risk of type 2 diabetes in the top fifth of the GGT was 6.8 times that of the bottom, and after adjustment for blood sugar, body weight, alcohol, exercise and other variables, it was still 4.8 times. In 1878 apparently healthy men, the hazard ratio for a first coronary event in the top quarter compared to the bottom quarter was 2.34, adjusted for blood pressure, blood lipids, diabetes, smoking and body weight, among other things. Across 1,667 people, every one standard deviation increase predicted new hypertension, with a hazard ratio of 1.20.

A review brings this together with glutathione metabolism and suggests that elevated GGT levels should be viewed as an indicator of inadequate antioxidant levels. This is an interpretation of the connections and not a measurement result on individual people.

And then the cross-check

The same picture with blood pressure. The GGT quarters there were strongly related to systolic and diastolic blood pressure; Calculated via gene variants, nothing remained. And for metabolic syndrome, the risk increased 3.81-fold across the GGT quarters in men. After additional adjustment for insulin resistance, the linear relationship was no longer statistically significant in either sex; only men in the top quartile maintained an increased risk compared to the bottom quartile.

The cross-check is different for one endpoint: for stroke, a Mendelian randomization found a possible causal connection with an odds ratio of 1.23. The paper itself notes that this has yet to be confirmed and relates to a European population.

The pattern is similar to that of HDL cholesterol: a strong indicator whose causal contribution largely disappears in the genetic cross-check. Mendelian randomization is not a final authority; it has its own assumptions. What follows from the data is not to ignore the value, but rather not to treat it as a goal: a high value is a reason to look, and lowering it without changing the cause has no proven benefit here.

What this means in strength training

• If transaminases are elevated, it is worth looking at the GGT. If it remains normal, a muscular origin of the transaminases becomes more likely; If it increases, the question shifts to the liver and bile. This rule has not been tested; it follows from the different behavior of the values ​​after load.
• If substances are swallowed, it should be included in the diagnosis. They and alkaline phosphatase are the values ​​that increase in cholestasis, and the guidelines for clarifying abnormal liver values ​​describe the disproportionately increased alkaline phosphatase compared to AST and ALT as a hallmark of cholestatic damage.
• A baseline before you start saves guesswork. The usual range is broad, and one's starting point within it is the most useful benchmark. There is no study here that proves this; it is an obvious precaution.
• Alcohol belongs in the information. Anyone who drinks on the weekend and measures on Monday is partly measuring the weekend.
• A persistently elevated GGT without oral substances and without alcohol is a reason to keep looking, and not just on the liver. The connections with blood sugar, blood pressure and cardiovascular diseases are clear in population studies, even if they are hardly confirmed as a cause.

Classification

The GGT is useful in strength training for a banal reason: it did not move in the present exercise study, while ALT and AST did. It is therefore a clue to the question where transaminases alone fail, namely whether an abnormal finding comes from the liver or from training. A study that tests the accuracy of this distinction on strength athletes is not included in the work used here.

Its second face is that of a general warning value, and caution is advised there. The size of the observed connections is impressive, and their causal interpretation does not hold up to the genetic cross-check in diabetes and blood pressure. In the case of stroke, however, such an analysis found a possible causal connection, which the authors themselves describe as still needing confirmation. A value that indicates a lot and whose causal part is open is a good reason to investigate and a dubious goal.

It remains unclear what a slightly increased GGT means in a training, slim, non-drinking person. The population studies were based on other collectives, and the training studies only measured the short-term response to a unit. The work cited here does not include a study that has followed strength athletes over the years.

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