Whey protein and the liver numbers of 59 young track athletes: they dipped a little on whey, but the biggest move came from nine runners on placebo

Hard training leaves marks in the blood. Enzymes usually read as signs of liver strain and muscle damage drift up, and sports nutrition has spent years asking whether protein can pull them back down. A trial published in the European Journal of Sport Science on 26 October adds an unusual angle: it put endurance and power athletes side by side.

The 59 volunteers were male track and field athletes with an average age of about 18, living and eating at a national training centre and training five times a week for two hours a session. The authors work in Tunisia and Switzerland, and the blood tests were run at the Pasteur Institute of Tunis. Twenty-nine did middle and long distance. Thirty were sprinters, jumpers and throwers. Within each camp, about two in three took 30 g of whey after training for eight weeks, and the rest took a carbohydrate powder matched for look and taste. So the groups were 20 and 20 on whey, but only 10 and 9 on placebo.

On whey, ALT, the enzyme most closely tied to the liver, fell from 17.5 to 15.2 units per litre in the power athletes and from 17.6 to 15.4 in the endurance athletes. AST fell from 27.1 to 22.9 and from 21.7 to 18.3. And these results did pass the test that counts in a trial, whey against placebo, with p below 0.001 for both enzymes.

Now look at what drove that gap. The nine endurance athletes on placebo went from 18.1 to 22.2 on ALT and from 23.0 to 29.6 on AST. Those are the largest shifts in either enzyme, in the smallest group in the trial. By our arithmetic, about two-thirds of the whey-placebo gap among endurance athletes comes from that rise, not from a fall on whey. The paper suggests oxidative and metabolic stress without nutritional support. That's possible, but it's an explanation offered after the fact, for nine people.

The muscle story is weaker than the summary makes it sound. Creatine kinase, or CK, dropped significantly on whey in both groups, from 409 to 362 and from 390 to 335, while it barely moved on placebo. But a fall inside one group isn't the same as beating placebo. The whey-against-placebo test for CK came in at p = 0.082, and for the inflammation marker CRP at p = 0.090, so neither cleared the bar. The authors say as much in the discussion, calling the CK effect confined to the whey subgroups rather than an overall effect of supplementation. Their abstract still leads with those falls.

There's also a question of what these enzymes are measuring here. AST is plentiful in muscle as well as liver, and the authors themselves say that part of the fall in both enzymes may simply follow from less muscle breakdown, rather than any protective effect on the liver. They didn't measure the markers that could separate the two. Nor were these worrying numbers to begin with. Even the highest group average for ALT, 22.2, sits below the 29 to 33 that US gastroenterology guidance gives as healthy for men, though that cut-off is debated. So this is no evidence that whey treats a liver problem, and it wasn't tested in anyone who had one.

Other gaps matter too. Nobody recorded what the athletes ate, so the authors can't rule out that whey was just topping up diets short on protein. They also note that the carbohydrate placebo may have had an effect of its own. Among the power athletes, the whey group started higher than the placebo group on ALT (17.5 against 13.5), AST and CK, which leaves room for high readings to drift back on their own, by our reading. Only men took part, there were only two blood draws, and performance wasn't measured.

What can you take from this? A modest one: in young men training hard, 30 g of whey a day came with no rise in these enzymes over eight weeks, and liver enzymes moved in a better direction than on a carbohydrate powder. That may be mildly reassuring for anyone who has heard that protein shakes strain the liver, within the narrow limits of this group. It isn't proof that whey protects the liver or speeds recovery, and the paper's call for individual protocols goes further than four small groups can carry. A larger trial, with diet recorded and liver-specific and muscle-specific markers measured, could settle what this one only hints at.