Lactate has long been treated as a waste product of hard-working muscle. The authors of this study point out that it is the highest-turnover metabolite circulating in mammals, and that many organs burn it for energy. To be used, it must first be converted to pyruvate, which feeds the tricarboxylic acid (TCA) cycle, the chain of reactions inside mitochondria that extracts energy from food. The textbook account places that conversion in the cytosol, the fluid that fills the cell. Pyruvate is then ferried into mitochondria by a dedicated protein, the mitochondrial pyruvate carrier, or MPC. A 2026 study in Nature by researchers at Rutgers, the University of Utah and Wake Forest argues that part of this route runs differently in the heart.

The work was done in mice. The team used carbon-13 stable isotope tracing. In this technique lactate is labelled with a heavier, non-radioactive form of carbon, so its fate can be followed through the cell's chemistry. In the heart muscle of mice whose MPC had been genetically deleted, the labelled lactate was still oxidised. That meant lactate had another way in.

The authors report that this alternative depends on monocarboxylate transporter 1, a protein called MCT1 and encoded by the Slc16a1 gene. Mitochondria isolated from heart muscle lacking MCT1 had trouble metabolising lactate, but their pyruvate metabolism did not show the same defect. Inside the mitochondria, an enzyme called mitochondrial lactate dehydrogenase converts the imported lactate. In doing so it generates NADH, a molecule that carries electrons to the oxygen-consuming machinery of respiration. The authors describe the process as an electron shuttle. They report that it supplies enough NADH to keep respiration running even when the TCA cycle itself is disrupted.

The consequences appeared when the hearts were put under strain. Mice whose hearts lacked MCT1 were exposed to a range of cardiac insults. They progressed rapidly to heart failure with reduced ejection fraction, a form of heart failure in which the main pumping chamber pushes out a smaller share of its blood with each beat. The authors conclude that importing and oxidising lactate inside mitochondria is one way carbohydrate enters the TCA cycle. In their account, this route helps sustain the heart's energy supply and preserve its structure and function under stress.

The findings come from genetically modified mice. The abstract does not say which cardiac insults were used, how large the effects were or how many animals were studied. It also does not address whether the same pathway operates in human hearts, or how much it contributes compared with the conventional pyruvate route in a healthy heart. This is basic research on metabolism and does not test any treatment.