The heart can burn lactate, a molecule often treated as a by-product of metabolism, by taking it straight into its energy-making compartments. That is the conclusion of a new study in Nature, and it challenges a standard picture of how heart cells use fuel.
The evidence comes mostly from mice. The paper, published in Nature in 2026, also reports that the key protein is present in human heart muscle cells. Only the abstract was available to us, and it does not state how many animals were studied. This article does not report details beyond what the abstract gives.
The heart is a flexible fuel user. According to the study, it can burn several fuels, including glucose and lactate, to meet its energy needs during changes in diet, exertion and injury. The textbook view is that carbohydrate fuels converge on a molecule called pyruvate. A transporter called the mitochondrial pyruvate carrier then moves pyruvate into mitochondria, the cell's power units. The researchers found that glucose-derived carbon was still burned in mouse heart muscle even when that carrier was genetically removed. Using genetic and drug tools, they showed that a different protein, MCT1, was required for this to happen. MCT1 is traditionally found on the cell's outer membrane. The study reports it also sits in the inner membrane of mitochondria in mouse and human heart muscle cells.
Inside mitochondria, MCT1 works with an enzyme called LDHB. Together, according to the authors, they convert lactate into pyruvate and NADH, which directly feed the electron transport chain, the final stage of energy production. The authors describe this as a parallel, lactate-based route for burning carbohydrate.
The pathway appeared to matter under stress. In mice, loss of MCT1 impaired lactate burning and disrupted the heart's metabolic flexibility. It also sped the development of heart failure and raised mortality after two kinds of challenge: overactivation of the body's stress-hormone signalling, and ischemia-reperfusion injury, in which blood flow to the heart is cut off and then restored.
A commentary in Nature on the work notes that lactate is abundant in human blood and has been studied for centuries, yet how cells handle it remains debated. It says the study provides "solid support for a conclusion that defies current dogma": that in the heart, lactate can enter mitochondria directly through a specific transporter, and that this is essential for cardiac function under stress.
For later-life heart health, the implications are not yet established. The abstract shows the pathway in mouse hearts and shows MCT1's location in human heart cells. It does not show that the pathway protects people, that it declines with age, or that it can be targeted by treatment. Any therapy based on this finding remains hypothetical.
What to watch next is whether researchers confirm this lactate route in living human hearts, and whether it changes in people with heart failure.
Sources: Nature (2026), Nature
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Mitochondria · Cardiovascular health