Lactic acid, the metabolic chemical that once got a bad rap for creating exercise "burn," just moved from sideshow to center stage. A new study places lactic acid in an important role within cells and may change how physicians treat a blood disorder associated with diabetes and AIDS.
During exercise, muscle cells demand more energy than the body can readily supply. Traditional physiology says that cells meet this demand by turning starch and sugar into a simpler chemical called pyruvate, which then enters either an aerobic or anaerobic metabolic pathway. Aerobic metabolism utilizes oxygen and creates far more energy for hungry muscles, but it's slow. So most of the waiting pyruvate goes down the oxygen-poor anaerobic road, becoming the once-maligned lactic acid, or lactate. After that, it's kicked out of the cell, at which point it gums up the tired muscle--at least in theory.
But five years ago, researchers showed that lactic acid has its benefits: During exercise, it helps to counteract high potassium levels, which lead to muscle fatigue (ScienceNOW, 20 August 2004). Now, using a powerful laser scanning microscope, George Brooks, an exercise metabolism expert at the University of California, Berkeley, and colleagues demonstrate that lactic acid is present in rat muscle cells regardless of oxygen content. What's more, the team discovered a set of proteins that seem to shuttle lactate to the cell's energy centers, the mitochondria. Previous work by Brooks's group showed that lactate can serve as a fuel, so the team suspects that these proteins help the cell utilize lactate as an alternative energy source, even when oxygen is present.
The findings may prove especially important to diabetics and AIDS patients, who often suffer from a potentially lethal buildup of lactic acid in the blood known as lactic acidosis. The traditional metabolic model assumes the buildup is related to lack of oxygen in the cell, so the common treatment has been to administer oxygen and bicarbonate buffers. Brooks says the new study, which will appear in the June issue of the American Journal of Physiology, indicates that the high acid content isn't due to a lack of oxygen, but rather a problem in the mitochondria processing the lactic acid. Adding more oxygen, he says, is unlikely to help the situation.
The findings "affect how we understand basic metabolism," says L. Bruce Gladden, an exercise biochemist at Auburn University in Alabama. But not everyone is convinced. Robert Robergs, a lactate specialist at the University of New Mexico in Albuquerque, says that just because lactate-friendly proteins gather around mitochondria doesn’t mean they are doing anything.