For years, lactic acid was considered the enemy of endurance athletes, a waste product that gummed up the works and would eventually cause muscles to grind to a halt. It was blamed for the burn of intense exertion and the soreness days after an event.

After years of trying to teach runners, cyclists and other long-haul athletes to avoid lactic acid production, scientists are now coming around to the fact they were wrong.

Slowly but surely, physiologists are accepting the theory proposed decades ago by Dr. George Brooks, an exercise physiologist and former collegiate runner: that lactic acid might help much more than it hurts.

The maligning of lactic acid stems from the work of Nobel prize winners A.V. Hill and Otto Meyerhof, who in the 1920s experimented with frogs to test their theories about lactic acid. The researchers cut a frog in half, cutting off the supply of oxygen to the leg muscles and stimulated the leg muscles to contract with electric shocks.

After a few contractions, the muscles seized up. The researchers saw that the muscles were full of lactic acid and concluded that the absence of oxygen led to the production of lactic acid, and with enough lactic acid, the muscles would stop working.

The theory persisted, and for years scientists and trainers believed that as long as you could work aerobically, that is, with sufficient oxygen delivery to the muscles, lactic acid production was kept to a minimum and you could continue to work at that level indefinitely.

It was further believed that at some level of exertion, the cardiovascular system couldn’t deliver enough oxygen to keep the muscles working aerobically, and the muscles shifted to anaerobic work, producing energy without requiring oxygen.

The byproduct of that anaerobic work was lactic acid, and with lactic acid buildup, muscles would tire and cease working. Lactic acid was also thought to be responsible for the burning felt in muscles during extreme exertion and for the soreness in muscles felt a day or two after a hard workout.

As a result, training methods were devised to keep the muscles from switching to anaerobic work. Go too hard, the mantra was, and you’ll tire out the muscles with too much lactic acid and have to cut short your training session. Even recovery strategies were geared towards helping clear the lactic acid from muscles.

Changing views

But there were certain things that just didn’t make sense to researchers. For one, lactic acid generally cleared from the muscles in the hours after working out. Why then would muscles be sore two days later?

Additionally, Brooks and other researchers discovered that training techniques that produce high volumes of lactic acid caused changes that would lower lactic acid levels in the bloodstream. Where was the lactic acid going?

And there was no evidence that muscles lacked oxygen, even during heavy exertion.

Brooks was eventually able to show that lactic acid, or technically lactate, moves out of the muscle cells into the blood and travels to various organs, including the liver and the brain, where it is burned with oxygen for energy. And he suspected the same was happening inside muscle cells.

Now he believes he’s found the missing link – a set of proteins that appear to shuttle the lactate in muscle cells into the mitochondria, the power plant of the cell. There it can burned with oxygen to produce more energy.

Now he believes he’s found the missing link – a set of proteins that appear to shuttle the lactate in muscle cells into the mitochondria, the power plants of the cell. There it can be burned with oxygen to produce more energy.

”This is a fundamental change in how people think about metabolism,” Brooks says. ”This shows us how lactate is the link between oxidative (or aerobic) and glycolytic, or anaerobic, metabolism.”

Brooks helped convince many of the nation’s experts that the body relies on a combination of the various energy-producing systems it had at its disposable. These processes were not distinct as previously thought.

When exercising at lower levels of intensity, muscles rely primarily on the aerobic cycle. Glucose in the bloodstream or glycogen from the muscles is broken down into pyruvic acid, which is then processed in the mitochondria of muscle cells to form adenosine triphosphate, or ATP, the main source of energy for muscles. The aerobic pathway is very efficient, producing six times more ATP from the same amount of glucose than the anaerobic cycle.

But the aerobic cycle is much slower, and as exercise intensity increases, the aerobic cycle can’t keep up with the demand for energy. Then the anaerobic cycle kicks in. Pyruvic acid outside of the mitochondria is converted into lactate, producing small amounts of ATP very quickly but only for a limited amount of time. The lactate, a byproduct of the anaerobic cycle, then seeps into the bloodstream to be used elsewhere.

At lower levels of exertion, there’s a balance between lactate production and lactate removal. But with increased reliance on anaerobic pathways, the lactate builds up faster than the cells can clear it. The athletes pass what’s known as the lactate threshold.

The higher intensity causes another shift from using primarily slow-twitch muscle fibers geared toward aerobic work, to more fast-twitch muscle that trends toward anaerobic work, leading to more lactate production.

Shuttle theory

Brooks’ latest research shows that if energy demands persist, the lactate is shuttled into the mitochondria where it can be burned with oxygen to give the muscles an additional source of energy.

Dr. Thomas Fahey, a professor of exercise physiology at California State University at Chico, says this use of lactate is why some runners experience a second wind.

”Our findings can help athletes and trainers design training regimens and also avoid overtraining, which can kill muscle cells,” Brooks says. ”Athletes may instinctively train in a way that builds up mitochondria, but if you never know the mechanism, you never know whether what you do is the right thing.”

Numerous studies have shown that lactate threshold is the best and most consistent predictor of performance in endurance events. Brooks says that ironically coaches have been way out in front of scientists on training methods, because they have seen what works.

”The world’s best athletes stay competitive by interval training,” Brooks says. ”The intense exercise generates big lactate loads and the body adapts by building up mitochondria to clear lactic acid quickly. If you use it up, it doesn’t accumulate.”

Interval training, which involves bouts of intense exercise to produce large amounts of lactic acid interspersed with easier exercise to allow the body to recover, helps the body to produce less lactate acid to begin with and to clear it faster when it does.

The high levels of lactate during hard exercise stimulate the cell’s mitochondria to grow in size. That helps to clear lactate faster. But since aerobic work relies on the mitochondria to process blood sugar, it also helps the muscles do more work aerobically, delaying lactate accumulation even further.

Typically, endurance athletes rotate from interval training above the lactate threshold, to exercising for longer duration at a lighter pace, to working at close to the lactate threshold continuously for shorter distances.

Good personal trainers or coaches can help you estimate your lactate threshold from your heart rate or from a perceived exertion scale. Exercise labs, such as the one at Central Oregon Community College, can conduct more precise tests to determine your lactate threshold.

A bad rap

Scientists now know the soreness that comes days after extreme exertion comes from inflammation, microscopic tears and other damage to muscles, not because of lactic acid. And the burn called acidosis you feel during heavy exertion? Even that’s not due to lactic acid.

Dr. Robert Robergs, an exercise physiologist with the University of New Mexico, explains that lactate production actually retards acidosis. In a review published in the American Journal of Physiology in 2004, Robergs describes how when ATP is broken down for energy, a single hydrogen ion is released, and these hydrogen ions are what caused the acid buildup, or the burn. As hydrogen ions accumulate in muscle cells, they combine with the pyruvate that hasn’t entered the mitochondria to create lactate. As a result, lactate production results in a drop in the number of hydrogen ions, delaying acidosis.

Far from causing acidosis, Robergs explains, lactate helps to mitigate the burn. Thus same endurance training that helps the body make better use of lactate, also helps to delay acidosis.

”If muscle did not produce lactate,” Robergs says, ”acidosis and muscle fatigue would occur more quickly, and exercise performance would be severely impaired.”