Lactic Acid – Friend or Foe?

Lactic Acid – Friend or Foe?

[Article by Tait Hearps of Sweat Elite]

Gasping, you drive hard with your arms as you come off the bend into the final straight. An intense burn began to permeate your body a few hundred metres ago, and now it is peaking, all-consuming. You can’t keep this up, your strength is fading. Your whole body is awash with lactic acid, drenched up to your eyeballs, which are popping out of your grimacing face.

A familiar feeling for anyone who has pushed themselves to their limit in a middle-distance race, and a feeling distinct from that which comes in the latter stages of a long-distance race. But, as I will explain in this piece, what most people think they know about lactic acid is, frankly, all wrong. Here we will examine this compound and debunk some myths about what it is and how it impacts fatigue, body soreness and recovery.

Correlation does not imply causation! A dictum hammered into every student of science since time immemorial, yet still overlooked with a frequency that is startling. One such oversight is what has led to the perpetuation of the idea that lactic acid is the evil and debilitating waste product of anaerobic metabolism.

Otto Meyerhof, a German biochemist, won the 1922 Nobel Prize for Physiology or Medicine for his discovery of the fixed relationship between the consumption of oxygen and the metabolism of lactic acid in the muscle, together with the English physiologist A.V. Hill.

Meyerhof studied glycolysis, the process by which glucose is broken down to produce the energy currency of the body, Adenosine Triphosphate (ATP). In his studies he discovered that repeated stimulation of frog leg muscles using an electric current resulted in the muscle eventually losing contractile function. When testing the muscles, it was found that the concentration of lactate was sky high. The inference was made that lactic acid therefore impeded muscle function, and many subsequent studies examining muscle physiology came to similar conclusions.    

Note that it was found that lactate, not lactic acid, was in high concentrations. This is an important difference and changes things a lot. Lactate is an anion, meaning it has a negative charge, and when paired with a proton (H⁺, a hydrogen ion) it forms the organic compound lactic acid. To get our bearings, we have to take a look at some of the physiology here.

We all know glucose is needed for energy when exercising. But it’s not glucose itself which is needed to power muscle contractions – we need ATP. Glucose, along with many other molecules, can be broken down, or oxidised, to generate ATP. This occurs in two main phases. The first chain of reactions that glucose goes through is glycolysis, in which glucose (a six carbon sugar) is split to eventually form two pyruvate molecules (a three carbon sugar), and two ATP molecules.

In the presence of oxygen these pyruvate molecules then undergo further breakdown in the mitochondria to produce carbon dioxide, and a lot more ATP. This aerobic respiration (in the presence of oxygen) is the most efficient way of generating ATP in the body. However, during sprint efforts the demand is such that there is not enough time to disseminate the oxygen required for aerobic metabolism to adequately supply ATP.

The result is that glycolysis then becomes the main mechanism for generating ATP. But to continue to break down glucose certain compounds must be regenerated, and in this process, protons are added to pyruvate, forming lactate (see diagram below).

There are a lot more specifics which go beyond the scope of what we will look at here today, but this is a basic overview of how lactate is formed. 

Note that lactate is formed by adding protons (hydrogen ions) to pyruvate. Protons are what make something acidic, and as an anion lactate then has the capacity to bind protons, thus acting as a buffer and reducing acidity. Acidosis of exercise is due to several mechanisms. It’s this acidosis which is suggested to cause the “burn” felt during hard exercise, and therefore lactate may actually serve to reduce the sensation of pain.     

In the past few decades one of the world’s leading scientists has been Dr George Brooks of UC Berkeley. He has made a slew of incredible findings in his research, including that lactate can actually be a fuel for muscles, the heart and the brain. This occurs by shuttling lactate to other cells, where it can either be used to regenerate pyruvate and undergo aerobic respiration in the mitochondria (often done in neighbouring muscle fibres), or to regenerate glucose using two lactate molecules (Cori’s cycle, predominantly occurring in the liver).

Type II muscle fibres are commonly called “fast twitch” fibres and these fibres are recruited readily in sprinting. Type II fibres have fewer mitochondria and generate more lactate than the type I fibres, which are more efficient at using oxygen and play more of a role in endurance efforts. Thus, when lactate has accumulated in type II fibres it may be shuttled to neighbouring type I fibres, acting as fuel to allow more ATP to be produced and prolong an effort. This shuttling can also transport lactate in the blood from exercising muscles to non-active muscles to provide a substrate for energy, as well as to the heart and brain. Lactate is proposed to even be involved in processes as complex as memory formation and neuroprotection.

Another interesting point coming from research is that acidosis is not the primary cause of muscular fatigue. Muscle fatigue is multifactorial, and studies have shown that lactate itself is likely not implicated in muscle fatigue at all.

Here is a great summary by Dr. Bruce Gladden:

“For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O₂ debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a ‘lactate revolution’ has occurred… It now appears that increased lactate production and concentration as a result of anoxia or dysoxia (hypoxia) are often the exception rather than the rule. Lactic acidosis is being re-evaluated as a factor in muscle fatigue… Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional and whole body metabolism.”

So, if not lactic acid, what does cause muscle fatigue? In the context of slowing down at the end of a relatively anaerobic – near maximal – effort, depletion of glucose does not account for the fatigue, that’s more relevant for endurance efforts (think of “the wall” towards the end of a marathon). It also appears that the state of acidosis observed in athletes at the end of these efforts is not responsible for the slowing, as muscle fibres have been shown to be minimally affected by acidic conditions at physiological temperatures.

There are a few theories to explain this loss of contractile force. One is that phosphate released when ATP (remember that this stands for adenosine triphosphate) is broken down to fuel muscle contractions, then goes on to decrease force generating capacity in subsequent contractions. Another is that reactive oxygen species (ROS) produced by muscle contractions then go onto interfere with further contractions. A final theory is that the loss of force is due to changes in calcium distribution in and around the muscle cells.

Sore the day after that hard workout? It’s a commonly held belief that accumulated lactic acid is responsible for delayed onset muscle soreness (DOMS) in the day(s) following a hard workout. However, scientists have examined the role of lactate in muscle soreness… The findings? Yet again, lactate has been unjustly vilified as an evil molecule. This has been known for a long time, with studies showing such evidence back in the 1980s, yet it’s something that is still perpetuated right to the top level of sport. DOMS is now believed to be due to microtrauma to muscle fibres and subsequent inflammatory responses. 

Another commonly held belief is that the warm down after a hard workout or the shake out the next day is important to ‘help get the lactic out of the legs’. However, again the science doesn’t back this up. Yes, walking or jogging does shorten the time it takes for lactate levels to return to normal, but this return to baseline occurs relatively quickly anyway. By the time someone is doing a shakeout the day after a race or hard session, the lactate generated by that effort has long ago left the muscles. And where is it going? This is where lactate being a fuel source again comes into play, according to Brooks, after ‘exhaustive’ exercise lactate then becomes the preferred energy source, being burned up by muscles that are no longer using anaerobic respiration, and by the liver to regenerate glucose.

This now brings us to the lactate threshold, which can be defined as the exercise intensity at which blood lactate concentrations rise exponentially. It has been identified in research as one of the best predictors of endurance performance. Closely linked to an athlete’s lactate threshold is their VO₂ max, which represents their ability to utilise oxygen. Increasing VO₂ max means that at a given intensity they are supplying more oxygen to working muscles and this makes the cells less reliant on anaerobic metabolism. And increasing lactate threshold means that an athlete can exercise at a greater intensity before lactate starts to accumulate. 

Here again it’s important to remember the dictum, “correlation does not imply causation”. We now know that this increase in lactate associated with the lactate threshold and the decline in performance we see when someone passes the threshold is not caused by the lactate. Rather, lactate is produced in step with other changes that result in declining performance. How to improve these? Intense training has been shown to improve both the lactate threshold and VO₂ max. Interestingly, one study found that strength training had the effect of increasing the lactate threshold but not the VO₂ max. 

We have covered a lot here, hopefully getting down into the weeds on this was interesting and hasn’t left you feeling a bit disoriented. Some of the science here is really hard to wrap your head around. But just to consolidate what has been covered, let’s summarise…

• Lactic acid won’t hurt you!
• Lactate acts as a buffer and can decrease acidity in muscles.
• Lactate acts as a fuel source for exercising muscles, as well as cardiac muscle and the brain.
• Lactic acid isn’t responsible for fatigue, acidosis appears to not be responsible either, the causes are complex, and understanding is still developing.
• By the time you’re doing your shakeout the day after a race or hard workout, the lactate is long gone.
• Improving lactate threshold is one of the best ways to improve performance.

What does all of this change? Not much really. We’ve busted some of the myths that have for too long shrouded lactic acid in a veil that belies its true nature. But that intense burn you’re all too familiar with will still come to haunt you and make your legs feel like jelly on the home straight of the next 800m race you run. You’ll know it’s not lactic acid causing it, and that the lactate in your legs is actually working as fuel, but it will still hurt.

Should you stop warming down after a tough workout? Probably not. The causes of fatigue are complex and it’s likely that cooling down does something that is really difficult to measure scientifically in the lab. People do a lot of things that are custom (or that someone else told them was a good idea), whether or not there’s a scientific backing. In the world of recovery, a safe bet is generally that if it feels good, do it. But there are some important lessons here, the obvious one being that it’s important to question ‘age-old wisdom’ from time to time. How many other commonly held beliefs don’t make sense or have been proven to be wrong since they were popularised, yet are still perpetuated? Probably more than you or I care to think about.