Lactic Acid Gives Lactate a Bad Rap

Coaches, trainers, and armchair aficionados often use “lactate” and “lactic acid” interchangeably when providing pejorative condolences to an athlete hitting the wall. Colloquially, people assume you mean the same thing when you use either term, but lactate vs. lactic acid is indeed very different.

The Misconception of Lactate vs Lactic Acid

High levels of lactate — or, as it is often called in popular sports culture, lactic acid — was once considered responsible for an athlete’s bonking in a race and/or practice. Simply put, it’s not. The presence of lactate is one of many trackable physiological markers that are found in exhausted athletes. Correlation is not causation.

The emphatic evidence is that very little lactate is produced during prolonged, continuous training. Yet it is this very type of exercise that can leave muscles sore for days. Post-exercise muscle fatigue is actually caused by ‘micro-tears’ to muscle fibers, free radical damage, and inflammation. But don’t go taking an ice bath just yet.

While the misnomer of lactate vs lactic acid still exists, many high-level athletes and coaches have caught up to decade-old research. Foreward thinking is to believe that lactate is an end product of anaerobic muscle metabolism. Its presence causes local muscle fatigue via an increase in acidity (decrease in pH) to the point where muscles can no longer operate under the increasingly ‘hostile’ environment. 

But more recently, lactate is believed to be an intermediate bridge between anaerobic and aerobic systems. It serves as both a direct and indirect fuel for muscle contraction. And may actually delay fatigue.

Muscles at work never reach a level of acidity that would directly cause fatigue, because lactic acid does not increase muscular acidosis.

When muscle cells were electrically innervated to give the illusion of a high physiological workload, complete mechanical failure never occurred. Implying that acidosis is an indicator of potential fatigue, but not directly responsible.

Blood lactate measurements best serve to inform training periodization for optimal recovery and performance. (or check the color of the athlete’s face and/or depth/speed of breath to save yourself a few dollars)

Mythical Status of Lactic Acid

Dr. George Brooks’ interest in lactate vs lactic acid unwittingly began in the 1960’s as an athlete.

While running the 400 meters at Queens College he experienced that all too familiar pain all athletes feel after 40 seconds of maximum effort. Those last 6-10 seconds feel as though the finish line is running from you.

In an attempt to rationalize the phenomena, Brook’s track coach would blame lactic acid for the burning sensation in his legs and the loss of performance.

Perhaps skeptical, or just intrigued by the assertion, Brooks would go on to earn a doctoral degree in exercise physiology. His field of study? The lactate transport shuttle or to the fox – ‘lactate vs lactic acid’.

Oversimplified, lactic acid is the metabolic waste created when lactate bonds with leftover hydrogen ions from anaerobic glycolysis. A primary requirement of bursts of effort when oxygen is typically limited.

Either because too much energy has been required for metabolic waste to be efficiently managed. Or the muscles have not primed themselves correctly for immediate needs.

Typically it can take an athlete 2 minutes to get aerobic systems firing on all cylinders. And in the meantime, a maximal, or near maximal performance, requires and produces lactate as the primary energy source.

Whatever one calls this relationship, it is not a waste product of anaerobic metabolism, as once believed. It’s a balancing act between anaerobic and aerobic performance requirements.

Both energy systems work in concert. A delicate dance that coaches can stress. And athletes can adapt to performance requirements.

Elevates Blood Lactate

It’s now widely accepted that lactate can serve as a fuel for musculature, vital organs, and the brain.

But Brooks first postulated that continuous training actually reduces the amount of lactate entering the bloodstream without affecting the amount of skeletal lactate created. Evidence that lactate is also used at the cellular level. 

While racing and working out it was thought that high-level athletes produced less lactate than the average joe. Now it appears that these athletes are better able to utilize lactate production without it finding its way into the bloodstream. This efficiency is why blood lactate tests show lower amounts.

A fact I can anecdotally attest to as I personally spent time taking blood lactate samples from the likes of Michael Phelps and others at USA Swimming competitions and practices. The aim was to improve recovery and inform training. The methodology was flawed.

Phelps’ superhuman ability to clear blood lactate was likely more correlated to the lactate produced during exercise being used in the mitochondria. Very little finding itself into the bloodstream. Phelps buffered production.

Intuitively, this would mean that he is either genetically more gifted at the process and/or trained to manage the exchange with incredible efficiency and biomechanical economy.

Away From Skeletal Lactate

Lactate is a highly mobile substrate that can permeate muscle cell membranes to find its way into the bloodstream. 

From there the lactate flows to other muscles (especially resting muscles and muscles working at lower intensities) and other organs—especially the heart, liver, and brain—and used as a fuel. Lactate that reaches the liver is even converted back into glucose and sent back to the hardest-working muscles to replenish depleting fuel stores.

Brooks began to suspect that the classical lactate vs lactic acid misconception was wrong when he traced radioactive isotopes in rats. The radioactive tracers found that their bodies consumed it faster than any other energy source. Enter the lactate shuttle concept.

During moderate-intensity exercise done over longer durations, most energy is created aerobically and produces no lactate.  Aerobic metabolism creates more energy, but takes longer and requires oxygen.

At high intensities, another pathway initializes more quickly, giving the muscle two parallel pathways to release energy. An athlete’s anaerobic potential allows for high speed and availability (but creates less) to keep up with muscle demands.

Here glycogen or glucose is broken down to lactate without oxygen, and then lactate is broken down to carbon dioxide and water with oxygen.

Into Applied Training vs Basic Understanding

As mentioned earlier, some of the world’s best endurance athletes, such as Michael Phelps, appear to produce significantly less blood lactate during intense exercise than lesser athletes. This makes sense if you believe that lactate is a toxic waste product that causes fatigue and does not help exercise performance in any way.

In all likelihood, the reason there is less lactate in the Phelps’ blood during intense exercise is not that his muscles produce less of it. Rather that they use more.

More likely, if the average endurance athlete allows lactate burned in the mitochondria to escape into the bloodstream at a slower rate than the average mile time. Conditionally, some very highly trained athletes, like Phelps, are even better at buffering lactate at the cellular level.

And the Usain Bolt’s of the world likely need never worry about lactate buffering and want to access immediate stores prior to a race. Lactate production at the cellular level.

To Find the Lactate Threshold in Practice

Think of it as being aware of the curve. Blood lactate accumulation remains ‘flat’ up until about 2mmol (lactate threshold) and exponentially grows past 4 mmol (OBLA)

When applied to actual accomplished work the lactate threshold is not all that high compared to how high blood lactate accumulation can happen.  An untrained person might hit 2mmol blood lactate from walking to the mailbox. In a sufficiently trained athlete it more closely correlates to the fastest swimming, cycling, or running speeds that continuous training allows. 

Challenge it with undulating periodization to allow for adequate recovery/stress during individual workouts and mesocycles to improve your performance(s) at LT. But again, LT is typically 2mmol and OBLA is 4mmol. I’ve recorded blood lactate levels in 50m world record holders at over 18mmol.

Most importantly, when challenging training with the appropriate periodization, researchers have found little correlation between blood lactate and muscle soreness post-workout.  Yet it is still worth noting, blood lactate awareness can be a rate-limiting physiological and psychological marker during exercise and performance.

And Manage ‘the burn’ During Competition

So what do athletes do to mitigate the burning in Dr. Brooks’ legs and the fading finish line in the distance?

Many turned to the ingestion of sodium bicarbonate to mitigate the acidosis. Think third grade science fair volcano project. Unfortunately, the metabolites have to leave somehow – and athletes typically find themselves uncomfortably attached to a toilet for a while post race.

As the understanding of lactate’s contribution has grown, others have become more fascinated with beta alanine’s possible role at the mitochondrial level. It would appear that interval training repeats between 30 seconds and 10 minutes can be improved (efficiency), but not individual performance speeds (economy). And that co-supplementation with sodium bicarb showed even greater gains.

All of this is to say, that the principle of specificity is incredibly important to incorporate. Or to paraphrase a contemporary of Brooks, Dr. Bruce Gladden, from his appearance on this ultrarunning podcast: If the goals is to be the best rocking chair performer. Get to rocking because the lactate levels are nearly inconsequential to performance.

The Race is Over. The Pain is Worse

Extreme exercise, not the rocking chair efforts Gladden alludes to, result in an inflammatory response to repeated mechanical overuse. Typically the feeling appears 24 hours after exercise and lasts for up to 72 hours, depending on the severity of the damage. This effect is now commonly referred to as delayed onset muscle soreness (DOMS).

And it would appear that the type of muscle contractions stressed the most appear to be a key factor in the development of DOMS. Plyometric movements, exploiting the stretch-shortening cycle may be most to blame for athletes who encounter severe consequences from overtraining – rhabdomyolysis.

And while anti-inflammatory drugs (NSAIDs) do appear to reduce perceived muscle soreness, they may slow adaptation to the exercise. By mitigating an athlete’s response to recovery, there is the possibility of unintended negative consequences to performance gains during the overall training plan.

Instead, if the discomfort does not rate at the rabdo level. Facilitate recovery with active warmdowns. During training use foam rollers (if they work for the Rock:) and their derivatives. When at a competition, try doing a similar exercise at increasingly slower speeds – eventually dipping below OBLA.

Embrace Lactate! Fear Lactic Acid?

Typically training was periodized to manage the amount of blood lactate production at high exercise intensities. And this was done so that the athlete can race without fatiguing due to ‘lactic acid’. 

But in the lactate vs lactic acid conversation, the highest priority of training should be to increase the body’s capacity to use lactate. And allow athletes to race faster through greater utilization.

How much supra-threshold training is enough to create new neuromotor exchanges to facilitate mechanical change and metabolic adaptation? The answer is back to the principle of specificity Dr. Gladden referenced. A couple of quick bullets

The overall numbers should also be applied at specific times in micro and mesoocycles so as to challenge and recover from the efforts during training. Lactate workouts featuring shorter intervals (threshold training) should come earlier in the training cycle and work up to VO2 max training.

The greatest blood lactate accumulation likely occurs in workouts consisting of :40-60 seconds bouts of maximal efforts with a work to rest ratio of approximately 1:6 or 1:10. As evidenced by a very high peak of blood lactate during the passive recovery phase. This is likely where Dr. Brooks should have focused his 400m training.

While challenging skeletal lactate buffering occurs with 90-95% max efforts of 20-:90 second bouts at a work to rest ratio of 1:1. This is where Phelps likely spent much of his ‘speed work’.

And limit these bouts to 48-72 hours between them and a total of 20-30 minutes.

Always note that lactate vs lactic acid is something to be understood. Not a boogeyman to psychologically fear.