Lactate and Lactic Acid production are routinely offered as the seemingly natural cause and effect parameters that lead to fatigue and a decrease in performance, but are they really the source of the problem?
By Matt McNamara
If you’ve read anything about training in the last ten years you’ve probably come across the idea of Lactate Threshold and a discussion of how lactic acid production limits performance. The argument often goes something like this:
“As exercise intensity increases lactic acid production rises at a rate that, eventually, overwhelms the bodies ability to buffer this build-up and a decrease in performance naturally follows.”
Heck, I’ve repeated the mantra myself time and again over the years, despite KNOWING that it was an incomplete explanation of what actually happens. The truth is it provides a simple, though not wholly inaccurate, way to explain the well-documented trends of decreasing performance with increasing lactate concentrations. The idea of cause and effect just sort of fit well. So rather than perpetuate mediocre understanding, let’s jump in and learn a bit more:
A Brief, Albeit Incomplete, History
Lactic Acid was first isolated by Swedish researcher Carl Wilhelm Scheel from a batch of sour milk in 1780 (hence the commonly used term “lactic” instead of the far sexier formal name of 2-hydroxypropanoic acid, but I digress). Otto Meyerhoff and Archibald Hill, Nobel Prize winners in 1922, demonstrated that Lactic Acid was actually produced as a side reaction of Glycolysis, a primary metabolic pathway that converts carbohydrate/glucose into pyruvate, in the process converting energy into ATP through a 10-step set of reactions. In the absence of oxygen this conversion is sustained with Lactic Acid. This anaerobic process releases a proton (H+).
This was a key finding as it seemed to offer a cause and effect relationship between lactate production (lactate is, essentially, the salt or base of Lactic Acid) and the extended concept of Lactic Acidosis, or a decrease in pH that results from the release of protons in the system (cell or bloodstream).
This cause and effect relationship was taken as fact by researchers throughout the 20th and into the 21st century. However, in reviewing past and current research, Robergs et al (2004) have shown that there was no actual empirical evidence to support the cause/effect relationship; rather it was largely based on statistical correlation and the reputation of the Nobel Laureates Meyerhoff and Hill (which was richly deserved, I might add).
So, if the cause and effect nature of lactate production and acidosis is not an accurate portrayal of the role of Lactate in the onset of acidosis, and therefore performance, what is?
Debunking Lactic Acidosis
In 2004 Roberg, et al wrote an extensive review of the literature that sought to debunk the long-standing cause and effect relationship between lactate production and metabolic acidosis. Their sixteen page review takes an exhaustive, and somewhat intimidating, look at the true biochemistry of metabolic acidosis.
For example they detail the role of the phosphagen, glycolytic and mitochondrial systems in producing ATP and the differences in how each manages any released protons. They also note the difference in the nature of the proton release in glycolysis depending on whether the carbohydrate was derived from blood glucose or muscle glycogen. Glycogen is less acidifying to muscle during intense exercise.
Roberg then goes on to detail the many benefits derived from lactate production including the alkalizing effect of LDH, Lactate Dehydrogenase, or that it then circulates away the lactate to other areas that need it including the kidney, liver, and heart, for use as a substrate.
Finally, they looked at the role of nonmitochondrial ATP production, via research by Gevers in 1977 and 1979. Gevers established that metabolic processes other than LDH might contribute to the removal of protons in the form of the turnover of ATP via glycolysis. In other words that non-mitochondrial ATP production was likely responsible for metabolic acidosis.
But here’s where lactate threshold based training comes in
Training Threshold
Lactate threshold based training is a great tool. More specifically using the combination of a powermeter and a threshold based training approach is a highly effective way to manage your training.
Andy Coggan recently hosted a webinar on Lactate Threshold via USA Cycling. In addition to a comprehensive look at the establishment, definitions, and relationships of training around one’s lactate threshold. Among the cool takeaways
The first is to see terminology like Lactate Threshold, Maximal Lactate Steady State, Onset Blood Lactate Accumulation, etc as talking about roughly the same range of intensity. It’s likely going to be between about 80-90% of your VO2max for sustained periods of time. This will raise your general metabolic fitness. Further specialization is ideal for targeting specific race preparation
Coggan also noted that it has been shown in a wide array of studies that many other factors and processes contribute to fatigue. Things like epinephrine/norepineprine (adrenaline/noradrenalin), plasma potassium, and cortisol level, etc. often show a similar threshold type profile to that of lactate.
Abiss and Laursen did a comprehensive look at fatigue in 2005. Models to Explain Fatigue During Prolonged Endurance Cycling looked at no fewer than 10 different models of fatigue including the cardiovascular/anaerobic model, neuromuscular biomechanical, thermoregulatory models, and several others. Their net conclusion is that any number of systems may contribute to fatigue in a specific way for a specific situation, but in general the limitation of the system is derived from oxygen delivery to the muscles. Since we established above that metabolic acidosis is not derived from lactic acid, but that lactate production is an important contributor to oxygen delivery, it time to embrace those burning quads and get to work improving that lactate tolerance.
Perhaps next time we’ll look at that – drop me a line if you’re interested in a part 2.
References:
1. Abbiss, Chris, Laursen, Paul – Models to Explain Fatigue During Prolonged Endurance Cycling. School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Australia. 2005
2. Coggan, Andy – Explaining Lactate Threshold. Webinar Presentation. 2010
3. Robergs, Robert A., Ghiasvand, Farzenah, Parker, Daryl – Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 287: R502–R516, 2004
