"Anaerobic Threshold" is a term thrown around by athletes and coaches alike with the same regularity as "hurt box" or "blocked". In reality the former has about as much physiological reality as the latter two, which of course is none. The physiological definition of a threshold is "a limit below which a stimulus causes no reaction". But, of course a threshold is a pretty easy concept to understand. It is the term "anaerobic" which perhaps is the confusing point to most. "Aerobic" pertains to metabolic processes requiring oxygen. The prefix "an" means without, and therefore "anaerobic" means metabolic processes without oxygen. Putting it all together, in the strictest sense, "anaerobic threshold" is a point above which we have metabolism without oxygen. The anaerobic threshold has therefore been used (mistakenly) to describe why lactate concentration increases non-linearly above a given exercise intensity, a point where exercise becomes difficult to sustain. I will discuss the physiological basis of the concept and why in reality it is not correct.
The anaerobic threshold theory is based on the idea that an oxygen deficit results in lactate production and accumulation and that breathing increases in an effort to buffer increasing acidity. The theory falls apart in a number of places. First and foremost, there is very little evidence that exercising muscle is ever deficient in oxygen. In reality, most measurements indicate that skeletal muscle maintains a critical level of oxygen. This makes intuitive sense because without oxygen most tissues will not survive. We are familiar with what happens when heart muscle goes without oxygen, a heart attack, so you would have to ask why skeletal muscle would allow the same to happen. A particularly insightful study made measurements of oxygen concentration in skeletal muscle during increasing intensities of exercise (Figure 1). The red line of the figure shows oxygen content inside the muscle at increasing exercise intensities (up to 100% VO2max). Notice that even though exercise intensity increases (on the x-axis) the oxygen content in the muscle does not change. However, as exercise intensity increases the amount of lactate efflux (blue line) does increase. Therefore, the rate of lactate release changes even though there is no change in oxygen content and therefore the increase in lactate release is not because of an "anaerobic threshold".
A second piece of evidence comes from a particular disease called McArdle's Syndrome. Patients with McArdle's lack the ability to produce lactate because they cannot break down glycogen in the muscle. These patients have obvious exercise limitations. However, when a graded exercise test is performed the patient will have a ventilatory change at a workload at which we would expect the "anaerobic threshold" to occur (see Hagberg 1982). However, these patients have no lactate production. Therefore, the change in ventilation is not caused by lactate accumulation in the blood as the anaerobic threshold predicts.
The reality of the situation is that lactate production in the muscle occurs under full aerobic (with oxygen) conditions. Lactate production does not equate with a lack of oxygen. Further, human muscle maintains oxygen content even at maximal exercise intensity. Finally, it is also important to realize that lactate concentration is determined on a two-way street. While a muscle produces lactate, it (and other muscles) are simultaneously using that lactate as an energy source. Therefore, the concentration of lactate in the blood is the sum of the production and use of lactate at any given time. In other words equating lactate concentration to only a process that produces lactate (such as anaerobic metabolism) is an oversimplification and will inevitably fail.
It is baffling why the "anaerobic threshold" term still exists among coaches and athletes. Perhaps it is the simplicity of the concept; harder exercise ® decreased oxygen ® increased lactate ® increased breathing ® fatigue. However, the simplicity is exactly that, an oversimplification that is not based on physiological realities. The central tenants of the concept have been indisputably destroyed as long as 25 years ago. In fact, whenever I hear "anaerobic threshold" from a coach, I immediately question their credibility. There does exist a threshold above which it is difficult to sustain exercise. However, this threshold does not have anything to do with a lack of oxygen. In the next column I will explain why it probably has little to do with lactic acid either, as most would lead you to believe.
Ben Miller is Senior Lecturer in Exercise Physiology. Ben did a PhD at the University of California – Berkeley and a Post-Doc at the Institute for Sports Medicine, Copenhagen before arriving in New Zealand. As a departure from his life in a closed scientific box safe from the realities of the world, he is a cyclist regularly taking his life in his own hands on the streets of Auckland and in the local club racing and criteriums. Ben's wife is much more successful at cycling having competed full-time in Europe and the US for the last 4 years.
Hagberg JM, Coyle EF, Carroll JE, Miller JM, Martin WH, Brooke MH. Exercise hyperventilation in patients with McArdle's disease.J Appl Physiol. 52(4):991-4, 1982.
Richardson RS, Noyszewski EA, Leigh JS, Wagner PD. Lactate efflux from exercising human skeletal muscle: role of intracellular PO2. J Appl Physiol. 85(2):627-34, 1998.