You may be familiar with that point during exercise where you can’t push yourself anymore. You start to feel that burning sensation in your limbs, causing you to slow down your pace.
Fitness professionals often associate this sensation with the lactate threshold, a term often used in conjunction with phrases like aerobic threshold, anaerobic threshold, and VO2 max. Although they may sound similar, each encompasses a unique concept that has different implications. To properly understand what this all means for your training, let’s discuss the science behind how your body makes energy to power exercise.
Your Energy Production
Our activity is fueled by the energy we consume from food. During rest and less intense bouts of exercise like distance running, the aerobic energy system works to produce adenosine triphosphate (ATP), our body’s currency for energy. This energy system breaks down either fat or carbohydrate to make ATP.
When activity levels increase, your body increases usage of the anaerobic energy system, which thrives off of carbohydrates stored in our muscles. It’s termed anaerobic because this process can occur with little to no oxygen present, like when you’re breathing heavily during tough training sessions (1). The by-products of this process include lactate and hydrogen ions (4).
A third energy system also thrives in anaerobic conditions. The ATP-CP, or phosphagen system, uses the energy stored in creatine phosphate (CP) to resynthesize ATP quickly (yes, that creatine). Ingested creatine is stored in our muscles as the energy-laden creatine phosphate, which serves as a reservoir for immediate ATP production. Unfortunately, this supply is short-lived and can only provide energy for activities that last up to around ten seconds, like a 100m sprint, as shown in Figure 1. When creatine phosphate stores run out, exercise effort must diminish to move into utilization of the anaerobic energy system.
Figure 1. The three energy systems contribute to athletic performance. The phosphagen system (ATP-CP) is used in the short term to fuel explosive movements. Anaerobically-created energy overlaps with use of the ATP-CP system to provide energy for activities lasting up to around 3 minutes. Aerobic glycolysis provides energy for longer-distance events by breaking down fat and some carbohydrate. Anaerobic and aerobic energy systems are constantly activated to some extent, representing a continuum of energy production. Figure adapted from (1).
The first point where lactate levels increase during exercise is loosely referred to as the aerobic threshold. The aerobic threshold also corresponds to an increase in breathing as a result of the increase in metabolic rate. The production of lactate occurs because the aerobic system supplies an inadequate amount of energy for the intensity of exercise. However lactate production isn’t all bad; it allows the anaerobic energy systems to continue producing energy past this point (4).
The aerobic threshold is of particular interest to athletes exercising at lower intensities for long durations such as marathon runners, triathletes, and cyclists. The longer duration of these events means that these athletes may want to consider training just below the aerobic threshold. If these athletes compete at too high of a pace they may fatigue earlier and be unable to maintain their pace throughout the event.
As exercise intensity increases, byproducts of anaerobic metabolism cause an increase in blood acidity, causing a surge in muscle fatigue. Fatigue is due to hydrogen ion accumulation, among several other factors, not the commonly implicated “lactic acid buildup” (2).
Above the aerobic threshold that we just discussed, there’s a period during which the body is able to handle the increase in blood acidity without a significant change in breathing rate. Nevertheless, as your body works harder, acidity levels in the blood exceed the capacity of the blood buffering systems and your brain is notified of this buildup in waste products.
The body compensates by breathing rapidly (hyperventilation) to help eliminate waste products. This is point is termed the anaerobic threshold and roughly coincides to the point before which blood lactate increases steadily with increasing exercise intensity (Figure 2). In other words, this is the point where anaerobic waste products that cause muscle fatigue begin to accumulate faster than they can be cleared from the blood stream. Exercise above this threshold is not sustainable and will quickly result in exhaustion (3).
Figure 2. Lactate levels gradually accumulate at any speed/activity level over the aerobic threshold. At and after the anaerobic threshold, lactate accumulates exponentially. Graph of simulated data adapted from Faude et al., 2009 (4).
Your Genes and Lactate Threshold
In one study, markers in two genes were found to influence anaerobic threshold development in a group of 136 middle-aged men and women from Germany (5). The genes implicated include PPARD and PPARGC1A, which have been shown to play a role in mitochondrial function, the energy powerhouse of our cells. Specifically, the study found that those with a certain genotype in a PPARD variant had increased mitochondrial activity.
Depending on your genotype at these two genetic markers, your lactate threshold levels may adapt to training differently compared to others. Low responders to lactate threshold training may adapt slower to endurance training compared to others, while high responders may be quicker to up their lactate threshold.
What does this mean for your training? Check out our quick guide below.
Training hard and dialing in your diet are fundamental to attaining optimal athleticism. Unlocking the genetic underpinnings of how your lactate threshold adapts to training is a major key in achieving your performance goals.
- Katch, V. L., McArdle, W. D., Katch, F. I., & McArdle, W. D. (2011). Essentials of exercise physiology. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health.
- Allen, D. G., Lamb, G. D., & Westerblad, H. (2008). Skeletal muscle fatigue: cellular mechanisms. Physiological Reviews, 88(1), 287–332.
Meyer, T., Lucía, A., Earnest, C. P., & Kindermann, W. (2005). A conceptual framework for performance diagnosis and training prescription from submaximal gas exchange parameters–theory and application. Int J Sports Med, 26, S38–48.
Faude, O., Kindermann, W., & Meyer, T. (2009). Lactate threshold concepts: how valid are they? Sports Med, 39(6), 469–490.
- Stefan, N., Thamer, C., Staiger, H., Machicao, F., Machann, J., Schick, F., … Häring, H.-U. (2007). Genetic variations in PPARD and PPARGC1A determine mitochondrial function and change in aerobic physical fitness and insulin sensitivity during lifestyle intervention. J Clin Endocrin Metab, 92(5), 1827–1833.