Lactate Threshold Training

The terms lactic acid and lactate, despite biochemical differences, are often used interchangeably. Fitness professionals have traditionally linked lactic acid or ‘the burn’ with an inability to continue an intensive exercise bout at a given intensity. Although the conditions within the exerciser’s muscle cells have shifted towards acidosis, lactate production itself does not directly create the discomfort (acidosis) experienced at higher intensities of exercise. It is the proton (H+) accumulation, coinciding with, but not caused by lactate production, that results in acidosis, impairing muscle contraction, and ultimately leading to the ‘burn’ and associated weariness (Robergs, Ghiasvand, Parker 2004). The increased proton accumulation occurs most notably from the splitting of ATP (the body’s energy liberating molecule) by the muscle protein filaments, in order to sustain vigorous muscle contraction. Interestingly, the lactate production is proposed to be a physiological event to ‘neutralize’ or ‘retard’ the exerciser’s muscle acidic environment (Robergs, Ghiasvand, Parker 2004). Thus, lactate accumulation, which for years has been associated with the cause of the burn, is actually a beneficial metabolic event aimed at diminishing the burn. Scientists denote conditioning at this physiological state as lactate threshold training.

Fitness professionals can utilize this knowledge to enhance the cardiovascular endurance performance of their students and clients. All world and Olympic endurance athletes incorporate lactate threshold training into their workouts. This article will explain and discuss how lactate threshold training principles can be incorporated into your training program.

Lactate Threshold and Endurance Performance

Traditionally, maximal oxygen uptake (VO2max) has been viewed as the key component to success in prolonged exercise activities (Bassett & Howley 2000). However, more recently scientists have reported that the lactate threshold is the most consistent predictor of performance in endurance events. Studies have repeatedly found high correlations between performance in endurance events such as running, cycling, and race-walking and the maximal steady-state workload at the lactate threshold (McKardle, Katch, & Katch 1996).

What is the Lactate Threshold?

At rest and under steady-state exercise conditions, there is a balance between blood lactate production and blood lactate removal (Brooks 2000). The lactate threshold refers to the intensity of exercise at which there is an abrupt increase in blood lactate levels (Roberts & Robergs 1997). Although the exact physiological factors of the lactate threshold are still being resolved, it is thought to involve the following key mechanisms (Roberts & Robergs 1997):

1) Decreased lactate removal

2) Increased fast-twitch motor unit recruitment

3) Imbalance between glycolysis and mitochondrial respiration

4) Ischemia (low blood flow) or hypoxia (low oxygen content in blood)

1) Lactate Removal

Although once viewed as a negative metabolic event, increased lactate production occurring exclusively during high-intensity exercise is natural (Robergs, Ghiasvand, Parker 2004). Even at rest a small degree of lactate production takes place, which indicates there must also exist lactate removal or else there would be lactate accumulation occurring at rest. The primary means of lactate removal include its uptake by the heart, liver, and kidneys as a metabolic fuel (Brooks 1985). Within the liver, lactate functions as a chemical building block for glucose production (known as gluconeogenesis), which is then released back into the bloodstream to be used as fuel (or substrate) elsewhere. Additionally, non-exercising or less active muscles are capable of lactate uptake and consumption. At exercise intensities above the lactate threshold, there is a mismatch between production and uptake, with the rate of lactate removal apparently lagging behind the rate of lactate production (Katz & Sahlin 1988).

2) Increased Fast-Twitch Motor Unit Recruitment

At low levels of intensity, primarily slow-twitch muscles are recruited to support the exercise workload. Slow-twitch muscle is characterized by a high aerobic endurance capacity that enhances mitochondrial respiration, which is the aerobic ATP energy production system. With increasing exercise intensity there is a shift towards the recruitment of fast-twitch muscles, which have metabolic characteristics that are geared towards glycolysis (an anaerobic energy pathway). The recruitment of these muscles will shift energy metabolism from mitochondrial respiration more towards glycolysis, which will eventually lead to increased lactate production (Anderson & Rhodes 1989).

3) Imbalance between Glycolysis and Mitochondrial Respiration

At increasing exercise intensities, there is an increased reliance on the rate in the transfer of glucose to pyruvate through the reactions of glycolysis. This is referred to as glycolytic flux. Pyruvate, which is the final product of glycolysis, can either enter the mitochondria for further biological breakdown (for eventual synthesis of energy) or be converted to lactate. There are some researchers who believe that at high rates of glycolysis, pyruvate is produced faster than it can enter into the mitochondria for mitochondrial respiration (Wasserman, Beaver, & Whipp 1986). Pyruvate that cannot enter the mitochondria will be converted to lactate, which can then be used as fuel elsewhere in the body (such as the liver or other muscles).

4) Ischemia and Hypoxia

For years, one of the primary causes of lactate production was thought to include low levels of blood flow (ischemia) or low levels of blood oxygen content (hypoxia) to exercising muscles (Roberts & Robergs 1997). However, there is no experimental data indicating ischemia or hypoxia in exercising muscles, even at very intense bouts of exercise (Brooks 1985).