The Science behind training your lactate system
Our understanding of how the body produces energy has changed vastly over time as new concepts and theories are unveiled, particularly in the last twenty-five years. We now recognise that the three metabolic energy systems do not work independently. Instead, we can think of all the energy systems being active during exercise, to a greater or lesser extent, all of the time. The relative contribution of each energy system to a particular physical activity will depend on the energy requirements, which will be directly related to the intensity and duration of the exercise.
The background science to the INSCYD testing protocol obviously involves the lactate system and how it functions. We look closely at the athletes lactate system, which we now understand works synergistically with the aerobic system and permits activity at greater intensity and duration than would be supported solely by the former concepts of 'aerobic processes'. We now know that the lactate system works all the time and is active in the presence of oxygen even though it does not require oxygen. In the past the lactate system was referred to as one of the 'anaerobic energy systems' and this led many people to the mistaken belief that it only operates when there was insufficient oxygen available.
The following diagram illustrates the current view of how the three metabolic energy systems contribute over time, if the body is operating maximally for that time period. For an illustration of how the three systems function over time at medium and low intensities as well as at high intensity.
Past Concepts of Lactate Formation
Much of what has been written in the past viewed the lactate energy system as being a purely anaerobic phenomenon, with lactic acid being produced and playing the role of a 'toxic by product' or 'waste product'. Until recently, lactic acid was thought by many coaches, physicians, educators and lay people to be responsible for a wide variety of athletic problems, such as fatigue and sore or cramped muscles. Research has done much to change these views over the past two and a half decades and the modern coach and athlete need to develop an understanding of the current concept of lactate energy provision and the implications that this has on metabolic energy production and on training itself.
It was originally believed that lactic acid formation only occurred under conditions where a supply of oxygen was unavailable. This concept of purely anaerobic energy production derived from early research studies. One of the pioneer biochemists, Louis Pasteur, studied the metabolism of simple, single celled, unicellular, organisms and compared the rates of glycolysis when air was present and when it was eliminated. He discovered that when oxygen was absent yeast broke down glucose and produced lactic acid. This is the well known 'Pasteur Effect' (Brooks GA, 1990).
Another old theory about lactic acid being the thing that stopped muscles from working was based on an experiment performed in countless Biology classes on dissected frog legs. After being subjected to electric shock the frog legs contracted a few times and then stopped contracting. On examination the motionless frog legs were found to be saturated with lactic acid and consequently this 'proved' that lactic acid was bad, since it was thought to have stopped the muscles from working.
Later, in 1923, a researcher by the name of A.V. Hill noted that when exercise intensity increased, lactate concentration in the blood rose slowly at first but at higher work levels, blood lactate rose rapidly. From this, he proposed that at low work rates oxygen delivery to the muscle by the blood was adequate. At higher work rates oxygen delivery was inadequate to meet the metabolic demand by the muscles and so anaerobic metabolism, with conversion of glycogen to lactic acid, came into operation to supplement energy supply. From this came the idea that the 'anaerobic lactic acid energy system' was switched on when the body ran out of oxygen.
We now know that lactic acid, as such, just does not exist in the body. As soon as it is formed it dissociates into a 'lactate bit' and an 'acidic bit' that are created in a one-to-one relationship. The lactate bit is definitely not a 'bad guy' but is instead a positive and central player in our metabolism and in how we produce energy.
Current Concepts on the Formation and Role of Lactate
In the past twenty-five years, research has been carried out specifically focussed on determining the metabolic role of lactate. This has been possible by injecting animals and willing research subjects with lactate that has been 'tagged' isotopically. Study of the dilution of the 'tagged' lactate has revealed that lactate production occurs within skeletal muscle during rest as well as during exercise (Brooks GA 1986). Lactate is not a metabolic dead-end and its formation does not mean that all the potential energy stored within the carbohydrate has been wasted. There are several possible fates for lactate, once formed, which result in utilisation, removal and clearing it from the body.
The lactate system is operating all of the time and not just when the body "runs out of oxygen". Lactate is, therefore, being produced in the body all of the time, at rest as well as during exercise.
On formation, lactate may follow one of several possibilities. It may:
be metabolised in the muscle in which it formed
enter the systemic circulation
Lactate produced within a muscle cell may be 'consumed' within that muscle cell. Perhaps a better word than consumed would be either metabolised back to pyruvate and moving, or moving as lactate, to the mitochondria and then oxidised within the mitochondria for the production of ATP. Lactate produced within a muscle cell may, additionally, leave that cell to be taken in and used in oxidative metabolism by other muscle cells within the same muscle. Oxidation of lactate is one of our most important energy sources. In highly oxidative muscle fibres, lactate is the preferred fuel source (Brooks GA, 1988). The relationship between pyruvate and lactate is a reversible one and not the 'dead-end' that used to be proposed for lactate produced by anaerobic glycolysis.
Any lactate that is produced may also leave the exercising muscle and enter the systemic circulation. In the systemic circulation the lactate has a variety of destinations and it may:
move to non-exercising skeletal muscle where it is 'stored' until required
be taken up by the heart and used for oxidative energy production in the cardiac muscle
be taken up by the liver to replenish glucose and glycogen stores
be taken up by the brain and used for oxidative energy production.
The dynamic action of lactate as a metabolite moving about within muscles and the systemic circulation to provide energy is what Dr George Brooks hypothesised in the 1980s, giving it the term 'The Lactate Shuttle'.
This concept of the lactate shuttle suggests that lactate is possibly the most important metabolic fuel used by muscle. The formation and distribution of fuel in the form of lactate provides a central means by which the formation of energy in the active muscles supply is achieved. Within the muscle cell there is a continual flux with pyruvate going to lactate and lactate going to pyruvate, in an actively reversible relationship.
The accepted understanding now is that muscle cells convert glucose to lactate preferentially since this is a rapid process and quickly permits access to energy production. Lactate becomes then an intermediary to help in the metabolism of carbohydrates from the diet. Apart from the speed of the process, lactate helps in this intermediary role by not stimulating insulin production or fat synthesis. The lactate is taken up and used as a fuel by the mitochondria, which are the 'energy factories' in muscle cells.
"Lactate is now recognised for its important metabolic functions and is a key substance used to provide energy, produce blood glucose and liver glycogen and promote survival in stressful situations. Oxidation of lactate is one of our most important energy sources. In highly oxidative muscle fibres, lactate is the preferred fuel source". Brooks GA, 1988
One of the challenges to the hypothesis of lactate contributing in some way to aerobic energy production was, "how does the lactate get into the mitochondria?" Research eventually identified special transporter proteins called monocarboxylate transporters, MCTs, that move the lactate into the mitochondria (Brooks GA, 2000). The MCTs constitute a family of proton-linked plasma membrane transporters that have been identified over the past decade and can carry molecules having one carboxylate group (monocarboxylate), such as lactate and pyruvate, across biological membranes. There are at least 14 MCTs that have been identified, although MCT1 and MCT4 seem to be most relevant to lactate and pyruvate transportation within cardiac and skeletal muscle.
As stated, the biological membranes that the MCTs can transport across include those around the mitochondria. As a result of this research, Brooks proposed a development of the original Lactate Shuttle hypothesis, "...the "lactate shuttle" hypothesis has been modified to include a new, intracellular component involving cytosolic to mitochondrial exchange." All of these research findings emphasise how aerobic metabolism and lactate metabolism operate synergistically, and side by side in the mitochondria. Once I heard of the discovery of the MCTs there was a moment when I thought about combining 'Lactate Dynamics Training' and the 'New Interval Training' under the banner of 'MCT Training' since these were probably the mediators of improved fuel production from lactate but there are more things at work here than purely MCTs but they do play a pivotal role in the fate of lactate.
The 'intracellular lactate shuttle' gained considerable support in 2006, as summarised in a UC Berkley press release: