Muscle fibres rely on four types of fuel sources, namely phosphocreatine, blood glucose, glycogen and fat. Some of the fat comes from stores within the muscle, whereas the majority of fat (or free fatty acids) comes from our fat stores. These fuels will go through processes that breaks it down to form energy for muscle contraction (in the form of ATP). These processes rely on the enzymes within the fibres and its mitochondria.
Collectively, metabolism refers to the fuel substrates and all the processes (including the mitochondria) within the muscle that contributes to energy production. There are literally thousands of enzymes within these four metabolic pathways (depicted on the right). Scientists have discovered marker enzymes (depicted as the stars) that can serve as indicators of how quickly a pathway can function. The greater the activity (speed – measured as µmol substrate per minute per gram tissue), the greater the flux, thus the greater the contribution of a specific pathway.
The fuel sources and their metabolism
The metabolism of one molecule of phosphocreatine can yield only 1 ATP, whereas one molecule of glucose can yield 2 ATPs, when converted to lactate. The moment mitochondria becomes involved (a process that requires oxygen), the more ATPs can be produced from that same glucose molecule. Instead of producing lactate, the glucose molecule is converted to carbon dioxide and water, yielding a net energy of 36 ATPs! That is much more efficient, but the process takes longer. Fat can only be metabolised by the mitochondria into carbon dioxide and water, but can yield between 120 to 130 ATPs. This latter process takes the longest. Therefore, it is merely a question of how quickly and how much ATP are required for muscle contraction. The higher the intensity of exercise (more force, quicker contraction), the quicker ATP is required. To illustrate, if a man sprints the 100 meters, the contraction of the muscles are so fast and strong that he would solely rely on phosphocreatine and the anaerobic breakdown of glucose and glycogen to lactate, to produce the required ATP. On the other hand, if he goes for a jog, the intensity of the exercise is low and these fuels have time to enter the mitochondria to yield greater amounts of ATP.
The different metabolic pathways described above are also reflected in the three fibre types. Each fibre type (being type I, type IIA or type IIX) is unique with regards to its own metabolism (figure on the right).
Type I fibres normally have the greatest number of mitochondria, thus CS and 3HAD activities are higher than the type IIA and IIX fibres. On the other hand, the LDH and PFK activities is higher in the type IIA and IIX fibres.
The type and amount of fuel stored complement the mitochondrial content of the fibres (see figure on the right) – the darker the blue, the greater the number of mitochondria). Type I fibres store more fat than type IIA and IIX fibres, whereas the latter fibre type stores more glycogen and phosphocreatine.
Therefore, the metabolism of the three muscle fibre types are geared towards its individual contractile properties. In other words, because type I fibres are slow in contraction speed, the amount of ATP required per time unit (e.g. minute) is less than for type IIA and type IIX fibres. This would mean that the fat and glucose have enough time to be metabolised by the mitochondria to yield the necessary amount of ATP.
Adaptation to exercise
However, exercise training can improve the metabolic pathways by increasing the amount of enzymes involved in the breakdown of the fuels. Effectively, the activity of the enzymes are increased to ultimately increase the total amount of ATP produced per time unit. This is clearly illustrated in the figure below. The values of each enzyme activity are expressed as the percentage change in activity relative to untrained muscle. Sprinting type exercise decreases the reliance of the muscle on fat (CS and 3HAD) and increases the capacity to produce lactate (PFK & LDH). For both endurance runners and cyclists, the opposite occurs, where the oxidative (or aerobic) capacity of the muscle increases substantially and a concomitant decrease in LDH activity. Many scientists believe that this decrease in the enzyme that produces lactate results in the lower lactate levels observed in the blood in response to longterm endurance exercise. The reason why PFK remains unchanged would be the argument that this enzyme sits high up in the glycolytic pathway. Irrespective whether a carbohydrate molecule will be metabolised via the Kreb’s cycle or metabolised to lactate, that same molecule must first go through the initial phase of the glycolytic pathway before any ATP is generated. It is also true that very few scientists have shown a real decrease or increase in PFK activity.
The following section focusses on the muscle fibre size and its impact on contraction.