Muscle structure

Muscle structureGenetic testing and muscle structure

Humans have two different types of muscles, type I and type II. Sprinters tend to have more type II muscles in their bodies – fast muscle fibres, or more active fibres, and long distance runners tend to have more effective type I muscles – slow muscle fibres.

A study by Australian scientists has included more than 400 top athletes divided into two groups. The first group included athletes from disciplines where mostly strength and speed are needed, and in the other group included those who required endurance. They discovered that, in the first group, people with two copies of a functioning ACTN3 gene prevailed, and, in the second group, people with two copies of a non-functioning ACTN3 gene prevailed. It has been, therefore, proven, that the mentioned gene determines the effectiveness of a specific type of muscle fibre. In addition to this gene, a mutation in the PPAR-alpha gene is also known. PPAR-alpha gene determines the representation of a specific type of muscle fibres in our body. By simultaneously analysing both genes it is possible to predict the activities that you are likely to be the most successful at.

More details about muscle structure

We know fast and slowly twitch muscle fibres. These two types of fibres differ in structure as well as their functioning. Slow muscle fibres produce energy mostly with cell respiration, and their main energy source are fats. They do not fatigue so easily, and are red coloured, because of the substance, called myoglobin. Fast muscle fibres, however, are rich in glycogene, and their energy source are not fats, but basic constituents, glucose and creatine phosphate. There can be a lack of oxygen in them, and lactic acid starts to form, making the muscles become tired.

While studying neuromuscular disease, Australian scientists have started to pay attention to the alpha-actinin (ACTN3) gene, the product of which is important for muscle cell contraction. They have discovered that the product of this gene is present only in fast muscle fibres. They have identified a mutation which causes the product of this gene to become inactive, and, therefore, ACTN3 is in such people absent. In the research, which included top athletes, they have discovered that sprinters mostly have two active copies of the ACTN3 gene, while long distance runners have two inactive variants of the gene. They have, thereby, proven the hypothesis that an active ACTN3 gene is required for the explosiveness of muscles. In a second research, the scientists have proven that fast twitch muscle fibres, in which the ACTN3 gene is inactive, use more oxygen than those that have at least one active copy of the gene present. A greater need for oxygen slows down the muscles. Muscle fibres with an inactive ACTN3 gene are supposedly weaker and smaller, but they also become fatigued much later.

PPAR alpha is also a known gene, for which scientists have claimed that it is more active in slow muscle fibres, which is logical, considering its function. Namely, PPFAR alpha regulates the activity of genes, responsible for oxidation of fats. Endurance training actually increases the consumption of fats and, through activity of the PPAR alpha gene, increases the oxidative capacity of muscles. Because of its role in regulating the activity of numerous genes which encode muscle enzymes, involved in the oxidation of fats, PPAR alpha is probably an important component of the adaptive response to endurance training. In this gene, there is a known mutation which influences the gene's activity and even influences the ratio of fast and slow twitch muscle fibres in our body. A changed sequence of the gene influences a lower activity of the PPAR alpha gene in slow twitch muscle fibres, and causes that the percentage of slow muscle fibres in our body decreases, while percentage of fast muscle fibres increases. A mutated variant of the gene is present mostly in athletes who, for their disciplines, need strength and explosiveness.