An Introduction To Skeletal Muscle Basics

Throughout our list of articles, we have quite a few posts explaining the mechanisms that can be used to generate energy to power muscle contractions, but here we’ll take a bit more of a look at how skeletal muscles actually function. The article below is a lightly edited excerpt from our Cycling Physiology and Training Science Guide.

We don’t go right into the very complex details around how skeletal muscles work, as this isn’t necessary to understand training. However, there are a few key basics that are useful to know and you can find some references at the bottom of the page should you want to do some of your own further reading.

 


So first, let’s look at the structure of muscles…

Muscle structure

You can think of a muscle as a big bunch of muscle cells, which are long thread-like structures made of protein. These cells are more commonly referred to as muscle ‘fibres’ due to their fibre-like structure.

The fibres are collected into larger bunches known as fascicles, and these fascicles are in turn grouped into muscles as shown below. The fibres themselves are made up of smaller threads – known as myofibrils, which contain the proteins that cause contraction.

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The contraction-causing proteins are known as ‘actin’, and ‘myosin’, and their structures are illustrated in the diagram below. The myosin filaments include heads that are shaped such that they can bind with the actin filaments.

 

 
 

 

The myosin heads have two positions: activated and inactivated. Chemical energy from ATP (a molecule used by the body to store and transfer energy) causes the myosin head to move to the activated position, where it is primed to bind with the actin binding sites.

However, even when primed, the myosin heads cannot ordinarily bind with the actin filaments, as they are blocked by proteins (troponin and tropomyosin). Thus, in order to cause muscular contraction, a nerve signal is also needed, which causes calcium to be released from elsewhere in the muscle structure, causing a reaction that unblocks the myosin heads. The activated myosin heads can then bind to the actin binding sites, pushing the actin filament along and causing muscular contraction.

In essence therefore, the fundamental requirements of muscular contraction are

(i) a supply of ATP and

(ii) neural stimulation.

This contraction process repeats until the nerve signal stops, or all ATP is exhausted.

Training can be used to affect both of these factors.

For example, training can influence the way ATP is produced, which in turn can help make contractions more powerful or more fatigue-resistant. Training can also increase the strength or frequency of neural stimulation, which can lead to stronger, more forceful muscle contractions. We’ll discuss these different responses to training later in this article.

Another thing it’s important to know is that muscle fibres come in different types:

  • Type I

  • Type IIa

  • Type IIx

Let’s take a look at each individually…

Type I

Type I muscle fibres (also known as slow twitch muscle fibres) have the smallest diameter, the slowest rate of contraction, and produce the least force. However, they also have the lowest fatiguability of all muscle fibre types, so can continue producing contractions for hours.

The reason for this is that they are very well adapted for aerobic metabolism and particularly fat oxidation. Relative to the other fibre types, they have a high density of capillaries, which can deliver a good supply of oxygen to the fibres.

They also have a high density of mitochondria (which is the site where aerobic metabolism takes place) and a high concentration of ‘myoglobin’ – which are the molecules that carry oxygen from the capillaries to the mitochondria.

They also typically store high concentrations of triglycerides (i.e. fats) within the muscle fibres and high concentrations of oxidative enzymes, and are thus primed and ready to produce energy through fat oxidation, which (unlike other metabolic pathways) is not associated with the production of fatiguing by-products and helps explain why these fibres are so fatigue-resistant. 

Type IIx

At the other end of the spectrum is Type IIx fibres (also known as ‘fast glycolytic’ fibres). These fibres, while actually only being of moderate size, are the most powerful fibres, because they can contract quickly and with a lot of force. Unlike Type I fibres, they have a minimal capillary and mitochondrial density, and very few myoglobin, and are thus not well adapted for aerobic respiration.

They do, however, have high concentrations of creatine phosphate, and enzymes linked with the phosphocreatine system (this is the system that can supply energy the fastest). They also have high stores of glycogen, and are thus well adapted to producing energy through the glycolytic system. 

Type IIa

Sitting between these two fibre types are the Type IIa fibres (also known as ‘fast oxidative’ fibres). These are the largest fibres and have attributes that lend themselves both to aerobic and anaerobic metabolism; although they are generally most adapted for carbohydrate rather than fat metabolism.

They therefore have a moderate capillary and mitochondrial density, and a moderate number of myoglobin for aerobic metabolism, but also a good store of creatine phosphate and glycogen. They have moderate force and contraction speed.

Fibre Recruitment

As the force demands increase, these muscle fibre types are activated in order from Type I to Type IIa to Type IIx. So, when only a small force is needed, only the Type I fibres are activated. When a larger force is needed, the Type IIa fibres begin to be recruited in addition to the Type I fibres. Then if a very high force (like a maximal sprint) is needed, then the Type IIx fibres are finally also recruited. 

Training and Fibre Type

The amounts of these different fibre types contained within a muscle are determined by (i) the specific muscle and its purpose (ii) genetics and (iii) training. In particular, Type IIa fibres can adapt so that they become more similar to Type I fibres, or more similar to Type IIx fibres, depending on the type of training undertaken.

Specific adaptations that can occur as a result of training can include increased density of capillaries around a muscle fibre, improved mitochondrial density, or changes in enzyme concentration and activity, which can for example improve the ability of a fibre to produce energy via fat or carbohydrate oxidation.

Neural Stimulation

As well as influencing muscle fibre composition and the pathways through which ATP is generated, training can also impact the neural stimulation of the muscles, and thus it’s worth spending a little time discussing this aspect of muscular contraction.

The nerve signal that unblocks the actin and myosin filaments, allowing contraction, comes from the central nervous system, and is carried by a ‘motor neuron’. Each motor neuron is connected to a number of muscle fibres, and when activated, will stimulate contraction across all connected fibres. The grouping of muscle fibres and associated nerve fibre is known as a ‘motor unit’. Each motor unit will contain a single type of muscle fibre only (e.g. a Type I motor unit will contain only Type I muscle fibres).

There are several neural factors that influence the force and power with which a muscle can contract, as well as the efficiency with which they contract, including:

1.  The number of motor units that can be recruited

2.  The frequency with which a motor unit can fire

3.  The synchronicity with which those motor units are activated

4.  The coordination of motor unit activation such that activation of antagonist muscles is down-regulated and the most optimal motor units are recruited for a given movement pattern

It’s clear therefore that neural adaptations can contribute to performance on the bike. Indeed, neural adaptations are actually the biggest contributor to improved muscular strength and power when beginning resistance and/or sprint training.


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References

Frontera, W. R., & Ochala, J. (2015). Skeletal muscle: a brief review of structure and function. Calcified tissue international, 96(3), 183-195.

Hansen, A. K., Fischer, C. P., Plomgaard, P., Andersen, J. L., Saltin, B., & Pedersen, B. K. (2005). Skeletal muscle adaptation: training twice every second day vs. training once daily. Journal of Applied Physiology, 98(1), 93-99.

MacIntosh, B. R., Gardiner, P. F., & McComas, A. J. (2006). Skeletal muscle: form and function. Human kinetics.

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