Sprinters are born, endurance runners are made?
You’re either born a sprinter or you’re not — the question isn’t as simple as it first seems. The answer depends on which level we’re talking about, what muscle fibers actually mean and what training can really change.
Are sprinters really born?
At the elite level — yes, I can say that without hesitation. Someone whose muscles are made up of 80% slow muscle fibers has very different prerequisites from someone whose figure is 48%. The gap is so large that even under ideal training conditions, these two people could never compete against each other. Exactly the same applies to sprinters and fast muscle fibers.
Fast and slow muscle fibers: what’s the difference?
Fast glycolytic fibers (type II) contract explosively but also fatigue quickly. They are characterized by high myosin ATPase activity and the ability to release calcium from the sarcoplasmic reticulum rapidly. These fibers have a large diameter, are innervated by large nerve cells and belong to large motor units. Their glycogen and creatine phosphate stores are large, while they contain few mitochondria.
Slow oxidative fibers (type I) are the opposite: more mitochondria, a denser capillary network and triglycerides as the primary energy source. They work for a long time and fatigue slowly.
The split isn’t black and white. Fast fibers are further divided into types II A and II B. II B is the extreme — short-lived, explosive, anaerobic. II A sits in between: it has characteristics of both fast and slow fibers.
| Fiber type | Slow I | Fast II A | Fast II B |
|---|---|---|---|
| Contraction time | Slow | Fast | Very fast |
| Motor neuron size | Small | Large | Very large |
| Fatigue resistance | High | Medium | Low |
| Type of activity | Aerobic | Longer-lasting anaerobic | Short-duration anaerobic |
| Force production | Low | High | Very high |
| Mitochondrial density | High | High | Low |
| Capillary density | High | Medium | Low |
| Oxidative capacity | High | High | Low |
| Glycolytic capacity | Low | High | High |
| Main energy source | Triglycerides | Phosphocreatine, glycogen | Phosphocreatine, glycogen |
Training to be a sprinter: what can be changed?
There’s one important nuance here. Even training doesn’t change a muscle fiber’s basic blueprint — fast fibers don’t become slow ones or vice versa. Metabolic shifts do occur, though.
Consistent, high-volume aerobic training prompts a metabolic shift of type II B fibers toward II A: more mitochondria form, and the capillary network and the amount of oxidative enzymes increase. The opposite process takes place with strength training — II A fibers shift toward II B, and the number of anaerobic enzymes grows, as do glycogen and phosphocreatine stores.
Aerobic capacity depends primarily on metabolic mechanisms, which respond well to training. So becoming an endurance runner is indeed possible to some extent. Developing sprinter-like qualities is harder, because in addition to metabolism, neural factors play an important role: the size of motor neurons, the composition of motor units, the higher excitation threshold of fast fibers. No training can change these neural aspects.
All in all: sprinter-like qualities can be improved to some extent, but endurance qualities are far more trainable — precisely because endurance capacity depends more on metabolism.
Sprinters are born — what does gene science say?
The genetic determination is supported by a discovery made by researchers at the Australian Institute of Sport: a gene called alpha-actinin. It has been established that sprinters carry the ACTN3 version of this gene and endurance runners the ACTN2 version. The actinin synthesized from ACTN3 is found only in fast muscle fibers — those that rely on glycogen and perform explosive movements. The ACTN2 variant is characteristic of slow fibers, which rely on fatty acids and work for a long time.
The experiment involved 300 world-class athletes. The result: 95% of elite sprinters carried at least one copy of the ACTN3 gene, and 50% had as many as two copies — one from each parent. Elite endurance runners tended to have a pair of ACTN2 versions.
FAQ
Can you become a sprinter through training?
Partly. Strength training shifts the metabolism of your fibers in a more sprinter-like direction, but training doesn’t change neural factors — which are critical in sprinting. To compete at the elite level, you need the right genes.
Is it easier to “become” an endurance runner than a sprinter?
Yes. Endurance capacity depends primarily on metabolic mechanisms, which respond well to training. In sprinting, neural factors also play a role, and these don’t adapt to training.
What does having the ACTN3 gene mean?
The ACTN3 gene is responsible for producing actinin in fast muscle fibers. This protein supports explosive, forceful movement. 95% of world-class sprinters have at least one copy of this gene.
This is the author’s subjective opinion.
Author: Silvar Rückenberg
Come and train! ArtGym
