Muscle fibre types
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Muscle Fibre Types: Why tapering after intense training boosts sprinting speed
What makes a winning sprinter? The answer to this apparently simple question is a complex one including such elements as mental approach, diet and even clothing. But since sprinting performance is heavily dependent on speed of limb movement, one of the biggest single factors contributing to success is physiology(1). The muscle fibres in the winning sprinter's legs are able to contract faster over the short period of the sprint than those of his or her less successful counterparts. Recent research findings have improved our knowledge of how human muscle adapts to training, and the extent to which muscle can alter its ability to meet the fast movement velocities demanded by sprinting performance.
A muscle consists of a bundle of cells known as fibres bound together by envelopes of a connective tissue called collagen. A single fibre comprises a membrane, many nuclei containing genetic information, and thousands of inner strands running the length of the fibre, called myofibrils. Muscle force production is accomplished through the interaction of two protein filaments that make up the myofibril: actin and myosin.
One component of the myosin filament, known as the myosin heavy chain (MHC), determines the functional abilities of the entire muscle fibre. This heavy chain exists in three forms: I, IIa and IIb. Type I fibres contain a predominance of type I MHC and are commonly called slow twitch, while fibre types IIa and IIb contain a predominance of type IIa and IIb MHC respectively, and are known as fast twitch. Slow twitch fibres are so-called because the maximum contraction velocity of a single fibre is approximately one tenth that of a type IIb fibre(2). Type I fibres also produce less maximum force than type IIb fibres(3). Type IIa fibres lie somewhere between type I and type IIb in their maximum contraction velocity and maximum force production.
Because of the high velocity of contraction and the large forces they produce, type IIb fibres are probably one of the key elements required for successful performances in speed-dependent pursuits like sprinting. It is therefore not surprising to find that successful sprint athletes possess more of these IIb fibres than the average person(4). But is this part of a sprinter's make-up pre-determined by genetics? Or can the proportion of type IIb fibres in muscle be increased through training?
Training effects on fibre type
Virtually all the available evidence suggests that the answer to the last question is no. In fact, it has been suggested that type IIb MHC and therefore IIb fibres constitute a 'default' fibre type setting in humans when activity is absent, and evidence of high proportions of this fibre type in paralysed muscle support this theory(5). It has also been known for some time that increases in activities like strength or power training can lead to conversion of muscle fibres. But, unfortunately, this conversion operates in one direction only, changing fast type IIb fibres into slower type IIa fibres(6). Moreover, if heavy loading of muscles continues for a month or more, virtually all type IIb fibres will transform to type IIa, with obvious consequences for sprinting potential(7).
What happens when heavy strength training stops? Do the newly formed type IIa fibres revert back to type IIb? The answer is yes, but recent research has revealed some extraordinary results to which a simple yes does not do justice. Scientists from the Copenhagen Muscle Research Centre examined training and detraining effects on muscle fibre type distribution(8). Biopsies (muscle samples) were taken from the vastus lateralis muscle of nine young sedentary males. All the subjects then undertook three months of heavy resistance training, aimed predominantly at the quadriceps muscle group, which ended with a second muscle biopsy. The subjects then abruptly ceased training and returned to their normal sedentary lifestyles before providing a third biopsy three months later.
Biopsies from the vastus lateralis were analysed for muscle fibre type distribution and number. As was expected, there was a decrease in the proportion of fast twitch IIb fibres (from around 9% to 2%) during the resistance training period. The researchers expected that the proportion of IIb fibres would simply be restored to pretraining values during the detraining period. However, they found to their surprise that the proportion actually doubled to around 18% after three months of sedentary living!
How heavy training followed by tapering produces 'overshoot'
So it seems that a pattern of heavy resistance training followed by decreased activity causes first a decrease then an overshoot in the proportion of the fastest fibre type in the trained/detrained muscle group. An explanation for this overshoot currently eludes researchers, but the findings accord with the theory that muscle fibres 'default' to type IIb with a (relatively) decreased level of activity(5).
Further research using trained athletes as subjects would add weight to these findings. But until then, sprinters may draw the following conclusions: a large increase in training volume for approximately three months will decrease the proportion of IIb fibres in the trained muscles; a subsequent reduction (not cessation) in training volume relative to the heavy resistance training phase should not only reverse this decrease but lead to a significant overshoot in the proportion of IIb fibres. In consequence, the potential for the rapid and forceful muscle contractions so crucial to sprint performance should be enhanced.
This conclusion is in line with the current training practices of many sprint athletes: a heavy resistance training phase followed by a taper in training volume and intensity in the lead up to the competitive season(9). And on the evidence of the Copenhagen research, others would be advised to follow their example, with three months of heavy resistance training followed by three months of relative detraining, with relatively reduced training volume in the run up to key targeted events.
However, as is usually the case, new research findings will probably refine these recommenda-tions over the coming years.
Alun Williams and Mick Wilkinson
References
1. New Studies in Athletics, 10 (1), 29-49
2. Journal of Physiology, 472, 595-614
3. Journal of Physiology, 495, 573-586.
4. Journal of Applied Physiology, 59, 1716.
5. Pflƒgers Archiv. European Journal of Physiology, 431, 513-518.
6. Journal of Applied Physiology, 74, 911-915.
7. Acta Physiologica Scandanavica, 151, 135-142
8. Muscle and Nerve, 23, 1095-1104.
9. Medicine and Science in Sports and Exercise, 27 (8), 1203-1209.
One component of the myosin filament, known as the myosin heavy chain (MHC), determines the functional abilities of the entire muscle fibre. This heavy chain exists in three forms: I, IIa and IIb. Type I fibres contain a predominance of type I MHC and are commonly called slow twitch, while fibre types IIa and IIb contain a predominance of type IIa and IIb MHC respectively, and are known as fast twitch. Slow twitch fibres are so-called because the maximum contraction velocity of a single fibre is approximately one tenth that of a type IIb fibre(2). Type I fibres also produce less maximum force than type IIb fibres(3). Type IIa fibres lie somewhere between type I and type IIb in their maximum contraction velocity and maximum force production.
Because of the high velocity of contraction and the large forces they produce, type IIb fibres are probably one of the key elements required for successful performances in speed-dependent pursuits like sprinting. It is therefore not surprising to find that successful sprint athletes possess more of these IIb fibres than the average person(4). But is this part of a sprinter's make-up pre-determined by genetics? Or can the proportion of type IIb fibres in muscle be increased through training?
Training effects on fibre type
Virtually all the available evidence suggests that the answer to the last question is no. In fact, it has been suggested that type IIb MHC and therefore IIb fibres constitute a 'default' fibre type setting in humans when activity is absent, and evidence of high proportions of this fibre type in paralysed muscle support this theory(5). It has also been known for some time that increases in activities like strength or power training can lead to conversion of muscle fibres. But, unfortunately, this conversion operates in one direction only, changing fast type IIb fibres into slower type IIa fibres(6). Moreover, if heavy loading of muscles continues for a month or more, virtually all type IIb fibres will transform to type IIa, with obvious consequences for sprinting potential(7).
What happens when heavy strength training stops? Do the newly formed type IIa fibres revert back to type IIb? The answer is yes, but recent research has revealed some extraordinary results to which a simple yes does not do justice. Scientists from the Copenhagen Muscle Research Centre examined training and detraining effects on muscle fibre type distribution(8). Biopsies (muscle samples) were taken from the vastus lateralis muscle of nine young sedentary males. All the subjects then undertook three months of heavy resistance training, aimed predominantly at the quadriceps muscle group, which ended with a second muscle biopsy. The subjects then abruptly ceased training and returned to their normal sedentary lifestyles before providing a third biopsy three months later.
Biopsies from the vastus lateralis were analysed for muscle fibre type distribution and number. As was expected, there was a decrease in the proportion of fast twitch IIb fibres (from around 9% to 2%) during the resistance training period. The researchers expected that the proportion of IIb fibres would simply be restored to pretraining values during the detraining period. However, they found to their surprise that the proportion actually doubled to around 18% after three months of sedentary living!
How heavy training followed by tapering produces 'overshoot'
So it seems that a pattern of heavy resistance training followed by decreased activity causes first a decrease then an overshoot in the proportion of the fastest fibre type in the trained/detrained muscle group. An explanation for this overshoot currently eludes researchers, but the findings accord with the theory that muscle fibres 'default' to type IIb with a (relatively) decreased level of activity(5).
Further research using trained athletes as subjects would add weight to these findings. But until then, sprinters may draw the following conclusions: a large increase in training volume for approximately three months will decrease the proportion of IIb fibres in the trained muscles; a subsequent reduction (not cessation) in training volume relative to the heavy resistance training phase should not only reverse this decrease but lead to a significant overshoot in the proportion of IIb fibres. In consequence, the potential for the rapid and forceful muscle contractions so crucial to sprint performance should be enhanced.
This conclusion is in line with the current training practices of many sprint athletes: a heavy resistance training phase followed by a taper in training volume and intensity in the lead up to the competitive season(9). And on the evidence of the Copenhagen research, others would be advised to follow their example, with three months of heavy resistance training followed by three months of relative detraining, with relatively reduced training volume in the run up to key targeted events.
However, as is usually the case, new research findings will probably refine these recommenda-tions over the coming years.
Alun Williams and Mick Wilkinson
References
1. New Studies in Athletics, 10 (1), 29-49
2. Journal of Physiology, 472, 595-614
3. Journal of Physiology, 495, 573-586.
4. Journal of Applied Physiology, 59, 1716.
5. Pflƒgers Archiv. European Journal of Physiology, 431, 513-518.
6. Journal of Applied Physiology, 74, 911-915.
7. Acta Physiologica Scandanavica, 151, 135-142
8. Muscle and Nerve, 23, 1095-1104.
9. Medicine and Science in Sports and Exercise, 27 (8), 1203-1209.
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