Ok. I’m at the point where I’m sick of everyone telling me what these muscle fibers do without understanding them. What are all the differences between these types of fibers?
That’s a hell of a question.
Basically, at root, the only real distinction you can make is neurologically. The variance between FT and ST fibers is more or less on a continuum based on activation/recruitment threshold. The higher the threshold, generally the greater force-producing capability-- there are some physiological differences between the two, size being the most notable.
However, a lot of that is based on peripheral adaptation. MHC expression especially, which is how fibers are classified as type I, IIa, and IIx, is highly variable according to activity level and specific function. Most fibers co-express several forms of MHC.
In all actuality, the IIx isoform, which most people associate with the “really fast” fibers is more an indicator of dis-use. This actually makes sense if you think about it though-- the highest-threshold fibers that IIx is most evident in are rarely “trained” by most people.
MHC expression is also only loosely related to metabolic activity. True, there is a general trend towards oxidative action in ST fibers and glycolytic action in FT fibers, but this again is more a result of how they function, as opposed to an innate property of the fiber.
In short-- once you get past the neural classification of the fiber, and beyond the extremes on each end of the continuum, you’re pretty much left with a lot of room for specific training to elicit any adaptations you might need.
PowermanDL-
This is a topic which is constantly raised and references to targetting the fast twitch fibers or preferentially targetting the type IIB fibers (presumably this is interchangeable with IIX? You also previously mentioned IId of which I have not heard) is commonplace in training advice so I think that it is important to understand what is being said.
My understanding from this and your previous posts is that;
1.The shift from IIB/X to type IIA is expected from training as essentially these fibers are untrained fibers( and if what you previously said about these fibers contracting “too” quickly is correct they are also “unwanted” fibers?) . On this point I am not entirely sure why they convert to IIA and why not for example simply become hypertrophied type IIB/X fibers.
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MHC expression as type I, IIA or IIB is “peripheral”. I am not sure if this means that there is some metabolic shift between the fibers which is not significant or less important than neural factors or whether peripheral means something else.
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The shift in MHC expression does not seem to have any performance implications.
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Neural activity is more important than MHC expression.
What is bothersome is that in for example the article on “Training principles for jumpers” by Moura and Moura cited in the previous thread the training structure seems to revolve around the very notions of MHC expression which may not be important e.g avoiding conversion to type I fibers, tapering to reconvert IIA to faster IIB fibers, selectively recruiting type IIB fibers etc , etc.
In other words they adopt a language which is popular in training literature but which from what I now understand is misleading or at best simplistic. Or have I totally misunderstood this whole issue?
IIb is the analog of IIx which is found in non-human mammals. IId is roughly the same thing as IIx, and IIRC is only a difference in nomenclature, though I’d have to check to be certain-- in any event, they are very similar if there is any difference between the two.
My understanding from this and your previous posts is that;
1.The shift from IIB/X to type IIA is expected from training as essentially these fibers are untrained fibers( and if what you previously said about these fibers contracting “too” quickly is correct they are also “unwanted” fibers?) . On this point I am not entirely sure why they convert to IIA and why not for example simply become hypertrophied type IIB/X fibers.
It has to do with the shortening velocity of the IIx isoform. Most everything out there now indicates that the shift from IIx --> IIa is common to all strength athletes, which likely indicates that the IIx isoform is in some way inappropriate for those athletes.
As I mentioned, MHC expression isn’t an innate property of a fiber. If you lablel a fiber “Type IIx” then go train in a specific fashion for two months, that fiber may no longer express the IIx isoform, or it might be coexpressing it with another.
The only true way to classify fibers is according to neural action and activation threshold. The rest is all a result of that.
- MHC expression as type I, IIA or IIB is “peripheral”. I am not sure if this means that there is some metabolic shift between the fibers which is not significant or less important than neural factors or whether peripheral means something else.
Peripheral, meaning at the level of the muscle itself (as opposed to central, in the nervous system).
This means that MHC expression is a result of how the muscle behaves, as signaled by the nervous system, as opposed to being a unique property of the fiber.
- The shift in MHC expression does not seem to have any performance implications.
Yes. MHC expression is a result of training adaptations, part of the process that causes performance gains, not a causal factor in and of itself.
- Neural activity is more important than MHC expression.
By far. As far as strength, speed, and explosiveness are concerned, the nervous system is king.
What is bothersome is that in for example the article on “Training principles for jumpers” by Moura and Moura cited in the previous thread the training structure seems to revolve around the very notions of MHC expression which may not be important e.g avoiding conversion to type I fibers, tapering to reconvert IIA to faster IIB fibers, selectively recruiting type IIB fibers etc , etc.
In my view of things, MHC expression is best used as a marker of how fibers are being trained.
It could be used to monitor performance and detraining (well, assuming you found some way besides muscle biopsies to check…), and it could be part of the “rebound” mechanism that occurs after periods of heavy loading.
In other words they adopt a language which is popular in training literature but which from what I now understand is misleading or at best simplistic. Or have I totally misunderstood this whole issue?
Nah, seems like you’ve pretty much got it.
As usual, when a few gurus get hold of a little bit of knowledge, they can very quickly bastardize it for everyone else-- so it’s no shock that a lot of this stuff is grossly misapplied in common usage.
Great posts, PowerMan! I completely agree.
Fibre conversion has been proven to be a good marker of talent and training effect by researchers’ such as Delecluse, Bosco et al. I have no references to hand but I will explain.
Individuals who are able to excel in power sports have the ability to convert type I fibers and type IIB fibers to type IIa in other words, after training some individuals will have a massive increase in type IIa fibers and a decrease in the other fibre expressions.
The not so talented may see a shift in THE wrong direction ie type IIb to IIa and then type IIa becoming more like type I. The implications are serious.
Individuals who adapt to training by causing fast fibres to become type I in behaviour are probably suited to power endurance/endurance events. This type of fiber switching is unidirectional as the conversion is from fast, medium fast to slow.
Individuals who adapt to taining by causing fast fibres type b to become type IIa and slow type I to become type IIa are suited to strength power, speed events. This type of fibre switching is known as bidirectional conversion.
All fibre type conversions are a result of the body trying to be efficient, trying to improve its thermodynamic qualities. Being able use both oxygen and glucose is more efficient. (type II are also known as fast oxidative glycolytic ). Energy to resynthesize glycogen and any net PCr that is broken down for short-term requirements is supplied by oxidation of the lactate generated, hence the reason why type IIb acquire IIa characteristics.
Though people who adapt in a unidirectional manner are disadvantaged, strength training and speed training done correctly and with proper regeneration periods are critical. First of all the strength and speed training can selectively increase the size of fast fibres to make up for any lack of fast fibre percentage in the beginning and after fibre conversion.
The regeneration periods will help stabilise hormonal profiles especially testosterone, adrenal and thyroid hormones as these three hormones are responsible for promoting fast fibre well being and even causing slow to fast conversions through different pathways.
Training correctly is essential. For example Tidow et al have discovered that when strength training emphasis is changed, over a set period, gains in power can be greater than when the training emphasis was unchanged.
A sequence of hypertrophy followed by maximum strength and then power/speed caused fast fibres to change.
During the hypertrophy stage fast fibres decreased while slow or medium fast predominated. During the max strength phase, the fibre conversion caused by the hypertrophy stayed the same, no change. During the power/ speed phase muscle fibre conversion back to the original distribution occured or in some individuals, increased.
(Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression
S. D. R. Harridge1,2, R. Bottinelli3, M. Canepari3, M. Pellegrino3, C. Reggiani3, M. Esbjörnsson4, P. D. Balsom1 and B. Saltin1,2
1 Department of Physiology and Pharmacology, Karolinska Institute, Stockholm; 2 Copenhagen Muscle Research Centre, Rigshospitalet, DK-2200 Copenhagen N, Denmark; 3 Institute of Human Physiology, University of Pavia, I-27100 Pavia, Italy; and 4 Department of Clinical Physiology, Huddinge Hospital, Karolinska Institute, S-114 86 Stockholm, Sweden
THE INCREASE IN MUSCLE POWER generation that results from training could be brought about by at least two different mechanisms. First, it can be brought about by an increase in the force-producing capability of the muscle, either through increased activation or through an increase in muscle size. Second, it can occur by increasing the speed at which a muscle can shorten against a given load.
A close coupling exists between the speed of muscle shortening and the expression of the different myosin heavy chain (MHC) isoforms. Muscle fibers that express the MHC-I isoform exhibit significantly slower maximal velocities of shortening (Vo) (24, 28) and power outputs (11) compared with fibers expressing the two fast MHC isoforms. Within the subgroups of fast isoforms, fibers that express the MHC-IIB isoform [which has recently been shown to be homologous to the MHC-IIX isoform found in small mammals (18, 34)] are significantly faster (24, 28) and can generate higher power outputs than fibers containing the MHC-IIA isoform (11, 36). Muscle speed of movement could be increased either by altering the relative expression of the fast and slow isoforms or by changing the coupling between isoform expression and function.
Skeletal muscle is a highly plastic tissue capable of altering its contractile proteins and its contractile properties with increased use, or with disuse (see Refs. 23 and 31 for reviews). The important role played by the activation pattern has been demonstrated by chronic electrical stimulation studies on animal muscle. Prolonged low-frequency electrical stimulation is capable of transforming “fast” contracting muscles into “slow” contracting muscles such that MHC isoform expression proceeds in the general direction MHC-IIB MHC-IIX MHC-IIA MHC-I (31). Although there is some evidence that intermittent high-frequency stimulation may alter the properties of denervated soleus muscles to resemble those of a faster muscle (6, 22), an increase in the expression of MHC-IIB seems only possible with disuse (5). However, a change in activation pattern is only one determinant of the muscular adaptation to exercise. In general, changes in activation pattern are also accompanied by increases in mechanical load and by alterations of metabolic homeostasis (10). In human training studies, whether endurance or power based, the most common observation has been the decrease in the proportion of type IIB fibers, determined histochemically (4, 23) or, more recently, in MHC-IIB content determined electrophoretically (1). Sprint training seems to represent a notable exception because there is some evidence of a “bidirectional” transformation to MHC-IIA from both MHC-IIB and MHC-I (3, 19). From this point of view, sprint training might be similar to the above-mentioned condition of intermittent high-frequency stimulation (6, 22).
With regard to the coupling between expression and function, we have recently demonstrated that single fibers containing a specific MHC isoform have the same Vo irrespective of whether they originate from a fast or a slow contracting muscle (24). We expect that the same holds true for fibers containing the same MHC isoform but isolated from muscles exposed to different levels of stimulation or mechanical activity. The point is questionable because there is some evidence that the coupling between MHC isoform and contractile characteristics may be altered by a change in activity (20, 35, 36).
Human training may take many forms; sprint training might be considered to be the most likely condition in which increases in speed, either through a shift in fiber-type distribution or through an altered coupling between fiber type and speed of shortening, might contribute to increased power generation, in addition to the increases in strength. In the present study our purpose was to test this possibility by determining whether high-intensity, short-duration sprint training could induce 1) an uncoupling between MHC expression and contactile properties of single fibers tested in vitro, 2) a change in the relative distribution of the different MHC isoforms within whole muscles, and 3) changes in the voluntary and electrically evoked contractile properties of whole muscles measured in vivo. )
(Acta Physiol Scand. 1994 Jun;151(2):135-42. Related Articles, Links
Myosin heavy chain isoforms in single fibres from m. vastus lateralis of sprinters: influence of training.
Andersen JL, Klitgaard H, Saltin B.
August Krogh Institute, University of Copenhagen, Denmark.
The myosin heavy chain (MHC) composition of single fibres from m. vastus lateralis of a group of male sprint athletes (n = 6) was analysed, before and after a three months period of intensive strength- and interval-training, using a sensitive gel electrophoretic technique. Significant improvements were observed after training in almost all of a series of performance tests. After training the sprinters revealed a decrease in fibres containing only MHC isoform I (52.0 +/- 3.0% vs. 41.2 +/- 4.7% (mean +/- SE) (P < 0.05)) and an increase in the amount of fibres containing only MHC isoform IIA (34.7 +/- 6.1% vs. 52.3 +/- 3.6% (P < 0.05)). Fibres showing co-existence of MHC isoforms IIA and IIB decreased with training (12.9 +/- 5.0% vs. 5.1 +/- 3.1% (P < 0.05)). Only one out of 1000 fibres analysed contained only MHC isoform IIB. In contrast, a higher amount of type IIB fibres (18.8 +/- 3.6% vs. 10.5 +/- 3.9%, (P < 0.05)) was observed with myofibrillar ATPase histochemistry. The majority of histochemically determined type IIB fibres of sprinters seems therefore to contain both MHC isoforms IIA and IIB. Sprint-training appears to induce an increased expression of MHC isoform IIA in skeletal muscles. This seems related to a bi-directional transformation from both MHC isoforms I and IIB towards MHC isoform IIA.
Publication Types:
Clinical Trial)
Stretch and force generation induce rapid hypertrophy and myosin isoform gene switching in adult skeletal muscle.
Goldspink G, Scutt A, Martindale J, Jaenicke T, Turay L, Gerlach GF.
Unit of Molecular and Cellular Biology, Royal Veterinary College, London University, U.K.
Using electrical stimulation to control force generation and limb immobilization to alter the degree of stretch, we have studied the role of mechanical activity in inducing hypertrophy and in determining fast and slow muscle fibre phenotype. Changes in gene expression were detected by analysing the RNA in hybridization studies employing cDNA probes specific for fast and slow myosin heavy chains and other genes. As a result of overload in the stretched position, the fast contracting tibialis anterior muscle in an adult rabbit is induced to synthesize much new protein and to grow by as much as 30% within a period as short as 4 days. This very rapid hypertrophy was found to be associated with an increase of up to 250% in the RNA content of the muscles and an abrupt change in the species of RNA produced. Both stretch alone and electrical stimulation alone caused repression of the fast-type genes and activation of the slow-type genes. it appears that the fast-type IIB genes are the default genes, but that the skeletal slow genes are expressed as a response to overload and stretch. These findings have implications as far as athletic training and rehabilitation are concerned.
PMID: 1716229 [PubMed - indexed for MEDLINE]
Fibre conversion is real, and it matters. What you will find is that superior training programs like CF’s already take care of the implications above whether by evolution or by calculated design.
It only matters as an indicator, as I mentioned.
Performance correlates to MHC expression, but MHC expression is not the causal factor.