Making muscles grow
Discussion
How often should you train them? Common concensus is maybe two times maximum over a seven day period. But, I've just come back from a holiday in France with no access to a gym, and apart from cycling every day, the only exercise I took was to do press ups and lots of them! I did at least 400 press ups every day for 14 days, so by my rough calculation that's over 5,000 press ups. Anyway, as a net result of this, my chest and triceps have put on a very large amount of growth and thickness, more so than I have ever achieved going to the gym. The thing I find confusing is common wisdom dictates that if you train a muscle every day you actually make it smaller.
Are high reps and daily training recommended for muscle growth, or over time would this do damage to the muscle tissue?
Are high reps and daily training recommended for muscle growth, or over time would this do damage to the muscle tissue?
If you train a muscle every day you will not make it smaller,you'll just overtrain it to the point of pain.Then you'll have to stop.
The training you have been doing is endurance training ie high reps low weight,and you're right it doesn't really force growth.For the overload principle to work
you really need significantly heavier weights and lower reps.However you have grown and this is because your body has adapted to the new demands placed on it,
ie press ups etc.This growth will tail off very quickly,but you will still be able to increase the number of reps,again overload this time though through reps.
As for times you can train a bodypart per week? For most large muscle groups,lats,glutes,quads etc once a week is generally considered enough,smaller groups more often.
The training you have been doing is endurance training ie high reps low weight,and you're right it doesn't really force growth.For the overload principle to work
you really need significantly heavier weights and lower reps.However you have grown and this is because your body has adapted to the new demands placed on it,
ie press ups etc.This growth will tail off very quickly,but you will still be able to increase the number of reps,again overload this time though through reps.
As for times you can train a bodypart per week? For most large muscle groups,lats,glutes,quads etc once a week is generally considered enough,smaller groups more often.
Interesting this!
When I started training (with Noah) most of the experts on the Ark and writing on the tablets recommended training each bodypart twice a week. Some, like many powerlifters, trained three times a week doing whole body sessions. Many of these folk were 'big' by any normal idea of size.
Then it seemed to shift to once a week or less, even to restricting any training to a few sessions/hours over 7 to 10 day periods, citing 'hard gainers' as the mass populace/audience. I've never been sure either way but suspect that even if 'once per week' is good for developing muscle size it won't be for developing any meaningful athletic ability.
I was doing push ups two or three times a week and after several yeas of not bench pressing could do more than I'd imagined during an experiment at Christmas. I've neglected them recently and on re-starting benching have lost 10% or so; the push ups must have helped.
When I started training (with Noah) most of the experts on the Ark and writing on the tablets recommended training each bodypart twice a week. Some, like many powerlifters, trained three times a week doing whole body sessions. Many of these folk were 'big' by any normal idea of size.
Then it seemed to shift to once a week or less, even to restricting any training to a few sessions/hours over 7 to 10 day periods, citing 'hard gainers' as the mass populace/audience. I've never been sure either way but suspect that even if 'once per week' is good for developing muscle size it won't be for developing any meaningful athletic ability.
I was doing push ups two or three times a week and after several yeas of not bench pressing could do more than I'd imagined during an experiment at Christmas. I've neglected them recently and on re-starting benching have lost 10% or so; the push ups must have helped.
mcelliott said:
How often should you train them? ... The thing I find confusing is common wisdom dictates that if you train a muscle every day you actually make it smaller.
That really isn't common. Nor is it wisdom. I'm not surprise you're confused! 
Muscular fitness is 2x per week (Minimum), around 10 different exercises per session.
Anyway, re: your results. It probably just means you're more of a slow twitch fibre person than a fast twitch fibre person. 400 press-ups a day, assuming around 100 per stint, is well into the muscular endurance training zone. ...And what you have actually discovered is the results you can get by massively varying your routine.
Before you can choose a training regime, it's handy to know what kind of muscular composition you have, otherwise wrong training for the wrong composition will yield poor results.
mattikake said:
Before you can choose a training regime, it's handy to know what kind of muscular composition you have, otherwise wrong training for the wrong composition will yield poor results.
I would have thought training is for a purpose or aim you have- be it strength/body building/endurance etc? I'd set the training as to what you want to achieve, rather than set the training around your body composition. How odd.didelydoo said:
I would have thought training is for a purpose or aim you have- be it strength/body building/endurance etc? I'd set the training as to what you want to achieve, rather than set the training around your body composition. How odd.
Depends - for many, the aim is "make me look good" rather than "excel at a sport I enjoy".RemainAllHoof said:
mattikake said:
Before you can choose a training regime, it's handy to know what kind of muscular composition you have, otherwise wrong training for the wrong composition will yield poor results.
How can you find out? Just doing various exercises until one proves to grow stuff more?Not to worry though as it is possible to force change from one to the other with serious training,("Muscle, Genes and Athletic Performance" Scientific
American) should you want.Are you a sprinter or a marathon runner? Short sharp bursts of power or more endurance based activity like hundreds of pressups? (as above)
As someone who trains for climbing I'd have thought fast twitch fibres,ie power,was more likely your muscle composition.
goldblum said:
As someone who trains for climbing I'd have thought fast twitch fibres,ie power,was more likely your muscle composition.
Yeah, I'm more just interested from a "scientific" viewpoint than specifically for my training. WRT climbing, it's partly power and partly endurance as you want to be able to perform well over extended periods of time (hours) not just a few minutes. Apparently, the ladies love this. 
RemainAllHoof said:
mattikake said:
Before you can choose a training regime, it's handy to know what kind of muscular composition you have, otherwise wrong training for the wrong composition will yield poor results.
How can you find out? Just doing various exercises until one proves to grow stuff more?
Re. the fibre composition/body types I've copied and pasted below details from an article I read a while back (can't find where/what it's called) that might be interesting?
Sorry about the length but it is detailed! The bit near the end about possible metabolic effects on decreasing training might relate to MC's 'holiday' growth?
Muscle Fibers
There are three primary muscle fiber types in humans -- Type I, Type IIA, and Type IIB. Type I are referred to as "slow twitch oxidative", Type IIA are "fast twitch oxidative" and Type IIB are "fast twitch glycolytic" (1). And as their names suggest, each type has very different functional characteristics. Type one fibers are characterized by low force/power/speed production and high endurance, Type IIB by high force/power/speed production and low endurance, while Type IIA fall in between (2, 3, 4). The advantages of a certain fiber composition on performance in various sports is both obvious and well established -- for example, marathon runners have 75% slow twitch fibers, while sprinters and weightlifters have 75% fast twitch (5, 6).
These characteristics are a result, primarily, of the fiber's Myosin Heavy Chain (MHC) composition, with MHC isoforms I, IIa and IIx corresponding with muscle fiber types I, IIA, and IIB, respectively (7) -- A small % of hybrid fibers co-expressing two isoforms also exist (8). Myosin Light Chains have been found to exert an effect on some of these properties, but they are minor, and not as well characterized or understood (9), thus we will be dealing with only the MHC.
MHC
MHC IIx possess a shortening velocity 5-10 times that of MHC I and are also faster than MHC IIa (10, 11, 12). Power production, particularly at high velocities, is higher with IIx than either IIa or I as well (11, 13). Force (strength) production has generally been shown to be greater in MHC IIx than IIa (14, 15), though one study found the opposit (16). Both MHC II types have been consistently shown to be superior to MHC I in all three areas (10-16). So, clearly, it is favorable for speed and strength athletes to posses a high % of MHC II, particularly IIx.
The Theory
MHC composition, and thus athletic potential, is thought to be determined to a great extent by genetics. However, various forms of mechanical and electrical stimulus (or lack thereof) have been shown to alter their expression, and it is this potential for manipulation that is the centerpiece of the system I am proposing. I will start with the two most interesting studies:
In the first study, subjects were put on a 3 month resistance training program, which was then followed by 3 months of detraining. Analysis of of the MHC composition of the vastus lateralis was done before training, after training, and following the detraining period (17).
Training resulted in a decrease in MHC IIx from 10% to 4% and an increase in MHC I from 49% to 51% -- the opposite of what we want as a speed/strength athlete. This fast to slow conversion has been well characterized in the literature -- both with bodybuilding type routines such as this, but also with routines typical of those used by power athletes. We will go into considerably more detail on this in a bit.
What is not as well characterized (and what is exciting) is what happened following the detraining period. At the end of the three months, MHC IIx had risen from 4% to 19%, while MHC I had dropped from 51% to 45%. Remember, MHC IIx started out at only 10% before training. This means a significant overshoot in MHC IIx occurred with detraining. Obviously, this is a speed/strength athletes dream.
In the second study (18), fifteen women were divided into two groups -- the first group (T) had undergone a 20 week resistance training program followed by 32 weeks of detraining prior to the study. The second group (U) was totally untrained. Both groups were subsequently put on a 6 week training program. Fiber type % measurements for T were taken before and after the 20 weeks of training, after the the 32 weeks of detraining, and again after the 6 week training period. For U, measurements were taken before and after the 6 week training program.
The initial 20 week program for T caused a reduction in IIB from 16% to 1%. The detraining period caused an increase from 1% to 24% -- another instance of overshoot. And considering the length of the detraining period, it is possible that a greater overshoot occurred but that levels were returning to baseline by week 32 (17).
However, this is not the most interesting part, as we will see. Following the subsequent 6 week program, the IIB % of U dropped from 24.9% to 6.7%, but T only dropped from 24.2 to 12.9%. There reduction was far less than that of the untrained group. The differences in type I are just as dramatic. T showed no increase in type I while U increased from 37.5% to 50.5%. In addition to the slow to fast overshoots we have seen, this suggests that the on/off cycling might be causing a resistance to fast to slow transformations. Hopefully, at this point, you have put two and two together and are wondering what might happen if we put together multiple on/off cycles.
I should note that these studies did use untrained subjects and the training protocol was not typical of that used by power athletes, thus if this were the only these studies, they could perhaps be written off. However, a number of other studies argue for the possibility of this being much more than an isolated occurrence, as we will see.
We will first take a look at several studies showing fast to slow conversions which will help us to determine possible mechanisms, not only to allow us to develop training strategies to minimize them, but also to give us some insight as to how the slow to fast changes might be made to occur, so as to facilitate and optimize them.
Fast to Slow
Studies in both man and animal have consistently shown a fast to slow (FTS) MHC response to resistance training, with not only endurance and bodybuilding type routines, but even with with routines typical of speed/strength athletes. We will not concern ourselves with endurance studies, except to say that it causes a rapid slowing of the phenotype (IIx to IIa and IIa to I) without concomitant increases in strength, thus it should be entirely avoided by those wishing to maximize speed, strength, and power (5, 19, 20).
I will not do an exhaustive presentation of the fast to slow literature, as many of the studies use identical design with identical results -- I will focus instead on presenting the different protocols that have produced fast to slow adaptations.
Hortabagyi et al showed a 12% reduction in MHC IIx and 13% increase in MHC I after 12 weeks using high volume maximal effort isokinetic contractions, with eccentric only, concentric only, as well as with mixed training (21).
In another study, using a twice a week heavy (6-8RM), light (10-12RM) split, MHC IIx was reduced from 18% to 7.1% and 18.9% to 6.1% in just 7 weeks in both men and women (22a). Interestingly, between the 7th and 9th week, it leveled off in both groups and the % actually increased slightly in the women. A similar reversal of the STF occurred from week 7 to 9 in another study, using the same training protocol, but which looked at fiber type % (22b).
Twelve weeks of a typical bodybuilding routine caused a 25% MHC IIx reduction along with a slight MHC I increase (23).
It is probably not a big surprise to many that the above training methods caused FTS. However, a study using sprinters (24), employing their normal sprint preparation programs might be. Subjects were tested, following a three week training break, for MHC content, and sprinting speed. This was followed by a three month training period. Type IIx was found to have decreased by about 50%. And this is with a pre-contest sprint preparation protocol.
But, before you decide to just quit training altogether, it should be noted that sprint times still improved slightly (we mustn't forget about the neural and cross sectional area components of speed/strength/power), and type I decreased by 25%. Anderson et. al. and Esbjornsson et. al. have found a similar bi-directional shift (IIX to IIa and I to IIa) with sprint training (24, 25).
Another study, employing multiple 3 second cycle sprints did not observe this, but rather showed the decrease in MHC IIx and increase in MHC I observed in all of the other studies (26).
Slow to Fast
Slow to Fast transitions in the literature are also abundant, however not that many human studies deal with any sort of resistance training setting, thus we will have to dip a bit into other areas such as immobilization, reduced electrical activity, and reduced gravity, as well as animal studies.
Detraining
Obviously, the studies most applicable to our purposes are those using detraining. We have previously mentioned 2 studies showing STF with extended detraining. Several detraining studies of shorter duration (2-4 weeks) have shown no STF transformation (27, 28). However, an analysis of MHC at the protein level have shown increases in MHC mRNA -- which is indicative of the early stages of IIa to IIb and I to IIa conversions -- in short term studies (21, 29). This makes sense given an MHC turnover time of 3-4 weeks (30). Thus, there is clearly evidence supporting STF given a detraining period of adequate length.
Immobilization
There is a lack of data on the effect of immobilization in humans, however, animal studies show STF transformations in as little as 2-7 days (31, 32).
Reduced Loading
Reduced loading situations such as space flight and its ground based counterpart, hindlimb unloading, result in rapid STF transitions. As little as 4 days of spaceflight in rats and 11 days in humans caused significant increases in MHC IIx and decreases in MHC I (33, 34). In another study, 17 days resulted in a doubling of the proportion of fast twitch fibers in the human soleus (35). While hindlimb unloading consistently shows STF is rats, it has been more mixed in humans (36).
Neural Inactivity
Reduced neural activity, such as that which occurs in spinal cord injury or transection, rapidly and reliably show STF transformation in both slow-twitch and fast twitch muscles, beginning as early as five days and showing profound changes within 3 months (37, 38, 39, 40).
Obviously, some of the above situations are not exactly 100% analogous to the type of detraining that is practical to a power athlete. However, what they do show, is that given the proper stimulus (or lack thereof), MHC content displays a great deal of plasticity, and in a short enough time to be practical for implementation into a power athlete's off-season program.
Mechanisms
Fast to Slow
The exact mechanisms behind the transformations observed is not conclusively known at this time. The most popular theory is that MHC IIx gene represents a default gene, which is switched under conditions of increased contractile activity (41, 42, 24). However, several studies have shown increased MHC IIx expression with certain types of training programs, most notably short duration sprinting (43), as well as with certain metabolic and hormonal conditions, including hyperthyroidism, hyperinsulinemia, leptin administration, and beta 2 adrenergic stimulation (44, 45, 46, 47). Thus, I think this view is flawed.
A more likely explanation is that the phenotype is adapted to its to meet the demands of its environment. Let's look at this from an evolutionary point of view -- in other words, what are the advantages of FTS vs. STF for the survival of the organism.
With resistance training, particularly employing strength training protocols, one would at first view the FTS as paradoxical in the face of mechanical overload. After all, that aspect, all else being equal, represents a weakening of the phenotype. However, on closer inspection, we find that it offers certain advantages, while still allowing the organism to adapt to the stimuli presented.
First, a FTS conversion would make the organism metabolically more efficient (48, 49), which is an obvious advantage in the times of scarcity in which we evolved. And, given that under non-training conditions, motor units associated with MHC IIx isoforms are only active 30-180 seconds per day, most current training programs are going to represent a significant increase in activity (50).
Second, the training stimulus with current protocols does not present a true maximal overload, particularly in regards to the eccentric component. This, along with the fact that some studies show MHC IIa fibers to produce equal or superior force at low velocities compared with MHC IIx (16), mean that a concentric/eccentric rep under typical strength training conditions (loads only as high as the concentric 1 RM and low velocities) could be adequately handled by a phenotype with a preferential IIa expression.
This makes it tempting to suggest loads equal to or greater than the ECCENTRIC 1 RM, however, speed of cross-bridging is less fiber type dependent (50b), thus it might overactivate and thus hypertrophy type I and IIa fibers. Therefore, we will leave this as an area for exploration at this point. The other method would be to employ only a concentric contraction at very high velocities (or perhaps at loads equal to the 1 RM).
Slow to Fast
The specific mechanisms responsible for STF at the micro level are not fully known. A couple of theories exist -- one involving the myogenic regulatory factor pathway and the other calcineurin:NF-AT pathway (36). However, these are very much speculative at present and are well beyond the scope of this today's article, thus we will not go into further detail, today.
At the macro level, we can once again turn to the advantage STF might produce for the organism. With the hormonal conditions mentioned above, it is fairly obvious. Beta 2 receptors are activated by epinephrine and norepinephrine, the so called "fight or flight" hormones. Clearly, a STF transformation of the phenotype would be advantageous for an organism that has to run away from a predator (or chase down its prey). This is likely what accounts for STF transformations that have occurred with short duration sprint training as well (51, 52).
As for hyperthyroidism, hyperinsulinemia, and leptin administration, what these all have in common is they are characteristic of the organism being in the "fed" state. Thus, the need for metabolic efficiency is done away with for the time being, leaving the organism free to assume a phenotype most conducive to the afore mentioned fight or flight situations.
With reduced mechanical loading and neural activity, the mechanism is likely the opposite of that which produces the FTS during training. In the face of reduced activity, thus reduced energy expenditure and need for muscular endurance, the afore mentioned metabolic efficiency would no longer be necessary for survival, thus the organism is free to once again assume the faster phenotype, which is clearly advantageous, all else being equal.
With detraining, it is likely that, from the body's vantage point, the abrupt withdrawal of stimulus following increased muscle activity with training is analogous to the near complete cessation of activity with immobilization/neural inactivation following normal activity (17). In other words, it "tricks" the body into thinking it can safely assume the metabolic inefficiencies that accompany the faster phenotype.
Muscle and Strength Losses
At this point, perhaps you are convinced of the possibility of slow to fast transformations but are concerned about the negative effects of the detraining period on muscle mass and strength. After all, spinal cord transection can accomplish STF, but it is not going to make anyone a great athlete. Fortunately, this is not a great concern. As I will show, both parameters rapidly return to normal levels (and above) when training is resumed.
The previously mentioned study by Staron et. al. (18) showed complete strength and power recovery after just 6 weeks of retraining following 20 weeks of detraining. Hortabagyi (21) and MacDougall (53) showed gains to beyond starting levels despite complete immobilization for extended periods. These are not surprising in light of data showing that majority of neural adaptation induced strength gains take place in the first 3-5 weeks of training (54). In addition, a couple studies have found that fiber areas of subjects trained for only a couple of months were equal to those of subjects trained for several years (54, 55). This has ramification that go far beyond what is presented today, but that is the subject of another article.
References
1. Bee G, Solomon MB, Czerwinski SM, Long C, Pursel VG Correlation between histochemically assessed fiber type distribution and isomyosin and myosin heavy chain content in porcine skeletal muscles. J Anim Sci 1999 Aug;77(8):2104-11
2. Bottinelli R, Reggiani C Human skeletal muscle fibres: molecular and functional diversity Prog Biophys Mol Biol 2000;73(2-4):195-262
3. Thorstensson A, Grimby G, Karlsson J Force-velocity relations and fiber composition in human knee extensor muscles. J Appl Physiol 1976 Jan;40(1):12-6
4. Inbar O, Kaiser P, Tesch P Relationships between leg muscle fiber type distribution and leg exercise performance. Int J Sports Med 1981 Aug;2(3):154-9
5. Tesch PA, Wright JE, Vogel JA, Daniels WL, Sharp DS, Sjodin B The influence of muscle metabolic characteristics on physical performance. Eur J Appl Physiol Occup Physiol 1985;54(3):237-43
6. Gollnick PD, Armstrong RB, Saubert CW, Piehl K, Saltin B J Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. Appl Physiol 1972 Sep;33(3):312-9
Sorry about the length but it is detailed! The bit near the end about possible metabolic effects on decreasing training might relate to MC's 'holiday' growth?
Muscle Fibers
There are three primary muscle fiber types in humans -- Type I, Type IIA, and Type IIB. Type I are referred to as "slow twitch oxidative", Type IIA are "fast twitch oxidative" and Type IIB are "fast twitch glycolytic" (1). And as their names suggest, each type has very different functional characteristics. Type one fibers are characterized by low force/power/speed production and high endurance, Type IIB by high force/power/speed production and low endurance, while Type IIA fall in between (2, 3, 4). The advantages of a certain fiber composition on performance in various sports is both obvious and well established -- for example, marathon runners have 75% slow twitch fibers, while sprinters and weightlifters have 75% fast twitch (5, 6).
These characteristics are a result, primarily, of the fiber's Myosin Heavy Chain (MHC) composition, with MHC isoforms I, IIa and IIx corresponding with muscle fiber types I, IIA, and IIB, respectively (7) -- A small % of hybrid fibers co-expressing two isoforms also exist (8). Myosin Light Chains have been found to exert an effect on some of these properties, but they are minor, and not as well characterized or understood (9), thus we will be dealing with only the MHC.
MHC
MHC IIx possess a shortening velocity 5-10 times that of MHC I and are also faster than MHC IIa (10, 11, 12). Power production, particularly at high velocities, is higher with IIx than either IIa or I as well (11, 13). Force (strength) production has generally been shown to be greater in MHC IIx than IIa (14, 15), though one study found the opposit (16). Both MHC II types have been consistently shown to be superior to MHC I in all three areas (10-16). So, clearly, it is favorable for speed and strength athletes to posses a high % of MHC II, particularly IIx.
The Theory
MHC composition, and thus athletic potential, is thought to be determined to a great extent by genetics. However, various forms of mechanical and electrical stimulus (or lack thereof) have been shown to alter their expression, and it is this potential for manipulation that is the centerpiece of the system I am proposing. I will start with the two most interesting studies:
In the first study, subjects were put on a 3 month resistance training program, which was then followed by 3 months of detraining. Analysis of of the MHC composition of the vastus lateralis was done before training, after training, and following the detraining period (17).
Training resulted in a decrease in MHC IIx from 10% to 4% and an increase in MHC I from 49% to 51% -- the opposite of what we want as a speed/strength athlete. This fast to slow conversion has been well characterized in the literature -- both with bodybuilding type routines such as this, but also with routines typical of those used by power athletes. We will go into considerably more detail on this in a bit.
What is not as well characterized (and what is exciting) is what happened following the detraining period. At the end of the three months, MHC IIx had risen from 4% to 19%, while MHC I had dropped from 51% to 45%. Remember, MHC IIx started out at only 10% before training. This means a significant overshoot in MHC IIx occurred with detraining. Obviously, this is a speed/strength athletes dream.
In the second study (18), fifteen women were divided into two groups -- the first group (T) had undergone a 20 week resistance training program followed by 32 weeks of detraining prior to the study. The second group (U) was totally untrained. Both groups were subsequently put on a 6 week training program. Fiber type % measurements for T were taken before and after the 20 weeks of training, after the the 32 weeks of detraining, and again after the 6 week training period. For U, measurements were taken before and after the 6 week training program.
The initial 20 week program for T caused a reduction in IIB from 16% to 1%. The detraining period caused an increase from 1% to 24% -- another instance of overshoot. And considering the length of the detraining period, it is possible that a greater overshoot occurred but that levels were returning to baseline by week 32 (17).
However, this is not the most interesting part, as we will see. Following the subsequent 6 week program, the IIB % of U dropped from 24.9% to 6.7%, but T only dropped from 24.2 to 12.9%. There reduction was far less than that of the untrained group. The differences in type I are just as dramatic. T showed no increase in type I while U increased from 37.5% to 50.5%. In addition to the slow to fast overshoots we have seen, this suggests that the on/off cycling might be causing a resistance to fast to slow transformations. Hopefully, at this point, you have put two and two together and are wondering what might happen if we put together multiple on/off cycles.
I should note that these studies did use untrained subjects and the training protocol was not typical of that used by power athletes, thus if this were the only these studies, they could perhaps be written off. However, a number of other studies argue for the possibility of this being much more than an isolated occurrence, as we will see.
We will first take a look at several studies showing fast to slow conversions which will help us to determine possible mechanisms, not only to allow us to develop training strategies to minimize them, but also to give us some insight as to how the slow to fast changes might be made to occur, so as to facilitate and optimize them.
Fast to Slow
Studies in both man and animal have consistently shown a fast to slow (FTS) MHC response to resistance training, with not only endurance and bodybuilding type routines, but even with with routines typical of speed/strength athletes. We will not concern ourselves with endurance studies, except to say that it causes a rapid slowing of the phenotype (IIx to IIa and IIa to I) without concomitant increases in strength, thus it should be entirely avoided by those wishing to maximize speed, strength, and power (5, 19, 20).
I will not do an exhaustive presentation of the fast to slow literature, as many of the studies use identical design with identical results -- I will focus instead on presenting the different protocols that have produced fast to slow adaptations.
Hortabagyi et al showed a 12% reduction in MHC IIx and 13% increase in MHC I after 12 weeks using high volume maximal effort isokinetic contractions, with eccentric only, concentric only, as well as with mixed training (21).
In another study, using a twice a week heavy (6-8RM), light (10-12RM) split, MHC IIx was reduced from 18% to 7.1% and 18.9% to 6.1% in just 7 weeks in both men and women (22a). Interestingly, between the 7th and 9th week, it leveled off in both groups and the % actually increased slightly in the women. A similar reversal of the STF occurred from week 7 to 9 in another study, using the same training protocol, but which looked at fiber type % (22b).
Twelve weeks of a typical bodybuilding routine caused a 25% MHC IIx reduction along with a slight MHC I increase (23).
It is probably not a big surprise to many that the above training methods caused FTS. However, a study using sprinters (24), employing their normal sprint preparation programs might be. Subjects were tested, following a three week training break, for MHC content, and sprinting speed. This was followed by a three month training period. Type IIx was found to have decreased by about 50%. And this is with a pre-contest sprint preparation protocol.
But, before you decide to just quit training altogether, it should be noted that sprint times still improved slightly (we mustn't forget about the neural and cross sectional area components of speed/strength/power), and type I decreased by 25%. Anderson et. al. and Esbjornsson et. al. have found a similar bi-directional shift (IIX to IIa and I to IIa) with sprint training (24, 25).
Another study, employing multiple 3 second cycle sprints did not observe this, but rather showed the decrease in MHC IIx and increase in MHC I observed in all of the other studies (26).
Slow to Fast
Slow to Fast transitions in the literature are also abundant, however not that many human studies deal with any sort of resistance training setting, thus we will have to dip a bit into other areas such as immobilization, reduced electrical activity, and reduced gravity, as well as animal studies.
Detraining
Obviously, the studies most applicable to our purposes are those using detraining. We have previously mentioned 2 studies showing STF with extended detraining. Several detraining studies of shorter duration (2-4 weeks) have shown no STF transformation (27, 28). However, an analysis of MHC at the protein level have shown increases in MHC mRNA -- which is indicative of the early stages of IIa to IIb and I to IIa conversions -- in short term studies (21, 29). This makes sense given an MHC turnover time of 3-4 weeks (30). Thus, there is clearly evidence supporting STF given a detraining period of adequate length.
Immobilization
There is a lack of data on the effect of immobilization in humans, however, animal studies show STF transformations in as little as 2-7 days (31, 32).
Reduced Loading
Reduced loading situations such as space flight and its ground based counterpart, hindlimb unloading, result in rapid STF transitions. As little as 4 days of spaceflight in rats and 11 days in humans caused significant increases in MHC IIx and decreases in MHC I (33, 34). In another study, 17 days resulted in a doubling of the proportion of fast twitch fibers in the human soleus (35). While hindlimb unloading consistently shows STF is rats, it has been more mixed in humans (36).
Neural Inactivity
Reduced neural activity, such as that which occurs in spinal cord injury or transection, rapidly and reliably show STF transformation in both slow-twitch and fast twitch muscles, beginning as early as five days and showing profound changes within 3 months (37, 38, 39, 40).
Obviously, some of the above situations are not exactly 100% analogous to the type of detraining that is practical to a power athlete. However, what they do show, is that given the proper stimulus (or lack thereof), MHC content displays a great deal of plasticity, and in a short enough time to be practical for implementation into a power athlete's off-season program.
Mechanisms
Fast to Slow
The exact mechanisms behind the transformations observed is not conclusively known at this time. The most popular theory is that MHC IIx gene represents a default gene, which is switched under conditions of increased contractile activity (41, 42, 24). However, several studies have shown increased MHC IIx expression with certain types of training programs, most notably short duration sprinting (43), as well as with certain metabolic and hormonal conditions, including hyperthyroidism, hyperinsulinemia, leptin administration, and beta 2 adrenergic stimulation (44, 45, 46, 47). Thus, I think this view is flawed.
A more likely explanation is that the phenotype is adapted to its to meet the demands of its environment. Let's look at this from an evolutionary point of view -- in other words, what are the advantages of FTS vs. STF for the survival of the organism.
With resistance training, particularly employing strength training protocols, one would at first view the FTS as paradoxical in the face of mechanical overload. After all, that aspect, all else being equal, represents a weakening of the phenotype. However, on closer inspection, we find that it offers certain advantages, while still allowing the organism to adapt to the stimuli presented.
First, a FTS conversion would make the organism metabolically more efficient (48, 49), which is an obvious advantage in the times of scarcity in which we evolved. And, given that under non-training conditions, motor units associated with MHC IIx isoforms are only active 30-180 seconds per day, most current training programs are going to represent a significant increase in activity (50).
Second, the training stimulus with current protocols does not present a true maximal overload, particularly in regards to the eccentric component. This, along with the fact that some studies show MHC IIa fibers to produce equal or superior force at low velocities compared with MHC IIx (16), mean that a concentric/eccentric rep under typical strength training conditions (loads only as high as the concentric 1 RM and low velocities) could be adequately handled by a phenotype with a preferential IIa expression.
This makes it tempting to suggest loads equal to or greater than the ECCENTRIC 1 RM, however, speed of cross-bridging is less fiber type dependent (50b), thus it might overactivate and thus hypertrophy type I and IIa fibers. Therefore, we will leave this as an area for exploration at this point. The other method would be to employ only a concentric contraction at very high velocities (or perhaps at loads equal to the 1 RM).
Slow to Fast
The specific mechanisms responsible for STF at the micro level are not fully known. A couple of theories exist -- one involving the myogenic regulatory factor pathway and the other calcineurin:NF-AT pathway (36). However, these are very much speculative at present and are well beyond the scope of this today's article, thus we will not go into further detail, today.
At the macro level, we can once again turn to the advantage STF might produce for the organism. With the hormonal conditions mentioned above, it is fairly obvious. Beta 2 receptors are activated by epinephrine and norepinephrine, the so called "fight or flight" hormones. Clearly, a STF transformation of the phenotype would be advantageous for an organism that has to run away from a predator (or chase down its prey). This is likely what accounts for STF transformations that have occurred with short duration sprint training as well (51, 52).
As for hyperthyroidism, hyperinsulinemia, and leptin administration, what these all have in common is they are characteristic of the organism being in the "fed" state. Thus, the need for metabolic efficiency is done away with for the time being, leaving the organism free to assume a phenotype most conducive to the afore mentioned fight or flight situations.
With reduced mechanical loading and neural activity, the mechanism is likely the opposite of that which produces the FTS during training. In the face of reduced activity, thus reduced energy expenditure and need for muscular endurance, the afore mentioned metabolic efficiency would no longer be necessary for survival, thus the organism is free to once again assume the faster phenotype, which is clearly advantageous, all else being equal.
With detraining, it is likely that, from the body's vantage point, the abrupt withdrawal of stimulus following increased muscle activity with training is analogous to the near complete cessation of activity with immobilization/neural inactivation following normal activity (17). In other words, it "tricks" the body into thinking it can safely assume the metabolic inefficiencies that accompany the faster phenotype.
Muscle and Strength Losses
At this point, perhaps you are convinced of the possibility of slow to fast transformations but are concerned about the negative effects of the detraining period on muscle mass and strength. After all, spinal cord transection can accomplish STF, but it is not going to make anyone a great athlete. Fortunately, this is not a great concern. As I will show, both parameters rapidly return to normal levels (and above) when training is resumed.
The previously mentioned study by Staron et. al. (18) showed complete strength and power recovery after just 6 weeks of retraining following 20 weeks of detraining. Hortabagyi (21) and MacDougall (53) showed gains to beyond starting levels despite complete immobilization for extended periods. These are not surprising in light of data showing that majority of neural adaptation induced strength gains take place in the first 3-5 weeks of training (54). In addition, a couple studies have found that fiber areas of subjects trained for only a couple of months were equal to those of subjects trained for several years (54, 55). This has ramification that go far beyond what is presented today, but that is the subject of another article.
References
1. Bee G, Solomon MB, Czerwinski SM, Long C, Pursel VG Correlation between histochemically assessed fiber type distribution and isomyosin and myosin heavy chain content in porcine skeletal muscles. J Anim Sci 1999 Aug;77(8):2104-11
2. Bottinelli R, Reggiani C Human skeletal muscle fibres: molecular and functional diversity Prog Biophys Mol Biol 2000;73(2-4):195-262
3. Thorstensson A, Grimby G, Karlsson J Force-velocity relations and fiber composition in human knee extensor muscles. J Appl Physiol 1976 Jan;40(1):12-6
4. Inbar O, Kaiser P, Tesch P Relationships between leg muscle fiber type distribution and leg exercise performance. Int J Sports Med 1981 Aug;2(3):154-9
5. Tesch PA, Wright JE, Vogel JA, Daniels WL, Sharp DS, Sjodin B The influence of muscle metabolic characteristics on physical performance. Eur J Appl Physiol Occup Physiol 1985;54(3):237-43
6. Gollnick PD, Armstrong RB, Saubert CW, Piehl K, Saltin B J Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. Appl Physiol 1972 Sep;33(3):312-9
goldblum said:
RemainAllHoof said:
mattikake said:
Before you can choose a training regime, it's handy to know what kind of muscular composition you have, otherwise wrong training for the wrong composition will yield poor results.
How can you find out? Just doing various exercises until one proves to grow stuff more?And short of a disection, you can only find out what you by your response to training. As it happens, I have developed a 6 month training scheme were anyone could work out their rough SO-FOG-FG proportions...
goldblum said:
Not to worry though as it is possible to force change from one to the other with serious training,("Muscle, Genes and Athletic Performance" Scientific American) should you want.
Interesting. I read SciAm quite a lot so must've missed that article and I'd have been well interested in that. By the accepted medical book (as opposed to SciAm's slight more sensationalist journalism!), the number slow (SO - Slow Oxidative) and fast (FG - Fast Glycotic) twitch fibres you have from birth cannot change - they are same as when you die regardless of training. FYI - seems worth pointing out that you never grow new muscle fibres, only increase the number of myosin (mostly affecting power and strength), size of the sarcoplasmic reticulum (mostly affecting hypertrophy), strength of the z-disc (mostly can affect all muscular effects!).
Only FOGs (Fast Oxidative Glycotic/Type 2b - the clue is in the name, can use Oxygen or Glycogen) have the ability to absorb SO or FG features, but due to this adaptive nature, of course will never be as efficient as a full SO or FG fibre.
FG and SO fibres will adapt to the wrong exercise - E.g. strength training a SO fibre will improve that fibre (because your body adapts to everything), but the results will be nothing compared to endurance training that fibre.
/selfplug Then you need to consider Somatotypes, form, routine, diet, and the training gets complex enough to need a Personal Trainer to work it all out for you.
/selfplug(NB: not lost interest in wiki article that spells "Fibre" incorrectly from the very start.
I guess the gist of the article is the result of a study that "the book" would describe as a bit maverick... But that's half the fun of science.)Edited by mattikake on Friday 29th July 14:29
It might have got the spelling of fiber (sic) incorrect but it doesn't mean it's necessarily worthless, or not based on any serious research, though the claims for such extreme benefits of de-loading do seem a bit far fetched.
I didn't get it from Wiki btw.
I do not need to read up on/study this stuff for professional reasons as you do but have read plenty, including published papers/journals (not just M&F) out of interest for many years + have the experience of different regimes on my own body. From all that, I would agree that the proportion of muscle fibre types remains fixed, that they serve different purposes/suit different athletic endeavours/respond to different forms of training differently etc.
For most of us training a particular way will suit one type better than another so it could be argued that we are neglecting overall development if we focus on just one style, or maybe that we should focus on the fibres we most need to benefit for our goals - endurance, fast-reaction/power development or cosmetic size gains?
From the stuff read, I have also spotted repeat references to the fact that the typical bodybuilding approach of medium/high reps - say, 10 to 15 a set, and medium to high set counts increases muscle size to a significant degree by increase in the volume taken by the muscle sarcoplasm you refer to, but that this has no benefit to strength/athletic performance. In other words that very large muscles so gained will not just be through fibre volume growth but through stuff (basically fluid) that has little apparent 'benefit' other than size.
Maybe this is why so many serious bodybuilding aficionados mention, often with surprise, that there are smaller guys who can lift more - seen it myself; wiry and/or densely muscled types who focus on lower rep/strength training approaches who are seriously strong and/or explosive
Why not outline your 'test your type' in 6 months clinic stuff for us, might be helpful...
I didn't get it from Wiki btw.
I do not need to read up on/study this stuff for professional reasons as you do but have read plenty, including published papers/journals (not just M&F) out of interest for many years + have the experience of different regimes on my own body. From all that, I would agree that the proportion of muscle fibre types remains fixed, that they serve different purposes/suit different athletic endeavours/respond to different forms of training differently etc.
For most of us training a particular way will suit one type better than another so it could be argued that we are neglecting overall development if we focus on just one style, or maybe that we should focus on the fibres we most need to benefit for our goals - endurance, fast-reaction/power development or cosmetic size gains?
From the stuff read, I have also spotted repeat references to the fact that the typical bodybuilding approach of medium/high reps - say, 10 to 15 a set, and medium to high set counts increases muscle size to a significant degree by increase in the volume taken by the muscle sarcoplasm you refer to, but that this has no benefit to strength/athletic performance. In other words that very large muscles so gained will not just be through fibre volume growth but through stuff (basically fluid) that has little apparent 'benefit' other than size.
Maybe this is why so many serious bodybuilding aficionados mention, often with surprise, that there are smaller guys who can lift more - seen it myself; wiry and/or densely muscled types who focus on lower rep/strength training approaches who are seriously strong and/or explosive
Why not outline your 'test your type' in 6 months clinic stuff for us, might be helpful...
Calculate % muscle fibre type:
Squat,Bench Press or Deadlift.
Armed with your 1 RM, use 80% of that weight for you next set. Perform and count the maximum number of repetitions you could perform with 80% of your 1 RM weight. How many did you do?
less than 7 repetitions = Fast twitch (FT) fibers
The muscle group is more likely to be 50% or more FT fibers.
greater than 12 repetitions = Slow twitch (ST) fibers
The muscle group is more likely to be 50% or more ST fibers.
This is available online from a number of sources.The only way (I'm aware of) to get a more accurate estimate is through medical tests or an (obviously invasive) biopsy.
Squat,Bench Press or Deadlift.
Armed with your 1 RM, use 80% of that weight for you next set. Perform and count the maximum number of repetitions you could perform with 80% of your 1 RM weight. How many did you do?
less than 7 repetitions = Fast twitch (FT) fibers
The muscle group is more likely to be 50% or more FT fibers.
greater than 12 repetitions = Slow twitch (ST) fibers
The muscle group is more likely to be 50% or more ST fibers.
This is available online from a number of sources.The only way (I'm aware of) to get a more accurate estimate is through medical tests or an (obviously invasive) biopsy.
^^^
This confirms my assumption that I am mainly - but not overly so? - a fast twitch type. Also, was always better relatively (still crap!) at sprinting rather then long distance running, whatever my weight. I used to run between 6 to 8 miles a night as part of the boxing training but Jesus, was I slow over those distances!
Gaining endurance on things like the high rep 'free squats' I do has come but needs to be worked for so hard compared with what I had put in to gain strength.
This confirms my assumption that I am mainly - but not overly so? - a fast twitch type. Also, was always better relatively (still crap!) at sprinting rather then long distance running, whatever my weight. I used to run between 6 to 8 miles a night as part of the boxing training but Jesus, was I slow over those distances!
Gaining endurance on things like the high rep 'free squats' I do has come but needs to be worked for so hard compared with what I had put in to gain strength.
RemainAllHoof said:
Thanks. Does that work for other muscles? I don't have the kit to do 1 RM safely.
Don't see why not.Try to keep the exercise compound if possible,but if you're performing isolation keep it strict for efficacy/accuracy of result.(ie bicep curlstand with back only an inch away from wall.)
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