Las fibras rojas pueden transformarse en fibras blancas por causa de la testosterona...
por supuesto produce un gran detrimento en la carga
Existe una relacion directa entre cargas altisimas con el aumento de la fuerza?
De una ves pongo el sst:
13. Does HST work for strength, SST, strength-Specific-Training
It takes quite a bit of time and effort to piece all the strength research together to form a big comprehensive picture with which to base an SST method. HST was not born overnight, neither would SST. Fortunately, there is a lot more applied strength research out there than there is hypertrophy research. The reason for this is that strength research is used to help countries fair better in international competition. This has been extremely important to most of the world for many decades...especially the Eastern block countries of the 70s and 80s. It is important to distinguish whether strength was the goal of the research or hypertrophy. Contrary to popular belief, they are not synonymous.
Remember, when training for strength, you are training the entire neuromuscular system. This requires special attention to not only the muscle tissue itself, but also to the nervous system and the emotional state of the lifter. These variables require certain training principles to achieve the most predictable increases in strength. But when training for muscular hypertrophy, your focus should only be in the muscle itself. Work it until it is “done”. Like kneading dough. You knead it until it is done. Getting a muscle to grow is a mechanical phenomenon. You will also find that your pumps are as good as ever (if your not dieting) when you work a muscle until it is done, no more, no less.
The whole point of HST (which others have already summarized aptly) is to:
1) Increase the frequency of loading each muscle to 3 times per week.
2) Continually increase the load. Zigzagging is fine as long as the general trend over time is upwards. If you don’t, the condition (which is to say, the resistance of the tissue to the mechanical strain of a given weight load) of the muscle will catch up with you and your growth will plateau. Growth with a given load will probably only produce gains for about 4-6 weeks. The lighter the load, the shorter the amount of time it will be able to induce muscle growth.
3) Use Strategic Deconditioning to enable a given load to once again induce muscle hypertrophy. This occurs once the tissue has been resensitized (i.e. made susceptible) to the mechanical strain of load bearing.
These are the principles (or characteristics) that distinguish a hypertrophy-specific program from a strength-specific program. Is it complicated? No. Need it be? No. Is there evidence to support the idea that these principles really do change the effect of a training program from inducing strength to inducing hypertrophy? Of course, otherwise I would never have brought it up.
In order to come up with a method that is "strength-specific" we first have to have an understanding of those factors involved in the production of voluntary strength. Here is a "brief" review of those factors that you must figure out how to manipulate if you are going to develop a strength-specific training method. (I took this from an article I wrote a few years ago so the references are not included. In a future article I will include those and newer references).
As an untrained individual begins a strength training program for the first time they will experience quite dramatic increases in muscular strength. These improvements in strength will continue almost linearly for about 8-12 weeks. The dominating mechanism of these initial strength gains are neurological in nature (Morianti,1979; Sale,1988). These adaptations take place with or without increases in muscle cross sectional area (CSA).
Some ways that a muscle may undergo neural adaptation include cross-education, increases in electromyographic (EMG) activity, reflex potentiation, alterations in the co-contraction of antagonist muscles, and improved coordination of synergist muscles.
The foundation for the development of strength is neuromuscular in nature. Increases in strength from resistance exercise has been attributed to several neural adaptations including altered recruitment patterns, rate coding, motor unit synchronization, reflex potentiation, prime mover antagonist activity, and prime mover agonist activity. Aside from incremental changes in the number of contractile filaments, voluntary force production is largely a matter of "activating" motor units. In order to ascertain the relative contribution of each of these mechanisms, various measurement techniques have been utilized. Hereafter we will briefly discuss each of these mechanisms as they relate to resistance training.
Recruitment of motor units can be measured with Electromyography (EMG). As a muscle contracts, the electrical signal initiated by the motor nerve can be detected with EMG. The intensity or magnitude of this signal is sometimes described as "neural drive". In order to explain increases in strength from resistance exercise, researchers have measured the changes in EMG activity in weight training subjects.
Hakkinen and co-workers have shown that there is an increase in EMG activity with strength training as well as a decrease in EMG activity upon cessation of training (Hakkinen,1983). Fourteen male subjects (20-30 yr) accustomed to weight training went through progressive strength training of combined concentric and eccentric contractions three times per week for 16 wk. The active training period was followed by an eight week detraining period. The training program consisted mainly of dynamic exercises for leg extensors with the loads of 80-120% of one maximum concentric repetition (1RM). Significant improvements in muscle function were observed in early conditioning; however, the increase in maximal force during the very late training period was greatly limited. Marked improvements in muscle strength were accompanied by significant increases in the neural activation (EMG) of the leg extensor muscles. The relationship between EMG and high absolute forces changed during the training period. The occurrence of these changes varied during the course of training. During detraining, there was a decline in EMG activity.
Now those who would argue that increases in strength are solely due to increased recruitment of motor units would have a difficult time defending themselves in light of other research. There is a method of measuring motor unit activity called "Interpolated Twitch Technique", or ITT. ITT is used to determine the extent of activation of the entire muscle. Merton (Merton, 1954) was the first to use this technique to describe whole muscle activation. He showed full activation of the adductor pollicis with fatigue in untrained subjects. Several other studies have since shown a similar ability of untrained subjects to voluntarily fully activate various muscle groups (Bellemare 1983, Chapman 1985, Gandevia 1988, Belanger 1981). This directly contradicts the theory of strength increases due to the ability to activate more motor units.
The activation of motor units is done in an asynchronous fashion, meaning that not all fibers contract at the same time within a given muscle. There is a hierarchy to the order of fiber recruitment in muscle tissue. Because fiber activation is not "analog" or variable in nature, in other words, a fiber is either fully activated or fully quiescent, the brain must control contraction intensity by altering the number of fibers it activates. In general, slow twitch fibers are activated first followed by larger fast twitch fibers. Now when muscles begin to fatigue the asynchronous firing of fibers become more and more synchronized (Butchal, 1950). This allows for greater force production. This synchronization of muscle fibers has been linked to increases in voluntary strength (Milner-Brown, 1975).
Now although increases in motor unit synchronization have been reported with training, studies involving artificial stimulation show that force development with asynchronous stimulation is greater and smoother (Clamann, 1988). In addition, researchers have shown that the rate of force development in brief maximal contractions is faster in voluntary than in evoked contractions (Miller, 1981). So from these studies we see that although synchronization of motor units can increase with training, asynchronous motor unit activation is more advantageous to rate and magnitude of force development than is synchronous activation.
Increases in "reflex potentiation" have also been linked to resistance training (Sale & Upton 1983, Sale & MacDougall 1983) as well as decreases with immobilization (Sale, 1982). The actual benefit, if any, of this adaptation is unclear. An increase in reflex potentiation would contribute to the voluntary EMG signal augmenting the motor or neuronal drive. Nevertheless, because untrained individuals have been shown to be able to fully recruit their motor units, the purpose of increased reflex potential remains undecided.
Finally, that activity of prime mover agonists and antagonists plays a role in directed voluntary strength. The obvious role of agonists is to assist the prime mover by guidance and stabilization. This could be termed "coordination". It is well known that any unaccustomed exercise requires practice in order to develop sufficient coordination to allow maximum efficiency of muscular effort. The role of antagonistic muscle groups is more complicated. They serve to prevent damage through co-contraction as well as ensure less resistance through relaxation to prime mover contractility.
The protective mechanisms function by way of golgi tendon organs (GTO). The GTO is sensitive to force output or tension within the muscle. They are located at the musculo-tendonous junction and are contained within a compressible collagenous capsule. Fibers of the GTO are connected directly to muscle fibers as well as to Type "Ib" inhibitory neurons within the muscle. The physical structure of the GTO allows it to be sensitive to stretch or load present in the muscle. Think of the notorious "Chinese finger trap". You first stick you fingers in each end. Then as you pull your fingers apart, the structure of the woven tube causes it shrink (or in the case of GTO it compresses) in diameter in order to stretch. The GTO works very much like this. When the collagen around the GTO is compressed because of contraction or stretch by the muscle, the Ib neurons generate an impulse that is proportional to the amount of GTO deformation. In this way the GTO can decrease contraction of a muscle being stretched in order to protect it from being torn. Likewise, GTO are thought to prevent unusually high contractions of a muscle in order to protect it from tearing itself apart. So in an antagonist muscle, the GTO can serve to inhibit co-contraction, facilitating contraction of the prime mover. In a prime mover, the GTO acts to prevent torn pecs, biceps and whatever else you are using to lift insanely heavy weights.
Another neuronal structure regulating involuntary muscle activity is the muscle spindle. The muscle spindle is found in greater abundance in the muscle belly as apposed to the musculotendonous junction. The muscle spindle also responds to stretch. However, the spindle is less like a Chinese finger trap and more like spring. When the muscle undergoes stretch, the center of the spindle is stretched. These spindles contain neurons that are sensitive to this stretching. Unlike with the GTO, when a muscle spindle is stretched its excitatory neurons fire in order to counteract the stretch.
When a stretch is imposed on a muscle, the Type-I sensory neuron sends impulses into the spinal cord and connects with interneurons, generating an excitatory local-graded potential that is sent back to the muscle being stretched. If the stretch is of sufficient magnitude and/or rate, a local graded impulse will be sent back to the same muscle with sufficient strength to initiate a contraction via alpha motoneurons. This reflex arc in known as the "stretch-reflex" and is characterized by a quick muscular contraction following a rapid stretch of the same muscle. Now this stretch reflex primarily functions in slow twitch muscle fibers.
Alterations in the sensitivity of these two regulatory mechanisms have been seen with training. Carolan (Carolan, 1992) showed a decrease in antagonist co-activation of the lex extensors with training. On the other hand, increases in co-activation have been seen in longitudinal studies comparing explosive trained athletes to non-explosive trained athletes (Osternig 1986, Barrata 1988). These somewhat contradictory results may reflect the possibility that co-activation alterations are very specific in nature and depend on things such as contraction velocity, range of motion, and training specific effects.
The nature of these changes is determined by the nature of the stimulus. If you regularly allow only very slow contractions of a given muscle (such as with Super Slow methods), that muscle will improve its ability to contract slowly, at times at the expense of its ability to contract rapidly and powerfully. If you train a muscle for endurance, it will improve the oxidative capacity and fatigue resistance of muscle fibers, and even begin to change the contractile properties of all fibers in favor of endurance-type activity. All this due to chronic, and specific neural activity patterns.
. Lo saque del enlace de abajo, no sabia que eran esas fibras y me parecia interesante ponerlo.