Training Effects on Muscle Tissue

[Joshua Naterman]

Source: http://www.wlinfo.com/training_effects_on_muscle_tissu.htm

Training Effects on Muscle Tissue (Excerpted from Appendix 2 - A Short Course in Anatomy, Physiology, Mechanics and Biomechanics)

Specific kinds of training can apparently cause a conversion among FT sub-types of fibers (e.g., Type IIB and Type IIA), but the available evidence does not suggest that Type I and II fibers are interconvertible. (Experimentally, the switching of motor neurons supplying fast and slow fibers has resulted in the gradual reversal of the speed with which the fibers contract.) It has been suggested that, on a practical level, the transformation from one muscle fiber type to another is impeded by a number of natural conditions. In the case of the transformation of slow twitch into fast twitch fibers, any transformation stimulated by training may be countered by the use of the trained muscles for postural reasons. (The low intensity and long- term kind of muscle action that is needed to maintain posture stimulates the slow-twitch qualities of the muscle, perhaps offsetting any stimulation for those muscles to transform into FT fibers.) The transformation of FT fiber types to ST is probably impeded by the fact that considerable effort is required in order to reach the threshold necessary to activate the FT muscles often enough to transfer them to a slower type.

Training appears to selectively hypertrophy muscle fiber types. Most of hypertrophy is due to increases in the diameter of fast glycolytic fibers. For example, one study of bodybuilders found that their Type II fibers were 58% larger than normal while their Type I fibers were only 38% larger. In weightlifters and powerlifters, hypertrophy is probably even more selective in favor of Type II hypertrophy (because of the emphasis of these athletes on low-repetition training). It should be noted that an increase in the diameter of the muscles fiber is caused primarily by increased synthesis of actin and myosin filaments, which leads to a greater opportunity for cross-bridge interaction and hence an increase in contractile strength.

Training with maximal and near-maximal weights may lead to the recruitment of the high-threshold neurons that are not normally within the realm of voluntary control (heavy training may also cause an increase motor unit firing rates). FT fibers (particularly type II B) are rarely recruited, but when they are, hypertrophy of them is relatively rapid. ST fibers appear to grow less easily. Partial splitting (hyperplasia) of muscle fibers (not myofibrils) is observed in surgically overloaded muscle but little evidence of such an occurrence in live human muscle exists. Nevertheless, hyperplasia through a lengthwise split of an enlarged muscle fiber may occur to some small extent with unusual levels of training stress.

Endurance training can increase the amount and size of mitochondria, the muscle's ATP-synthesizing capacity, as well as capillarization within muscle tissue. Resistance training generally has no effect on the ratio of capillaries to muscle fibers, but capillary density within a muscle falls as hypertrophying muscle fibers comprise a greater share of total muscle. Bodybuilders who employ high reps in their training may be an exception to this rule (for these athletes the capillary density may not change).

It takes time for the influences of training to cause a change in the composition of muscle fibers. The half life of contractile proteins has been estimated to be seven to fifteen days. This is the time it takes for half of the contractile proteins to be synthesized (with synthesis taking place in FT fibers faster than it does in ST fibers). Therefore, the training effects on muscle tissue cannot begin to take widespread effect for several weeks.

Muscle fibers can adapt to stresses placed on them by increasing in length as well a girth (the former by adding sacromeres in series to the same muscle fiber). For example, the immobilization of muscles in a shortened position will result in a decrease in the number of sacromeres along the fiber in series (immobilization in the lengthened position has the opposite effect). It appears that length has a greater effect than tension on the number of sacromeres.

I have emphasized a few key points. I thought this was interesting, and that some people here may enjoy the information! All spelling errors have been faithfully copied from the source page.

[Joshua Naterman]

With IGF use, one is able to cause this hyperplasia which actually increases the number of muscle cells present in the tissue. Weight training with or without anabolic steroid use enables these new cells to mature in size and strength. In addition, animal tests have shown that stretching a muscle can trigger hyperplasia, though this phenomenon has yet to be confirmed in humans. Hyperplasia may also be induced through specific power output training for athletic performance, thus increasing the number of muscle fibers instead of increasing the size of a single fiber.

This is from Wikipedia. I followed up by checking the sources at PubMed, and this is accurate. There is a large body of research papers that say hyperplasia, the formation of NEW MUSCLE FIBERS, can occur from progressive stretch overload(like fascial stretching, iso-extreme, weighted pike stretch, etc), high power output training (maximal sprints, depth jumps, rebounds, and plyometrics), and general exercise.

[JL]

Good find. I can't remember reading any information on the time it takes to synthesize muscle.