How do muscle cells multiply
|Muscle fibers differ in their speed of contraction. For this, the chemical composition of the myosin molecule is decisive, specifically its largest subcomponent, the so-called heavy chain. It occurs in three different forms in adults: the isoforms I, IIa and IIx (also called IId). This subdivision then also applies to theCorresponding muscle fibers: If they contain one of the two types of type II, one speaks of fast fibers, whereas type I is called slow. This classification is entirely justified when you consider that the sluggish fiber type shortens about ten times more slowly than the fastest of the fast ones, namely Type IIx. The speed of Type IIa fibers is in between. In addition to the three pure fiber types, there are also mixed fibers, each with two different myosin isoforms. Their functional properties are generally based on the dominant type of myosin.|
The contraction speed of the muscle fibers is influenced by the different speed at which the heavy myosin chain worksAdenosine triphosphate (ATP) is split and thus consumed. This substance is the universal energy supplier of all cells. Since type I fibers break down their ATP more slowly and primarily regain it via an oxygen-consuming metabolic pathway, they are particularly suitable for endurance sports such as long-distance running, cycling or swimming. Fast fibers, on the other hand, with their high consumption, tire more quickly, but can briefly mobilize more reserves via an oxygen-free - anaerobic - metabolic pathway. They therefore play a key role in short-term activities such as weightlifting or sprinting.
The average healthy adult has about as many slow fibers as fast, for example in the anterior thigh muscle, the four-headed thigh extensor. However, there are also great individual differences in the structure of muscles of the same type. In the thigh muscle, for example, we found a range from only 19 percent slow fibers to a remarkable 95 percent - ideal for the marathon, but bad for the hundred meter run.
Muscle fibers, i.e. muscle cells, are unable to multiply through cell division. If they are lost through illness or old age, no new ones can arise (see appendix). A muscle can only gain mass if its existing fibers thicken. And that happens mainly through the production of additional myofibrils. This production is stimulated by physical exertion, for example through training. It puts mechanical stress on tendons and other structures connected to the muscle. In the end, different genes are activated via a cascade of signal proteins, which in turn induce the increased formation of contractile proteins. These are mostly myosin and actin for building new myofibrils.
However, a vehemently increased protein synthesis requires more cell nuclei in muscle fibers - also in order to maintain a certain ratio between the then rapidly growing cell volume and the number of nuclei. However, since neither these nuclei nor the muscle fibers can divide themselves, the organism falls back on divisible satellite cells. These lie on the outside of the muscle fibers or may migrate to them in the form of other stem cells. If necessary, they can merge with their larger neighbors and thus support their growth in thickness through "core donation".
Remarkably, this source of new cell nuclei always gushes particularly strongly when hard muscle training has strained the fibers. According to a common theory, tiny cracks, so-called micro-lesions, occur in the process, which act like a magnet on the spider-shaped satellite cells. These migrate to the injured region and there begin to produce protein material for repair. They also share. Some of them merge with the fibers, others remain outside as satellites. The donated cell nuclei, which incidentally cannot be distinguished from the ones already contained, create the conditions for the large-scale production of further proteins and thus of additional myofibrils in the fiber.
For production, the muscle cell, just like any other cell, falls back on the building instructions of the relevant genes in the cell nucleus. From there a copy goes to the protein factories in the cell plasma. Experts refer to the steps from gene to protein as expression.
The stuff muscles are made of
The scientific interest in skeletal muscles focuses on two questions that are particularly interesting for athletes: How can muscles be built up through training and other stimuli, and how can one type of fiber be converted into another?
The prehistory goes back to the sixties. At that time, several scientists, among them the 1963 Nobel Prize for Medicine, John C. Eccles of the Australian National University in Canberra, showed that slow and fast types of fibers can be converted into one another in animal skeletal muscles. The researchers mainly used what is known as cross innervation. They swapped the nerves between an overall slow and an overall fast muscle. Amazingly, their contraction properties were reversed. The researchers also stimulated a muscle electrically over a longer period of time in order to activate it. Or they cut his nerve to do the opposite.
In the seventies and eighties, the focus shifted to human muscles and there, above all, to the question of the extent to which our muscle fibers can also change their size and properties. This ability, commonly known as plasticity, manifests itself in the extreme after paraplegia. The muscles in question then rapidly dwindle because the lack of nerve impulses make them inactive. The muscle type also changes somewhat unexpectedly; in such a way that the proportion of the slow myosin variant is significantly reduced in favor of the faster.
As we have shown, among other things, after five to ten years of paralysis a certain "sub-muscle" of the four-part thigh extensor - the outer thigh muscle - often contains almost no slow myosin, while on average half of its cells are of the slow type. From this we concluded that incoming electrical impulses are required so that muscle cells can always reproduce their slow myosin. In fact, for example, artificial electrical stimulation of the paralyzed muscles can slightly increase the proportion of slow myosin again.
Fiber types also change in healthy muscles. For example, repeated heavy weight training - such as working with weights - changes the number of fast IIx fibers: They convert into medium-fast IIa fibers. Instead of the IIx gene, the IIa gene is then read in their cell nuclei. If someone does this kind of strength training for at least four weeks, then even all fast fibers will convert to medium-fast fibers. At the same time, they produce more proteins, so that the individual muscle cells become thicker.
In the early 1990s, Geoffrey Goidspink of the Royal Free Hospital in London suggested that the expression of the IIx gene be regarded as a kind of basic setting. The results of various studies supported his hypothesis: On the one hand, people who sit a lot have a higher content of myosin IIx in their muscles than people who are active in sports; on the other hand, the concentration of myosin IIa increases with muscle activity.
But what happens after the end of a training period? Do the muscle cells then gradually switch back to their basic IIx setting? The answer is basically yes, but in a detour, as our study with nine young inactive Danes showed.
To begin with, we took an initial tissue sample from the outer part of the thigh extensor. The proportion of fast myosin Ilx averaged nine percent. The second collection took place after three months of strength training to strengthen the thigh extensor, a third then three months after the end of training, from which the test subjects had resumed their old way of life. As expected, the percentage of the fast IIx isoform decreased in the muscle during strength training, from an average of nine to about two percent. To our surprise, however, after three months of inactivity, it not only rose again to the starting value, but far beyond it: to an average of 18 percent (see diagram on this page above). We did not take any more samples afterwards; but we assume that the myosin-IIx content will eventually return to its "resting value" of around nine percent after a few more months.
From slow to fast fibers?
We are still lacking a conclusive explanation for this excessive reaction. However, some practical conclusions can be drawn from the experiment. For example, sprinters who want to massively increase the proportion of their fastest muscle fibers would be well advised to reduce the existing proportion first through training and then wait for the doubling during a fading phase. In fact, many sprinters simply reduce their training program before a competition based on experience, without knowing the physiological background.
The mutual conversion of the two fast muscle fiber types IIa and IIx therefore takes place depending on the physical activity. But is it also possible to convert from slow to fast fibers - from type I to type II - and vice versa? Numerous earlier experiments on this on human muscles had negative results. It was only at the beginning of the 1990s that we discovered the first indications that hard training can also convert slow fibers of type IIa into medium-fast fibers. Our subjects during a three month study were elite sprinters. They did their normal exercise program.
Around the same time, Mona Esbörnsson and her colleagues from the Karolinska Institute in Stockholm presented similar results from a study with twelve participants who were not high-performance athletes. This suggests that intensive weight training, supplemented by other anaerobic exercises, such as the training of elite sprinters, not only converts fast fibers into medium-fast ones, but also from slow fibers to medium-fast ones.
But is the reverse also feasible for humans? So can medium-fast fibers be transformed into slow fibers through special exercises? This question has not yet been clearly answered by any investigation. But that does not rule out the possibility of such a conversion. As mentioned, top athletes in endurance sports generally have a remarkably high proportion of slow fibers in their main muscle packages - up to 95 percent. However, it is still unclear whether these people were born with numerous type I fibers and accordingly felt drawn to endurance sports or whether they gradually worked through the high proportion. We only know that converting medium-fast to slow fibers, if possible, takes significantly longer than converting fast to medium-fast fibers.
Perhaps gifted marathon runners or sprinters really have an extraordinary muscle composition from birth: Then future long distance runners would of course be characterized by a relatively high type I fiber density and future sprinters by a low one. But if you still feel drawn to the short haul, you shouldn't give up. Scientists have found that with appropriate strength training, the type II fibers thicken twice as much as the others. Therefore, weight training significantly increases the area that Type II fibers take up on the cross-section of a muscle without changing the ratio of fast to slow fibers. However, it is precisely the area ratio between the two that is decisive for the functional properties of the muscle: the larger the cross-sectional area covered by fast fibers, the faster the entire muscle is. Thus, at least every sprinter has the opportunity to optimize the properties of his muscles through strength training in this regard ...
All in all, the conversion of IIa to I-fibers is difficult to achieve through training, but in the not too distant future this could become possible through genetic engineering. ... "
Spectrum of Science 3/2001
Movement theory | Training theory | Sports sociology / psychology
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