Theory and Practice of Physical Culture 1990 issue#5 p.11-14
Mechanisms of muscle fiber adaptations to physical stress and possibile methods of controlling that process.
B. A. Nikitiuk, N. G. Samoilov
Keywords: adaptation, hypertrophy, hyperplasia, muscle fiber, physical stress, muscle activity.
Expansion of human adaptation limits to natural and produced conditions, increased resistance and workload capability are dictated by the needs of modern society. That is why the task of searching for the optimal conditions for reaching these goals and methods of regulating these processes holds great, not only medicinally-biological but also, social value.
The axial premise in the teachings of adaptation is the ability of a random system and organism to wholly expand it’s biochemical(1), physiological(7) and morphological(13) parameters. Mechanisms of adaptogenesis are complex, but one thing is clear - it’s origins must be searched on a molecular level of the organization, in the cells’ genetic apparatus(3). In research materials of F.Z.
Meyerson(7) who established the connection between the volume of functional stress and the cell’s genetic apparatus(3) it was shown that increase of the function always leads to the activation of the genetic apparatus, increased speed of transcription, translation, protein biosynthesis and formation of certain structures. The same author had proposed the notion of Functional Structure Intensity(FSI) the basic tenet of which is that the volume of the function is always determined by a specific unit of mass of the working organ.
Derivatively the higher the function intensity the more physical structures must form to support it. However, such quantitative increases of functions, dependant on the growing number of structures, will not proceed indefinitely. In other words the process has certain limits. To prove the aforementioned limits of adaptation a methodology of our search was developed. It’s key is in the stereological analysis of structural reconstructions with varying intensities of the active factor(which was chosen to be physical stress - PS).
This was accomplished utilizing a complex of methods which allow us to trace the quantity of not only devastated but formed structures as well.
Materials and methods.
The experiment is set on 3-month old male rats of the Vistar line. PS was modeled with running on a tread ban with varying speed(from 20 to 60m/min) and duration(from 20 to 60 days).
After decapitation half-thin[?] cuts of skeletal muscle(??? and general finger extensor) colored with 1% methylene blue and 1% boric on water. Ultra thin slicing of muscle tissue were performed using the UMPT-3 ultratome[sic] and observed with the EVM-100 BR microscope. Stereological analysis was processed on standard positives with the method of L. M.
Nepomniaschih et al(9). A count of following muscle components was conducted: volumetric portion of myofibrils(MF), volumetric portion of mitochondria(MC) and their sum MF++MC.
Quantitative account of destructive changes conducted on gystological[sic?] muscle extracts colored with hematoxylin-eosin with the aid of an ocular micrometer with built-in net of 150 squares 20mkm2[square mkm] each. Quantitative results processed with the method of variation statistic(8).
Results and discussion.
According to wide-spread opinion the more intense the PS the greater increase of activation of the function moving apparatus(i.e. FSI). The latter also implies obligatory growth of the number of structures which supply the reinforced function. However, as it was revealed, this is far from being true. When comparing portions of myofibrils vs mitochondria there is a determined a strict dependence of their quantity to the intensity of PS.(see Table)
Data presented in the table testifies: the greater the intensity of PS, and it’s accumulation over time, the less structures responsible for muscle contractions are formed.
At the same time the number of muscle fibers being destroyed increases. Now if we take into account the myriad of data of national and foreign researchers(2, 23, 25 and others) showing that increasing intensity of physical stress results in hypertrophy of muscle fibers and an increase in their number through hyperplasia(4, 11, 21, 27) then it might seem that our facts are contradictory to the aforementioned.
But a more thorough analysis of what occurred allowed to determine that with increase of intensity of PS and the speed of it’s accumulation, hypertrophy of muscle fibers does indeed occur - their increased numbers and destruction(image 1.) with concurrent decrease of contractile structures in their sarcoplasm. All these positions are illustrated on the proposed schema(image 2). It must be noted that a volumetric unit of hypertrophied muscle fibers contain less foundational organelles of sarcoplasm: myofibrils and mitochondria.
Increased girth of these kinds of muscle fibers occurs mainly due to the volume of sarcoplasm. At the same time, with low intensity and speed of physical stress accumulation, a volumetric unit of muscle fiber contains more myofibrils and mitochondria. From this the first type of hyperplasia can be called sarcoplasmic and the other - myofibrillar-mitochondric.
It was later shown that the execution of an amount of work by hypertrophied muscle fibers requires a larger volume of tissue then regular muscle fibers.
Therefore, according to the results, hypertrophy of muscle fibers is a process of weak effectiveness for increasing work capability. However it does take place. From this a naturally occurring question arises: why does it occur and where does it end? In other words, what is the fate of hypertrophied muscle fibers?
Muscle fiber hypertrophy is, without a doubt, an adaptive process. Contractile activation of muscle fibers demands an increased inflow of energy which on this level of organization is ladled via splitting of macroergic substances synthesized by the mitochondria. The necessity of larger energy consumption leads to a reaction in the mitochondria which consists of their hemorrhaging and surface area growth of the inner membrane(18).
That is precisely the path of this situation that is consistently sensible, as significantly less energy and “building material” is spent than it would to form new small mitochondria. Under these conditions, following the laws of thermodynamics, the mitochondria, as a whole system spends a minimum amount of energy to preserve an already established condition, i.e. it’s wholeness.
With a high speed of accumulation of PS over time there is observed an intensification of this process: mitochondria increase in size(19, 20, 22). The increases in their size, and especially in the number of crystals, for a period of time activates the synthesis of ATP and provides the working muscle fibers with energy.
However, the size increase of mitochondria lowers their numbers per volumetric unit of sarcoplasm which results in a decrease of energy which sustains this volume of muscle fiber(5, 26). Growth of mitochondria as a cause leads to a chain of events. Decline of ATP concentration per unit of surface area leads to a decrease of volumetric portion of contractile structures - myofibrils.
Energetic deficiency is quickly reflected on the construction of new structures. Lower quantity of ATP per unit of volume is the reason behind the intensification of destructive processes, which is what our research has shown. The role of energetic deficiency in weakening the cellular-genetic apparatus is reflected in the work(24). Consequently, the less energy is produced(in light of worsening of biosynthesis processes coming from the genetic apparatus) the weaker the process of new structure formation will be.
It is established that 3-month rats at a running speed of 20m/min the volumetric portion of myofibrils equals 81,45+0,27 and a speed increase to 50m/min(during this the mitochondria swell up and their volume increases by 4,5-7%) makes it fall to 78,93+0,33. In other words, the quantity of newly-formed myofibrils declines.
The second derivative of mitochondria growth is the induced enlargement of sarcoplasmic components as the environment supplying their functions. A wide-known biologic conformity, established by I.I. Schmalghausen(16), concludes that a quantitative increase of environmental elements, their surplus, is the main condition for positive movement in any living system. A graphic expression of this conformity can be found in the mathematical model of Volter-Lotka.
From analyzing image #3 it is clear that growth of elements of the executive system “induces” a quantitative increase in the supplying system. Because of that, growth of the mitochondria leads to an abundant synthesis of sarcoplasmic components supplying it as well as sarcoplcasmic hyperplasia and hypertrophy of muscle fibers. And the hypertrophy of muscle fibers with a decrease of myofibrils per unit of volume occurs with high intensity PS.
This process is an induced one and it temporarily allows for extreme activation of functions. It is realized through an extensive path and by it’s results can be determined as a “non-rational” adaptation(10).
Hypertrophy of a muscle fiber is a process the result of which is a significant falling behind of fiber surface area growth compared to it’s volume. And since in living systems there exists a strict interrelation between volume and surface area (14) the disturbance of this interrelation serves as one of the main reasons of shrinkage of this fervently growing volume. An example is a well known position, formulated by Gertvig, about the violation of nuclear-plasmic relation in a cell which causes mitosis.
A famous specialist on mitosis D. Mezia thinks that a quantitative inconsistency between the growth of the core volume and the falling behind of it’s surface area along with the correlation with cytoplasm are one of the main reasons of cell division. With hypertrophy of a muscle fiber it is precisely the disturbance of the interrelation of it’s vigorously growing volume to the falling behind surface area that is the condition of it’s split and reversion of the above interrelation to it’s original level(see image 2).
An overly large intensity of physical stress very often leads to accumulation of poisonous byproducts, depletion of energy resources, which impedes the splitting of hypertrophied fiber and it demolishes. Here are the two possible ways of thickened muscle fiber transformations. The process is presented on image 2.
Low and medium intensities of PS accumulation require lesser energy consumption which allows every component of muscle fiber to fully recuperate, doesn't cause any significant destructive processes and stimulates(and for this there is enough plastic material and energy) the formation of new non-hypertrophied(minor) organelles. Also their numbers per unit of sarcoplasm are high(see table).
Minor organelles have a large surface of interaction with the surrounding(satisfactory to them) environment. And in consequence of high concentration of working elements per unit of sarcoplasmic volume the minor organelles can accomplish significantly more work per unit of time.
Consequently, myofibriliar-mitochondrial hyperplasia doesn’t lead to excessive hypertrophy of muscle fibers and, naturally, does not cause all the consequences of this process. In conjunction to this, medium intensity and speed of PS accumulation over time lead to an “intensive” path of development and can be viewed as a “rational” adaptation.
Intensification of the function can be provided by two methods: 1) by increasing the number of working components; 2) by increase of the coefficient of their utilization. With "rational" form of adaptation both of these methods are being utilized simultaneously. Also execution of a unit of work with a lesser volume of muscle fiber(compared to hypertrophied) testifies of the economic use of building material and energy, which conforms to one of the principles of "rational" adaptation(10).
Increased quantity of ultra-structures responsible for contraction and it’s energetics create a surplus of elements which, by information theory, is a condition of biological dependability of any system(6, 15). It must be remembered that any function is “materialized” and it’s expansion requires a increase of the number of structures which will work.
However since this numeric increase has limits there exist margins of adaptation to environmental factors and physical stresses as well. It is established that quantitative growth of the main working structures of muscle fibers with step-pattern PS equals 5-11%(12). In order to reach the limit level of volumetric portions of myofibrils and mitochondria per unit of muscle fiber volume a certain amount of time is required during which the intensity of motor activity must grow. However, of critical importance is it’s growth per unit of time.
Therefore to intentionally control the formation of structures the most important principle should be accepted to be the account of the quantities of both forming and demolishing structures(which is possible by taking biopsies from sports athletes with subsequent stereological analysis). Only under such conditions can we forewarn excessive development of destructive processes, as even with their presence the athlete is able to overcome tremendous strain by maximally increasing the coefficient of utilization of undamaged elements.
However if these stresses are to continue for any significant amount of time there will immutably be a downfall(tear of tissues, traumas of suspendatory-mobility apparatus etc.). Under these conditions morphological control of tissue states can provide an invaluable service which will determine it’s such important prophylactic role. Only this approach can provide an unfolding of processes in tissues via the “rational” type of adaptation and will serve as a dependable method of trauma prevention and preservation of long lasting physical capability.
Received on 19.02.1990
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