Physiology of excitable tissues. General physiology of the central nervous system

PHYSIOLOGY OF EXCITABLE TISSUES

Lecture 3

Composition (muscle composition)

The ratio of slow to fast muscle fibers in different muscles is not the same and in different people it is also different. The more fast fibers

The ratio of muscle fibers is genetically programmed. The transition of fast muscle fibers to slow and vice versa does not occur during life.

Under natural conditions, the muscle is rarely in a relaxed state, as it is in good shape.

The ability of a muscle to maintain a state of some tension for a long time and stably with minimal energy expenditure is called tone. For example, the neck muscles support the head all day long. In some diseases of the nervous system, the tone may be disturbed.

The structure of the muscle fiber

The length of the muscle fiber is 12-14 cm. It contains many nuclei. Its membrane is called the sarcolemma, which curves into the interior of the fiber. The contents of the muscle fiber is called sarcoplasm. As part of the sarcoplasm, myofibrils, myoglobin, glycogen, sarcoplasmic reticulum (a system of longitudinal tubules and elongated sacs that contain calcium) are isolated.

Myofibrils are grouped into bundles and pass through the entire fiber without interruption. They are divided into dark and light discs. Dark disks are called anisotropic, while light disks are called isotropic. Light stripes in the center have a Z-membrane, and dark H-stripes. The section of the myofibril between the two Z-membranes is called the sarcomere.

Each myofibril consists of actin (thin) and myosin (thick) filaments. On actin filaments are proteins troponin (have a high affinity for calcium ions) and tropomyosin. At the ends of myosin filaments there are myosin heads that form transverse bridges with actin filaments.

Muscle contraction theory (thread sliding)

Muscle contraction is associated with the occurrence of an action potential on the membrane of the muscle fiber, which propagates along the sarcolemma and enters the interior of the fiber. The propagating nerve impulse promotes the release of calcium ions from the sarcoplasmic reticulum. Calcium ions released from the reticulum bind to troponin and tropomyosin. These proteins change their position on the actin filaments. As a result of this process, the obstacle that inhibited the interaction of actin and myosin fibers is eliminated. Myosin heads attach to actin filaments and carry out longitudinal traction. As a result, actin filaments slide between myosin filaments.

Binding of troponin by calcium leads to the release of myosin-ATPase, which breaks down the ATP molecule and energy is released. The resulting ADP molecule and inorganic phosphate are removed from the head, and a new ATP molecule is formed in their place. The released energy is used to break the connection between the actin and myosin cross-bridge.

This cycle can be repeated as long as there are calcium and ATP ions in the sarcoplasm.

Muscle fatigue.

Fatigue is a temporary decrease in performance that occurs during work and disappears after rest.

Reasons for fatigue:

1. Accumulation of metabolic products (lactic acid) in the muscles, which leads to inhibition of action potential generation.

2. Oxygen starvation, i.e. oxygen cannot be delivered to the muscle.

3. Depletion of energy.

4. Central nervous theory of fatigue. According to this theory, fatigue of nerve cells occurs faster than that of muscles.

5. Fatigue of synapses through which impulses are transmitted to the muscles.

In general, there is no first or last reason. They all operate at the same time.

Muscle hypertrophy and atrophy

Muscle hypertrophy is an increase in the mass of muscle tissue during systematic intensive work. There are two types of hypertrophy:

1. Myofibrillar type. It develops during static work (weight lifting). With this type of hypertrophy, the number of myofibrils increases and muscle strength increases significantly. For example, weightlifters.

2. Sarcoplasmic type - an increase in the volume of the sarcoplasm (glycogen, creatinine phosphate, myoglobin, the number of capillaries). With this type of hypertrophy, endurance develops. For example, long-distance runners.

Muscle atrophy develops when it is inactive. Atrophy is promoted by bed rest, transection of tendons, diseases of the nervous system, plaster cast.

Smooth muscles

Smooth muscles are found in the walls of blood vessels, skin, and internal organs.

From striated muscle tissue smooth muscles differ in that they do not have ordered actin and myosin myofibrils. Smooth muscle junctions are close contacts between membranes at a great distance, which are called nexuses. Thus, they form a network that acts as a whole.

Smooth muscles provide slow movements and long tonic contractions. For example, pendulum and peristaltic contractions of the intestine. Smooth muscles provide the tone of the arteries and arterioles.

According to the functional value, they are divided into two types:

1. Visceral (internal). They are located in the gastrointestinal tract and urinary system.

2. Unitary. Consist of units called units that contain big number muscle cells. Unitary smooth muscles are found in the walls of blood vessels, in the pupil, lens, and skin.

The activity of smooth muscles is under the influence of the sympathetic and parasympathetic divisions of the ANS.

Visceral smooth muscle is able to contract without direct nerve influences. There is no constant resting membrane potential in smooth muscles, it constantly drifts and averages -50 mV. Drift occurs spontaneously, without any influence, and when the resting membrane potential reaches a critical level, an action potential arises, which causes muscle contraction. The duration of the action potential reaches several seconds, so the contraction can also last several seconds. The resulting excitation then spreads through the nexus to neighboring areas, causing them to contract.

The speed of excitation according to nerve fibers to smooth muscles is 3-5 cm per second.

Spontaneous (independent) activity is associated with stretching of smooth muscle cells, and when they stretch, an action potential occurs. The frequency of occurrence of action potentials depends on the degree of stretching of the fiber. For example, peristaltic contractions of the intestine are intensified when its walls are stretched with chyme.

Unitary muscles mainly contract under the influence of nerve impulses, but spontaneous contractions are sometimes possible. A single nerve impulse is not capable of causing a response. For its occurrence, it is necessary to sum up several impulses.

For all smooth muscles, during the generation of excitation, activation of calcium channels is characteristic, therefore, in smooth muscles, all processes are slower than in skeletal ones.

Humoral regulation of smooth muscle contraction. The force of contraction of smooth muscles is influenced by adrenaline, which causes a prolonged contraction. Smooth muscles are able to respond to the action of biological substances in the blood. In contrast, skeletal muscles respond to the action of substances only through the synapse.

Smooth muscles consume little energy and have the property of plasticity. Plasticity is the ability of a muscle to maintain its given length without changing tension. This property is very important for the functioning of the bladder.

The action of biologically active substances on smooth muscles located in various organs is not unambiguous. So, acetylcholine excites smooth muscles that are in the internal organs, but inhibits in the vessels; adrenaline is able to relax the non-pregnant uterus, but causes contraction of the pregnant one.

With muscle atrophy, their tissues are weakened and reduced in volume. Muscle atrophy can occur as a result of inactivity, malnutrition, illness or injury. In most cases, atrophied muscles can be strengthened through special exercises, diet, and lifestyle changes.

Steps

Part 1

What is muscle atrophy

Learn about what muscle wasting means. Muscle atrophy is a medical term that describes the reduction in muscle volume and their disappearance in a particular area of ​​the body.

Learn more about dysfunctional atrophy (atrophy from inactivity), which is the main cause of muscle wasting. Muscles can atrophy due to the fact that they are not used at all or are used very rarely, as a result of which muscle tissue degrades, contracts and becomes damaged. This usually occurs as a result of injury, a sedentary lifestyle, or an illness that prevents certain muscles from working.

• Dysfunctional muscle atrophy can develop as a result of extremely poor nutrition. For example, muscle tissue can atrophy and disappear in prisoners of war and people suffering from eating disorders such as anorexia.
• This type of muscle atrophy can also be observed in people who have a sedentary job, as well as in those who are physically inactive.
• Severe injuries, such as damage to the spine or brain, can leave a person bedridden and result in muscle atrophy. Even less severe injuries, such as a broken bone or torn ligament, can limit mobility and also cause dysfunctional muscle atrophy.
• Diseases that limit a person's ability to exercise and be active include rheumatoid arthritis, which causes inflammation of the joints, and osteoarthritis, which leads to weakening of the bones. With these diseases, movements are often accompanied by a feeling of discomfort, pain, or even become impossible, which leads to muscle atrophy.
• In many cases, dysfunctional muscle atrophy can be reversed by strengthening and building muscle by increasing physical activity.

1. Learn about the causes of neurogenic atrophy. Neurogenic muscular atrophy occurs as a result of disease or damage to the nerves in the muscles. Although this type of atrophy is less common than dysfunctional atrophy, it is more difficult to treat because in many cases it cannot be eliminated simply by increasing the load on the muscles. The following diseases often lead to neurogenic atrophy:

   Recognize the symptoms of muscle atrophy. It is important to identify the symptoms of muscle atrophy as early as possible in order to immediately begin to eliminate it. The main symptoms include the following:

   • Muscle weakness, reduction in their volume.
   • The skin surrounding the affected muscles appears flabby and drooping.
   • Performing activities such as lifting various objects, moving the atrophied area and exercising is associated with difficulties, although there were no problems with this before.
   • Pain in the affected area.
   • Back pain and difficulty walking.
   • Feeling of stiffness and heaviness in the damaged area.
   • It can be difficult for a person without medical education to determine the symptoms of neurogenic atrophy. The most obvious symptoms of this type of atrophy include slouching, stiffness of the spine, and limited mobility of the neck.

2. If you think you have muscle atrophy, seek medical attention. If you suspect muscle atrophy, try to consult your doctor without delay. He will be able to identify the causes, make the correct diagnosis and prescribe the appropriate treatment.

   Seek help from other professionals. Depending on the cause of your muscle atrophy, your doctor may recommend that you see a physical therapist, dietitian, or personal trainer who can help you improve your condition with specific exercises, diet, and lifestyle changes.

   Find personal trainer or a physiotherapist. Although you can do some exercises on your own in an attempt to stop muscle wasting, it's best to do it under the guidance of a qualified instructor or trainer to make sure you're doing it right.

   • The coach will begin by evaluating your physical state and then teach you special exercises, allowing to strengthen and build up muscles in the atrophied area. He will evaluate the effectiveness of training and, if necessary, correct them.

3. Start with small loads, gradually increasing the intensity. Since most people with atrophied muscles start exercise after a long period of low physical activity, you should start with small loads. Remember that your body is not as strong as before atrophy.

   Start with aquatic exercise or aquatic rehabilitation. Swimming and water exercises are often recommended for patients recovering from muscle atrophy, as this type of exercise helps reduce muscle pain, quickly tone atrophied muscles, restore muscle memory and relax damaged muscles. Although these exercises are best performed under the guidance of a specialist, below are a few basic steps to start your workout with.

4. Walk around the pool. After going into the water about waist-deep, try to walk in it for 10 minutes. This safe exercise helps to develop the muscles of the lower body.

   • Over time, increase the duration and depth.
   • You can also use an inflatable ring, paddle or water dumbbells for more water resistance. These devices will help you strengthen the muscles of your torso and upper body.

5. Perform knee raises in the pool. Rest your back against the wall of the pool, standing on the bottom with both feet. Then lift one leg, bending it at the knee as if you were marching in place. Raising the knee to the level of the pelvis, straighten the leg, stretching it forward.

   • Do the exercise 10 times, then repeat it with a change of leg.
   • Increase the number of repetitions over time.

6. Do push-ups in the water. Standing facing the wall of the pool, place your hands on its edge, holding them shoulder-width apart. Raise yourself on your hands, leaning out of the water about halfway. Hold this position for a few seconds, then lower yourself back into the water.

   • For an easier version of this exercise, place your hands on the edge of the pool, spreading them shoulder-width apart. Then, bending your elbows, lean towards the wall of the pool.

7. Go to exercise with own weight. As you progress, add ground-based bodyweight exercises to your workouts.

   • Beginners can start with 8-12 repetitions of the exercises below. These exercises are aimed at developing the main muscle groups.
   • To strengthen atrophied muscles, do these exercises three times a week.

8. Learn do squats . To do this, stand up straight with your arms outstretched in front of you. Gently and slowly bend your knees, as if sitting down on an imaginary chair. After holding this position for a few seconds, straighten your legs, returning to the starting position.

   • Keep your balance on your heels and make sure your knees don't go forward past your toes.

9. Fulfill one leg lunge squat . To do this, stand up straight with your hands on your hips. Pull in your belly.

   • Take a wide step forward with your right foot. While doing this, keep your back straight. Raise your heel, resting your toe on the floor.
   • Bend both knees at a 90 degree angle at the same time. You can control your posture by watching yourself in the mirror.
   • Lower your heel to the floor and straighten up. Return to the starting position by pulling the right leg back and repeat the exercise for the left leg.
   • Remember to keep your back straight.

10. Try lowering to train triceps. Use a stable bench or chair for this. Sit on a bench or chair and lean on the edges with your hands, spreading them shoulder-width apart.

    • Stretching your legs out in front of you, slowly slide forward, leaning on your hands. Straighten your arms so that the main load falls on the triceps.
    • Gently bend your elbows, keeping your back close to the bench. As you lower yourself down, firmly hold onto the edges of the bench with your hands.

11. Fulfill basic abdominal exercises . To do this, lie on your back on a mat or rug. Without lifting your feet off the floor, bend your knees.

    • In this case, you can cross your arms over your chest, or bring them behind your neck or head. Try to lift your shoulders up by tensing your muscles abdominals.
    • Hold this position for a few seconds, then lower yourself onto your back and repeat the exercise.

12. Try weight training. Use expanders or strength training equipment for this. These exercises should only be started after you have successfully mastered the bodyweight exercises above. Also try to figure out which weight-bearing exercises help strengthen the muscle group you need.

    • The bench press can be done with expanders. Lying on your back on a bench, stretch the expanders in front of you, as if lifting dumbbells up.
    • Start with lighter expanders. Feeling that the exercise is given to you quite easily, change the expander to a heavier one. This way you can gradually increase the load.

13. Incorporate aerobic exercise into your workouts. Complement the above exercises with aerobic exercises, which also help strengthen atrophied muscles. Try to do regular walking and other cardio exercises.

    • Start with a 10-15 minute daily walk. Gradually increase the speed, bring the duration of the walk to 30 minutes, after which you can move on to daily jogging.

14. Do not forget stretch muscles . After each session, stretch your muscles to increase their range of motion. Spend 5-10 minutes stretching your muscles after each workout. You can stretch the muscles and separately from training.

    • Try to stretch all the major muscle groups, giving each for 15-30 seconds.
    • Start by stretching your back and upper body. Then move on to the muscles of the neck, forearms, wrists and triceps. Do not forget about the muscles of the chest, abdomen and buttocks. After that, work on the muscles of the thighs, ankles and feet.

15. Learn some special stretches. Below are some stretching exercises individual groups muscles.

    • Neck stretch. Tilt your head forward and, stretching your neck, move it to the left, right, back and forward again. Do not roll your head in circles as this is not safe.
    • Shoulder stretch. Place your left hand on your chest. Grab her forearm with your right hand. Pull it until you feel a stretch in your left shoulder. Push your left hand in the opposite direction, squeezing the muscles of the shoulder. Do the same with the right hand.
    • Triceps stretch. Raise right hand. Bending it at the elbow, bring it back, reaching for the area between the shoulder blades. Place your left hand on your right elbow and pull it towards your head.
    • Wrist stretch. Stretch your arm forward and slightly pull your palm back, holding it with your other hand. Repeat the same with the palm of the other hand.
    • Knee stretch. Sit cross-legged. Stretch one leg in front of you and try to reach the foot, holding it for a few seconds. Return to the starting position and repeat the exercise with the second leg.
    • Lumbar stretch. Lie on your back. Bending one leg at the knee, lift it to your chest. Repeat the exercise with the second leg.
    • Leg stretch. Lie on your back and stretch both legs up. With your hands on the back of your thighs, pull your legs up to your face.

Systematic intensive work of the muscle leads to an increase in the mass of muscle tissue. This phenomenon is called working muscle hypertrophy. Hypertrophy is based on an increase in the mass of the protoplasm of muscle fibers, leading to their thickening. This increases the content of proteins and glycogen, as well as substances that deliver energy used in muscle contraction - adenosine triphosphate and creatine phosphate.

Apparently, in connection with this, the strength and speed of contraction of a hypertrophied muscle is higher than that of a non-hypertrophied one.

The increase in muscle mass in trained people, in whom many muscles are hypertrophied, leads to the fact that the musculature of the body can be 50% of body weight (instead of the usual 35-40%).

Hypertrophy develops if a person daily performs muscular work for a long time that requires a lot of stress (strength load). Muscular work performed without much effort, even if it continues for a very long time, to muscle hypertrophy does not lead.

The opposite of working hypertrophy is muscle atrophy from inactivity. It develops in all cases when the muscle for some reason loses the ability to perform its normal work. This happens, for example, with prolonged immobilization of a limb in a plaster cast, with a patient staying in bed for a long time, with transection of a tendon, as a result of which the muscle ceases to work against the load, etc.

With atrophy, the diameter of muscle fibers and the content of contractile proteins, glycogen, ATP and other substances important for contractile activity in them fall sharply.

With the resumption of normal muscle work, atrophy gradually disappears.

A special type of muscle atrophy is observed during muscle denervation, i.e., after the transection of its motor nerve.

If you have already tried to figure out how muscles grow, then most likely you are already confused in incomprehensible terms, and many sources give conflicting information.
I will try to tell in a simple and accessible form what's what - what types of muscle fibers exist, how they "turn on", what types of hypertrophy exist, what workouts can achieve muscle growth and what it depends on.

Muscle structure is very complex, so we're going to simplify a lot. The article was prepared specifically for beginners, we will not dig deep.

The structure and composition of muscles.

It should be understood that muscles are made up of several components. Protein only makes up 20-25% of the total muscle mass. The rest is the muscle fiber supply system, which includes: glycogen (carbohydrate storage), water, minerals, creatine phosphate, mitochondria (for energy production), capillaries, some fat in the form of intramuscular triglycerides, etc., that is, in fact, muscles 70-80% are water.

Types of hypertrophy.

Only if we are talking about muscle growth is it customary to use the term hypertrophy. Hypertrophy is an increase in the size of the muscle fibers themselves. There is also the term "Hyperplasia" - an increase in the number of muscle fibers, but we will not talk about it.
An interesting, and very important point for us - there are two types of hypertrophy:

Sarcoplasmic.
Myofibrillar.

Myofibrillar hypertrophy is an increase in the size of the fibers themselves, their protein component. This is "True" muscle growth. To start this type of hypertrophy, it is necessary to create a powerful stimulus of great effort (strength training. Protein synthesis is a rather energy-consuming process, so it is very important not only to create a stimulus with strength training, but also to properly organize nutrition.

Sarcoplasmic hypertrophy is an increase in the volume of everything else that makes up the muscle: glycogen, water, minerals, etc. The main stimulus is the depletion of these energy resources (especially glycogen. This causes the cell to replenish glycogen (and therefore water, since glycogen is stored in the body in the "Wet" form, retaining 3-4 g of water per gram) and replenish them in excess, so that the muscles appear larger.Regular high-rep training also increases the capillary network, mitochondria and all other non-contractile elements, which additionally visually increase muscle size.

Types of muscle fibers.

There are two main types of muscle fibers - type I fibers and type II fibers (often intermediate types of fibers are also distinguished, but we will simplify.

Type I fibers are called slow muscle fibers (SMF) or red fibers, type II fibers are called fast muscle fibers (bmw) or white fibers.

But it should be understood that the very words "Fast" and "slow" fibers refer to the speed at which muscle fibers can generate force. MMV are reduced in 0.1 seconds, and BMW in 0.05. But this does not mean at all that the speed of the exercise affects which fibers will be included in the work. That is why the terms BMW and MMV bring confusion and misunderstanding of the very essence of the work of the muscular system.

The classification into slow and fast fibers is based on the activity of atphase (an enzyme necessary for muscle contraction. The higher the activity, the more powerful the contraction. Slow fibers have a much lower atphase rate, that's all.

Fibers also differ in the type of energy supply: oxidative and glycolytic. Oxidative - means that it works by oxidizing fatty acids and glucose and oxygen is needed for their work, and glycolytic ones work on anaerobic (without oxygen access) glycolysis. Oxidative fibers are more enduring and least strong, while glycolytic ones have an extremely short duration of work (about a minute), but they have the greatest power and contraction force.

motor units.

In general, muscles are not tensed by specific individual fibers. Muscular system uses the so-called motor units(de) - several muscle fibers that are innervated by one motor neuron. Accordingly, de is divided into high-threshold motor units (vpde) and low-threshold motor units (npde. They also correspond to BMW and MMV.

They have a motor neuron with a small cell body that innervates 300 to 800 muscle fibers. Npde have a low activation threshold, so they are included in the work first.

They are innervated by motor neurons that have a large body and have a high input resistance, so they are activated last.

With the development of effort from weak to strong, a stable order of recruitment ("Inclusion") is observed de: first npde --.

Sarcoplasmic muscle hypertrophy. Not all muscles are the same

One of the main problems in training strength athletes (American football players, baseball players, basketball players, wrestlers and even powerlifters), in my opinion, is too much emphasis on exercises with 10-15 reps per set. This kind of training has a place in the preparation of athletes, but it needs to be given less attention. For example, linemen (in American football, these are big guys who stand on the line and have to break through / prevent breaking through to point guards) need to gain mass so that they are not kicked all over the field. The “bodybuilding” high rep approach can be very helpful during the season to prevent loss. muscle mass, as well as to restore the lost mass after the end of the playing season. There is also scientific evidence that large muscles are easier to make strong in the future if you start training for strength indicators. The main thing to remember is that this type of hypertrophy has nothing to do with explosive strength and movements such as punching, running, throwing, jumping, or maximizing strength in one movement. That is why bodybuilders who work primarily on type IIA fibers and gain growth in non-contractile muscle components (sarcoplasmic volume, capillary density and mitochondrial growth) are not the fastest and strongest athletes in the world. And this is despite the fact that they have an average more muscle than any other athlete! I believe that in such hypertrophy form prevails over function.

Muscular hypertrophy is an increase in muscle mass, as well as their cross-sectional area. This happens when the overload increases rapidly. The heart and skeletal muscles can get used to the constant increase in workload. Muscle tissue cells begin to more effectively transfer force through the tendons to the bones. The overall picture of this process is very complex and is still not fully understood by doctors.

In muscle hypertrophy, the mass and cross-sectional area of ​​the muscles is due to an increase in the size of individual muscle fibers, while their length remains the same.

Each skeletal muscle performs two functions: contracting (to move the body), stabilizing (to maintain position). It can contract with varying amounts of tension to do the job. During hypertrophy, various variable stresses occur in the muscle, which forces it to adapt. It does this by increasing the size as well as the number of contractile proteins that make up the myofibrils within each fiber. This contributes to an increase in individual fibers and their strength.

Hypertrophy changes:

• speed of muscle contraction;
• maximum work force;
• resistance to fatigue.

The nature of adaptation can be different depending on different systems of response to loads.

Hypertrophy can be called a combination of local and peripheral events that are coordinated with each other. The main regulatory signals for them are mechanical, hormonal, nervous and metabolic factors.

Types of hypertrophy

The main types of hypertrophy:

• myofibrillar (when the muscles increase due to the growth and increase in the number of myofibrils. They fit more densely in the fiber. More often this type of hypertrophy occurs with type IIB fast fibers).
• sarcoplasmic (when the muscles increase due to an increase in the volume of the sarcoplasm, that is, the part that does not contract. The amount of mitochondria, glycogen, creatine phosphate, etc. increases in the fibers. More often this type occurs with slow type I muscles, as well as fast oxidative types IIA).

Mechanisms of hypertrophy

Scientists put forward several theories that explain the mechanisms of myofibrillar-type hypertrophy. These hypotheses include:

• acidosis;
• hypoxia;
• Mechanical damage.

The acidosis hypothesis suggests that the main stimulus that starts the process of hypertrophy is the accumulation of lactic acid in the muscle. It damages the sarcolemma of the muscle fibers and the membranes of the organelles. At the same time, calcium ions appear in the fiber, which activate proteolytic enzymes that break down proteins.

The hypoxia hypothesis says that the main reason is the lack of oxygen for some time. This happens when you train with a lot of weight. The lack of oxygen, and then active saturation with it, damages the fiber membranes, which entails saturation with calcium ions, etc.

The hypothesis of mechanical damage suggests that the main factor is damage to contractile proteins, which occurs with strong muscle tension.

Androgens play an important role in the growth of muscle volume. Women also produce them, but to a lesser extent. The more of these hormones the body produces, the faster the muscles grow.

Hypertrophy Factors

There are a few mandatory conditions, without which this process cannot begin:

• synthesis of contractile proteins;
• ribonucleic acid;
• hyperplasia (an increase in the number of fibers);
• androgenic anabolic steroids.

Degree score

The degree of hypertrophy can be assessed by measuring its mass and volume. These days, this can be done with a CT or MRI. The specialist must evaluate the change maximum value cross section of the muscle.

Skeletal muscle hypertrophy. Workout type

Functional hypertrophy skeletal muscle of a person depends on the type of training, which also affects the work of either type I or type II fibers. The simple conclusion from this is that light, low-intensity bodyweight training will include most type I work, as a result of which, the cross-sectional area of ​​\u200b\u200bthe muscle remains practically unchanged. Strength, high-speed training with large weights includes type II work, which significantly increases the cross-sectional area.

In addition, there are two types of hypertrophy:

• Myofibrillar;
• Sarcoplasmic.

In order not to go into the details of the structure, let's just clarify that the sarcoplasm is the liquid content around the fibers, the myofibrils are thin threads that run along the muscle fiber. You can see the difference more clearly in the picture.

So - the type of training also affects the type of muscle growth. Low-intensity long-term training leads to sarcoplasmic hypertrophy, i.e. increase the volume of the sarcoplasm, in which the amount of glycogen and creatine phosphate increases. This increases endurance and allows you to make the next workout longer. So, for example, hypertrophy occurs in long-distance runners. Myofibrillar hypertrophy occurs under the influence of strength training and leads to an increase in the myofibrils themselves and, accordingly, in the cross-sectional area.

However, in its pure form, neither the first nor the second is found. There is always a mixed type. But in strength training the second prevails, in aerobic - the first.

There are two types of muscle hypertrophy - true and false. False muscle hypertrophy is a negative process when an external increase in muscle mass occurs due to an increase in body fat, obesity.

True muscle hypertrophy is the result that fans aspire to power types sports, characterized by an increase in muscle cells and muscle volume - both in general and in individual muscle groups.

Such muscle growth is of two types - myofibrillar and antispasmodic.

Knowledge is a tool to achieve results. Knowing what hypertrophy is and how to use the biological process to improve the body will allow you to achieve high performance, acquire excellent muscles as in the classroom. gyms as well as self-training at home.

Myofibrillar type

Myofibrillar-type muscle hypertrophy, characterized by dry muscles, is achieved by an increase in the number, size and density of the myofibrils that make up the contractile tissue.

The increase in such muscle structures contributes to an increase in strength and power. Myofibrillar type hypertrophy is used in powerlifting, weightlifting and arm wrestling.

The myofibrillar type of muscle hypertrophy is typical for fast fibers that perform high-speed actions, powerful, "explosive" but quickly tired.

When performing exercises aimed at switching on the mechanism of this type of hypertrophy, the muscles must be given rest between the performed approaches, lasting from 1 to 3 minutes.

For muscle growth according to the myofibrillar type, it is recommended to train with sports equipment heavy weight and low reps. The duration of the training, as a rule, does not exceed an hour and is built in such a way that muscle groups got rest for.

In order for the muscles not to adapt to the loads, the training plan should include training with an increase in the number of approaches, using lighter sports equipment.

Sarcoplasmic type

Sarcoplasmic muscle hypertrophy, which is characterized by voluminous but less dense muscles, is achieved by an increase in the nutrient fluid surrounding the muscle fibers.

Muscle growth occurs due to metabolic reactions occurring in muscle cells and thickening of the capillary network of muscles that occur during exercise.

Muscle hypertrophy of the sarcoplasmic type involves slow, low-speed muscle fibers capable of performing long-term movements. Quite insignificant, but overall endurance and muscle relief increase.

This type of training is performed with light and medium-weight sports equipment and can last from one and a half to two hours. For classes, they are carried out at a high pace, using a relatively large number of approaches (up to 12) and a short rest between repetitions.

For muscle growth, their useful, true hypertrophy, there are certain recommendations:

1. The use of two types of loads when performing an exercise - with a high and low number of repetitions.
2. Periodic change of training programs. As a rule, one training program carried out for no more than two months.
3. Building training according to an accentuated type aimed at one muscle group.
4. Gradual increase in the weight of sports equipment.
5. A prerequisite for muscle growth is high-quality nutrition, which should not only be high in calories, but also contain required amount proteins, fats, vitamins and minerals.

Performance simple terms will allow you to develop high-quality muscles without the problems of excessive overloads and with pleasure.

What is Sarcoplasmic Hypertrophy?

Myofibrillar hypertrophy of muscle fibers - an increase in the volume of muscle fibers due to an increase in the volume of myofibrils. ... Sarcoplasmic hypertrophy of muscle fibers - an increase in the volume of muscle fibers due to a predominant increase in the volume of the sarcoplasm, i.e., their non-contractile part.

Etiological factors in these patients were: unilateral type of chewing, trauma during sports competitions, boxing. For some, this disease began gradually, imperceptibly, the compression of the jaws gradually increased. For the final diagnosis in patients on the area of ​​the convex hypertrophied muscle, we apply a layer of barium and perform X-ray cinematography in a direct projection, r. full face, and the patient was asked to squeeze and unclench the dentition. With muscle hypertrophy, swelling of the cheek increases sharply with compression and noticeably decreases with unclenching of the jaws.
With this pathology, a plastic mouthguard was made for the entire dentition mandible with an increase in bite by 3.0 mm. Muscle relaxants (mydocalm. sonapaks) were prescribed under the control of electromyography. Selective electromyostimulation of weakened muscle groups was carried out, the patient was recommended to eat on the opposite side.

Rice. 118. Patient K., 45 years old. Diagnosis: parafunction of the muscles that lift the lower jaw, occlusal-articulation dysfunctional TMJ syndrome.
A - there is a generalized increased abrasion of the teeth of the lower jaw.
B - increased abrasion of the upper frontal teeth.
C - a patient after prosthetics of teeth with the creation of a dense fissure-tubercular contact of all teeth. Explanation in the text.
Treatment of patients with unilateral hypertonicity of the lateral pterygoid muscle
At the beginning of treatment for a month, the patients were prescribed myogymnastics with the mixing of the lower jaw to the midline of the linden and even a little more. In this position of the jaw, the patients made vertical movements 3 times a day for 15 minutes during

1. x weeks. Then an apparatus with a lateral inclined plane was made. Treatment was carried out for 4-5 months.

In addition to orthopedic treatment, patients were prescribed massage in the area of ​​the temporal and proper chewing muscles. Electrophoresis with 5% potassium iodide solution in the TMJ area. After treatment, all pathological symptoms were eliminated. The movements of the lower jaw became smooth, without mixing to the side.
Treatment of patients with bruxism and lateral shift of another etiology was carried out with a plate with an occlusal patch and an inclined plane.

Working muscle hypertrophy and inactivity atrophy

Systematic intensive work of the muscle leads to an increase in the mass of muscle tissue. This phenomenon is called working muscle hypertrophy. Hypertrophy is based on an increase in the mass of the protoplasm of muscle fibers, leading to their thickening. This increases the content of proteins and glycogen, as well as substances that deliver energy used in muscle contraction - adenosine triphosphate and creatine phosphate.

Apparently, in connection with this, the strength and speed of contraction of a hypertrophied muscle is higher than that of a non-hypertrophied one.

The increase in muscle mass in trained people, in whom many muscles are hypertrophied, leads to the fact that the musculature of the body can be 50% of body weight (instead of the usual 35-40%).

Hypertrophy develops if a person daily performs muscular work for a long time that requires a lot of stress (strength load). Muscular work performed without much effort, even if it lasts a very long time, does not lead to muscle hypertrophy.

The opposite of working hypertrophy is muscle atrophy from inactivity. It develops in all cases when the muscle for some reason loses the ability to perform its normal work. This happens, for example, with prolonged immobilization of a limb in a plaster cast, with a patient staying in bed for a long time, with transection of a tendon, as a result of which the muscle ceases to work against the load, etc.

With atrophy, the diameter of muscle fibers and the content of contractile proteins, glycogen, ATP and other substances important for contractile activity in them fall sharply.

With the resumption of normal muscle work, atrophy gradually disappears.

A special type of muscle atrophy is observed during muscle denervation, i.e., after the transection of its motor nerve.

What is cardiac hypertrophy?

HYPERTROPHY OF THE HEART - an increase in the volume of the heart muscle due to the thickening of the wall of the ventricles (the muscle fibers thicken and the size of their nuclei increases). ... In athletes, the muscle of the left and, to a lesser extent, the right ventricle of the heart hypertrophies.

Human skeletal muscle hypertrophy. INTRODUCTION

Myofibrillar hypertrophy - adaptation of human skeletal muscles to power loads with directionality training process to increase their volume or strength. It has been established that with this type of hypertrophy, the number and volume of myofibrils, the main elements of the muscle fiber, increase.

The aim of the study was to develop a concept describing the mechanisms of myofibrillar hypertrophy of human skeletal muscles under the influence of force-oriented loads.

Muscle atrophy. Causes of muscle atrophy

Primary muscle atrophy is caused by damage to the muscle itself. The cause of the disease in this case may be unfavorable heredity, which is expressed in metabolic disorders in the form of a congenital defect in muscle enzymes or high permeability of cell membranes. Environmental factors that provoke the onset of the pathological process also have a significant impact. These include physical overstrain, infectious process, trauma. The most pronounced primary muscle atrophy in myopathy.

The cause of muscle atrophy can be an injury to the nerve trunks, an infectious process that occurs with damage to the motor cells of the spinal cord, such as poliomyelitis and polio-like diseases.

Sometimes the pathological process is hereditary. In this case, the distal extremities are affected, and the process itself proceeds more slowly and is of a benign nature.

In the etiology of the disease, the following factors are distinguished: malignant tumors, paralysis of the spinal cord or peripheral nerves. Often, muscle atrophy develops against the background of various injuries, starvation, intoxication, as a result of a slowdown in metabolic processes as the body ages, prolonged motor inactivity for any reason, as a consequence of chronic diseases.

If the spinal cord and large nerve trunks are affected, then neuropathic muscle atrophy develops. With thrombosis of large vessels or impaired blood flow in muscle tissue as a result of mechanical or pathological damage, an ischemic form develops. The cause of the functional form is absolute, often partial motor inactivity due to pathological processes in the body - arthritis. poliomyelitis and poliomyelitis-like diseases.

Almost all body movements associated with the simultaneous contraction of the agonist and antagonist muscles on opposite sides of the joints, which is called the coactivation of the agonist and antagonist muscles. Coactivation is controlled by the motor centers of the brain and spinal cord.

The position of each part body, such as arms or legs, is determined by the relative degrees of contraction of the muscle groups of agonists and antagonists. Suppose that the arm or leg should be in the middle position. To do this, the muscles agonists and antagonists are excited approximately to the same extent. Recall that a muscle contracts with more force when lengthening than when shortened: a muscle develops maximum contractile force at its full functional length, and develops almost no force at half its original length. Therefore, an elongated muscle on one side of the joint can contract with much more force than a shorter muscle on the opposite side.

As arm or leg move in the direction of their middle position, the force of contraction is more longus muscle decreases, while the force of contraction is more short muscle increases until both forces are equal to each other. At this point, the movement of the arm or leg stops. Thus, by changing the degree of activation of the agonist and antagonist muscles, the nervous system controls the position of the arm or leg.

All muscles of the body are constantly reconstructed adapting to their intended function. Their diameter, length, developed strength, vascular supply and even types of muscle fibers change (to a small extent). This reconstruction process is often carried out quite quickly - within a few weeks. Animal experiments have shown that in some small, active muscles, contractile proteins can be replaced within as little as 2 weeks.
Muscle hypertrophy and atrophy. An increase in total muscle mass is called muscle hypertrophy, and a decrease is called muscle atrophy.

Muscular hypertrophy is almost always the result of an increase in the number of actin and myosin filaments in each muscle fiber, which leads to their enlargement. This is called simple fiber hypertrophy. The degree of hypertrophy increases significantly if the muscle is loaded during contraction. For the development of significant hypertrophy, only a few strong contractions per day for 6-10 weeks are enough.

Mechanism, by which strong contraction leads to hypertrophy is not clear. It is known, however, that with the development of hypertrophy, the synthesis of muscle contractile proteins is sharply accelerated. This contributes to a gradual increase in the number of actin and myosin filaments in myofibrils, the number of which often increases to 50%. It has also been noted that some myofibrils in hypertrophied muscle are themselves split with the formation of new myofibrils, but the importance of this process in normal muscle hypertrophy is still unknown.

Along with the increase in size myofibril enzymatic energy-producing systems are also enhanced. This is especially pronounced in the enzymes for glycolysis, which provides a rapid energy delivery during a powerful short-term muscle contraction.

If in for many weeks the muscle is not used, the rate of decay of contractile proteins in its fibers becomes higher than the rate of their recovery. As a result, muscle atrophy develops.

Muscle Length Adjustment. When muscles are stretched beyond their normal length, another type of hypertrophy develops. This leads to the addition of new sarcomeres at the ends of the muscle fibers where they attach to tendons. It is known that in a newly developing muscle, new sarcomeres can be added very quickly - up to several sarcomeres per minute, which characterizes the possible rate of development of this type of hypertrophy. Conversely, if the muscle consistently remains shorter than normal length, the sarcomeres at the ends of the muscle fibers may actually disappear. Through these processes, muscles are constantly remodeled to be of the appropriate length for proper muscle contraction.

Hyperplasia of muscle fibers. When a muscle develops excessive contraction force (in rare cases), in addition to fiber hypertrophy, their absolute number also increases. This increase in the number of fibers is called hyperplasia. During this process, a linear splitting of the pre-enlarged fibers takes place.