yogabook / movement physiology / muscle

The muscle

General and structure

The muscle (from Latin musculus: mouse) is an organ capable of contraction and relaxation, which attaches to bones or soft tissue structures such as connective tissue to enable movements of the body, both in the musculoskeletal system and in other organs, such as

• in the peristalsis of digestion (wave-like contractions to transport chyme or faeces)
• as a sphincter (sphincter)
• as a pump (heart)
• as a regulator of vascular tension, e.g. in blood vessels.

Smooth and striated muscles

A distinction is made between:

smooth muscles

in the walls of all cavity organs except the heart. It lacks the microscopically visible transverse striations of the skeletal muscles and cannot be contracted voluntarily. It controls itself or is subject to the influence of hormones, neurotransmitters, other messenger substances, the autonomic or enteric nervous system.

striated muscles

including cardiac muscles and skeletal muscles, muscles of the tongue, larynx and diaphragm . Of all these, the heart alone is not subject to voluntary control. In the case of skeletal muscles, the insertion points are usually referred to as the origin and insertion ; the origin, at least in the limbs, is the point/area closer to the center of the body. This is often consistent with the view that the origin is the punctum fixum (fixed point) and the insertion is the punctum mobile (moving point), although the rectus femoris, for example , is a counterexample. The origin is also not clear, as the Biceps brachii or Triceps brachii shows. In the shoulder girdle , the fixation to the trunk is usually referred to as the origin when the muscle moves the scapula (trunkoscapular muscles) or the arm (trunkouhmeral muscles). Likewise the fixation to the scapula is called origin when the muscle moves the arm (scapulohumeral muscles) relative to the scapula . If a muscle attaches to the end of a bone ( epiphysis ), the transition is slightly cartilaginous , which offers minimal elasticity; if it attaches to a bone shaft ( Diaphysis ), minimal damping is achieved by the interweaving of the collagen fibers of the tendon with the elastic fibers of the connective tissue outer layer (stratum fibrosum) of the periosteum (bone skin).

Muscle fibres

A skeletal muscle consists of several muscle fiber (secondary) bundles separated by a fascia (perimysium). The secondary bundles consist of several primary bundles . The secondary bundles are surrounded by perimysium externum , which pulls inward with septa and as perimysium internum surrounds the primary bundles . The individual approximately 20 µm wide muscle fibers (myocytes), which make up a primary bundle approximately 40 – 80 µm wide (similar to a human hair), are each surrounded by endomysium .

The muscle fibers are usually up to 15 cm long, in the case of the M. sartorius also 30-40 cm long cells: myocytes. The myocytes have several cell nuclei that control a certain “area of ​​influence” (MND: MyoNuclear Domain). The MND can be enlarged through strength training. Myocytes contain thousands of thread-like parallel myofibrils as cell organelles. The myofibrils consist of many microfilaments attached one after the other, the actual contractile elements of the muscle. When colored under the microscope, these appear to be lying side by side along the length of the myofibril, hence the name striated muscles.

sarcomere

The smallest contractile functional unit of a muscle is the sarcomere. In most muscles, there are more than 1000 sarcomeres in a row in the myofibrils. Depending on the degree of contraction of the muscle (and thus depending on the innervation), the sarcomeres are between a minimum of just over 1 µm and a maximum of just under 5 µm in length. Its average resting length is 2-2.5 µm. In vivo, a sarcomere hardly reaches a length of more than 4 µm. They are bordered in the longitudinal direction by Z-discs on which actin filaments are suspended, which have a larger number of possible binding sites for another protein, myosin, in the longitudinal direction. The myosin filaments are attached to another disc, the M-disc, in the (longitudinal) centre of the sarcomere, so that the myosin filaments protrude into the spaces between the actin filaments. The myosin filaments each consist of approx. 300 myosin proteins with tails twisted together in pairs, each with a neck and a head. This is why they are also referred to as thick filaments, while the much thinner actin filaments are called thin filaments. The actin filaments are in the form of a double helix, to which an attached tropomyosin thread is attached at rest in such a way that it covers the binding sites for myosin. The troponin attached to the tropomyosin can swivel the filament to one side so that the binding sites are exposed. At rest, the myosin head is at a low-energy angle of 45° to the tail (and to the actin). An ATP molecule is attached to it. For a more detailed description of the sarcomere, see Wikipedia.

Cross-bridge cycle

Through hydrolysis of the ATP attached to the myosin head to ADP plus a phosphate residue, the head is positioned at an angle of 90° to the tail. Mg is involved in this reaction. If Ca now flows in from the sarcoplasmic reticulum after a nerve impulse and binds to troponin, this swings the tropomyosin thread to one side so that the myosin can bind to the nearest actin binding site. This binding is called a cross-bridge. Now the myosin head releases the still bound ADP and the phosphate residue, causing the neck to abruptly change its angle back to the low-energy 45° position. This movement is known as a power stroke. The empty binding site for ATP on the myosin head is reoccupied with ATP, whereupon the head detaches from the actin and returns to the 90° position, from which it can bind again if a binding site released by the tropomyosin is nearby. At the same time, the Ca is released from the troponin, whereupon the tropomyosin blocks the binding sites again. The resulting cycle is called a cross-bridge cycle. Cross-bridge cycles last between about 10 and 100 ms. Around 50 cycles can be completed within one second, which can shorten the muscle by half if it was previously at a long sarcomere length. How long cross-bridge cycles are carried out in succession depends on the Ca influx and thus on the innervation. The membrane of the sarcoplasmic reticulum contains channels for the sudden release of Ca for the initiation of cross-bridge cycles as well as Ca pumps for reabsorption. It therefore also serves as a Ca store or reservoir. As the myosin heads do not synchronise their force beats and releases with each other and therefore there are always enough myosin heads bound to the actin, the myosin filament cannot slip back on the actin. The neurotransmitter that transmits the nerve impulse for contraction to the muscle is acetylcholine. A concentric contraction therefore results from the fact that the myosin and actin filaments continue to interlock through repeated cross-bridge cycles and pull the Z-discs towards the M-discs. One cross-bridge cycle brings about 1% of the possible contraction of the muscle. After the nerve impulse, the muscle contracts within 20 ms.
As calcium and magnesium are involved in the mechanism, an imbalance of these electrolytes can have a direct influence on the performance of the muscle and may also cause cramps (Ca deficiency).

Titin

Titin (connectin ) filaments traverse the sarcomere from the Z-discs to the myosin filaments and thus keep them in position parallel to the actin proteins. Titin contains 10% elastic areas that make the muscle stretchy. It is not involved in the contraction itself, but it determines the elasticity and speed of contraction and prevents an unphysiological increase in length of the muscle. At 36 megadaltons (1 dalton is 1/12 the mass of a carbon atom and therefore about the mass of a nucleon), it is the largest known human protein. At the edges of the sarcomeres there is an area that myosin does not reach.
The area around the M disk that does not come into contact with actin is called the H zone (Hensen zone). The I-Band /Zone (isotropic, simply refractive) is the band surrrounding the Z-disc comprising only actin and titin. The remaining area is called the A-band (anisotropic). The discs and zones are therefore arranged as follows: Z – I – A – H – M – H – A – I – Z . To put it simply, the contraction occurs by docking myosin to actin, whereby the angle of the head of the myosin filament changes, resulting in a movement of the myosin relative to the actin.

The trigger for contraction is a nerve impulse . Calcium and magnesium are involved in the mechanism, so that an imbalance of these electrolytes has a direct influence on the performance of the muscle and may cause cramps. is also ATP necessary, which is split into ADP and a phosphate residue and must be replaced. Such a “ cross-bridge cycle ” lasts approx. 10 – 100 ms and shortens a sarcomere by 1-2 µm, but the cycle can be repeated several times. whereby the muscle or the individual sarcomere can shorten by around 50% within one second through around 50 cycles.

Sarcomere length

The sarcomere length is the current length of the sarcomere , i.e. the distance between two Z-disks and thus a measure of how far a muscle can still contract or how far it can still stretch. The average resting length of a sarcomere is around 2 – 2.5 µm, at just over 1 µm the muscle is completely contracted and no further contraction or shortening of the muscle is possible. The maximum length of a muscle is reached at just over 4 µm.

Contractions types

When contracts , a distinction is made between:

• Isotonic : the muscle shortens without changing force , as happens when lifting an object very slowly
• Isometric : The length of the muscle remains constant regardless of the force exerted . Examples: Attempting to lift an object that is too heavy or attempting to open a locked door
• auxotonic : both force and length change.
• eccentric (see here)
• concentric (see here)

The myosin filaments have two heads. In a concentric contraction, only one of the two binds, and in an eccentric contraction both, which explains why a muscle during an eccentric contraction has noticeably more strength .

Heads and bellies

A muscle can not only have multiple heads like the biceps or triceps brachii , but also multiple bellies like the rectus abdominis . The contractile bellies are separated from each other by non-contractile tendon tissue (Inscriptions).

Fibre types

The muscle fibers of skeletal muscles are divided into red fibers and white fibers . The red muscles have more muscle fibers with oxidative energy production, so they are well suited for endurance performance, but have significantly less strength , the white ones are better for speed and gravity performance. The relationship is genetically predisposed and can be influenced to a limited extent through training. People with a higher proportion of white fibers respond better to training stimuli, their muscles are more visible, but their muscles tire more quickly.

The fibre composition of a muscle is genetically predisposed. Basically, trunk muscles are rich in type 1 fibres, while the muscles of the limb arm, for example, are mainly of type 2a and 2x.Through strength training, type 2a and type 2x fibres in particular hypertrophy and type 2x partly convert to type 2a.Type 1 fibres hardly hypertrophy, but do become stronger. A transformation from both sides is known from sprint training: both type 1 and type 2 fibres partially transform into type 2a fibres.Endurance training, on the other hand, causes (to varying degrees) improved capillarisation and mitochondrial proliferation (mitochondrial biogenesis) in all three types. There is also a conversion from type FF to type FR and type FR to type ST. In fact, the innervation of types 1 and 2 also differs in that type 2 is innervated by faster nerve pathways. In top cross-country skiers, for example, a change from type 2 fibres to type 1 fibres has been demonstrated, such that a similar capillarisation and a similar mitochondrial volume are achieved.

Pennation

Pennation refers to the property of muscles that their fibers do not run parallel to the longitudinal extent of the muscle. With single pinnation (unipennatus) the deviation is uniform, with multiple pinnation it occurs in different ways. Due to pinnation, the physiological cross section (section orthogonal to the course of the fibers) increases compared to the anatomical cross section (orthogonal section through the macroscopic course of the muscle). Pinnation means that the direction of the fibers is different from the connecting line between the origin and insertion, which means that with the same muscle thickness (anatomical cross-section), a larger number of muscle fibers can attach to the tendons, which increases the force transmitted to the tendons and also increases the lifting height of the muscle. The feathering angle changes with the contraction . slightly
Example: if a muscle is feathered by 45°, it loses factor cos (45°), i.e. about 30% of its strength due to the changed direction of the muscle fibers, but the physiological cross section increases by a factor of 3, so that the gain in strength , which is transferred to the tendons is a factor of 2.1. The average force of around 40 N / cm² has therefore increased to 84 N / cm² diameter. With greater force naturally increases the maximum power and thus the maximum contraction speed

Contraction

The contraction of a muscle or muscle contraction refers to the process in which a muscle exerts contraction force beyond its resting innervation by consuming more energy (compared to the resting state) in the form of hydrolysis of ATP to ADP. A chemical reaction of the protein myosin, which is attached to the middle disc of the sarcomere, causes a geometric change in its head, which docks onto variable sites of the protein actin, which is attached to the Z-disc bordering the sarcomere, leading to a shortening of the sarcomere.
The process from one force impact to the next is known as the cross-bridge cycle. A distinction is made between concentric, eccentric, isometric and isotonic contraction. If nothing else is specified, contraction is generally understood to mean concentric contraction. For a more detailed description, see the structure of the sarcomere and the description of the contraction mechanism on Wikipedia.

Contractions types

Eccentric contraction

Muscle contraction in which the interlocking of actin and myosin in the sarcomeres is reduced, i.e. the distance between the M and Z discs increases, so that the distance between the origin and insertion of the muscle increases. In addition to the eccentric contraction, there are also concentric, isometric and isotonic contractions. The eccentric contraction is also known as the pliometric contraction (plio: Greek: long). Today following properties of eccentric contraction are known:

• vermehrte Kraftentfaltung
• strukturelle Mehrbelastung der aktivierten Muskelfasern
• günstige Energiebilanz (low cost, high force)
• Einfluß auf die willkürliche Innervation, verändertes neuromuskulären Innervationsmusters
• Neigung zu überlastungsbedingten Verletzungen der Muskulatur
• erhöhtes Risiko artikulären und periartikulärer Verletzungen sowie der Sehnen
• Effektive Trainingsform um der Sarkopenie entgegenzuwirken und das Osteoporose-Risiko zu mindern
• günstig in der Therapie von Tendopathien sowie zur Prävention von Muskelverletzungen

Walker et al (7) zeigten in einer 10-wöchigen Studie, daß vor allem exzentrisches Training (die konzentrische Bewegungen wurde den Probanden massiv erleichtert) mit 40% höheren Gewichten einen vergleichbaren Aufbau an Muskelmasse gegenüber klassischem Krafttraining aufwies, aber in der Zunahme der Maximalkraft überlegen war.

Isometric contraction

Muscle contraction in which the position of actin and myosin in the sarcomeres and the distance between the M and Z discs remain unchanged and therefore the distance between the origin and insertion of the muscle remains the same. In addition to isometric contraction, there is also eccentric, concentric and isotonic contraction.

Isotonic contraction

Muscle contraction in which the tension of the muscles(contraction force) remains the same. Whether an eccentric or concentric contraction results, i.e. whether and how the distance between the origin and insertion of the muscle changes, depends on the external resistance to the contraction. This includes not only forces acting on the body from the outside but also the tension of the antagonist(s). In addition to isotonic contraction, there is also concentric, eccentric and isometric contraction.

Concentric contraction

Muscle contraction in which the actin and myosin in the sarcomeres interlock further, reducing the distance between the M and Z discs and thus reducing the distance between the origin and insertion of the muscle. In addition to concentric contraction, there is also eccentric, isometric and isotonic contraction. Concentric contraction is also known as miometric contraction (mio: gr.: short). During concentric contraction against a certain resistance, a muscle develops less force than during eccentric contraction. This dependence is also speed-dependent, which was described by Hill in the equation of the same name, which states that speed is inversely related to force, see under , force-velocity-function

Contraction force

The force with which a muscle contracts, i.e. pulls its insertion and origin towards each other. The easiest way to understand the contraction force is as the axial tensile load applied in one (some muscles of the musculoskeletal system do not attach to both ends with tendons, but possibly directly to bones) or both tendons, the tendon force.

The contraction force of a muscle depends on how many motor units are activated and how many muscle fibers they contain (ranging from around 100 to 3000). A motor unit includes a single motor neuron along with all the muscle fibers innervated by it. The motor units with few muscle fibers allow a fine gradation of force (muscles of the eyes and some of the fingers), those with many fibers belong to muscles that a lot of force can exert , e.g. quadriceps . When a muscle contraction increases in strength, small motor units are first used (recruited), then larger ones (Hennemann’s principle). The fibers of individual motor units do not lie next to each other but are distributed throughout the muscle. For maximum force development, the neuronal impulse frequency is increased so that individual contractions overlap and their force adds up.

If the musculoskeletal system is given a task, all relevant muscles must provide a certain amount of force, the motor force. The maximum achievable motor force depends on various influencing factors, including psychophysical factors such as motivation and inhibiting factors such as fear. Apart from these factors, there are essentially three areas that influence the achievable force:

1. neuronal influences:
   • Recruitment: how many motor units can be recruited at the same time?
   • Frequency: how quickly can the nerve impulses stimulate the muscles to contract (number of action potentials: motor units from ST fibres are innervated at up to 20 Hz, units with FT fibres at up to 50 Hz)?
   • Synchronisation of motor neurones: increase in simultaneously active motor neurones
   • Inhibition reduction
   • Reflex support
2. muscular influences:
   • Muscle cross-section (hypertrophy)
   • Muscle fibre composition (distribution of fibre types, see below)
   • Muscle fibre characteristics
   • Metabolic quality
   • Capillarisation
   • Muscle elasticity
3. anthropometric or biomechanical conditions:
   • Leverage ratios, e.g. as force arm: distance chord – centre of rotation
   • Joint condition
   • Vision elasticity
   • external conditions that may play a role, such as surface and footwear

Force-length function (muscle- strength curve)

See also here . The muscle strength that can be achieved isometrically depends on the possible number of cross-bridges between actin and myosin. This in turn depends on the current length of the sarcomere . Below about 1.27 µm and above about 3.65 µm the muscle can no longer generate any significant force . The functional dependence of the maximum isometric force on the length of the sarcomere is roughly described by an upside-down parabola that is slightly stretched towards greater lengths. In reality, however, it is polygonal because the increase and decrease in force depends linearly on the integer number of bridges that can be reached. The maximum force is achieved at an average sarcomere length of around 2.8 µm. If, in addition to the by contraction generated active force is also , the passive force that an “averagely stretched” muscle applies against further stretching towards the end of its maximum sarcomere length considered, then this curve typically increases slightly above a local minimum (depending on the individual state of stretch). 4 µm strongly again.

Force-velocity relation

The maximum muscle performance (remember: performance = work / time = force * speed) is the product of the shortening speed and the achievable muscle strength. The muscle performance that can be achieved remains the same at all possible speeds, a slow concentric contraction enables greater strength isometrically than a fast one, more strength is available than concentrically and even more eccentrically. This is described by a curve with an inflection point in the isometric contraction . At maximum speed the achievable force is zero, the fastest possible eccentric contraction enables maximum force – with maximum risk of injury.
Muscle training takes place mainly, but not only, in the right part of the curve and allows an increase in muscle performance . Training can be roughly divided into maximum strength training and speed strength training. If the axes in the Hill diagram (Hill, 1938) are swapped, there is an increase in leg A through maximum strength training (training with >= 90% of maximum strength ) and an increase in leg B through speed strength training. This means that in the case of gravity , both a higher load can be moved at the same speed and a higher speed can be achieved with the same load. For the speed force it means that a higher load can be moved at the same speed or a higher speed can be achieved with the same load. Furthermore, the Hill model is only valid under strong conditions, especially only when viewed isometrically , which is why it is being replaced by the Häufle model, which provides a viscoelastic (shock absorber-like) element parallel to the contractile element and reflects real measurement data much better.

Pre-stretching

Prestretch refers to the muscle length (more precisely: sarcomere length) at the beginning of the contraction . For maximum force development, myosin heads must be connected to an actin filament, which is the case below about 2 – 2.2 µm. From around 3.6 µm, actin and myosin no longer have a connection, contraction so in order to enable , synergists of this muscle have to change the joint positions appropriately. Mathematically, the maximum possible contraction of the muscle is around 60%, but in practice this is more like 30%

Articularity

Monoarticular

The single-jointedness of a muscle, i.e. the property of a muscle to span exactly one joint and cause a movement in this joint. In general, a muscle or tendon of the musculoskeletal system causes flexion of the joint on the inside of which it runs.

biarticular

Two-jointedness of a muscle, i.e. the property of a muscle to span exactly two joints and cause a movement in these. The movement can be the same in both joints (flexion or extension) as e.g. in finger joints or the spine, or flexion in one joint and extension in the neighboring joint (example: rectus femoris muscle). However, this is more due to the nomenclature: the rectus femoris pulls the lower leg ventrally in relation to the thigh, just as it pulls the thigh ventrally in relation to the pelvis. In this sense, it is a movement in the same direction. However, the movement possibilities and habits of humans suggest that the dorsal movement of the lower leg in relation to the thigh should be described as flexion in the same way as the ventral movement of the thigh in relation to the pelvis.
However, there is also a case in which a muscle causes geometrically opposing movements. The lumbricals flex the metacarpophalangeal joints (MCP) and extend the proximal interphalangeal joints (PIP). This is possible because the executing tendons switch to the other side: from palmar in the MCP to dorsal in the PIP.
In addition to biarticular muscles, there are also monoarticular (covering one joint) and polyarticular (covering more than two joints) muscles.

Polyarticular

Multi-articularity of a muscle, i.e. the property of a muscle to span more than two joints and cause movement in them

Training

The effects you strive for when training include among other things:

• Hypertrophy : Enlargement of the muscle fiber (growth in thickness, increased number of parallel sarcomeres )
• Hyperplasia : Increase in muscle fibers, the ability to do this in humans is controversial
• Longitudinal adaptation : depending on the ROM used , the serial number of sarcomeres can be reduced (e.g. immobilization at a rather short distance from the origin approach) or increased (especially through training or active contraction beyond everyday stress with a large ROM ). The increase in serial sarcomeres increases muscle performance and thus the contraction force and the unloaded maximum shortening speed, even without radial hypertrophy (increase in cross-section). The first results came from Lynn and Morgan in 1994 in experiments with the vastus intermedius of rats. Vigorous eccentric training at large sarcomere lengths results in damage to the sarcomeres apparently also be repaired with an increase in serial sarcomeres , which can shifts . As a result, the working range of the individual sarcomeres slightly and their stability increases somewhat, which means a somewhat reduced susceptibility to injury.

Incentives for muscle building

There are three important factors for building muscle:

1. Training with growth stimuli (heavy weight with little repetition)
2. Regeneration : the electrolytes lost through sweating are quickly replaced, replenishing the glycogen stores takes a little longer and benefits from the supply of carbohydrates. This part of regeneration takes hours to days and requires a constant supply of protein, ideally starting no later than 20 minutes after training. Resynthesizing mitochondrial proteins takes longer than replenishing glycogen stores. Regeneration depends heavily on sleep intensity and nutrition.
3. Nutrition

Training once a week is just enough for maintenance training. In addition to the well-known forms of training, which involve constant, increasing or decreasing weights per training unit, a study shows that wave-shaped training is promising, a split training in which each muscle group is trained three times a week with different intensities and numbers of repetitions, each once with 85 %, 70% and 55% of maximum strength.

The number of repetitions plays a much smaller role than the intensity and the TUT (time under tension). Isometric contractions enable large gains in strength in a short period of time, but are not suitable as a sole training method. The resulting major metabolic stress is an important hypertrophy stimulus. Reducing the outflow and inflow of blood can also increase the hypertrophy stimulus (KAATSU training, in which a blood pressure cuff compresses the tissue and thus the vessels.)
When it comes to the duration of the training stimulus, a distinction is made according to TUT:
< 20 s: maximum force
20 – 50 s: Hypertrophy area
> 50 s: strength endurance

Jo Weider, der sich sein Leben lang mit Krafttraining und Bodybuilding beschäftigt und mit vielen Athleten aus diesem Bereich zusammengearbeitet hat und unter anderem für den Erfolg von Arnold Schwarzenegger mitverantwortlich war, hat eine Sammlung von „Trainigs-Prinzipien“ erstellt, die seiner Erfahrug nach die wichtigsten Prinzipien für Stimuli zu Hypertrophie und Kraftzuwachs zusammenfassen, siehe hier.

Supercompensation theory

After completing regeneration from heavier training or intensive physical work of a non-sporting nature, the body is said to ensure a slight increase in performance. This theory is known as supercompensation theory. Supercompensation therefore describes the (rather limited) phase of increased performance as well as the effect as such. The body tries to arm itself a little against the type of demand or overload. The supercompensation phase begins immediately after complete regeneration, the performance level slowly rises by a small amount up to a maximum increase, only to then slowly fall again and finally return to the original performance level you had before the training. Now, of course, you would want to place the next training session directly into the maximum of supercompensation in order to exploit this effect again at a slightly higher level. And again and again. However, the increase in performance does not develope proportionally without end, but probably follows more of a logarithmic curve, so that the achievable increase decreases further and further towards the end or disproportionately more effort has to be put in for the same increase. The supercompensation curve must therefore be taken into account for optimal training, although this is difficult to predict or calculate in general terms. They are very individual and depend on the type and intensity of training.

So, according to the supercompensation theory, there are three phases:

1. Training with loss of performance during training,
2. Regeneration with recovery to the original performance level
3. Adaptation phase with supercompensation , which approaches zero again towards the end of the adaptation phase. There is an excess of anabolic recovery processes here. The supercompensation is reversible within a relatively short period of time.

The mechanisms that lead to the phenomenon of supercompensation have not yet been sufficiently clarified, nor has the mechanism of hypertrophy been adequately explained. One component of this will be the increased storage of glycogen, another an increase in protein synthesis. The increase in protein synthesis within the muscle cells is caused by:

1. Anabolic steroids (endogenous or exogenous)
2. resulting microtraumas in the muscles
3. metabolic stimuli such as oxygen deficiency

This causes the muscle fiber to hypertrophy: the cross section grows.
A timely replenishment of the glycogen stores in the muscle cells through carbohydrate intake shortens the regeneration time. This causes degraded ATP to be resynthesized. A protein-rich diet promotes protein synthesis and leads to a positive net protein balance.

Combination exercises

Bench presses, but especially pull-ups, squats and deadlifts, are classic combination exercises in which several muscle groups work at the same time. This produces a higher output of growth hormone than isolated exercise. At least 40-50% of the exercises should be combination exercises.

Endurance sports versus strength sports and muscle building

If you’re aiming to build muscle and strength, you shouldn’t do too much endurance exercise, as it doesn’t contribute much but reduces a lot of resources. Running in the days between a three-way split does not allow for optimal muscle building, but rather delays it. If you value endurance sports, you should limit it to 3 * 20 minutes per week. If there is consistent progress in strength despite endurance training , it can be assumed that endurance sports are not (too much) disruptive.

More information

Incomplete short range movements, if performed in rather short sarcomere lengths, lead to a loss in the training effect. They reduce the TUT at the same speed and tend to shorten the muscles even more.
Momentum has no place in strength training. Taking too long a rest period of more than two to three minutes between sets is counterproductive. Holistic exercises like squats are superior to machine exercises. If the muscles are sufficiently warmed up, the speed of contraction can be increased: explosive movements activate more fast-twitch muscle fibers. However, the increased risk of injury must also be taken into account. The associated eccentric contraction can occur much more slowly. Rest in terms of exertion is not indicated during strength training. If strength deficits become visible, they should be addressed quickly.
Smoking reduces oxygen supply through the supply of carbon monoxide and thus performance and training success. Alcohol reduces testosterone and leads to a decrease in muscle mass.
Carbohydrates and proteins should be consumed after training. If the carbohydrates are missing, the body breaks down proteins in order to obtain glucose from protein via gluconeogenesis. A recommended ratio between carbohydrates and proteins after training is 4:1. According to a meta-study by Schoenfeld et al. (2013), however, it is not the time but only the daily amount of protein that is crucial for muscle growth. Regular and sufficient sleep at unchanged times is supportive; breaks in this regularity are detrimental. The last exercise and the last caffeine should be about 4 to 6 hours before sleep. Consuming too much sugar leads to blood sugar spikes, which make you feel full and prevent or reduce the absorption of valuable food.

Sufficient drinking supports protein metabolism, especially important when large amounts of protein are consumed. Roughly speaking, 5-6 times 25-30 g of protein per day are recommended, or according to other recommendations 4 times a day 0.4 g per kg of body weight per meal. Formulas are usually used that take body weight into account, with most figures being 1.4 – 2 g of protein per kg of body weight, which is around twice as much as the 0.8 g per kg of body weight recommended by the German Nutrition Society for people who do not do muscle-building strength training, but at best moderate recreational sport. A slightly higher protein intake of 1 g is recommended for people aged 65 and over in order to better counteract sarcopenia. A protein intake that exceeds these specifications harbours risks, for example for the kidneys.

Training intensity levels

The aerobic threshold (also known as lactate equivalent or baseline lactate) is defined as the intensity of exertion above which the body can no longer produce energy purely aerobically during prolonged exercise. For most people, it is 2 mmol/l of lactate, while 1-2 mmol/l are produced at rest.In spirometry, this corresponds approximately to the VAT (ventilatory anaerobic transition), the threshold at which the metabolism becomes partially anaerobic . Up to this point, fats and carbohydrates are used to generate energy. The IAS (individual aerobic threshold) as the point of the first lactate increase can be slightly different. Afterwards, only KH is used for further energy production. Depending on the training condition, more or less oxygen is delivered. With a good oxygen supply, a lot of energy is generated and only water and CO2 are produced as metabolic products that can be easily transported away as blood gases. If the oxygen supply is poor, little energy is produced and a lot of lactate (lactic acid) is produced, which makes the muscle increasingly acidic; the lactate can reach a certain level (steady state) are metabolized in real time by the brain and liver. The steady state depends on how good the oxygen supply and the penetration of the muscles with the smallest vessels is (capillarisation). Both parameters are improved through regular endurance training (at least 3/week), and the liver’s lactate metabolism performance also improves.
If the performance requirement continues or lasts for a longer period of time, the system decompensates and the anaerobic threshold (the highest possible exercise intensity defined that can be maintained without increasing acidification is 4 mmol/l lactate in the blood, can deviate slightly from this individually as IANS [Individual Anaerobic Threshold]). exceeded. The hyperacidity of the muscle irritates nerve cells, the muscle begins to hurt, fatigue and cramps can occur. The anaerobic threshold cannot be exceeded for long, especially since it also influences motivation. This phase can therefore only cover a final spurt. The recovery phase required afterwards is relatively long.
Some of the adaptations that trained athletes exhibit:
Higher VO₂ max, improved capillarization of the muscles, higher possible lactate concentrations, shortened regeneration phase, i.e. earlier restoration of performance, increased perspiration to avoid performance-inhibiting heat build-up due to metabolic heat (exothermic metabolism) in the muscles.
Through endurance training, these parameters can be shifted towards competitive athletes; a continuous stimulus in the area of ​​the steady state (anaerobic threshold) is optimal, where quick and sustainable adaptations and increases in performance can be achieved. While a competitive athlete can still gain aerobic energy at 80% VO₂ max, this is only possible for the underweight athlete at 50% VO₂ max. This measurement is usually relative to body weight as ml/min/kg and can be determined in clinical tests equal to the O₂ intake at the time the performance requirement is discontinued. The normal value depends on gender and decreases with age.
The following serve as further measurements:
– de carbon dioxide levy
– the minute ventilation volume VE as a product of tidal volume and breathing frequency. As with the regulation of blood flow, as the performance requirement increases, first the breathing depth, i.e. the tidal volume and then the breathing frequency increases. In the case of obstructive or restrictive airway diseases, these patterns may be altered.
– the respiratory quotient RER (respiratory exchange rate) as a quotient of VCO2 and VO2, which is between 0.7 for pure fat burning and 1 for pure carbohydrate burning. At high load intensities, the quotient exceeds 1
– the anaerobic threshold AT determined by the lactate test
– the ventilatory threshold VT or VAT (ventilatory [anaerobic] threshold), i.e. the point from which respiration increases non-linearly and metabolic acidosis must occur, which occurs from a further break point RCP (respiratory compensation point) in the RER, because it increases H+ must be exhaled.
In order to test performance according to these parameters, the following conditions, among others, must be met:
– last infection at least 14 days ago, good general health and motivation
– 48 hour alcohol abstinence
– at least 48 hours after the last exhaustive exercise
– Caffeine and nicotine consumption as usual
– Temp. 18°-24°, humidity 30%-60%.

Training zones

• Very Light: 50-60% Health Zone Promoting Health
• Slightly: 60-70% fat burning zone activation of fat metabolism, Improving basic endurance
• Moderate: 70-80% Aerobic training Increase endurance capacity, Aerobic fitness
• Intensive: 80-90% Anaerobic Training Improving Lactate Tolerance, Training, for maximum performance increase
• Maximum: 90-100% competition zone improvement in maximum performance and speed

During anaerobic training, only carbohydrates are burned; the white muscle fibers are recruited instead of the red ones. Sprints , competitive sports, and strength training are typical, while light endurance sports such as jogging and swimming are typical of aerobic training. The goals of aerobic training are to build muscle and increase performance instead of burning fat and increasing endurance.

Overtraining

Overtraining (see also here ) is the effect that results from repeated retraining before the end of the regeneration phase. The muscle then does not return to its original performance level, let alone to the level of maximum supercompensation. 40 – 72 hours should pass between (intensive) training of a muscle. See also here.

Sore muscles

Muscle soreness (actually catarrh), see also here , is the pain phenomenon that occurs as a result of mechanical damage to Z-discs. Due to high loads, especially eccentric contractions (which can be up to 40% stronger than concentric contractions), especially braking movements, the Z-discs develop cracks. This is followed by an aseptic inflammatory process with infiltration of water and the formation of a slight edema. In the process, proteins continue to degenerate and autophagy sets in. Since the muscle fibers do not have pain receptors (but they do have stretch receptors), pain only occurs after a delay of 12 – 24 hours when certain substances involved in the inflammatory process emerge from the sarcomere and come into contact with nerve endings.

The explanation that it is a lactic acid deposit is outdated: the half-life of lactate is 20 minutes, so the delayed onset of muscle soreness does not correspond to its breakdown. In addition, muscle soreness occurs especially during strength training, during which little lactate is produced. However, the 400m run, which produces a lot of lactate, usually results in less muscle soreness .

Stretching before or after intense muscle demand does not have a major impact on the development of muscle soreness . However, a good warm-up reduces the risk of injury and improves performance.
Gentle (not vigorous) massages reduce the expected muscle soreness a little because they promote blood circulation; vigorous massages are counterproductive because they mechanically irritate the muscles too much. Heat treatments relieve pain and promote healing because they increase blood circulation. Larger doses of protein taken preventatively or after exercise alleviate muscle soreness , with BCAA (branched-chain amino acids) having the best effect.

Muscle failure

There are three levels of muscle failure :

• concentric failure : the inability to further concentric contraction
• isometric failure : the inability an isometric contraction to continue holding
• Eccentric failure : the inability to continue contracting the muscle in a controlled eccentric manner, for example slowly releasing a weight toward the floor.

During heavy training with a large weight, all three stages of failure would normally be provokable one after the other,
if in the last repetition, where at which point a concentric contraction is no longer possible (concentric failure). If thereafter the isometric contraction is held for as long as possible isometric failure will occur. If then an attempt is made to perform the eccentric contraction as slowly as desired, this will lead to eccentric failure.

The three stages of muscle failure can be easily understood with the following simple experiment, which provokes the stages of muscle failure one after the other: lift a weight of the order of 80-90% of your “maximum strength”, for example in the sense of a bicep curl, over and over again for as long as possible. At some point, the energy reserves stored in the muscle will be too low to lift the weight again. The fuels delivered via the bloodstream cannot cover the energy requirements required at this weight in real time anyway, so the dumbbell visibly stops “halfway”. The phenomenon observed is concentric muscle failure . If you try to hold the weight in this position, you will notice that at some point this is no longer possible, then isometric muscle failure occurs. The attempt to lower the weight as slowly as you like will also come to an unwanted end due to increasing exhaustion, it will eventually come to an end Eccentric muscle failure : the impossibility of lowering the weight in a controlled manner with eccentric muscle contraction . The reason for this behavior lies, of course, in muscle physiology: even holding an object against the effects of gravity requires constant muscle work of alternating fiber bundles and thus uses energy. So, unlike what is possible in technical systems, there is no mechanism through which the muscle “locks into place” so that holding it no longer requires any additional energy. In the sense that muscle failure represents a supply that is no longer possible in real time, it has a kind of analogy with the aerobic threshold, at which oxygen can no longer be absorbed according to consumption. The above experiment also shows that a concentrically that can be achieved force is smaller than the force that can be achieved isometrically and that this in turn is smaller than an eccentric one , whereby the difference between the forces that can be achieved compared to isometric force is greater, the larger it is concentric or eccentric contraction speed.

For effective training some training instructors claim that more or less frequent muscle failure is necessary. However, the only thing that is certain is that “super-threshold stimuli” are necessary. A certain degree of caution is required when it comes to training until muscle failure : the muscle must be very well warmed up and the risk of injury is significantly increased in the mode in which the weight can no longer be controlled well. In addition, training to muscle failure places great demands on the CNS. For locally exhaustive training, 48 hours of regeneration is the lower limit.

Longitudinal muscle adaptation

The number of sarcomeres in a myofibril is not a fixed value that remains constant throughout life. The use of the musculoskeletal system does have an influence on this. For example, muscles that are immobilized in a short sarcomere length over a longer period of time (usually as a result of trauma) reduce the number of serial sarcomeres (i.e. those lying one behind the other in the myofibril), thus reducing their number. Similarly, more frequent intensive use of the muscle in larger sarcomere length is likely to increase the number of serial sarcomeres. This is referred to as longitudinal muscle adaptation, in contrast to the long-known growth in muscle thickness through training, in which the number of parallel sarcomeres increases. The consequences of the (reversible, see above) longitudinal muscle adaptation result from the fact that more sarcomeres in a row now perform the same work as before and, as far as is known today, are all positive:

1. favorable shift of the working range of the individual sarcomeres in terms of the force-length function
2. Slight increase in muscle performance
3. Slight increase in maximum strength
4. Slight increase in maximum contraction speed
5. Slightly reduced susceptibility to injury

For examples of poses that typically cause longitudinal muscle adaptation, see the explanation under muscle soreness.

Pre-activation

Pre-activation refers to the training principle in which the relevant muscles are challenged with a minimum intensity (medium or higher) shortly before a planned performance (around 5 minutes) so that they are more efficient for the planned activity. Pre-activation can be performed quickly or isometrically. In the literature you will find information on intensity between 30% and 70% of maximum strength.

Several mechanisms are responsible for this:
– increased phosphorylation of myosin chains enables better and faster contractions
– improved motoreural excitability
– a more favorable muscle feathering angle increases potential strength
Hopping, skipping, rope jumping, pulling exercises with fitness bands, isometric maximum contractions in the range of 3*10-15 s or a minute in total are beneficial.

The time of optimal pre-activation should be somewhere between 30 seconds and a few minutes. If the pre-activation is too intense, the muscle will already be slightly fatigued by the time the actual performance is due to take place. If it is too far away from the planned performance, the pre-activation effect has already partially worn off.

Stretching

The connective tissue structures of the muscles are only stressed when they are strongly stretched, their wavy fibers are stretched (creep effect), and extended stretching capacity can be used for up to an hour. The muscle fibers have stretch receptors (muscle spindles) that report the state of stretch to the brain. Stretching the muscles can reduce the stimulus threshold of the receptors. Regular stretching and strength exercises lead to a strengthening of the stabilizing titin.

A distinction is made between mobility as the amplitude (angular range in the joints) that can be actively achieved, whereas flexibility is the amplitude that can be achieved passively.

It is assumed that a stretched muscle has the same maximum force as a shortened one, but over a larger area. In other words: the force -length curve is stretched because there is optimal filament overlap over a longer area. It is further assumed that a muscle adapts to frequently performed movements and moves its maximum force to where it is used most forcefully: strength training near maximum length will shift the force maximum there, strength training near maximum contraction it towards maximum contraction will also shift and shorten the muscle. It is also obvious that a more stretched muscle has a lower resting tension.

Stretching sensation / pain

Pain sensation triggered by stretching, i.e. transferring a muscle into borderline large or increasingly larger sarcomere lengths, typically radiating in the direction of the muscle course. Physiologically, stretching pain is scalable from NRS 0 to 10 and subsides significantly within seconds after the end of the application of force to the muscle with only a short reverberation. The proprioceptors that report stretch pain are the muscle spindles.

Stretching tenderness/painfulness / pain on stretching

Stretching tenderness refers to the ability of a part of the musculoskeletal system (usually the muscle and its tendon) to show tenderness under actively (by force application of the antagonists) or passively induced stretching of the muscle, which goes beyond the physiological level of stretching sensation or shows a different quality of pain. Various diseases of the muscle (e.g. ruptures, strains, muscle bruises) or the tendon (e.g. insertional tendinopathies, tendovaginitis) can be associated with pain on stretching.

Relaxations points and insufficiency

Relaxation points

The passive relaxation point is the degree of stretching of the muscle at which the titin filaments no longer exert any force to contract the muscle, which is the case at around 2.8 µm.
The active relaxation point is the point at which the muscle can no longer generate any force for further contraction because the myosin heads accumulate in front of the Z-disc, which is the case at around 1.3 µm.

Insufficiency

Active insufficiency

State of complete contraction of a muscle, i.e. complete interlocking of actin and myosin filaments, which does not allow any further active concentric contraction and thus movement caused by this muscle itself in a joint which this muscle spans, although the covered joint or the spanned joints themselves are not yet in the end position (reaching a soft-elastic, firm-elastic or hard-elastic limit of movement), i.e. the joint can be moved further by another muscle or passively (from outside, externally).
Active insufficiency is always pathological in single-joint muscles but is more common in double-jointed (or polyarticular) muscles,

Passive insufficiency

State of a muscle not being fully contracted, that is, not being actively insufficient, i.e. actin and myosin filaments have not fully interlocked, but being prevented from further contraction by a lack of flexibility of its (more precisely: one of its partial) antagonists.
Passive insufficiency means that a muscle could continue to shorten and move in a joint, but its antagonist (s) prevents this.
The occurrence of passive insufficiency is mostly pathological in monoarticular muscles and physiological in biarticular and polyarticular muscles.

Sarcopenia

The effect that a person’s muscle mass decreases with age, given otherwise fairly constant parameters, is known as sarcopenia. This effect is in the order of 1-2%. Sarcopenia necessarily entails restrictions on the quality of life and development, as well as increased risks, such as a fall or bone fractures that promotes sarcopenia in osteoporosis , which occur much more easily . Depending on the extent, everyday activities such as lifting and moving objects, various tasks requiring strength and even locomotion, especially faster walking or climbing stairs, can also be significantly impaired by sarcopenia. A study shows that the risk of death is correlated with the degree of sarcopenia. According to current knowledge, the best method against sarcopenia is strength training of any kind. It is of no greater importance whether the exercises are carried out against external resistance such as weights or resistance bands or, if possible, against your own body weight. However, after a long period of abstinence from sports, this should be allowed to creep in.

Serial:
M. Sartorius ,
rectus abdominis
Parallel:
Biceps Brachii,
Glutaeus Maximus
feathering:
Semimembranosus (simple)
Plantaris (double)
Deltoid (multiple)

Torque

The most important joints of the musculoskeletal system have centers of rotation (three-dimensional mobility) or axes of rotation (one-dimensional mobility). changes in many joints As already explained in the script about the scientific principles, the distance between the tendon of a muscle and the relevant center of rotation . This means a change in the physical lever arm, on which the force is exerted, i.e. the force arm, which changes the torque . shown above The force -length function describes the change in the achievable force over the (sarmocer) length. However, since movements are usually rotary movements in the joint, the lever arm , which changes over the angle , also plays a role as a multiplicative factor in the torque that can be achieved .