A muscle can produce two mechanical effects on the human skeleton. He either stabilizes joints and body areas or he moves bones. For this to succeed, the force generated in the muscle must be transferred to the bone. This task is taken over by the tendons.
The total muscle consists of several subunits, such as muscle bundles, muscle fiber bundles, muscle fibers and at the lowest level the muscle cells, also called fibrils. In addition to cell organelles, these include thousands of cascaded sarcomeres, the smallest functional units of a muscle. Each sarcomere can contract and thus develop power. The total force of a muscle thus results from the sum of the power generation of the participating sarcomeres.
The functional center of each sarcomere is the actin myosin complex. Actin and myosin are proteins that are linked by cross bridges. The thinner Aktin strands are attached to the outer boundaries of the sarcomere, the thicker myosin molecules are each between two Aktinfäden.
If a nerve impulse arrives at the muscle, calcium is released and the sarcomeres are shortened or strained while consuming energy. The myosin units pull the actinic units to the center of the sarcomere by a rudder movement of their heads. The effect on the entire muscle depends on how many sarcomeres are contracted.
Contractions cause 2 effects in the muscle. On the one hand strength is developed, on the other hand heat is created.
The musculature has a poor mechanical efficiency. About 80% of energy expenditure in muscular work flows into the heat, only 20% in the generation of power. The heat produced, however, makes an important contribution to the regulation of body temperature and the optimization of metabolic processes.
The force developed by the contraction is transmitted via the tendons to the approaches on the bone and either leads to a movement in the involved joints or to an increased tension. Whether a movement arises depends on the goal, which is tracked in the movement programs in the brain and transmitted via nerve impulses to the muscles. If the goal is the execution of movements, all muscle chains are automatically switched on, which are necessary for the adequate action, inhibitory influences are switched off. If you want to hold a certain position, the command is for muscles to stabilize body parts and joints.
An important role in this process plays the interaction between agonists (acting muscles) and their counterparts (antagonists). This creates 3 possible types of contractions.
In isometric contraction, the tension in the muscle increases, but there is no movement, as the antagonists or an external resistance does not allow it. Ideally, the agonists and their opponents work together. This form of muscle work is important for all static loads, for example to stabilize the back or joints.
Concentric contractions cause movement in the joint, shortening the active muscle and allowing the antagonists to move. This form of muscle work is the most mechanically light and most beneficial to stimulate muscle metabolism.
Eccentric contractions occur when the muscle controls movements that prolong it. He has to do a lot of mechanical work, because he contracts while the number of cross bridges between actin and myosin is less and less. All braking activities are part of this contraction form.
A typical dysfunction of the muscle and contraction is muscle weakness (atrophy). It usually arises because a muscle is not used enough (inactivity atrophy). This phenomenon is typical for bedridden patients or immobilization of limbs (gypsum). The contractile force of the muscles and the muscle cross-section decrease, the function is more or less severely affected depending on severity and duration. Another trigger for inactivity is injury or other irritation, such as painful irritation of tendons. In this case, the brain turns on gentle programs that cause less muscle to be used. Inactivity atrophies can be regenerated if they do not last too long.
The contractility of the muscles depends on the nerve stimuli they receive from the brain. If these remain off, no contraction can take place. Nerve conduction can either be impaired centrally (brain or spinal cord) or peripheral (peripheral nervous system) or completely damaged. The result is an incomplete or complete paralysis. Causes may be injuries (paraplegia), herniated discs or inflammatory (MS, poliomyelitis) and metabolic diseases (polyneuropathy, amyotrophic lateral sclerosis).
Diseases that affect the ability to contract and have their cause in the muscle itself or at the transition between nerve and muscle, are summarized under the term muscular dystrophy. Common to all is the symptomatology, possibly visible atrophy, increasing weakness and rapid fatigue. In addition, pain often accompanies movement as the disease progresses, as the effort for the weakened muscles increases. Typical of muscular dystrophies is also the progressive transformation in muscle tissue. The contractile elements are increasingly being replaced by connective tissue, which causes not only an increasing weakness, but also a progressive immobility (contracture).
The cause of these diseases are genetic defects that cause irreparable damage to the muscle cells, which greatly reduces protein formation in the muscle or completely blocks it. Muscular dystrophies are rare diseases that are still not curable.