Skeletal muscle
Skeletal muscle is a type of
striated muscle, attached to the
skeleton. Skeletal muscles are used to facilitate movement, by applying force to
bones and joints; via
contraction. They generally contract
voluntarily , although they can contract involuntarily.
Muscles have an elongated, cylindrical
shape, and are
multinucleated . The
nuclei of these muscles are located in the peripheral aspect of the cell, just under the
plasma membrane, which vacates the central part of the
muscle fiber for
myofibrils.
Encyclopedia
Skeletal muscle is a type of
striated muscle, attached to the
skeleton. Skeletal muscles are used to facilitate movement, by applying force to
bones and joints; via
contraction. They generally contract
voluntarily , although they can contract involuntarily.
Muscles have an elongated, cylindrical
shape, and are
multinucleated . The
nuclei of these muscles are located in the peripheral aspect of the cell, just under the
plasma membrane, which vacates the central part of the
muscle fiber for
myofibrils. This unique arrangement of the nuclei allows for higher efficiency.
Skeletal muscles usually have one end attached to a relatively stationary bone, and the other end is attached across a joint, to another bone .
There are two types of fibers for skeletal muscles: Type I and Type II. Type I fibers appear reddish. They are good for endurance and are slow to tire because they use
oxidative metabolism. Type II fibers are whitish; they are used for short bursts of speed and power, use anaerobic metabolism, and are therefore quicker to tire.
How skeletal muscle works
The strength of skeletal muscle is directly proportional to its length and cross-sectional area. The strength of a joint, however, is determined by a number of
biomechanical principles, including the distance between muscle insertions and pivot points and
muscle size. Muscles are normally arranged in opposition so that as one group of muscles contract, another group 'relaxes' or lengthens. Antagonism in the transmission of nerve impulses to the muscles means that it is impossible to stimulate the contraction of two antagonistic muscles at any one time. During ballistic motions such as throwing, the antagonist muscles act to 'brake' the agonist muscles throughout the contraction, particularly at the end of the motion. In the example of throwing, the chest and front of the shoulder contract to pull the arm forward, while the muscles in the back and rear of the shoulder also contract and undergo eccentric contraction to slow the motion down to avoid injury. Part of the training process is learning to relax the antagonist muscles to increase the force output of the chest and anterior shoulder.
Skeletal muscle cells are stimulated by
acetylcholine, which is released at
neuromuscular junctions by motor neurons. Once the cells are "excited", their
sarcoplasmic reticulums will release ionic calcium , this interacts with the myofibrils and, thus, induces muscular contraction . Besides calcium, this process requires
adenosine triphosphate . The ATP is produced by
metabolizing creatine phosphate and
glycogen, which are stored within the muscle cells; as well by metabolizing
glucose and
fatty acids, obtained from
blood and within the cell.
Each motor neuron "controls" a group of muscle cells, known as "motor units". When more strength is required than can be obtained from a single motor unit, more units will be stimulated; this is known as "motor unit recruitment". If more strength is required than can be obtained from the current degree of unit contraction, the motor neurons will send additional stimuli; this causes a process of contractile summation, which increases the degree of contraction. If a muscle is maximally contracted, it is said to be in a state of tetanic contraction.
Red and white fibers
Skeletal muscles contain two types of fibers, which differ in the mechanism they use to produce ATP; the amount of each type of fibre varies from muscle to muscle and from person to person.
- Red fibers have more mitochondria, store oxygen in myoglobin, rely on aerobic metabolism, have a greater capillary to volume ratio and are associated with endurance; these produce ATP more slowly. Marathon runners tend to have more red fibers, generally through a combination of genetics and training.
- White fibers have fewer mitochondria, are capable of more powerful contractions, metabolize ATP more quickly, have a lower capillary to volume ratio , and are more likely to accumulate lactic acid. Weightlifters and sprinters tend to have more white fibers.
Characteristics of muscle types
| Fibre Type | Type I fibres | Type II a fibres | Type II b fibres |
|---|
| Contraction time | Slow | Fast | Very fast |
| Size of motor neuron | Small | Large | Very large |
| Resistance to fatigue | High | Intermediate | Low |
| Activity Used for | Aerobic | Long-term anaerobic | Short-term anaerobic |
| Force production | Low | High | Very high |
| Mitochondrial density | High | High | Low |
| Capillary density | High | Intermediate | Low |
| Oxidative capacity | High | High | Low |
| Glycolytic capacity | Low | High | High |
| Major storage fuel | Triglycerides | Creatine phosphate, glycogen | Creatine phosphate, glycogen |
Genes that define skeletal muscle phenotype
Skeletal muscle fiber-type phenotype is regulated by several independent signaling pathways. These include pathways involved with the Ras/mitogen-activated protein kinase , calcineurin, calcium/calmodulin-dependent protein kinase IV, and the peroxisome proliferator ? coactivator 1 . The Ras/MAPK signaling pathway links the motor neurons and signaling systems, coupling excitation and transcription regulation to promote the nerve-dependent induction of the slow program in regenerating muscle. Calcineurin, a Ca2+/calmodulin-activated phosphatase implicated in nerve activity-dependent fiber-type specification in skeletal muscle, directly controls the phosphorylation state of the transcription factor NFAT, allowing for its translocation to the nucleus and leading to the activation of slow-type muscle proteins in cooperation with myocyte enhancer factor 2 proteins and other regulatory proteins. Calcium-dependent Ca2+/calmodulin kinase activity is also upregulated by slow motor neuron activity, possibly because it amplifies the slow-type calcineurin-generated responses by promoting MEF2 transactivator functions and enhancing oxidative capacity through stimulation of mitochondrial biogenesis.
Contraction-induced changes in intracellular calcium or reactive oxygen species provide signals to diverse pathways that include the MAPKs, calcineurin and calcium/calmodulin-dependent protein kinase IV to activate transcription factors that regulate gene expression and enzyme activity in skeletal muscle.
PGC1-a, a transcriptional coactivator of nuclear receptors important to the regulation of a number of mitochondrial genes involved in oxidative metabolism, directly interacts with MEF2 to synergistically activate selective ST muscle genes and also serves as a target for calcineurin signaling. A peroxisome proliferator-activated receptor d -mediated transcriptional pathway is involved in the regulation of the skeletal musclefiber phenotype. Mice that harbor an activated form of PPARd display an “endurance” phenotype, with a coordinated increase in oxidative enzymes and mitochondrial biogenesis and an increased proportion of ST fibers. Thus—through functional genomics—calcineurin, calmodulin-dependent kinase, PGC-1a, and activated PPARd form the basis of a signaling network that controls skeletal muscle fiber-type transformation and metabolic profiles that protect against insulin resistance and obesity.
The transition from aerobic to anaerobic metabolism during intense work requires that several systems are rapidly activated to ensure a constant supply of ATP for the working muscles. These include a switch from fat-based to carbohydrate-based fuels, a redistribution of blood flow from nonworking to exercising muscles, and the removal of several of the byproducts of anaerobic metabolism, such as carbon dioxide and lactic acid. Some of these responses are governed by transcriptional control of the FT glycolytic phenotype. For example, skeletal muscle reprogramming from a ST glycolytic phenotype to a FT glycolytic phenotype involves the Six1/Eya1 complex, composed of members of the Six protein family. Moreover, the Hypoxia Inducible Factor-1a has been identified as a master regulator for the expression of genes involved in essential hypoxic responses that maintain ATP levels in cells. Ablation of HIF-1a in skeletal muscle was associated with an increase in the activity of bob-limiting enzymes of the mitochondria, indicating that the citric acid cycle and increased fatty acid oxidation may be compensating for decreased flow through the glycolytic pathway in these animals. However, hypoxia-mediated HIF-1a responses are also linked to the regulation of mitochondrial dysfunction through the formation of excessive reactive oxygen species in mitochondria.
See also
- Myopathy—muscle pathology/diseases, Muscle atrophy, Muscle
