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The efficiency is defined as the ratio of mechanical work output to the total metabolic cost, as can be calculated from oxygen consumption.

The latter two losses are dependent on the type of exercise and the type of muscle fibers being used fast-twitch or slow-twitch.

For an overall efficiency of 20 percent, one watt of mechanical power is equivalent to 4. For example, one manufacturer of rowing equipment calibrates its rowing ergometer to count burned calories as equal to four times the actual mechanical work, plus kcal per hour, [18] this amounts to about 20 percent efficiency at watts of mechanical output.

These can be synthesized experimentally using work loop analysis. Muscle is a result of three factors that overlap: physiological strength muscle size, cross sectional area, available crossbridging, responses to training , neurological strength how strong or weak is the signal that tells the muscle to contract , and mechanical strength muscle's force angle on the lever, moment arm length, joint capabilities.

The force generated by a contraction can be measured non-invasively using either mechanomyography or phonomyography , be measured in vivo using tendon strain if a prominent tendon is present , or be measured directly using more invasive methods.

The strength of any given muscle, in terms of force exerted on the skeleton, depends upon length, shortening speed , cross sectional area, pennation , sarcomere length, myosin isoforms, and neural activation of motor units.

Significant reductions in muscle strength can indicate underlying pathology, with the chart at right used as a guide.

Since three factors affect muscular strength simultaneously and muscles never work individually, it is misleading to compare strength in individual muscles, and state that one is the "strongest".

But below are several muscles whose strength is noteworthy for different reasons. Exercise is often recommended as a means of improving motor skills , fitness , muscle and bone strength, and joint function.

Exercise has several effects upon muscles, connective tissue , bone, and the nerves that stimulate the muscles. One such effect is muscle hypertrophy , an increase in size of muscle due to an increase in the number of muscle fibers or cross-sectional area of myofibrils.

Generally, there are two types of exercise regimes, aerobic and anaerobic. Aerobic exercise e. Aerobic activities rely on the aerobic respiration i.

Muscles involved in aerobic exercises contain a higher percentage of Type I or slow-twitch muscle fibers, which primarily contain mitochondrial and oxidation enzymes associated with aerobic respiration.

The anaerobic activities predominately use Type II, fast-twitch, muscle fibers. Many exercises are partially aerobic and anaerobic; for example, soccer and rock climbing.

The presence of lactic acid has an inhibitory effect on ATP generation within the muscle. It can even stop ATP production if the intracellular concentration becomes too high.

However, endurance training mitigates the buildup of lactic acid through increased capillarization and myoglobin.

Once moved out of muscles, lactic acid can be used by other muscles or body tissues as a source of energy, or transported to the liver where it is converted back to pyruvate.

In addition to increasing the level of lactic acid, strenuous exercise results in the loss of potassium ions in muscle.

This may facilitate the recovery of muscle function by protecting against fatigue. Delayed onset muscle soreness is pain or discomfort that may be felt one to three days after exercising and generally subsides two to three days after which.

Once thought to be caused by lactic acid build-up, a more recent theory is that it is caused by tiny tears in the muscle fibers caused by eccentric contraction , or unaccustomed training levels.

Since lactic acid disperses fairly rapidly, it could not explain pain experienced days after exercise. Independent of strength and performance measures, muscles can be induced to grow larger by a number of factors, including hormone signaling, developmental factors, strength training , and disease.

Contrary to popular belief, the number of muscle fibres cannot be increased through exercise. Instead, muscles grow larger through a combination of muscle cell growth as new protein filaments are added along with additional mass provided by undifferentiated satellite cells alongside the existing muscle cells.

Biological factors such as age and hormone levels can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an accelerated rate as the levels of growth-stimulating hormones produced by the body increase.

Natural hypertrophy normally stops at full growth in the late teens. As testosterone is one of the body's major growth hormones, on average, men find hypertrophy much easier to achieve than women.

Taking additional testosterone or other anabolic steroids will increase muscular hypertrophy. Muscular, spinal and neural factors all affect muscle building.

Sometimes a person may notice an increase in strength in a given muscle even though only its opposite has been subject to exercise, such as when a bodybuilder finds her left biceps stronger after completing a regimen focusing only on the right biceps.

This phenomenon is called cross education. During ordinary living activities, between 1 and 2 percent of muscle is broken down and rebuilt daily.

Inactivity and starvation in mammals lead to atrophy of skeletal muscle, a decrease in muscle mass that may be accompanied by a smaller number and size of the muscle cells as well as lower protein content.

In humans, prolonged periods of immobilization, as in the cases of bed rest or astronauts flying in space, are known to result in muscle weakening and atrophy.

During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass, known as sarcopenia. The exact cause of sarcopenia is unknown, but it may be due to a combination of the gradual failure in the "satellite cells" that help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors that are necessary to maintain muscle mass and satellite cell survival.

Sarcopenia is a normal aspect of aging, and is not actually a disease state yet can be linked to many injuries in the elderly population as well as decreasing quality of life.

There are also many diseases and conditions that cause muscle atrophy. Examples include cancer and AIDS , which induce a body wasting syndrome called cachexia.

Other syndromes or conditions that can induce skeletal muscle atrophy are congestive heart disease and some diseases of the liver. In general, problems with nervous control can cause spasticity or paralysis , depending on the location and nature of the problem.

A large proportion of neurological disorders , ranging from cerebrovascular accident stroke and Parkinson's disease to Creutzfeldt—Jakob disease , can lead to problems with movement or motor coordination.

Symptoms of muscle diseases may include weakness , spasticity, myoclonus and myalgia. Diagnostic procedures that may reveal muscular disorders include testing creatine kinase levels in the blood and electromyography measuring electrical activity in muscles.

In some cases, muscle biopsy may be done to identify a myopathy , as well as genetic testing to identify DNA abnormalities associated with specific myopathies and dystrophies.

A non-invasive elastography technique that measures muscle noise is undergoing experimentation to provide a way of monitoring neuromuscular disease. The sound produced by a muscle comes from the shortening of actomyosin filaments along the axis of the muscle.

During contraction , the muscle shortens along its longitudinal axis and expands across the transverse axis , producing vibrations at the surface.

The evolutionary origin of muscle cells in metazoans is a highly debated topic. In one line of thought scientists have believed that muscle cells evolved once and thus all animals with muscles cells have a single common ancestor.

In the other line of thought, scientists believe muscles cells evolved more than once and any morphological or structural similarities are due to convergent evolution and genes that predate the evolution of muscle and even the mesoderm —the germ layer from which many scientists believe true muscle cells derive.

Schmid and Seipel argue that the origin of muscle cells is a monophyletic trait that occurred concurrently with the development of the digestive and nervous systems of all animals and that this origin can be traced to a single metazoan ancestor in which muscle cells are present.

They argue that molecular and morphological similarities between the muscles cells in cnidaria and ctenophora are similar enough to those of bilaterians that there would be one ancestor in metazoans from which muscle cells derive.

In this case, Schmid and Seipel argue that the last common ancestor of bilateria, ctenophora, and cnidaria was a triploblast or an organism with three germ layers and that diploblasty , meaning an organism with two germ layers, evolved secondarily due to their observation of the lack of mesoderm or muscle found in most cnidarians and ctenophores.

By comparing the morphology of cnidarians and ctenophores to bilaterians, Schmid and Seipel were able to conclude that there were myoblast -like structures in the tentacles and gut of some species of cnidarians and in the tentacles of ctenophores.

Since this is a structure unique to muscle cells, these scientists determined based on the data collected by their peers that this is a marker for striated muscles similar to that observed in bilaterians.

The authors also remark that the muscle cells found in cnidarians and ctenophores are often contests due to the origin of these muscle cells being the ectoderm rather than the mesoderm or mesendoderm.

The origin of true muscles cells is argued by others to be the endoderm portion of the mesoderm and the endoderm.

However, Schmid and Seipel counter this skepticism about whether or not the muscle cells found in ctenophores and cnidarians are true muscle cells by considering that cnidarians develop through a medusa stage and polyp stage.

They observe that in the hydrozoan medusa stage there is a layer of cells that separate from the distal side of the ectoderm to form the striated muscle cells in a way that seems similar to that of the mesoderm and call this third separated layer of cells the ectocodon.

They also argue that not all muscle cells are derived from the mesendoderm in bilaterians with key examples being that in both the eye muscles of vertebrates and the muscles of spiralians these cells derive from the ectodermal mesoderm rather than the endodermal mesoderm.

Furthermore, Schmid and Seipel argue that since myogenesis does occur in cnidarians with the help of molecular regulatory elements found in the specification of muscles cells in bilaterians that there is evidence for a single origin for striated muscle.

In contrast to this argument for a single origin of muscle cells, Steinmetz et al. This author uses an example of the contractile elements present in the porifera or sponges that do truly lack this striated muscle containing this protein.

Furthermore, Steinmetz et al. Steimetz et al. Thus, the usage of any of these structural or regulatory elements in determining whether or not the muscle cells of the cnidarians and ctenophores are similar enough to the muscle cells of the bilaterians to confirm a single lineage is questionable according to Steinmetz et al.

Furthermore, Steinmetz et all showed that the localization of this duplicated set of genes that serve both the function of facilitating the formation of striated muscle genes and cell regulation and movement genes were already separated into striated myhc and non-muscle myhc.

This separation of the duplicated set of genes is shown through the localization of the striated myhc to the contractile vacuole in sponges while the non-muscle myhc was more diffusely expressed during developmental cell shape and change.

Steinmetz et al. Thus, Steinmetz et al. Furthermore, the Z-disc seemed to have evolved differently even within bilaterians and there is a great deal diversity of proteins developed even between this clade, showing a large degree of radiation for muscle cells.

Through this divergence of the Z-disc , Steimetz et al. Through further molecular marker testing, Steinmetz et al. Through this analysis the authors conclude that due to the lack of elements that bilaterians muscles are dependent on for structure and usage, nonbilaterian muscles must be of a different origin with a different set regulatory and structural proteins.

In another take on the argument, Andrikou and Arnone use the newly available data on gene regulatory networks to look at how the hierarchy of genes and morphogens and other mechanism of tissue specification diverge and are similar among early deuterostomes and protostomes.

By understanding not only what genes are present in all bilaterians but also the time and place of deployment of these genes, Andrikou and Arnone discuss a deeper understanding of the evolution of myogenesis.

In their paper Andrikou and Arnone argue that to truly understand the evolution of muscle cells the function of transcriptional regulators must be understood in the context of other external and internal interactions.

Through their analysis, Andrikou and Arnone found that there were conserved orthologues of the gene regulatory network in both invertebrate bilaterians and in cnidarians.

They argue that having this common, general regulatory circuit allowed for a high degree of divergence from a single well functioning network.

Andrikou and Arnone found that the orthologues of genes found in vertebrates had been changed through different types of structural mutations in the invertebrate deuterostomes and protostomes, and they argue that these structural changes in the genes allowed for a large divergence of muscle function and muscle formation in these species.

Andrikou and Arnone were able to recognize not only any difference due to mutation in the genes found in vertebrates and invertebrates but also the integration of species specific genes that could also cause divergence from the original gene regulatory network function.

Thus, although a common muscle patterning system has been determined, they argue that this could be due to a more ancestral gene regulatory network being coopted several times across lineages with additional genes and mutations causing very divergent development of muscles.

Thus it seems that myogenic patterning framework may be an ancestral trait. However, Andrikou and Arnone explain that the basic muscle patterning structure must also be considered in combination with the cis regulatory elements present at different times during development.

In contrast with the high level of gene family apparatuses structure, Andrikou and Arnone found that the cis regulatory elements were not well conserved both in time and place in the network which could show a large degree of divergence in the formation of muscle cells.

Through this analysis, it seems that the myogenic GRN is an ancestral GRN with actual changes in myogenic function and structure possibly being linked to later coopts of genes at different times and places.

Vertebrate smooth muscle was found to have evolved independently from the skeletal and cardiac muscle types.

From Wikipedia, the free encyclopedia. For other uses, see Muscle disambiguation. Contractile soft tissue of mammals. Main article: Muscle tissue.

Main articles: Myocyte and Sarcomere. See also: List of muscles of the human body. Main article: Muscular system.

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