A 2007 study, conducted by Blazevich  et al. , reiterated and added an extra dimension to Aagaard  et al. ’s conclusions. [ 6 ] [ 7 ]  Blazevich  et al.  examined the effect of 10-week concentric or eccentric knee extension training on architectural properties of the human quadriceps with the purpose of uncovering the mechanical stimulus involved in architecture adaptation. Both modes of exercise resulted in increased peak concentric and eccentric strength. Concentric training, however, results in higher peak concentric strength. Ultrasonography suggests vastus medialus and vastus lateris muscle fiber length increase similarly following eccentric and concentric training, with the changes occurring abruptly over the first 5 weeks of the training program. Because fiber length was independent of training type, Blazevich  et al.  believe distance of operation determines the optimal fiber length. This muscle property is important in determining the  angle-torque  relationship of a muscle. The study supported the pennation angle trends uncovered by Aagaard  et al. ; in addition, Blazevich  et al.  concluded that the vastus lateris fascicle angle changes are independent of training type and modulates strongly with volume. This suggests fiber length and pennation angle modifications occur via separate mechanical stimuli, i.e. distance of operation and muscle volume respectively. Furthermore, these angle changes occur over a relatively long time scale as the pennation angle increased until the cessation of the training program at week 10. Blazevich  et al.  predict the increase in pennation angle seen after eccentric or concentric training allow the pennate muscle to attach more fibers to the associated aponeurosis as well as increase PCSA and AGR. Architectural modifications to pennate muscles shift the position at which the muscle operates on the force-velocity and force-length curves to regions best suited for the muscle's function. An increase in pennation angle theoretically increases both the PCSA and AGR of a given pennate muscle, allowing the muscle to generate higher forces while operating at higher optimal speeds. An increase to fiber length would allow the muscle to function at longer lengths. [ 6 ] [ 7 ]


A 2009 study utilizing  magnetic resonance imaging  and  ultrasonography  discovered strain and pennation angle heterogeneity within the  medial gastrocnemius  pennate muscle during differing modes of contraction. Parameters of fascicle location and contraction type (eccentric or passive), determined the magnitude of strain experienced by differing regions of the MG. [ 6 ]
 Fascicle  ends nearest the deep MG  aponeurosis  (Achilles tendon) showed an increase in strain from the  proximal to distal  portions of the MG muscle. The converse was seen in the fascicle ends adjacent to the superficial aponeurosis, which decreased in fiber strain from proximal to distal portions of the MG muscle. These trends may have been due to changes in CSA of the muscle at the proximal and distal ends of the MG, resulting in regions of high stress and strain concentration. [ 6 ]
This regional variability in strain was accompanied by a statistically significant increase in AGR and resting pennation angle from distal to proximal portions of the muscle. Furthermore, greater changes in pennation angle were visible at the proximal end of the MG. The experimental AGR values modulated positively with the pennation angle as well as the distance between the deep and superficial apopneuroses and may have been affected by regional patterns in orthogonal bulging. These trends highlight the complexity of muscle physiology, as different regions of muscles may contract with diverse contractile properties, such as strain and AGR. [ 6 ]


Arm recoil  is a  neurological examination  of  neonate  for detecting the  muscle tone . [ 1 ] [ 2 ]


The baby is placed supine, with forearm flexed at elbow. The elbow (forearm) is extended by pulling the hand; then released. [ 3 ]


How quickly the forearm returns to flexed original position and the amount of flexion will designate a score. [ 1 ]


The greater the tone development (flexor tone), the brisker the recoil will be. [ 1 ]  This correlates to more advanced gestational age on the  Ballard Scale . [ 4 ]


Leg recoil can be assessed following the same principle. [ 5 ]


This  muscle  article is a  stub . You can help Wikipedia by  expanding it .


This  medical  diagnostic article is a  stub . You can help Wikipedia by  expanding it .


The  arrector pili muscles , also known as  hair erector muscles , [ 1 ]  are small muscles attached to  hair follicles  in  mammals . Contraction of these muscles causes the hairs to stand on end, [ 2 ]  known colloquially as  goose bumps  (piloerection). [ 3 ]


Each arrector pili is composed of a bundle of  smooth muscle  fibres which attach to several follicles (a follicular unit). [ 4 ]  Each is innervated by the sympathetic division of the  autonomic nervous system . [ 4 ]  The muscle attaches to the follicular stem cell niche in the follicular bulge, [ 3 ] [ 4 ] [ 5 ]  splitting at their deep end to encircle the follicle. [ 6 ]


The contraction of the muscle is involuntary. Stresses such as  cold ,  fear  etc. may stimulate the  sympathetic nervous system , and thus cause muscle contraction. [ 4 ]


Contraction of arrector pili muscles have a principal function in the majority of mammals of providing thermal insulation. [ 4 ]  Air becomes trapped between the erect hairs, helping the animal retain heat.


Many animals experience contraction of the arrector pili muscle in response to a perceived threat. This helps the animal seem more larger and more intimidating as a result. [ 7 ]


Pressure exerted by the muscle may cause  sebum  to be forced along the hair follicle towards the surface, protecting the hair. [ 8 ]


Arrector pili muscles also stabilise the base of the  hair follicle . [ 5 ] [ 6 ]


Skin conditions such as  leprosy  can damage arrector pili muscles, preventing their contraction. [ 9 ]  Inducing contraction of the arrector pili muscles via an  α1-adrenergic receptor  agonist has been shown to reduce hair shedding as a result of  traction alopecia [ 10 ]


The term "arrector pili" comes from Latin. It translates to "hair erector". [ 1 ]


Asynchronous muscles  are muscles in which there is no one-to-one relationship between electrical stimulation and mechanical contraction. These muscles are found in 75% of  flying insects  and have  convergently evolved  7-10 times. [ 1 ]  Unlike their synchronous counterparts that contract once per neural signal, mechanical oscillations trigger force production in asynchronous muscles. Typically, the rate of mechanical contraction is an order of magnitude greater than electrical signals. [ 1 ]  Although they achieve greater force output and higher efficiency at high frequencies, they have limited applications because of their dependence on mechanical stretch.


The exact molecular mechanisms used by asynchronous muscles are unknown, but it is believed that asynchronous muscles have no unique molecular structures as compared to their synchronous counterparts. A study investigating the asynchronous power muscles in  bumblebees  with  X-ray diffraction  videos showed that  actin  and  myosin  alone are sufficient for generating asynchronous behavior. [ 2 ]  This finding helps explain how asynchronous muscles independently evolved across insect  taxa . [ 1 ]  More recent work using similar X-ray diffraction techniques in  Lethocerus  discovered that troponin bridges may play a critical role in stretch activation. As the muscle is stretched, these bridges move tropomyosin to reveal myosin-actin binding sites. [ 3 ]  The muscle can only produce force when these sites are activated.


Several changes to asynchronous muscles' macroscopic structure provide it with high force production and efficiency at high contraction frequencies. A critical adaptation is that asynchronous muscles maintain a tonic level of calcium instead of cycling calcium between contractions. This is evident in their  long twitch duration . This is due to relatively spare  sarcoplasmic reticulum . Because of requirements for high force production,  myofiber  and  myofibril  diameters are increased and the large amount of ATP necessary leads to high  mitochondria  densities. [ 1 ]  In  Cotinus mutabilis ,  asynchronous muscles are composed of 58.1% myofibril, 36.7% mitochondria, and 1.6%  sarcoplasmic reticulum . In comparison, synchronous muscles in  Schistocerca americana  are composed of 65% myofibril, 23.5% mitochondria and 9.6% sarcoplasmic reticulum. [ 1 ]  Although synchronous muscle has a higher percentage of myofibril, the cross-sectional area of asynchronous myofibril is 3.7 μm 2  as opposed to 0.82 μm 2  in synchronous muscle for the previously described species. [ 1 ]


The defining characteristic of asynchronous muscles is that there is no direct relationship between neural activation and  muscle contraction . Typically, the number of muscle contractions is an order of magnitude greater than the number of action potentials sent to the muscle. Instead of directly controlling force generation, neural signals maintain [Ca 2+ ] above a threshold for stretch-activation to occur. [ 4 ]  For asynchronous muscles, neural inputs are typically thought of as an "on-off" switch while mechanical stimulus leads to individual muscle contractions. However, recent studies using genetically engineered  Drosophila  revealed correlations between [Ca 2+ ] and force production. [ 5 ]  Further work has shown bilateral calcium asymmetries in  Drosophila . [ 4 ]  These results indicate that there is some level of neural control beyond a simple "on" or "off" state.


Delayed stretch activation and delayed shortening deactivation allow asynchronous muscles to generate positive work under cyclic  oscillations . [ 6 ]  When the muscle shortens, force drops and continues dropping even when the muscle length remains constant. Similarly, when the muscle lengthens, force increases and continues increasing after the muscle length remains constant. [ 1 ]  Because of these delays, the work produced by the muscle during shortening is greater than the work absorbed during lengthening, therefore producing positive work. In contrast, synchronous muscles absorb work under similar conditions. [ 1 ]  Both types of muscles consume ATP to drive force production and produce work. [ 6 ]


Long twitch duration is a functional consequence of the macroscopic properties of asynchronous muscle. Because asynchronous muscle can generate power without cycling calcium between contractions, the required rate of calcium regulation is significantly slower. In addition to the reduction in sarcoplasmic reticulum, relatively large myofibril diameters lead to increased diffusion times of Ca 2+ .Under isometric twitch experiments, asynchronous muscle in  Cotinus mutabilis  were found to have a twitch duration of 125 ms. In the same study, synchronous muscle in  Schistocerca americana  had a twitch duration of 40 ms. [ 1 ]  Therefore, asynchronous muscles respond slowly to neural stimulus. In the case of insect flight, electrical stimulation alone is too slow for muscle control. For  Cotinus mutabilis , the twitch duration is ten times as long as a wingbeat period. [ 1 ]


Asynchronous muscles produce work when they undergo mechanical oscillations provided there is sufficient Ca 2+ . [ 1 ] [ 6 ]  This can be achieved in one of two ways. First, two antagonistic muscles can be configured with elastic structures such that the contraction of one muscle stretches the other, causing it to activate and vice versa. This configuration is found in the power muscles of flying insects. [ 7 ]  Second, a single asynchronous muscle can deform an elastic element which then stretches the muscle and causes the muscle to contract again. This setup is used by  Drosophila  to oscillate mechanosensory organs known as  halteres . [ 8 ]  As long as neural stimulus turn the muscles "on", both systems will continue to oscillate. These systems can be thought of as  resonant  systems, for which the oscillation frequency is dependent on the  elasticity ,  damping , and force applied to the system. [ 9 ]


In a simplified case, this can be thought of as a linearly damped  harmonic oscillator , for which the damped resonant frequency is


ω
 =

 (

 k
 m

 )

 (
 1
 −

 ζ

 2

 )

 .

 {\displaystyle \omega ={\sqrt {{\bigg (}{\frac {k}{m}}{\bigg )}(1-\zeta ^{2})}}.}


The damping ratio,  ζ ,  is dependent on c, the damping coefficient, m, the mass of the system, and k, the stiffness of the system as shown


ζ
 =

 c

 2

 m
 k

 .

 {\displaystyle \zeta ={\frac {c}{2{\sqrt {mk}}}}.}


Asynchronous muscles sacrifice neural control and flexibility in exchange for high force production and efficiency. Given the long twitch duration of asynchronous muscle, neural control is too slow to power flight. For instance, the asynchronous muscles in  Cotinus mutabilis  contract ten times faster than expected given their twitch duration. [ 1 ]  Because these muscles rely on stretch activation, they must be configured such that they can be stretched by an external force. Furthermore, they are only useful when evolutionary pressures select for a muscle that reactively contracts against an imposed stretch. For example, in grasping tasks, it would be detrimental for antagonist muscles to spontaneously contract. Despite these disadvantages, asynchronous muscles are beneficial for high frequency oscillations. They are more efficient than synchronous muscles because they do not require costly calcium regulation. [ 6 ]  This allows for changes in their  macroscopic structure  for increased force production.


Miniaturization of  insects  leads to high wingbeat frequencies with  midges  reaching wingbeat frequencies of 1000 Hz. [ 10 ]  Because of their high force production and efficiency, asynchronous muscles are used to power  insect flight  in 75% of species. These insects possess two pairs of  antagonistic  asynchronous muscles that produce the majority of the power required for flight. These muscles are oriented such that as one pair contracts, it deforms the thorax and stretches the other pair, causing the second pair to contract. [ 7 ]  The same thoracic deformations oscillate the wings. By utilizing the elastic thorax to store and return energy during wing deceleration and subsequent acceleration,  Drosophila  is able to reduce energetic costs by 10%. [ 11 ]  This leads to a highly-efficient resonant system.


When wingbeat frequencies match the resonant frequency of the muscle-thorax system, flight is most efficient. In order to change wingbeat frequencies to avoid obstacles or generate more lift, insects use smaller "control" muscles such as the pleurosternal muscles to stiffen the thorax. [ 9 ]  From the equations in the  Resonant properties  section, it is clear that the natural frequency of the system increases with stiffness. Therefore, modulating the stiffness of the thorax leads to changes in wingbeat frequency.


Although heart muscles are not strictly asynchronous, they exhibit delayed stretch activation properties. As  cardiac muscle  is lengthened, there is an instantaneous rise in force caused by elastic, spring-like elements in the muscle. After a time delay, the muscle generates a second rise in force, which is caused by delayed stretch activation as seen in purely asynchronous muscle. [ 12 ]  This property benefits heart function by maintaining  papillary muscle  tension during the entire  systolic  cycle well after the electrical wave has passed. [ 12 ]  Through stretch activation, the heart can rapidly adapt to changes in heart rates.


Because of challenges arising from miniaturization such as poor scaling of electric motors, researchers have turned towards insects to develop centimeter-scale flying robots. [ 13 ]  Although the actuators in the  RoboBee  are not asynchronous, they use elastic elements to transmit forces from its "muscles" ( piezoelectric  actuators) to flap the wings. Similar to flying insects, they exploit resonance to improve efficiency by 50%. [ 14 ]


The  axillary spaces  are  anatomic spaces . [ 1 ]  through which axillary contents leave the axilla. [ 2 ]  They consist of the  quadrangular space ,  triangular space , and  triangular interval . It is bounded by  teres major ,  teres minor , medial border of the  humerus , and long head of  triceps brachii . [ 3 ]


They should not be confused with the true "axillary space" within the borders of the axilla.


The true axilla is a conical space with its apex at the Cervico-axillary Canal, Base at the axillary fascia and skin of the armpit.  When viewed in an axillary plane (axillary cut), it is more triangle with:  Medial Wall:  Serratus Anterior,  Anterior Wall:   pectoral muscles,  Posterior Wall:  subscapularis muscle, where the "apex" of the triangle is the humerus [ 4 ] [ 5 ]


This space is in the posterior wall of the axilla.  It is a quadrangular space bounded laterally by surgical neck of the humerus, medially by long head of triceps brachii and inferiorly by  teres major . It is bounded superiorly by  subscapularis  in front, capsule of the shoulder joint in the middle, and behind by  teres minor . The  axillary nerve  and  posterior humeral circumflex artery  and vein pass through this space. [ 3 ]


This space (sin.  medial triangular space ) is also in the posterior wall of the axilla.  It is a triangular space bounded medially by teres minor, laterally by long head of triceps brachii, and inferiorly by teres major. The  scapular circumflex artery  and scapular circumflex vein pass through this space. [ 3 ]


This space (a.k.a.  lateral triangular space ) is in the inferior to the posterior wall of the axilla. The  triangular interval  is bounded medially by long head of triceps brachii, laterally by medial border of humerus (some say the lateral head of the triceps), and superiorly by teres major. The  radial nerve  and  profunda brachii artery   and vein passes through this space. [ 3 ]


The  Axioappendicular muscles  are the muscles that extend between the  axial  and (superior or inferior)  appendicular skeletons . There are two groups, the  anterior axioappendicular muscles  and the  posterior axioappendicular muscles .


The anterior axioappendicular muscles are the: [ 1 ] [ 2 ]


The posterior axioappendicular muscles are described as two sub-groups: [ 1 ] [ 3 ]


Ballistic movement  can be defined as  muscle  contractions that exhibit maximum velocities and accelerations over a very short period of time. They exhibit high firing rates, high force production, and very brief contraction times.


The  muscle contraction  of a ballistic muscle movement can exhibit a  muscle coactivation  of concurrent agonist  [ 1 ]  and antagonist muscles or the characteristic triphasic agonist/antagonist/agonist muscle activation. [ 2 ]   Electromyography  (EMG) recordings of demonstrate the triphasic muscle activation begins with a brief agonist motor unit activation signal with firing rates of 60 to 120 Hz that may last for 100ms and occurs 50 to 100ms before movement begins.  The firing rates of  ballistic movements are much higher than that of slow ramp movements (5–15 Hz). The brief agonist muscle contraction is thus followed by antagonist muscle unit activation. The degree of antagonist muscle unit activation is dependent on the task at hand unlike the first agonist muscle activation which is independent to environmental stimuli. The function of the antagonist muscle contraction is believed to control the amplitude and timing of ballistic movements. Antagonist muscle contraction may serve to prevent injury to joints by preventing the limb from overextending itself and also function to control the distance and time the limb is being moved. Experiments involving ballistic movement of small amplitudes show a marked increase in antagonist muscle activation and experiments where distance moved is not controlled antagonist muscle activation was decreased or absent. [ 2 ]  The second agonist muscle activation is suggested to terminate the negative acceleration of the antagonist muscle contraction and thus the ballistic movement.


Ballistic movements are often powered through  elastic energy  storage and subsequent recovery mechanisms.  The  power  required to produce the extremely rapid velocities of ballistic movements is made possible through muscle work being stored in elastic elements (such as  tendons ,  aponeuroses , or even muscle).  Muscle work is applied to these elastic elements over a relatively slow period of time, and is released very rapidly. [ 3 ]  Higher power output is produced because the energy is released in a much shorter amount of time than it is stored.  In this sense the power of the muscles is actually amplified.  When energy is produced by muscle contraction, stored in a tendon, then released to increase mechanical energy of the body (or body segment), muscle power is amplified. It is important to note, however, that the term power ‘amplification’ may be deceptive. In animals,  elastic mechanisms  never add energy to the system; they amplify power in the sense that the energy is released more rapidly than it is stored. [ 4 ]


Ballistic systems are capable of power outputs that are significantly greater than that of the muscles associated with the actual movement.  One prime example of this is tongue projection in  salamanders . [ 5 ]   This decoupling of muscle work from body/limb work is a major benefit of elastic energy storage mechanisms.  Another benefit resulting from this decoupling is decreased thermal dependence of ballistic movement. [ 6 ]  Deban and Lappin analyzed the prey capture behavior of  toads  (Bufo terrestris), which involves two types of movement: elastically powered, ballistic movement (mouth opening and tongue projection) and muscle-powered movement (tongue retraction and mouth closing). The toad feeding was observed across a range of temperatures (11–35 °C), and the kinematic, dynamic, and electromyographic variables were measured and analyzed. Over the 11–35 °C temperature range, the ballistic movements had  Q 10  values very close to 1 (Q 10  = 0.99–1.25), signifying thermal independence and supporting the main hypothesis. The muscle-powered movements had a higher temperature coefficient (Q 10  = 1.77–2.26), signifying thermal dependence.


Another example of a thermally independent ballistic movement is tongue projection in  chameleons . [ 7 ]  It was discovered that veiled chameleons (Chamaeleo calyptratus) were able to perform this high-performance tongue projection, and successful prey capture, across a wide range of temperatures (15 °C–35 °C).  Anderson and Deban also found a contrast between thermal dependence of tongue projection and retraction (which is not elastically-powered).  This further supports the hypothesis that the elastic recoil mechanism is responsible for the decreased thermal dependence of ballistic tongue projection.


In trap-jaw ants ( Odontomachus  bauri) ballistic movement can be seen in their extremely rapid mandible strikes. The trap-jaw ants mandible has an average closing speed of 38.4 m/s and can produce forces that are 371-504 times the weight of the ant. The ants use these extremely powerful mandible strikes in several novel ways. When the ant attacks a larger animal it will strike the animal and at the same time use the force from the strike to propel itself away from the animal. When facing prey of similar size such as another ant the strike actually results in both animals being propelled away from each other. When the ant is trying to flee from a predator it will strike at the substrate and propel itself vertically into the air. [ 8 ]


In crickets ( Acheta domesticus ) ballistic movements can be seen in the way they jump. The kicks that propel the cricket occur over a period of only 2-6ms, but during the 18-40ms prior to the kick the potential energy required is built up by the co-contraction of the antagonistic extensor and flexor tibiae. The crickets can also use these same ballistic movements for swimming. [ 9 ]


In the cone snail ( Conus catus ) ballistic movement can be seen in the way that it fires is harpoon-like radular tooth into its prey. After the cone snail’s proboscis comes in contact with its prey the tooth is ejected 240-295 ms later. It is believed that the propulsion of the tooth is accomplished by pressurizing the fluid space behind the tooth. [ 10 ]


In  Salamanders ,  Toads , and  Chameleons  ballistic movement can be seen in their tongue projection which is controlled by an elastic recoil mechanism. The orientation of the muscle fibers is significant because it is what allows ballistic movements to be possible.  In chameleons, the  muscle fibers  used for ballistic tongue movements were found to be in a spiral orientation, with an equal amount of fibers oriented clockwise and anti-clockwise to prevent torsional movement of the tongue during projection.  The internal fiber angles are approximately 45 degrees, which is the theoretical optimum to create an equal strain throughout the accelerator muscles. [ 11 ]


In salamanders of the genus  Hydromantes , the pattern of muscle activation has been mapped.   The main muscles used for ballistic tongue movements in these salamanders are the subarcualis rectus (SAR) muscles.  These SAR muscles can be further divided into anterior (SARA) and posterior (SARP).  The first muscle to be activated is the SARA, which is located near the back of the head.  The SARA remains active until the tongue makes contact with the prey.  Next, the posterior SARP, located further back on the medial and lateral sides of the salamander is activated.  Then the middle SARP is activated and the anterior SARP is the last to be activated.  The time between activation shortens and duration of activation increases with increasing prey distance. Ballistic tongues have evolved two times previously in the Hemidactyliini and Bolitoglossini genera.  The exact mechanisms of tongue projection vary slightly throughout the taxa, but the resulting projections have remained relatively constant. [ 12 ]


Frogs  do not have a specialized muscular structure for tongue projection.  They are able to bypass this issue by using very rapid jaw movement to project the tongue forward.  Present in all frogs are the two mandibular muscles that are used to control the jaw and, therefore, tongue projection.  The m. genioglossus is used to protract the tongue and the m.hyoglossus is the tongue retractor.  Both of these muscles have longitudinally oriented fibers, which is in contrast to the spiral oriented fibers of the chameleon. [ 13 ]


In human, ballistic movements involve spontaneous propulsion of the limbs. [ 14 ]  This can be seen in daily routines such as reach and strike reactions, which are atomic by nature. Pointing gestures and placing an object are reach reactions; they have low acceleration and deceleration. On the other hand, punching and throwing are strike reactions; they are characterized by high acceleration and deceleration. These movements have highly variable target locations, and they are referred to as “ballistic” in  kinesiology . During ballistic movement an initial impulse is needed to accelerate the limb (hand/foot) toward the target, then a decelerating impulse act as a brake to stop the movement.  These movements are characterized by a bell-shaped velocity profile. The Bayesian Model (see  Bayesian network ), which was developed to perform recognition without pose-tracking, explains human ballistic movement as a sequence of movements between objects and the environment. Each movement is independent from precedent and subsequent one, in varying context. Fast single joints movement in humans is controlled by a series of activation of agonist, antagonist and then agonist muscles; this process is called triphasic activation.  Those movements are executed “with a pattern of bursts in the agonist and antagonist muscles of fairly constant duration but different amplitude…” (Acornero et al. 1984). [ 15 ]  Any ballistic movement involving two joints will require an agonist and an antagonist burst; this can be viewed as the building blocks for different types of ballistic movements.


Balloonist theory  was a theory in early  neuroscience  that attempted to explain  muscle  movement by asserting that muscles contract by inflating with air or fluid. The Roman and Greek physician  Galen  believed that muscles contracted due to a fluid flowing into them, and for 1500 years afterward, it was believed that nerves were hollow and that they carried fluid. [ 1 ]   René Descartes , who was interested in  hydraulics  and used fluid pressure to explain various aspects of  physiology  such as the  reflex arc , proposed that "animal spirits" flowed into muscle and were responsible for their contraction. [ 2 ]  In the model, which Descartes used to explain  reflexes , the spirits would flow from the  ventricles of the brain , through the nerves, and to the muscles to animate the latter. [ 3 ]


In 1667,  Thomas Willis  proposed that muscles may expand by the reaction of animal spirits with vital spirits.  He hypothesized that this reaction would produce air in a manner similar to the reaction that causes an explosion, causing muscles to swell and produce movement.
This theory has now been  superseded  by the mainstream scientific community due to the establishment of neuroscience, which is supported by empirical evidence.


In 1667,  Jan Swammerdam , a Dutch  anatomist  famous for working with insects, struck the first important blow against the balloonist theory.  Swammerdam, who was the first to experiment on  nerve-muscle preparations , showed that muscles do not increase in size when they contract (and he supposed if a substance such as animal spirits flowed into muscles, their volume should increase when they contract).  Swammerdam placed severed frog thigh muscle in an airtight syringe with a small amount of water in the tip. [ 3 ]   He could thus determine whether there was a change the volume of the muscle when it contracted by observing a change in the level of the water (image at right). [ 3 ]  When Swammerdam caused the muscle to contract by irritating the nerve, the water level did not rise but rather was lowered by a minute amount; this showed that no air or fluid could be flowing into the muscle. [ 3 ]   Swammerdam did not believe the results of his own experiment, suggesting that they were the result of artifact. [ 3 ]   However, he concluded in his book  The Book of Nature II  that "motion or irritation of the nerve alone is necessary to produce muscular motion". [ 3 ]  This idea was an important step toward the current understanding of how nerves actually cause muscle contraction. [ 3 ]


Balloonist theory took a second hit from  Francis Glisson  who performed an experiment in which a man flexed a muscle under water. The water level did not go up (in fact it went down slightly), further supporting the conclusion that no air or fluid could be entering the muscle.


Giovanni Alfonso Borelli  performed an experiment to test the idea that muscle is inflated by air. He slit the muscle of an animal under water and watched to see whether bubbles of air would rise to the surface. Since no bubbles were seen to rise, this experiment helped to refute the balloonist theory.


The invention of the  microscope  allowed preparations of nerves to be viewed at high magnification, showing that they are not hollow.


In 1791,  Luigi Galvani  learned that frogs' muscles could be made to move by the application of  electricity .  This finding provided a basis for the current understanding that electrical energy (carried by  ions ), and not air or fluid, is the impetus behind muscle movement.


Biarticular muscles  are  muscles  that cross two  joints  rather than just one, such as the  hamstrings  which cross both the  hip  and the  knee . The function of these muscles is complex and often depends upon both their anatomy and the activity of other muscles at the joints in question. Their role in movement is poorly understood.


Biarticular muscles cross two joints in series, usually in a limb. The details of the origin (proximal attachment) and insertion (distal attachment) can play a large role in determining muscle function. For instance, the human  gastrocnemius  technically spans both the knee and ankle joints.  However, the origin point of the muscle is so close to the axis of rotation of the knee joint that the muscle's effective  lever arm  would be very small, especially compared to its large lever arm at the ankle. [ citation needed ]  As a result, even though it spans two joints, the strong bias in lever arms allows it to function primarily as an ankle plantar flexor. Other muscles, such as the  hamstrings , do not display such biases, so their function is not immediately evident from anatomy alone. Another important concept of biarticular muscles (consider the rectus femoris muscle for this example) is the change in muscle length when motion at the proximal and distal ends of the muscle is happening. For example, in the propulsive phase of a jump, the thigh is extended at the coxal joint, and the shank (lower leg) is extended at the tibiofemoral joint. These joint positions cause the rectus femoris muscle to remain unchanged in net length, because the proximal (Eccentric action) and distal (concentric action) attachments are contradicting one another.


Biarticular muscles can fulfill a range of functions during movement.  By contracting  isometrically  (without changing length), they put the joint into a  four-bar linkage , allowing the contraction of muscles at one joint to move the other by a fixed amount.  Unlike four-bar linkages in which all elements are bone and angle relationships are fixed by the relative bone lengths, the biarticular muscle can hold the joint at many different lengths, creating a range of four-bar properties as needed.


Biarticular muscles can also transfer mechanical power between distal and proximal joints, though the direction and magnitude of this transfer varies with anatomy, muscle activity level, and joint angles.  This is a crucial consideration when analyzing an organism's movement using  inverse dynamics .


Calcium-induced calcium release  ( CICR ) describes a biological process whereby  calcium  is able to activate calcium release from intracellular Ca 2+  stores (e.g.,  endoplasmic reticulum  or  sarcoplasmic reticulum ). Although CICR was first proposed for  skeletal muscle  in the 1970s, [ 1 ]  it is now known that CICR is unlikely to be the primary mechanism for activating  SR  calcium release. Instead, CICR is thought to be crucial for  excitation-contraction coupling  in  cardiac muscle . [ 2 ]  It is now obvious that CICR is a widely occurring cellular signaling process present even in many non-muscle cells, such as in the insulin-secreting pancreatic  beta cells , [ 3 ]  epithelium, and many other cells. [ 4 ]  Since CICR is a  positive-feedback system , it has been of great interest to elucidate the mechanism(s) responsible for its termination.


Excitation-contraction coupling  in myocardium relies on sarcolemma depolarization and subsequent Ca 2+  entry  to trigger Ca 2+  release from the  sarcoplasmic reticulum . When an  action potential  depolarizes the cell membrane, voltage-gated Ca 2+  channels (e.g.,  L-type calcium channels ) are activated. CICR occurs when the resulting Ca 2+  influx activates  ryanodine receptors  on the  SR  membrane, which causes more Ca 2+  to be released into the cytosol. [ 4 ] [ 5 ]  In cardiac muscle, the result of CICR is observed as a spatio-temporally restricted  Ca 2+  spark . The result of CICR across the cell causes the significant increase in cytosolic Ca 2+  that is important in activating muscle contraction.


Cardiac muscle  (also called  heart muscle  or  myocardium ) is one of three types of  vertebrate   muscle tissues , the others being  skeletal muscle  and  smooth muscle . It is an involuntary,  striated muscle  that constitutes the main tissue of the  wall of the heart . The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall (the  pericardium ) and the inner layer (the  endocardium ), with blood supplied via the  coronary circulation .  It is composed of individual cardiac muscle cells joined by  intercalated discs , and encased by  collagen fibers  and other substances that form the  extracellular matrix .


Cardiac muscle  contracts  in a similar manner to  skeletal muscle , although with some important differences.  Electrical stimulation in the form of a  cardiac action potential   triggers the release of calcium from the cell's internal calcium store, the  sarcoplasmic reticulum .  The rise in calcium causes the cell's  myofilaments  to slide past each other in a process called  excitation-contraction coupling .
Diseases of the heart muscle known as  cardiomyopathies  are of major importance.  These include  ischemic  conditions caused by a restricted blood supply to the muscle such as  angina , and  myocardial infarction .


Cardiac muscle tissue or myocardium forms the bulk of the heart. The heart wall is a three-layered structure with a thick layer of myocardium sandwiched between the inner  endocardium  and the outer  epicardium  (also known as the visceral pericardium). The inner endocardium lines the cardiac chambers, covers the  cardiac valves , and joins with the  endothelium  that lines the blood vessels that connect to the heart. On the outer aspect of the myocardium is the  epicardium  which forms part of the  pericardial sac  that surrounds, protects, and lubricates the heart. [ 1 ]


Within the myocardium, there are several sheets of cardiac muscle cells or cardiomyocytes.  The sheets of muscle that wrap around the left ventricle closest to the endocardium are oriented perpendicularly to those closest to the epicardium.  When these sheets contract in a coordinated manner they allow the ventricle to squeeze in several directions simultaneously – longitudinally (becoming shorter from apex to base), radially (becoming narrower from side to side), and with a twisting motion (similar to wringing out a damp cloth) to squeeze the maximum possible amount of blood out of the heart with each heartbeat. [ 2 ]


Contracting heart muscle uses a lot of energy, and therefore requires a constant flow of blood to provide  oxygen  and nutrients.   Blood  is brought to the myocardium by the  coronary arteries .  These originate from the  aortic root  and lie on the outer or epicardial surface of the heart.  Blood is then drained away by the  coronary veins  into the  right atrium . [ 1 ]


Cardiac muscle cells  (also called  cardiomyocytes ) are the contractile  myocytes  of the cardiac muscle. The cells are surrounded by an  extracellular matrix  produced by supporting  fibroblast  cells. Specialised modified cardiomyocytes known as  pacemaker cells , set the rhythm of the heart contractions. The pacemaker cells are only weakly contractile without sarcomeres, and are connected to neighboring contractile cells via  gap junctions . [ 3 ]  They are located in the  sinoatrial node  (the primary pacemaker) positioned on the wall of the  right atrium , near the entrance of the  superior vena cava . [ 4 ]  Other pacemaker cells are found in the atrioventricular node (secondary pacemaker).


Pacemaker cells carry the impulses that are responsible for the beating of the heart.  They are distributed throughout the heart and are responsible for several functions.  First, they are responsible for being able to  spontaneously generate  and send out  electrical impulses .  They also must be able to receive and respond to electrical impulses from the brain.  Lastly, they must be able to transfer electrical impulses from cell to cell. [ 5 ]  Pacemaker cells in the sinoatrial node, and atrioventricular node are smaller and conduct at a relatively slow rate between the cells. Specialized conductive cells in the  bundle of His , and the  Purkinje fibers  are larger in diameter and conduct signals at a fast rate. [ 6 ]


The Purkinje fibers rapidly conduct electrical signals;  coronary arteries  to bring nutrients to the muscle cells, and  veins  and a  capillary  network to take away waste products. [ 7 ]


Cardiac muscle cells are the contracting cells that allow the heart to pump.  Each cardiomyocyte needs to contract in coordination with its neighboring cells - known as a  functional syncytium  - working to efficiently pump blood from the heart, and if this coordination breaks down then – despite individual cells contracting – the heart may not pump at all, such as may occur during  abnormal heart rhythms  such as  ventricular fibrillation . [ 8 ]


Viewed through a microscope, cardiac muscle cells are roughly rectangular, measuring 100–150μm by 30–40μm. [ 9 ]  Individual cardiac muscle cells are joined at their ends by  intercalated discs  to form long fibers.  Each cell contains  myofibrils , specialized protein contractile fibers of  actin  and  myosin  that slide past each other.  These are organized into  sarcomeres , the fundamental contractile units of muscle cells.  The regular organization of myofibrils into sarcomeres gives cardiac muscle cells a striped or  striated  appearance when looked at through a microscope, similar to skeletal muscle. These striations are caused by lighter  I bands  composed mainly of actin, and darker  A bands  composed mainly of myosin. [ 7 ]


Cardiomyocytes contain  T-tubules , pouches of  cell membrane  that run from the cell surface to the cell's interior which help to improve the efficiency of contraction.  The majority of these cells contain only one  nucleus  (some may have two central nuclei), unlike skeletal muscle cells which contain  many nuclei . Cardiac muscle cells contain many  mitochondria  which provide the energy needed for the cell in the form of  adenosine triphosphate  (ATP), making them highly resistant to fatigue. [ 9 ] [ 7 ]


T-tubules  are microscopic tubes that run from the cell surface to deep within the cell.  They are continuous with the cell membrane, are composed of the same  phospholipid bilayer , and are open at the cell surface to the  extracellular fluid  that surrounds the cell. T-tubules in cardiac muscle are bigger and wider than those in  skeletal muscle , but fewer in number. [ 9 ]  In the centre of the cell they join, running into and along the cell as a transverse-axial network.  Inside the cell they lie close to the cell's internal calcium store, the  sarcoplasmic reticulum .  Here, a single tubule pairs with part of the sarcoplasmic reticulum called a terminal cisterna in a combination known as a  diad . [ 10 ]


The functions of T-tubules include rapidly transmitting electrical impulses known as  action potentials  from the cell surface to the cell's core, and helping to regulate the concentration of calcium within the cell in a process known as  excitation-contraction coupling . [ 9 ]  They are also involved in mechano-electric feedback, [ 11 ]  as evident from cell contraction induced T-tubular content exchange (advection-assisted diffusion), [ 12 ]  which was confirmed by confocal and 3D electron tomography observations. [ 13 ]


The  cardiac syncytium  is a network of cardiomyocytes connected by  intercalated discs  that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an  atrial syncytium  and a  ventricular syncytium  that are connected by cardiac connection fibres. [ 14 ]  Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the  all or none law . [ 15 ]


Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical  syncytium  (in contrast to the skeletal muscle, which becomes a multicellular syncytium during  embryonic development ). The discs are responsible mainly for force transmission during muscle contraction.  Intercalated discs consist of three different types of cell-cell junctions: the actin filament anchoring  fascia adherens junctions , the intermediate filament anchoring  desmosomes , and  gap junctions . [ 16 ]  They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. The three types of junction act together as a single  area composita . [ 16 ] [ 17 ] [ 18 ] [ 19 ]


Under  light microscopy , intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section. [ 20 ]


Cardiac fibroblasts are vital supporting cells within cardiac muscle.  They are unable to provide forceful contractions like  cardiomyocytes , but instead are largely responsible for creating and maintaining the extracellular matrix which surrounds the cardiomyocytes. [ 7 ]   Fibroblasts play a crucial role in responding to injury, such as a  myocardial infarction .  Following injury, fibroblasts can become activated and turn into  myofibroblasts  – cells which exhibit behaviour somewhere between a fibroblast (generating extracellular matrix) and a  smooth muscle cell  (ability to contract).  In this capacity, fibroblasts can repair an injury by creating collagen while gently contracting to pull the edges of the injured area together. [ 21 ]


Fibroblasts are smaller but more numerous than cardiomyocytes, and several fibroblasts can be attached to a cardiomyocyte at once.  When attached to a cardiomyocyte they can influence the electrical currents passing across the muscle cell's surface membrane, and in the context are referred to as being electrically coupled, [ 22 ]  as originally shown in vitro in the 1960s, [ 23 ]  and ultimately confirmed in native cardiac tissue with the help of optogenetic techniques. [ 24 ]  Other potential roles for fibroblasts include electrical insulation of the  cardiac conduction system , and the ability to transform into other cell types including cardiomyocytes  and  adipocytes . [ 21 ]


The  extracellular matrix  (ECM) surrounds the cardiomyocyte and fibroblasts.  The ECM is composed of proteins including  collagen  and  elastin  along with  polysaccharides  (sugar chains) known as  glycosaminoglycans . [ 7 ]  Together, these substances give support and strength to the muscle cells, create elasticity in cardiac muscle, and keep the muscle cells hydrated by binding water molecules.


The matrix in immediate contact with the muscle cells is referred to as the  basement membrane , mainly composed of  type IV collagen  and  laminin .  Cardiomyocytes are linked to the basement membrane via specialised  glycoproteins  called  integrins . [ 25 ]


Humans are born with a set number of heart muscle cells, or cardiomyocytes, which increase in size as the heart grows larger during childhood development. Evidence suggests that cardiomyocytes are slowly turned over during aging, but less than 50% of the cardiomyocytes present at birth are replaced during a normal life span. [ 26 ]  The growth of individual cardiomyocytes not only occurs during normal heart development, it also occurs in response to extensive exercise ( athletic heart syndrome ), heart disease, or heart muscle injury such as after a myocardial infarction. A healthy adult cardiomyocyte has a cylindrical shape that is approximately 100μm long and 10–25μm in diameter.  Cardiomyocyte hypertrophy occurs through sarcomerogenesis, the creation of new sarcomere units in the cell.  During heart volume overload, cardiomyocytes grow through eccentric hypertrophy. [ 27 ]  The cardiomyocytes extend lengthwise but have the same diameter, resulting in ventricular dilation.  During heart pressure overload, cardiomyocytes grow through concentric hypertrophy. [ 27 ]  The cardiomyocytes grow larger in diameter but have the same length, resulting in heart wall thickening.


The physiology of cardiac muscle shares many similarities with that of  skeletal muscle .  The primary function of both muscle types is to contract, and in both cases, a contraction begins with a characteristic flow of  ions  across the  cell membrane  known as an  action potential .  The  cardiac action potential  subsequently triggers muscle contraction by increasing the concentration of  calcium  within the cytosol.


The  cardiac cycle  is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called  diastole , following a period of robust contraction and pumping of blood, dubbed  systole . After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again.


The rest phase is considered polarized. The  resting potential  during this phase of the beat separates the ions such as sodium, potassium, and calcium. Myocardial cells possess the property of automaticity or spontaneous  depolarization . This is the direct result of a membrane which allows sodium ions to slowly enter the cell until the threshold is reached for depolarization. Calcium ions follow and extend the depolarization even further. Once calcium stops moving inward, potassium ions move out slowly to produce repolarization. The very slow repolarization of the CMC membrane is responsible for the long refractory period. [ 28 ] [ 29 ]


However, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle.  In cardiac muscle, the action potential comprises an inward flow of both sodium and calcium ions.  The flow of sodium ions is rapid but very short-lived, while the flow of calcium is sustained and gives the plateau phase characteristic of cardiac muscle action potentials.  The comparatively small flow of calcium through the  L-type calcium channels  triggers a much larger release of calcium from the sarcoplasmic reticulum in a phenomenon known as   calcium-induced calcium release .  In contrast, in skeletal muscle, minimal calcium flows into the cell during action potential and instead the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane.  This difference can be illustrated by the observation that cardiac muscle fibers require calcium to be present in the solution surrounding the cell to contract, while skeletal muscle fibers will contract without extracellular calcium.


During contraction of a cardiac muscle cell, the long protein  myofilaments  oriented along the length of the cell slide over each other in what is known as the  sliding filament theory .  There are two kinds of myofilaments, thick filaments composed of the protein  myosin , and thin filaments composed of the proteins  actin ,  troponin  and  tropomyosin .  As the thick and thin filaments slide past each other the cell becomes shorter and fatter.  In a mechanism known as  cross-bridge cycling , calcium ions bind to the protein troponin, which along with tropomyosin then uncover key binding sites on actin.  Myosin, in the thick filament, can then bind to actin, pulling the thick filaments along the thin filaments.  When the concentration of calcium within the cell falls, troponin and tropomyosin once again cover the binding sites on actin, causing the cell to relax.


It was commonly believed that cardiac muscle cells could not be regenerated. However, this was contradicted by a report published in 2009. [ 30 ]  Olaf Bergmann and his colleagues at the  Karolinska Institute  in  Stockholm  tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality.  By using DNA samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69% of the heart muscle cells of a 50-year-old were generated after they were born. [ 30 ]


One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process. [ 31 ]


In the 2000s, the discovery of adult endogenous cardiac stem cells was reported, and studies were published that claimed that various stem cell lineages, including  bone marrow stem cells  were able to differentiate into cardiomyocytes, and could be used to treat  heart failure . [ 32 ] [ 33 ]
However, other teams were unable to replicate these findings, and many of the original studies were later  retracted  for scientific fraud. [ 34 ] [ 35 ]


Cardiac muscle forms both the atria and the ventricles of the heart.  Although this muscle tissue is very similar between cardiac chambers, some differences exist.  The myocardium found in the ventricles is thick to allow forceful contractions, while the myocardium in the atria is much thinner. The individual myocytes that make up the myocardium also differ between cardiac chambers.  Ventricular cardiomyocytes are longer and wider, with a denser  T-tubule  network.  Although the fundamental mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the calcium transient is smaller and decays more rapidly in atrial myocytes, with a corresponding increase in  calcium buffering  capacity. [ 36 ]  The complement of ion channels differs between chambers, leading to longer action potential durations and effective refractory periods in the ventricles. Certain ion currents such as  I K(UR)  are highly specific to atrial cardiomyocytes, making them a potential target for treatments for  atrial fibrillation . [ 37 ]


Diseases affecting cardiac muscle, known as  cardiomyopathies , are the leading cause of death in  developed countries . [ 38 ]  The most common condition is  coronary artery disease , in which the  blood supply to the heart is reduced . The  coronary arteries  become narrowed by  the formation of atherosclerotic plaques . [ 39 ]  If these narrowings become severe enough to partially restrict blood flow, the syndrome of  angina  pectoris may occur. [ 39 ]  This typically causes chest pain during exertion that is relieved by rest. If a coronary artery suddenly becomes very narrowed or completely blocked, interrupting or severely reducing blood flow through the vessel, a  myocardial infarction  or heart attack occurs. [ 40 ]  If the blockage is not relieved promptly by  medication ,  percutaneous coronary intervention , or  surgery , then a heart muscle region may become permanently scarred and damaged. [ 41 ]  Specific cardiomyopathies include: increased  left ventricular mass  ( hypertrophic cardiomyopathy ), [ 42 ]  abnormally large ( dilated cardiomyopathy ), [ 43 ]  or abnormally stiff ( restrictive cardiomyopathy ). [ 44 ]  Some of these conditions are caused by genetic mutations and can be inherited. [ 45 ]


Heart muscle can also become damaged despite a normal blood supply. The heart muscle may become inflamed in a condition called  myocarditis , [ 46 ]  most commonly caused by a viral infection [ 47 ]  but sometimes caused by the body's own  immune system . [ 48 ]  Heart muscle can also be damaged by drugs such as alcohol, long standing high blood pressure or  hypertension , or persistent abnormal  heart racing . [ 49 ]
Many of these conditions, if severe enough, can damage the heart so much that the pumping function of the heart is reduced. If the heart is no longer able to pump enough blood to meet the body's needs, this is described as  heart failure . [ 49 ]


Significant damage to cardiac muscle cells is referred to as  myocytolysis  which is considered a type of cellular  necrosis  defined as either coagulative or colliquative. [ 50 ] [ 51 ]


The  central  governor  is a proposed process in the brain that regulates exercise in regard to a neurally calculated safe  exertion by the body. In particular, physical activity is controlled so that its intensity cannot threaten the body’s  homeostasis  by causing  anoxic  damage to the  heart muscle . The central governor limits exercise by reducing the neural recruitment of muscle fibers. This reduced recruitment causes the sensation of  fatigue . The existence of a central governor was suggested to explain fatigue after prolonged strenuous exercise in long-distance running and other endurance sports, but its ideas could also apply to other causes of exertion-induced fatigue.


The existence of a central governor was proposed by  Tim Noakes  in 1997, but a similar idea was suggested in 1924 by  Archibald Hill . It was first published as a full theory by Tim Noakes, Alan St Clair Gibson and Vicki Lambert in five linked articles in the British Journal of Sports Medicine in 2004-2005 [ 1 ]


In contrast to this idea is the one that fatigue is due to peripheral "limitation" or "catastrophe." In this view, regulation by fatigue occurs as a consequence of a failure of homeostasis directly in muscles.


The 1922  Nobel Prize in Physiology or Medicine  winner  Archibald Hill  proposed in 1924 that the heart was protected from anoxia in strenuous exercise by the existence of a governor.


the heart is able to regulate its output, to some extent, in accordance with the degree of saturation of the arterial blood ... we suggest that, in the body (either in the heart muscle itself or in the nervous system), there is some mechanism which causes a slowing of the circulation as soon as a serious degree of unsaturation occurs, and  vice versa . This mechanism would tend, to some degree, to act as a ‘governor’, maintaining a reasonably high degree of saturation of the blood: the breathing of a gas mixture rich in oxygen would produce a greater degree of saturation of the blood and so allow the output to increase until the ‘governor’ stopped it again. We realise the danger of a hypothesis partly suggested by teleological reasoning: in this case, however, we can see no other explanation of our experimental results pp. 163 [ 2 ]


This hypothesis was disregarded and further research upon exercise fatigue was modeled in terms of it being due to a mechanical failure of the exercising muscles ("peripheral muscle fatigue"). This failure was caused either by an inadequate oxygen supply to the exercising muscles, lactic acid buildup, or total energy depletion in the exhausted muscles. [ 3 ]


Tim Noakes , a professor of exercise and sports science at the  University of Cape Town , in 1997 [ 4 ]  has renewed Hill’s argument on the basis of modern research. Along with collaborators Alan St Clair Gibson and Vicki Lambert, they suggested that the power output by muscles during exercise is continuously adjusted in regard to calculations made by the brain in regard to a safe level of exertion. These neural calculations factor in earlier experience with strenuous exercise, the planning duration of the exercise, and the present metabolic state of the body. These brain models [ 5 ]  ensure that body homeostasis is protected, and an emergency reserve margin is maintained. [ 6 ] [ 7 ] [ 8 ] [ 9 ]  This neural control adjusts the number of activated skeletal muscle motor units, a control which is subjectively experienced as  fatigue . This process, though occurring in the brain, is outside conscious control.


the rising perception of discomfort produced by exhausting exercise progressively reduces the conscious desire to over-ride this control mechanism, which, if it were to be reduced, would lead to the recruitment of more motor units. Thus the presence of conscious over-ride would be undesirable because it would increase or maintain the exercise intensity, thereby threatening homoeostasis ... as exercise performance is centrally regulated by the CNS, then fatigue should no longer be considered a physical event but rather a sensation or emotion, separate from an overt physical manifestation—for example, the reduction in force output by the active muscles. Rather we now suggest that the physical manifestation of any increasing perception of fatigue may simply be an alteration in the subconsciously regulated pace at which the exercise is performed. Hence the novel suggestion is that the conventional understanding of fatigue is flawed because it makes no distinction between the sensation itself and the physical expression of that sensation which, we suggest, is the alteration in the subconsciously regulated pacing strategy consequent on changing motor unit recruitment/derecruitment by the CNS. [ 10 ]


Noakes, St Clair Gibson and Lambert created the idea of the central governor in the context of prolonged endurance exercise. However, they have noted that the central processes involved might also underlie the existence of other kinds of fatigue:


This new interpretation is the first to allow a more reasonable description of a number of phenomena that defy rational explanation according to the traditional ‘‘limitations’’ models of fatigue. These include, among many others, the chronic fatigue syndrome, in which affected individuals experience evident fatigue at rest, and the role of psychological and motivational factors,  centrally (brain) acting pharmaceutical agents,  hypnosis, shouting or sudden unexpected gunshots,  or other forms of distraction including music or premeditated deception on human exercise performance. [ 11 ]


In support of this, placebos (which must be mediated by a central process) have a powerful effect upon not only fatigue in prolonged exercise, [ 12 ] [ 13 ]  but also upon short term endurance exercise such as sprint speed, [ 14 ]  the maximum weight that could be lifted with leg extension, [ 15 ]  and the tolerance of  ischemic  pain and power when a tourniqueted hand squeezes a spring exerciser 12 times. [ 16 ]


The existence of a central governor over physiology has been questioned since ‘physiological catastrophes’ can and do occur in athletes (important examples in  marathons  have been  Dorando Pietri ,  Jim Peters  and  Gabriela Andersen-Schiess ). This suggests that humans can over-ride ‘the central governor’. [ 17 ]  Moreover, a variety of peripheral factors in addition to those such as lactic acid build up can impair muscle power and might act to protect against "catastrophe". [ 18 ]  Another objection is that models incorporating conscious control also provide an alternative explanation  [ 19 ]  (see Noakes’ reply). [ 20 ]


Exercise fatigue has also been attributed to the direct effects of exercise upon the brain such as increased cerebral levels of  serotonin , reduced level of  glutamate  secondary to uptake of ammonia in the brain, brain hyperthermia, and  glycogen  depletion in brain cells. [ 21 ] [ 22 ]


Composite  or  hybrid muscles  are those muscles which have more than one set of fibers but perform the same function and are usually supplied by different nerves for different set of fibers. [ 1 ] [ 2 ]


Certain muscles are commonly confused with composite muscles which they are not. Examples are:


Concentric hypertrophy  is a  hypertrophic  growth of a  hollow organ  without overall enlargement, [ 1 ]  in which the walls of the organ are thickened and its capacity or volume is diminished.


Sarcomeres  are added in parallel, as for example occurs in  hypertrophic cardiomyopathy . [ citation needed ]


In the  heart , concentric hypertrophy is related to increased  pressure overload  of the heart, often due to  hypertension  and/or  aortic stenosis . The consequence is a decrease in  ventricular  compliance and  diastolic dysfunction , followed eventually by  ventricular failure  and  systolic dysfunction . [ citation needed ]


Laplace's law  for a sphere states wall stress (T) is proportionate to the product of the  transmural pressure  (P) and cavitary radius (r) and inversely proportionate to wall thickness (W): In response to the pressure overload left ventricular wall thickness markedly increases—while the cavitary radius remains relatively unchanged. These compensatory changes, termed "concentric hypertrophy," reduce the increase in wall tension observed in aortic stenosis. [ citation needed ]


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also known as superior tendon of abdominal cavity.


The  conjoint tendon  (previously known as the  inguinal aponeurotic falx ) is a sheath of  connective tissue  formed from the lower part of the common  aponeurosis  of the  abdominal internal oblique muscle  and the  transversus abdominis muscle , joining the muscle to the  pelvis . It forms the medial part of the posterior wall of the  inguinal canal .


The conjoint tendon is formed from the lower part of the common aponeurosis of the  abdominal internal oblique muscle  and the  transversus abdominis muscle . [ 1 ]  It inserts into the  pubic crest  and the  pectineal line  immediately behind the  superficial inguinal ring . [ 1 ]  It is usually conjoint with the tendon of the  internal oblique muscle , but they may be separate as well. It forms the medial part of the posterior wall of the  inguinal canal . [ 1 ]


The conjoint tendon serves to protect what would otherwise be a weak point in the  abdominal wall . [ 1 ]  A weakening of the conjoint tendon can precipitate a direct inguinal hernia. [ 1 ] [ 2 ]


A  direct inguinal hernia  will protrude through  Hesselbach's triangle , whose borders are the  rectus abdominis  (medially),  inferior epigastric artery  and  inferior epigastric vein  (superolaterally), and the  inguinal ligament  (inferiorly).  The hernia lies medial to the inferior epigastric artery. [ 3 ]  This is in contrast to an  indirect inguinal hernia , which will protrude laterally to the inferior epigastric artery and is most commonly due to an embryological defect in the closure of the deep inguinal ring.


The conjoint tendon is also known as the inguinal aponeurotic falx, and Henle's ligament. [ 4 ]


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The  core  or  trunk  is the  axial  (central) part of an  organism 's  body . In common parlance, the term is broadly considered to be synonymous with the  torso , but academically it also includes the  head  and  neck .   Functional movements  are highly dependent on this part of the body, and lack of core muscular development can result in a predisposition to injury. [ 1 ]  The major muscles of the core reside in the area of the belly and the mid- and lower back (not the shoulders), and peripherally include [ clarification needed ]  the hips, the shoulders and the neck.


Major muscles included are the  pelvic floor  muscles,  transversus abdominis ,  multifidus ,  internal  and  external obliques ,  rectus abdominis ,  erector spinae  (sacrospinalis) especially the  longissimus thoracis , and the  diaphragm .  The lumbar muscles, quadratus Lumborum (deep portion), deep rotators, as well as cervical muscles, rectus capitus anterior and lateralis, longus coli may also be considered members of the core group. [ 2 ]


Minor core muscles include the  latissimus dorsi ,  gluteus maximus , and  trapezius .


The core is used to stabilize the thorax and the pelvis during dynamic movement and it also provides internal pressure to expel substances (vomit, feces, carbon-laden air, etc.).


The core is traditionally assumed to originate most full-body functional movement, including most sports.  In addition, the core determines to a large part a person's  posture .  In all, the human anatomy is built to take force upon the bones and direct autonomic force, through various joints, in the desired direction.  The core muscles align the  spine ,  ribs , and  pelvis  of a person to resist a specific force, whether static or dynamic.  [ 3 ]


Static core functionality is the ability of one's core to align the skeleton to resist a force that does not change.


An example of static core function is firing a rifle in the  prone position . To maintain accuracy, the shooter must be able to transfer their body weight and the weight of the rifle into the earth.  Any attempt of the shooter to create a dynamic motion of the sights (muscle the sights onto the target vs. allowing the posture to aim) will result in a jerky posture where the sights do not sit still on the target. For the shooter to maintain accuracy, the muscles cannot exert force on the rifle, and the skeleton must be aligned to set the rifle (and therefore the sights) onto the target.  The core, while resting on the ground and relatively far away from the rifle, is nevertheless aligning the spine and pelvis to which the shoulder and arms and neck are connected.  For these peripheral elements to remain static,  and not move unnecessarily, the spine, pelvis, and rib cage must be aligned towards this end.  Thus the core muscles provide support of the  axial skeleton  (skull, spine, and tailbone) in an alignment where the upper body can provide a steady, solid base for the rifle to remain motionless.


The nature of dynamic movement must take into account our skeletal structure (as a lever) in addition to the force of external resistance, and consequently incorporates a vastly different complex of muscles and joints versus a static position.


Because of this functional design, during dynamic movement there is more dependence on core musculature than just skeletal rigidity as in a static situation.  This is because the purpose of the movement is not to resist a static, unchanging resistance, but to resist a force that changes its  plane of motion .  By incorporating movement, the bones of the body must absorb the resistance in a fluid manner, and thus tendons, ligaments, muscles, and innervation take on different responsibilities.  These responsibilities include postural reactions to changes in speed (quickness of a contraction), motion (reaction time of a contraction), and power (amount of resistance resisted in a period of time).


An example of this is walking on a slope.  The body must resist gravity while moving in a direction, and balancing itself on uneven ground.  This forces the body to align the bones in a way that balances the body while at the same time achieving momentum through pushing against the ground in the opposite direction of the desired movement.  Initially, it may seem that the legs are the prime movers of this action, but without balance, the legs will only cause the person to fall over.  Therefore, the prime mover of walking is achieving core stability, and then the legs move this stable core by using the leg muscles.


Within the muscle tissue of animals and humans, contraction and relaxation of the muscle cells ( myocytes ) is a highly regulated and rhythmic process. In cardiomyocytes, or cardiac muscle cells, muscular contraction takes place due to movement at a structure referred to as the  diad , sometimes spelled "dyad." The dyad is the connection of transverse- tubules ( t-tubules ) and the junctional  sarcoplasmic reticulum  (jSR). [ 1 ]  Like skeletal muscle contractions, Calcium (Ca 2+ ) ions are required for  polarization  and  depolarization  through a  voltage-gated calcium channel . The rapid influx of calcium into the cell signals for the cells to contract. When the calcium intake travels through an entire muscle, it will trigger a united muscular contraction. This process is known as  excitation-contraction coupling . [ 2 ]  This contraction pushes blood inside the heart and from the heart to other regions of the body.


Myocytes  are incredibly specialized cells with only a select number of different organelle types. A myocyte is composed of multiple  myofibrils , which contain the “contractile units” of the muscle known as a  sarcomere . [ 3 ]  These sarcomeres are arranged in adjacent formations along the myofibrils. Similarly to the plasma membrane of other cells, the  sarcolemma  protects and surrounds the myocytes. The two cellular components that perform the “sliding filament” contraction are  myosin  and  actin , also referred to as the thick and thin filaments respectively [ 2 ]  The striations viewed using microscopy of the cardiac muscle are a result of the contrast between the thick and thin filaments. The z-line defines the borders of each sarcomere and act as the connection point between the thin filaments. The t-tubules and sarcoplasmic reticulum are used in conjunction to receive and direct the calcium ions and cause contraction. Once contracted, the clear H-zone between the actin filaments disappears as the filaments move towards each other.


Cardiomyocytes  are a particular form of myocyte, only present in heart tissue. Along with the basic myocyte elements, these cells also contain one to four nuclei and a large amount of  Adenosine Triphosphate  (ATP). [ 2 ]  These additions aid in the heart's resistance to fatigue to consistently pump blood throughout the body to deliver oxygen. Most muscle cells contain a  triad , which is a joining of 2 terminal cisternae of the sarcoplasmic reticulum and one t- tubule. However, cardiac muscle cells contain a  diad , which is a linking of only one sarcoplasmic reticulum with its respective t-tubule. Another notable distinction between all muscle cells and cardiac muscle cells is the presence of  intercalated discs . These tight connections between the cardiomyocytes allows for the accelerated sending of action potential signals to perform the rapid, rhythmic contraction of the heart muscle.


One of the most incredible attributes of cardiac muscle is the ability to automatically beat. This means that even when isolated, for example on a petri dish in an in- vitro setting, the tissue is able to contract and release. This is due to the presence of “ pacemaker cells ,” which originate from the  sinoatrial node . This structure allows for spontaneous depolarization, sending signals throughout the tissue.


Within the sarcolemma of the myocyte, there are specific invaginations referred to as  transverse- tubules . These structures attached to the sarcomere z-lines help to promote interaction between the  extracellular space  and the interior of the cell. [ 1 ]  Connecting these tubules to the Z line allows for a closer range of excitation- contraction coupling within the cell. [ 1 ]  Within the t-tubules, distinct ion channels and cellular proteins are present within the t- tubule bilayer that allow movement of calcium influx from the extracellular space into the myocyte to initiate depolarization and contraction. Once traveling through the t- tubules, the calcium arrives at the sarcoplasmic reticulum.


Within the lumen of the cardiac myocyte, the  sarcoplasmic reticulum  serves as the area of controlling the amount of calcium influx into the interior of the cell. [ 4 ]  After traveling through the t- tubule, the calcium is stored in the sarcoplasmic reticulum to maintain low concentration of calcium inside the lumen. Upon contraction of this muscle, the cell is depolarized and the calcium is released into the lumen to create the  excitation-contraction coupling . Once the initial calcium is released, a wave of additional calcium is discharged from the sarcoplasmic reticulum to maintain the contraction integrity.


The tension felt in muscles from prolonged contraction can be attributed to extended release of calcium ions through the sarcoplasmic reticulum. By absorbing calcium ions after contraction, the sarcoplasmic reticulum can regulate muscle fatigue and prevent overuse damage within the body.


Voltage- gated calcium channels  play a critical role in controlling the influx of calcium ions into the myocyte in response to the changing  action potential  of the sarcoplasmic membrane. [ 5 ]  The increase in action potential of the cell indicates depolarization of the cell, directly opening the ion channels to cause muscular contraction. When the action potential decreases, the ion channels close, preventing any calcium influx and further muscular contraction. This fluctuation within the myocyte contributes to the rhythmic “pacemaking” of the cardiac tissue.


There are two classes of voltage- gated calcium channels,  L- type  and  T- type . [ 5 ]   L-type calcium channels  are more commonly found in myocardial tissue throughout the heart whereas  T-type calcium channels  are more concentrated in the pacemaker cells of the  sinoatrial node . These channels also have slightly different activation levels. The L- type responds to a more positive action potential while the T- type channels are triggered at a more negative action potential. Discrepancies and/ or malfunctioning of these gates can contribute to a number of cardiac conditions, such as bradycardia.


Because the structural organization of the myocyte is very complex and specific, changes to their arrangement and/ or function can cause  cardiac illnesses  or  defects . For example, a leading cause of  heart failure  can be attributed to the lack of t- tubule and sarcoplasmic reticulum junctions or a decreased distance between the structures. [ 6 ]  This change in structure causes the excitation- coupling response in the myocyte to either lessen significantly or be completely diminished. Therefore, few to no heart contractions would take place causing heart failure. On the contrary, an increase in the distance of the junction can create an increased excitation- coupling response, shown in both  hypertension  and  cardiomyopathy . [ 6 ]  These conditions are proof that even the smallest changes in a complex structure can have long- range consequences.


Elastic mechanisms in animals  are very important in the movement of  vertebrate  animals. The  muscles  that control vertebrate locomotion are affiliated with tissues that are springy, such as  tendons , which lie within the muscles and connective tissue. A  spring  can be a mechanism for different actions involved in hopping, running, walking, and serve in other diverse functions such as  metabolic energy conservation, attenuation of muscle power production, and amplification of muscle power production. [ 1 ]


When a body is running, walking or hopping, it uses springs as a way to store energy which indicates that elastic mechanisms have a great influence on its dynamics. [ 2 ]  When a force is applied to a spring it bends and stores energy in the form of elastic  strain energy  and when it recoils after the force has been released,  this energy is released as well. [ 1 ]  Elastic proteins provide the property of elasticity which gives the spring the ability to bend reversibly without the loss of energy, and the ability to bend to large strains with small force. [ 3 ]  Elastic proteins also contain high resilience and low stiffness which helps with the function of elastic strain energy.


While running, tendons are able to reduce the metabolic rate of muscle activity by reducing the volume of the muscle that is active to produce force. The timing of muscle activation is very important for utilizing the mechanical and energetic benefits of tendon elasticity. [ 4 ]  Power  attenuation  by the use of the tendons can allow the muscle-tendon system the ability to absorb energy at a rate beyond the muscles maximum capacity to absorb energy. Power amplification mechanisms are able to work because the spring and muscles contain different intrinsic limits of power. Muscles in a skeletal system can be limited in their maximum power production. Power  amplification  by the use of the tendons allows the muscle to produce power beyond the muscle's capacity. [ 1 ]  The mechanical functions of tendons contain a structural basis and are not subjected to limitation of power production.


From previous experimental studies on large animals, it was noted that during active locomotion mammals save much of the energy they would otherwise need for running by means of elastic structures in their legs. Measurements been made of the rates of oxygen consumption of various animals, as they walked, ran or hopped, revealed that at high speeds animals seem to save more than a half the metabolic energy they would otherwise need for locomotion. [ 5 ]  A notable example is jumping in kangaroos. When hopping at slow speeds, their uses of energy increase linearly, but at high speeds, kangaroos can move as cheaply (from an energetic perspective) as if they were moving at slower speeds. [ 6 ]


Deep research into the anatomy of large mammals such as, kangaroos and other large  ungulates   such as deer and gazelle, suggests strongly that some sort of elastic mechanism is important for this energetic savings. [ 6 ]  Previous combination of careful experiments, with anatomical (e.g. tendon dimensions), mechanical (e.g. force plate recordings) and mathematical calculations revealed that a significant fraction of the work done with each step could be provided by the spring-like action of tendons, rather than by muscle work. [ 1 ]
When the animal's foot contacts the surface of the ground during high speed locomotion, the  tendon  or  ligament  is pressed tightly together, storing  elastic energy  much like a compressed spring. As the foot gets of the ground, the pressure on the compressed tendons and ligaments is released, and elastic recoil from these spring like structures provides additional force to propel the animal thus resulting in energetic savings. [ 6 ]  Simple calculations based kangaroo hopping and forces involved in hopping show how storage of elastic strain energy can save twenty to thirty percent of metabolic energy required for hopping. Measurements of oxygen consumption with fluctuations of kinetic and  gravitational potential energy , indicate elastic savings of at least fifty four percent at high speeds. [ 5 ]


It is important to take under consideration that metabolic benefits of elastic structures are probably most apparent for larger animals, rather than small organisms such as insects. This results from a simple fact, that larger animals can exert much higher forces on their tendons and ligaments during movement, compared to small animals. [ 6 ]


In  eccentric contractions , elastic tendons have the ability to operate as power  attenuation . Tendons exhibit power attenuation that allows the muscle-tendon systems to absorb energy. This rate exceeds the muscle's maximum capacity for energy. In comparison, power amplification of tendons allow for greater output of power that can exceed the capacity of their respective muscle. This elastic mechanism can lead to the following reductions by lengthening muscles: peak  power  input, lengthening  velocity , and  force . Muscle damage has been correlated with these factors. However, the shuttling of energy through tendons before it is absorbed by muscles has been shown to provide a protective mechanism against that damage. [ 1 ]  However, large accumulations of elastic energy storage over time may negatively affect the timing of recoil. This results in power attenuation. [ 7 ]


Though muscles produce and absorb mechanical power, tendons still have an integral role for dissipation of  mechanical energy .  This action is essential for activities like deceleration, when landing from a jump or downhill running. R.I. Griffiths conducted cross-experiments of isolated muscle-tendon preparations with  in vivo  studies in 1991 to keep muscles  isometric  during muscle-tendon unit lengthening. This was achieved with the practice of rapid stretches applied to muscle-tendon units which are then absorbed by the stretch of tendons. Experimenters explain this phenomenon by the idea that muscles are susceptible to damage when actively lengthened and this practice acts as a mechanical buffer against it. [ 1 ]  In addition,  in vivo  experiments it has been found that the elastic mechanism gives protection to musculoskeletal structure exceeding the  sarcomere . Due to this fact, forces developed in active muscles eventually decide the forces on tendons such as bones, joints, and  ligaments . [ 7 ]


Similarly, tendons are unable to entirely insulate muscles from dynamic extension. Tendons affect muscles when muscles lengthen, which affects peak forces experienced due to energy absorbing actions in the muscle tendon unit. Active lengthening of muscle fibers results in both an accumulation and loss of energy. Even though energy is briefly stored in stretched elastic elements are also released, there is an overall net gain. This shows that muscle fibers are effective in both power production and for energy consumption utilized by the body or individual body segments with muscle-tendon units. [ 1 ]


Tendons,  connective tissues , and molecular structures within a skeletal system can act as power amplifiers by storing energy gradually and releasing it rapidly. This  amplification  process is possible because spring-like tendons are not limited by the same rate limits imposed upon muscles by their intrinsic enzymatic processes. The process of amplification begins when a muscle contracts steadily, storing elastic strain energy in the tendon. Once the energy is completely stored, the tendon releases it in a much shorter time span than was required to create it within the muscle. The tendon is actually producing energy at a level slightly below the work done by the contracting muscle, but because power is equivalent to work over time, the considerably shorter time increases the power significantly. [ 1 ]


This phenomenon has been observed in numerous  vertebrate  behaviors, one of the most notable being jumping. Observed in kangaroos, bush babies, birds, frogs, and various species of antelope, jumping relies on this system because the action is inherently limited in the time that is available to produce power once the body has begun to accelerate. Once the body loses contact with the ground there is no way for the organism to continue to produce force. [ 6 ]  Substantial improvement in acceleration resulting from these mechanisms have been observed in jumping fleas, accelerating turkeys, the striking of mantis shrimp, and the running of horses whose bicep brachii power output is amplified fifty times by the use of catapult-like behavior of the tendon. [ 1 ] [ 6 ] [ 8 ]


Feeding mechanisms also benefit from spring-like power amplifiers within the skeletal system. The depressor mandibulae of toads rely on this mechanism to produce catapult-like tongue projection. [ 1 ]   More dramatically, the  ballistic  tongue projection utilized by chameleons and some salamanders utilize elastic mechanisms to produce mass-specific power outputs more than five times higher than those reported for most fast muscles. [ 9 ] [ 10 ] [ 11 ]  In chameleons, it is significant to note that the retractor muscles utilized in prey capture decreased in power output by 600% over a 20 °C temperature range while the  tongue  projection mechanism, which utilizes the elastic energy storage, decreased a mere 50%, demonstrating that these elastic mechanisms do not simply amplify the power output, but they also extend the temperature range in which power outputs may be amplified. [ 12 ]


The  endomysium , meaning  within the muscle , is a wispy layer of  areolar connective tissue  that ensheaths each individual  muscle fiber , or  muscle cell . [ 1 ] [ 2 ] [ 3 ]  It also contains  capillaries  and  nerves . It overlies the muscle fiber's  cell membrane : the  sarcolemma . Endomysium is the deepest and smallest component of  muscle connective tissue . This thin layer helps provide an appropriate chemical environment for the exchange of  calcium ,  sodium , and  potassium , which is essential for the excitation and subsequent contraction of a muscle fiber.


Endomysium combines with  perimysium  and  epimysium  to create the collagen fibers of  tendons , providing the tissue connection between muscles and bones by indirect attachment. [ 4 ]  It connects with perimysium using intermittent perimysial junction plates. [ 5 ]


Collagen  is the major protein that composes connective tissues like endomysium. [ 6 ]  Endomysium has been shown to contain mainly  type I  and  type III  collagen components, and  type IV  and  type V  in very minor amounts. [ 7 ]  Others have found type IV and type V more common. [ 2 ]


The term  cardiac skeleton  is sometimes considered synonymous with endomysium in the  heart , but cardiac skeleton also refers to the combination of the endomysium and  perimysium .


Anti-endomysial antibodies  (EMA) are present in  celiac disease . [ 8 ]  They do not cause any direct symptoms to muscles, but detection of EMA is useful in the diagnosis of the disease. [ 9 ]


In adult  vertebrates , trunk muscles can be broadly divided into  hypaxial  muscles, which lie  ventral  to the horizontal  septum  of the  vertebrae  and  epaxial  muscles, which lie  dorsal  to the septum. [ 1 ]  Hypaxial muscles include some vertebral muscles, the  diaphragm , the abdominal muscles, and all limb muscles.  The  serratus posterior inferior  and  serratus posterior superior  are innervated by the  ventral primary ramus  and are hypaxial muscles. Epaxial muscles include other (dorsal) muscles associated with the vertebrae, ribs, and base of the skull.  In humans, the  erector spinae , the  transversospinales   (including the  multifidus ,  semispinalis  and  rotatores ), the  splenius  and  suboccipital  muscles are the only epaxial muscles.


Hypaxial and epaxial muscles develop directly from  somitic  cells. Differentiation of hypaxial and epaxial muscles is postulated to have evolved as a new trait in vertebrate animals. [ 2 ]


The hypaxial muscles are located on the ventral side of the body, often below the horizontal  septum  in many species (primarily fish and amphibians). In all species, the hypaxial muscles are  innervated  by the  ventral ramus  (branch) of the spinal nerves, while the epaxial muscles are innervated by the  dorsal ramus . [ citation needed ]


Epimysium  ( plural   epimysia [ 1 ] ) (Greek  epi-  for on, upon, or above + Greek  mys  for muscle) is the fibrous tissue envelope that surrounds  muscle . [ 2 ]  It is a layer of  dense irregular connective tissue  which ensheaths the entire  muscle  and protects muscles from friction against other muscles and bones. [ 3 ]  It also allows a muscle to contract and move powerfully while maintaining its structural integrity. [ 4 ]


It is continuous with  fascia  and other connective tissue wrappings of muscle including the  endomysium  and  perimysium . It is also continuous with tendons, where it becomes thicker and  collagenous .


While the epimysium is irregular on muscles, it is regular on tendons.


An  extensor expansion  ( extensor hood , [ 1 ]   dorsal expansion ,  dorsal hood ,  dorsal aponeurosis [ citation needed ] ) is the special connective attachments by which the  extensor tendons  insert into the  phalanges .


These flattened tendons ( aponeurosis ) of extensor muscles span the proximal and middle phalanges. [ 2 ]


At the distal end of the  metacarpal , the extensor tendon will expand to form a hood, which covers the back and sides of the head of the metacarpal and the proximal  phalanx .


The expansion soon divides into three bands:


The extensor expansion allows for contractile forces from the  extensor compartment  muscles to be transferred to the phalanges. It also balances the forces across the phalanges. [ 1 ]


The  external anal sphincter  (or  sphincter ani externus ) is an oval tube of  skeletal muscle fibers . [ 1 ]  Distally, it is adherent to the  skin  surrounding the margin of the  anus . [ 2 ]  It exhibits a resting state of tonical contraction [ 1 ]  and also contracts during the  bulbospongiosus reflex . [ 3 ] [ 4 ] [ 5 ] [ 6 ]


The external anal sphincter is far more substantial than the internal anal sphincter. The proximal portion of external anal sphincter overlaps the internal anal sphincter (which terminates distally a little distance proximal to the anal orifice) superficially; where the two overlap, they are separated by the intervening  conjoint longitudinal muscle . [ 1 ]


Historically, the sphincter was described as consisting of three parts (deep, superficial, and subcontinuous). This is not supported by current anatomical knowledge. Some sources still describe it in two layers, deep (or proximal) and superficial (or distal or subcutaneous). [ 1 ]


Some of the muscles fibres decussate at the anterior midline and posterior midline, so forming an anterior commissure and posterior commissure. [ 1 ]


The muscle attaches anteriorly onto the  perineal body , and posteriorly onto the anococcygeal ligament. [ 1 ]


The sphincter receives innervation from the bilaterally paired  inferior anal nerve  (each a branch of the  pudendal nerve  which is derived from ventral rami of S2-S4). It may also receive additional motor innervation from the  nerve to levator ani . [ 1 ]


The sphincter consists mostly of  slow twitch fibers  that allow extended continuous contraction. [ 1 ]


This article incorporates text in the  public domain  from  page 425  of the 20th edition of   Gray's Anatomy   (1918)


Extrafusal muscle fibers  are the standard  skeletal muscle fibers  that are innervated by  alpha motor neurons  and generate tension by contracting, thereby allowing for skeletal movement. They make up the large mass of skeletal  striated muscle tissue  and are attached to bone by fibrous tissue extensions ( tendons ).


Each alpha motor neuron and the extrafusal muscle fibers innervated by it make up a  motor unit . [ 1 ]  The connection between the alpha motor neuron and the extrafusal muscle fiber is a  neuromuscular junction , where the neuron's signal, the  action potential , is transduced to the muscle fiber by the  neurotransmitter   acetylcholine .


Extrafusal muscle fibers are not to be confused with  intrafusal muscle fibers , which are innervated by sensory nerve endings in central noncontractile parts and by  gamma motor neurons  in contractile ends and thus serve as a sensory  proprioceptor .


Extrafusal muscle fibers can be generated in vitro (in a dish) from   pluripotent stem cells  through  directed differentiation . [ 2 ]  This allows study of their formation and physiology.


Galvanism  is a term invented by the late 18th-century physicist and chemist  Alessandro Volta  to refer to the generation of electric current by chemical action. [ 2 ]  The term also came to refer to the discoveries of its namesake,  Luigi Galvani , specifically the generation of electric current within biological organisms and the contraction/convulsion of biological muscle tissue upon contact with electric current. [ 3 ]  While Volta theorized and later demonstrated the phenomenon of his "Galvanism" to be replicable with otherwise inert materials, Galvani thought his discovery to be a confirmation of the existence of "animal electricity," a vital force which gave life to organic matter. [ 4 ]


Galvanic phenomena were described in the literature before it was understood that they were of an electrical nature. In 1752, when the Swiss mathematician and physicist  Johann Georg Sulzer  placed his tongue between a piece of lead and a piece of silver, joined at their edges, he perceived a taste similar to that of  iron(II) sulfate . Neither of the metals alone produced this taste. He realized that the contact between the metals probably did not produce a solution of either on the tongue. He did, however, not realize that this was an electrical phenomenon. [ 5 ]  He concluded that the contact between the metals caused their particles to vibrate, producing this taste by stimulating the nerves of the tongue. [ 6 ]


If we join two pieces, one of lead, and the other of silver, so that the two edges join, and if we approach them with the tongue we will feel some taste, quite similar to the taste of vitriol of iron [iron(II) sulfate], while each piece apart gives no trace of this taste. It is not probable that through this junction of the two metals, any solution of one or the other occurs, and that the dissolved particles penetrate the tongue. We must therefore conclude that the junction of these metals produces in one or the other, or in both, a vibration in their particles, and that this vibration, which must necessarily affect the nerves of the tongue, produces there the taste mentioned.


According to popular legend, Galvani discovered the effects of electricity on muscle tissue when investigating an unrelated phenomenon which required skinned frogs in the 1780s and 1790s. His assistant is claimed to have accidentally touched a scalpel to the sciatic nerve of the frog and this resulted in a spark and animation of its legs. [ 7 ]  This was building on the theories of  Giovanni Battista Beccaria ,  Felice Fontana ,  Leopoldo Marco Antonio Caldani , and  Tommaso Laghi  [ it ] . [ 3 ]  Galvani was investigating the effects of distant atmospheric electricity (lightning) on prepared frog legs when he discovered the legs convulsed not only when lightning struck but also when he pressed the brass hooks attached to the frog's spinal cord to the iron railing they were suspended from. [ 8 ]  In his laboratory, Galvani later discovered that he could replicate this phenomenon by touching metal electrodes of brass connected to the frog's spinal cord to an iron plate. He concluded that this was proof of "animal electricity," the electric power which animated living things. [ 3 ]


Alessandro Volta, a contemporary physicist, believed that the effect was explicable not by any vital force but rather it was the presence of two different metals that was generating the electricity. Volta demonstrated his theory by creating the first chemical electric battery. [ 9 ]  Despite their differences in opinion, Volta named the phenomenon of the chemical generation of electricity "Galvanism" after Galvani. [ 2 ]


On March 27, 1791, Galvani published a book about his work on animal electricity. It contained comprehensive details of his 11 years of research and experimentation on the topic. [ 10 ]


The 1797 edition of  Gren ’s Grundriss der Naturlehre  provides the first explicit definition of 'galvanism' as clearly reflecting Volta’s opinion in the following terms:


Galvani from Bologna was the first to observe muscular motions elicited by the contact between two different metals; after him, the phenomena of this sort were termed and included under the name of Galvanism. [ 11 ]