How Are Muscle Cells Adapted To Their Function

The adaptations of the muscle cell are: Multiple Nuclei : Because the muscle cells are long fibers, they are connected or fused together. The fusion causes the cells to have multiple nuclei, which help your body move. Nerve responsiveness: These muscle cells will respond when it is time to move.

What are the adaptations of a muscle?

ENDURANCE TRAINING – Endurance training leads to adaptations in both the cardiovascular and musculoskeletal system that supports an overall increase in exercise capacity and performance (Brooks 2011). The local adaptations in skeletal muscle, such as increased mitochondrial biogenesis and capillary density, aid in the body’s ability to transport and use oxygen to generate energy and therefore delay the onset of muscle fatigue during prolonged aerobic performance ( Joyner and Coyle 2008 ).

The mitochondrion is the main organelle for energy production through the generation of adenosine triphosphate (ATP) via the electron transport system (ETS), using substrates generated in the tricarboxylic acid (TCA) cycle ( Egan and Zierath 2013 ; Bishop et al.2014 ). Recent studies have begun to investigate the impact of exercise-induced mitochondrial biogenesis adaptations from the perspective of mitochondrial content and function with varying exercise intensity paradigms ( Serpiello et al.2012 ; Granata et al.2016a, b ; MacInnis et al.2016 ).

Studies investigating the role of the intensity and volume of exercise on mitochondrial adaptations have been conducted using long slow-distance (LSD) training, sprint interval training (; ∼30 sec maximal bouts) and high-intensity interval training (HIIT; 1–4 min all-out bouts) ( Gibala et al.2014 ).

• Traditional LSD training entails an individual sustaining a submaximal workload for a long period of time, or successfully completing a fixed distance/time through a higher than average power output ( Coyle 1995 ).
• On the other hand, HIIT and SIT require the individual to perform repeated bouts at close to maximal intensity for a short period of time with a reduced training volume ( Laursen and Jenkins 2002 ; Gibala et al.2006 ).

Many studies have highlighted similarities in adaptations for mitochondria markers (e.g., peroxisome proliferator-activated receptor γ coactivator 1α ) and skeletal muscle oxidative capacity in both training models ( Gibala et al.2009 ; Little et al.2010b, 2011 ; Jacobs et al.2013b ; Cochran et al.2014 ), and, therefore, HIIT/SIT has been proposed as a time-effective strategy for enhancing aerobic adaptations ( Gibala and McGee 2008 ; Gillen and Gibala 2013 ).

More recent studies have begun to directly address the importance of exercise intensity versus volume in relation to mitochondrial content and function ( Daussin et al.2008 ; Jacobs et al.2013b ; Cochran et al.2014 ; Granata et al.2016b ; MacInnis et al.2016 ). Granata and colleagues (2016b) used all three exercise protocols (LSD, HIIT, and SIT), matching volume in the traditional and HIIT groups, on young moderately trained men.

After 4 wk of training, the investigators observed a 25% increase in maximal mitochondrial respiration only in the SIT group, with no changes seen in either the LSD or HIIT groups. The increased level of mitochondrial respiration within the SIT group was accompanied by changes in PGC-1α, p53, and PHF20 protein content.

• PHF20 is important for both stabilizing and up-regulating p53 ( Cui et al.2012 ; Park et al.2012 ), whereas p53 is a tumor suppressor and involved in the regulation of mitochondrial function ( Matoba et al.2006 ; Park et al.2009 ).
• In contrast to the Granata study, HIIT alone has been shown to influence mitochondrial content and respiration ( Daussin et al.2008 ; Jacobs et al.2013b ).

Jacobs et al. (2013b) observed increased mitochondrial respiration along with alterations in content (measured by cytochrome c oxidase activity) culminating in increased exercise capacity after only 2 wk of HIIT training. Further support for mitochondrial adaptations with HIIT comes from a within-subject study that showed 2 wk of training resulted in increased mitochondrial volume density and respiration ( MacInnis et al.2016 ).

• The discrepancies between these studies may be because of differences in subject training status, experimental design, and methodological measures implemented for assessing mitochondrial adaptations.
• The optimal study to conclusively address this issue would use all three training models and a within-subject crossover design.

When the intensity of training is maintained and only the volume manipulated, the mitochondrial adaptation differs again, using a design in which 10 subjects performed HIIT once a day three times a week, then twice a day three times a week, followed by once a day two times a week.

Granata and colleagues ( Granata et al.2016b ) showed that mitochondrial respiration and citrate synthase (CS) activity increased (∼50%) during only the high-volume training period. The increase in mitochondrial respiration was accompanied by increased ETS and regulatory proteins, such as PGC-1α, p53, and PHF20.

Following 2 wk of decreased training volume, mitochondrial-specific respiration remained high, with a slight decrease in CS activity being the only sign of detraining. Overall, these studies suggest that high-intensity training is important for increasing mitochondrial activity, whereas a greater training volume is needed to increase mitochondrial mass ( Fig.1 ) ( MacInnis et al.2016 ). Schematic diagram of training intensity and volume on mitochondrial respiration versus content adaptations through endurance training. Recent evidence suggests that increases in exercise intensity (sprint interval training ; high-intensity interval training ) lead to enhanced mitochondrial respiration and function, whereas prolonged low-intensity and high-volume (long slow-distance training) endurance exercise appears to aid in increased mitochondrial content within skeletal muscle.

• Classically, PGC-1α has been anointed as the “master regulator of mitochondrial biogenesis” and a fundamental component of exercise-induced adaptations with endurance training ( Baar et al.2002 ; Pilegaard et al.2003 ; Little et al.2010a ).
• In recent years, another protein, p53, has emerged as a key player in substrate metabolism and mitochondrial biogenesis ( Park et al.2009 ; Saleem and Hood 2013 ; Bartlett et al.2014 ).

p53 was the first tumor suppressor protein discovered ( Baker et al.1989 ; Nigro et al.1989 ). In this role, p53 regulates cell-cycle arrest, apoptosis, angiogenesis, DNA repair, and cell senescence ( Levine et al.2006 ). Initial studies using mouse knockout (KO) models lacking p53 identified a further role for this protein in controlling mitochondrial content, with KO mice displaying reduced mitochondria in both subsarcolemmal and intermyofibrillar compartments, together with reduced COX activity and PGC-1α compared with wild-type animals ( Saleem et al.2009 ).

Furthermore, the loss of p53 and subsequent decrease in mitochondrial content and function resulted in reduced exercise capacity and performance ( Park et al.2009 ). The current proposed mechanisms for how p53 may regulate mitochondrial biogenesis is through targeting the mitochondrial genome and specifically interacting with mitochondrial transcription factor A (Tfam) ( Saleem and Hood 2013 ).

Saleem and Hood (2013) reported that, with acute exercise and muscle contraction, p53 translocates from the nucleus and positively modulates Tfam activity. In terms of current human data, Bartlett et al. (2012) observed increased p53 phosphorylation 3 h postexercise, although this alteration in p53 phosphorylation occurred after acute bouts of both continuous endurance and HIIT exercise.

In contrast, Granata and colleagues showed that p53 increases with maximal sprint training, whereas HIIT or continuous endurance training has no effect on p53 content ( Granata et al.2016b ). It is important to note that the regulation of p53 may not only be influenced by exercise intensity but also the nutritional status of the working muscle during training sessions, for example, reduced carbohydrate availability ( Bartlett et al.2013 ).

Future research is required to understand the time course of p53 activation and involvement in mitochondrial biogenesis with respect to endurance exercise ( Bartlett et al.2014 ). Understanding this signaling cascade will not only be important from a human performance perspective but also from a health standpoint in which exercise might be used to support treatments in cancer therapy ( Saleem and Hood 2013 ).

1. In addition to alterations in oxygen delivery, substrate metabolism, and mitochondrial mass within skeletal muscle after endurance training, other factors contribute toward the resulting enhanced exercise performance and improved running economy ( Saunders et al.2004 ; Barnes and Kilding 2015 ).
2. One such factor is the stiffness of the muscle–extracellular matrix (ECM)–tendon unit, because adaptations within this system will enhance the body’s ability to store and use elastic energy more efficiently.

An increase in elastic energy storage and recoil results in decreased ground contact time and reduced energy cost ( Arampatzis et al.2006 ; Fletcher et al.2010 ). Indeed, runners who display and/or develop a longer and stiffer musculotendonous system appear to have a lower oxygen uptake (VO 2 ) when performing at submaximal running velocities ( Craib et al.1996 ; Albracht and Arampatzis 2013 ; Barnes et al.2014 ).

A second factor contributing to improved running and cycling economy is neural adaptation. Muscle recruitment patterns vary greatly between highly trained individuals and novice counterparts ( Paavolainen et al.1999b, c ; Chapman et al.2008 ). Highly trained individuals may have the capacity to elicit increased muscle coactivation, leg stiffness, and greater eccentric to concentric muscle activity, which allows for more efficient usage of stored elastic energy, lowering the metabolic cost of exercise ( Paavolainen et al.1999b ; Heise et al.2008 ).

In contrast, stretching interventions used to enhance flexibility tend to decrease economy, although these results have been equivocal ( Craib et al.1996 ; Nelson et al.2001 ; Shrier 2004 ). Some of the possible reasons for the contrasting evidence with stretching include the length of intervention program (acute vs.

Chronic), the influence of gender in pooled studies, methodological designs, and treadmill familiarization ( Craib et al.1996 ; Nelson et al.2001 ; Shrier 2004 ; Allison et al.2008 ; Trehearn and Buresh 2009 ). Training to improve the connective tissue stiffness and neuromuscular components is quite different than classic endurance training.

Here, training is based on strength/power and plyometric exercises to heighten the neuromuscular adaptations (e.g., muscle activation, motor unit recruitment) and the stiffness of the muscle–ECM–tendon unit ( Storen et al.2008 ; Yamamoto et al.2008 ; Beattie et al.2014 ).

1. A good example of this work is an early study by Paavolainen and colleagues (1999a) who investigated the impact of explosive-type strength training in well-trained endurance athletes on endurance performance (5-km time trial, running economy, etc.).
2. After 9 wk of training, the investigators reported a 3% improvement in 5-km time trial with a tendency to decrease VO 2max,

The improved performance resulted largely from improvements in running economy. Subsequent research has highlighted an additive effect of incorporating a strength-training program into the training of predominately endurance-trained athletes, both during preseason and in season ( Rønnestad et al.2010 ).

The proposed mechanisms for these improvements in endurance performance are improved neural function (maximal voluntary contraction, rate of force development ), increases in type IIA muscle fibers (less fatigable), and increased muscle–ECM–tendon stiffness ( Aagaard and Andersen 2010 ; Aagaard et al.2011 ).

Further, the addition of strength training has been observed to improve exercise economy better than endurance training alone ( Sunde et al.2010 ; Beattie et al.2014 ; Vikmoen et al.2015 ) and the inclusion of strength training may enhance performance during the later stages of competition ( Rønnestad et al.2011 ).

One way to distinguish between the muscle–ECM–stiffness and neural adaptations would be to perform the strength/plyometric training on one leg and determine whether cross-limb transfer has resulted in improved performance in the opposite limb indicative of a neural adaptation (see below). However, these experiments have yet to be performed with endurance-type exercise.

Further, caution is warranted for strength training to improve endurance performance as there is also evidence to suggest that increasing endurance and strength training volume together may lead to impairments in both adaptations and performance ( Hickson 1980 ; Rønnestad et al.2012 ; Jones et al.2013 ).

The last adaptation to endurance exercise training that we would like to highlight is muscle hypertrophy and growth ( Harber et al.2009b, 2012 ; Konopka and Harber 2014 ). Over a 12-wk endurance-training program, muscle mass has been reported to increase by 7% to 11% ( Konopka et al.2010 ; Trappe et al.2011 ; Harber et al.2012 ).

This increase in muscle mass is comparable to resistance exercise training over the same time period ( Trappe et al.2011 ; Mitchell et al.2012 ). These reported increases in muscle mass with endurance training have been predominately observed in the quadriceps muscle, the mode of exercise used was cycling, and the individuals undertaking training had a limited level of exercise experience and/or sedentary lifestyle ( Konopka and Harber 2014 ).

1. Nonetheless, it appears that hypertrophy occurs in the quadriceps muscle with classical motor endurance training if the frequency of training and load are high enough ( Konopka and Harber 2014 ).
2. From a mechanistic perspective, acute studies have reported increases in muscle protein synthesis (MPS) with aerobic exercise, independent of age ( Short et al.2004 ; Harber et al.2009a, 2010 ; Durham et al.2010 ).

For example, Short and colleagues (2004) observed a 22% increase in MPS with 4 mo of cycling (up to 45 min at 80% peak heart rate, 3–4 days/wk). The observed increases in MPS with aerobic exercise do not appear to be driven by complex 1 of the mechanistic target of rapamycin complex 1 (mTORC1) ( Durham et al.2010 ; Philp et al.2015 ).

Using rapamycin (an inhibitor of mTORC1 activation), Philp and colleagues (2015) reported increases in muscle and mitochondrial protein synthesis rates following endurance exercise in rats, even when mTORC1 signaling was completely suppressed. The findings by Philp and colleagues are in contrast with previous findings reporting increased MPS and mTORC1 activation with aerobic exercise ( Mascher et al.2011 ; Edgett et al.2013 ; Di Donato et al.2014 ).

As mentioned previously with other facets of endurance adaptation, the impact of exercise intensity, modality, and level of muscle fiber recruitment may be a potential explanation for the contrast in findings between studies. Specifically, hypertrophy has been observed almost exclusively following training for cycling.

Are muscle cells adapted?

A muscle cell is a cell adapted to cause movement. Muscle cells possess special contractile proteins (protein filaments) that can shorten the cell, generating force. There are different types of muscle cells that are adapted to their specific functions, but they all have certain features in common.

What helps the muscle cell function?

Aerobic Metabolism – This type of metabolism refers to the utilization of oxygen for the muscle energy or “fuel” to produce muscle contraction and subsequent force production. The presence of oxygen allows the muscle energy systems to produce the chemical ATP from the breakdown of glucose, providing the energy to carry out the muscle contraction.

What are 3 adaptations of?

The three types of adaptation include structural, physiological, and behavioral.

What are 3 different types of adaptations?

7.2 Types of Adaptations Once an adaptation occurs, it generally falls into one of three main types: structural, physiological, or behavioral. We unpack these below.

How are muscle cells modified?

MUSCLE DIFFERENTIATION – Muscle cell differentiation begins with the conversion of mesodermal precursor cells into single-cell myoblasts, which then fuse to form myocytes. Further fusion of the myocytes produces multinucleate myotubes. Several different myogenic bHLH transcription factors are required for this process, and these factors recruit both HATs and HDACs to promoter regions to regulate transcription of target genes.57, 58 Two HAT families have been linked to the muscle differentiation program, CBP/p300 59–62 and GCN5/PCAF.59, 63 Class I HDACs such as HDAC1 are also important in preventing precocious muscle cell-specific gene expression and differentiation.

• CBP/p300 HAT activity is critical for myogenic differentiation in cultured cells.64 Expression of dominant negative alleles of these HATs or direct inhibition of their enzymatic activities by specific peptide inhibitors prevents muscle cell fusion.
• In addition, loss of CBP/p300 activity is associated with loss of expression of myosin heavy chain (MHC) and muscle creatine kinase (MCK), which are both markers for late muscle cells.

Thus, CBP/p300 are required for specific events during the late stages of muscle cell differentiation. These functions are likely through the modification of histones at genes activated by bHLH factors such as MyoD, which is involved in the initial step of myoblast determination.

• However, CBP/p300 and PCAF might also directly regulate the functions of MyoD during myoblast differentiation by acetylation of this factor.
• Both PCAF 65 and CBP/p300 64 can acetylate MyoD in vitro at conserved lysines to increase its DNA binding affinity.
• Acetylation of MyoD by PCAF, but not CBP/p300, is required for the ability of MyoD to induce transcription and stimulate myogenic conversion in vivo.59, 65 This indicates that MyoD uses both the CBP/p300 and PCAF HATs at unique steps during muscle cell differentiation.

The removal of acetyl moieties from histones and other factors also plays a key role in regulating muscle cell differentiation. In undifferentiated, dividing cells MyoD is associated with HDAC1, which likely deacetylates histones at MyoD targets to keep them repressed.

How are muscle cells unique?

Muscle Cell Structure and Composition – The differentiated muscle cell in postnatal muscle is the muscle fiber, a highly specialized, long, cylindrical cell that can range in diameter from 10 to 100 mm and in length from millimeters up to many centimeters.

The primary differences in fibers of different species are fiber length and number of fibers per muscle. Each fiber is surrounded by a 7.5- to 10-nm-thick plasmalemma, called the sarcolemma. The sarcolemma is a lipid bilayer like the cell membranes of other cells and has a lipid composition of roughly 60 percent protein, 20 percent phospholipid, and 20 percent cholesterol.

Surrounding the sarcolemma is the basal lamina, or basement membrane. This somewhat amorphous structure, 50 to 70 nm thick, is composed of mucopolysaccharides and collagen (types III and V). The cell membrane of muscle has a specialized structure—the motor endplate—which accommodates interaction with an axon from a motoneuron.

In addition, the membrane maintains an electrical potential that is propagated from the motor endplate, down the membrane, and finally into the cell by a complex set of invaginations that form the transverse tubular system. Muscle fibers contain the major organelles present in most cells. The most striking difference between muscle cells and the majority of other cells is their multinucleated nature.

Depending on its size, an individual fiber may contain hundreds of nuclei. They are found just beneath the sarcolemma and seem to be randomly distributed along the length of the fiber. Mitochondria are present between the contractile elements of muscle; their concentration varies with the metabolic activity of the particular fiber.

• Ribosomes are dispersed within the cytoplasm, but very few are associated with endoplasmic reticulum, primarily because muscle fibers synthesize few secreted proteins.
• The endoplasmic reticulum in muscle has formed a specialized set of membrane structures called the sarcoplasmic reticulum.
• The primary function of this structure is regulation of free calcium ion concentration.

When free calcium ion concentration is maintained below approximately 0.1 mM, contraction does not occur. But when the membrane is depolarized, the action potential reaches the interior of the cell through the transverse tubular system, calcium is released from the sarcoplasmic reticulum, the concentration approaches 1 mM, and contraction is activated.

1. Lysosomes are not readily seen in muscle fibers, although lysosomal enzymes are present.
2. The lysosomes are most likely sequestered in the sarcoplasmic reticulum.
3. By far the most unique subcellular aspect of muscle fibers is the contractile machinery, the myofibril.
4. This is an aggregation of 12 to 14 proteins into highly organized contractile threads that are insoluble at the ionic strength of the cytoplasm in muscle cells.

It is noteworthy that this specialized set of proteins constitutes about 55 percent of the total protein in muscle. Consequently, many developmental studies of muscle have focused on myofibrillar protein gene expression and synthesis, which are discussed later in this paper.

• Myofibrils are composed of two main classes of filaments: thick filaments and thin filaments.
• Thick filaments measure approximately 15 nm by 1,500 nm.
• The major protein in thick filaments is myosin, which has the active site that hydrolyzes adenosine triphosphate (ATP) and the site that binds to actin in the thin filament.

The thin filament is roughly 6 nm by 1,000 nm and is composed of actin, which forms the beaded backbone of the filament, and tropomyosin and troponin, which perform regulatory functions. At one end, thin filaments insert into a protein lattice called the Z-line; at the other end, they overlay with thick filaments in a hexagonal array.

Additional small-diameter filament systems are present within myofibrils to provide an elastic component. Also, an intermediate-diameter filament system, found outside the periphery of the myofibril, links adjacent myofibrils and maintains their contractile units in register. Specific details of the ultrastructure of myofibrils and the biochemical properties of this interdigitating array of filaments can be found in Goll et al.

(1984). These features of muscle cells are common to all skeletal muscle fibers, but specific fibers have differentiated somewhat depending on their purpose. Some populations of fibers are primarily responsible for rapid contractions on an intermittent basis, while others have slower contraction speed and sustain contractile activity over extended periods of time.

Muscle fiber types have been described extensively in many species; and their biochemical, physiological, and morphological differences are significant to problems of muscle growth and meat quality. A generalized scheme for describing fiber types classifies them on the basis of their contraction speed and on the energy metabolism pathways primarily used to provide energy for contraction.

Peter et al. (1972) provided one of the most descriptive classification systems by grouping fibers into three general categories. Fibers that were dependent on oxidative metabolism and had slower contraction speeds were classified as slow-twitch, oxidative fibers (so).

Fibers with faster contraction times that were dependent on anaerobic, or glycolytic, energy metabolism pathways were termed fast-twitch, glycolytic fibers (FG). A third broad category contained fast-twitch fibers that had glycolytic metabolic capabilities but also a significant capacity for oxidative metabolism; these were termed fast-twitch, oxidative-glycolytic fibers (FOG).

Contraction speed is correlated with myosin adenosine triphosphatase (ATPase) activity and, therefore, with the particular myosin isozymes synthesized by the fiber. Other myofibrillar protein isoform variations may also be associated with contractile properties.

The complexity and degree of development of the sarcoplasmic reticulum, t-tubule system, and neuromuscular junctions have all been associated with contraction speed and fiber class. As expected, mitochondrial content and glycolytic enzyme content vary, among fiber types, as do energy substrates such as glycogen and triglyceride.

Aspects of fiber type variation that affect muscle growth include the notable differences in fiber size that generally correlate with muscle fiber type. SO fibers are smaller in diameter than FG fibers, and FOG fibers tend to be intermediate in size. Smaller fiber diameters may facilitate efficient gas exchange in oxidative fibers.

In addition, SO fibers tend to have higher nuclei concentrations and, therefore, lower protein concentrations per nucleus. Satellite cell frequency, however, is reportedly higher for SO fibers (Kelly, 1978b). Because individual muscles vary in fiber type composition, factors that differentially affect the development or growth of specific fiber types can result in alterations in muscle mass (for example, the transition from FG to FOG that can accompany aerobic conditioning).

Reductions in fiber diameter and, consequently, muscle mass would be expected. Alterations in gene expression and in quantitative aspects of protein metabolism that are responsible for such fiber type transitions are poorly understood. Chemical composition of muscle tissue can be quite variable, and the primary source of variation is intramuscular adipose tissue.

It is clear that most of the variation in major constituents is minimized when expressed on a fat-free basis. Some compositional variation can be found in association with aging, but, in general, it is attributable to changes in moisture content. Skeletal muscle from very young animals has a high moisture content that decreases with maturity.

As a result, protein concentration increases with maturity. Subtle changes in other constituents, such as glycogen, can vary among muscles and species, but these differences may not have major nutritional significance when considering the composition of muscle as a food.

• The primary lipid fraction contributing to muscle tissue variation is triglyceride, which is stored in adipocytes within the muscle.
• These depositions are commonly referred to as marbling, and within the range of marbling found in the longissimus muscle of beef, the ether-extractable lipid (primarily triglyceride) varies from 1.77 to 10.42 percent on a wet weight basis (Savell et al., 1986).

Cholesterol content, on the other hand, is less variable. This can best be understood in light of its role in muscle tissue. Cholesterol is an integral part of cell membranes, mainly the plasma membrane. On a tissue basis across maturity groups and marbling contents within maturity groups, cholesterol content of beef muscle does not vary (Stromer et al., 1966).

1. In addition, the amount of cholesterol per gram of whole steak was not significantly different among the five yield grades examined by Rhee et al. (1982).
2. Furthermore, neither breed type nor nutritional background affected cholesterol content of lean muscle tissue in beef cows (Eichhorn et al., 1986).

It is possible to find variation in cholesterol content of meat, however, because adipose tissue tends to have a higher cholesterol concentration than do muscle fibers. Consequently, variations in the amount of subcutaneous or inter-muscular fat consumed with the lean portion can alter cholesterol intake.

It has been calculated that 37 to 56 percent of the cholesterol in a cooked rib steak of beef originates from subcutaneous and inter-muscular adipose tissue (Rhee et al., 1982). In looking only at muscle cells, however, significant variations in cholesterol content have not been seen, even among most of the species used for muscle foods (Reiser, 1975; Watt and Merrill, 1963).

This is also true for the amino acid composition of muscle. The majority of muscle cell proteins are myofibrillar and are very highly conserved across species. In addressing topics such as alteration of tissue composition to enhance nutritional quality, it is important to keep in mind that the biology of the animal or tissue must come first.

What are the key features of muscle cells?

MUSCLES-STRUCTURE AND FUNCTION Functions of muscle tissue

Movement: Our body’s skeleton gives enough rigidity to our body that skeletal muscles can yank and pull on it, resulting in body movements such as walking, chewing, running, lifting, manipulating objects with our hands, and picking our noses. Maintenance of posture: Without much conscious control, our muscles generate a constant contractile force that allows us to maintain an erect or seated position, or posture. Respiration: Our muscular system automatically drives movement of air into and out of our body. Heat generation: Contraction of muscle tissue generates heat, which is essential for maintenance of temperature homeostasis. For instance, if our core body temperature falls, we shiver to generate more heat. Communication: Muscle tissue allows us to talk, gesture, write, and convey our emotional state by doing such things as smiling or frowning. Constriction of organs and blood vessels: Nutrients move through our digestive tract, urine is passed out of the body, and secretions are propelled out of glands by contraction of smooth muscle. Constriction or relaxation of blood vessels regulates blood pressure and blood distribution throughout the body. Pumping blood: Blood moves through the blood vessels because our heart tirelessly receives blood and delivers it to all body tissues and organs, This isn’t a complete list. Among the many possible examples are the facts that muscles help protect fragile internal organs by enclosing them, and are also critical in maintaining the integrity of body cavities. For example, fetuses with incompletely formed diaphragms have abdominal contents herniate (protrude) up into the thoracic cavity, which inhibits normal lung growth and development. Even though this is an incomplete list, an appreciation of some of these basic muscle functions will help you as we proceed.

Properties of muscle tissue All muscle cells share several properties: contractility, excitability, extensibility, and elasticity:

Contractility is the ability of muscle cells to forcefully shorten. For instance, in order to flex (decrease the angle of a joint) your elbow you need to contract (shorten) the biceps brachii and other elbow flexor muscles in the anterior arm. Notice that in order to extend your elbow, the posterior arm extensor muscles need to contract. Thus, muscles can only pull, never push. Excitability is the ability to respond to a stimulus, which may be delivered from a motor neuron or a hormone. Extensibility is the ability of a muscle to be stretched. For instance, let’s reconsider our elbow flexing motion we discussed earlier. In order to be able to flex the elbow, the elbow extensor muscles must extend in order to allow flexion to occur. Lack of extensibility is known as spasticity. Elasticity is the ability to recoil or bounce back to the muscle’s original length after being stretched.

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How are muscle cells controlled?

Motor Units and Muscle Receptors (Section 3, Chapter 1) Neuroscience Online 1.1 What is Motor Control?

Figure 1.1 Sensory receptors provide information about the environment, which is then used to produce action to change the environment. Sometimes the pathway from sensation to action is direct, as in a reflex. In most cases, however, cognitive processing occurs to make actions adaptive and appropriate for the particular situation.

Much of the brain and nervous system is devoted to the processing of sensory input, in order to construct detailed representations of the external environment. Through vision, audition, somatosensation, and the other senses, we perceive the world and our relationship to it.

This elaborate processing would be of limited value, however, unless we had a way to act upon the environment that we are sensing, whether that action consist of running away from a predator; seeking shelter against the rain; searching for food when one is hungry; moving one’s lips and vocal cords in order to communicate with others; or performing the countless other varieties of actions that make up our daily lives.

In some cases the relationship between the sensory input and the motor output are simple and direct; for example, touching a hot stove elicits an immediate withdrawal of the hand (Figure 1.1). Usually, however, our conscious actions require not only sensory input but a host of other cognitive processes that allow us to choose the most appropriate motor output for the given circumstances.

1. Volition. The motor system must generate movements that are adaptive and that accomplish the goals of the organism. These goals are evaluated and set by high-order areas of the brain. The motor system must transform the goals into the appropriate activations of muscles to perform the desired movements.
2. Coordination of signals to many muscle groups. Few movements are restricted to the activation of a single muscle. For example, the act of moving your hand from inside your pocket to a position in front of you requires the coordinated activity of the shoulder, elbow, and wrist. Making the same movement while removing a 2-lb weight from your pocket may result in the same trajectory of your hand, but will require different sets of forces on the muscles that make the movement. The task of the motor system is to determine the necessary forces and coordination at each joint in order to produce the final, smooth motion of the arm.
3. Proprioception. In order to make a desired movement (e.g., raising your hand to ask a question), it is essential for the motor system to know the starting position of the hand. Raising one’s hand from a resting position on a desk, compared to a resting position on top of the head, results in the same final position of the arm, but these two movements require different patterns of muscle activation. The motor system has a set of sensory inputs (called proprioceptors) that inform it of the length of muscles and the forces being applied to them; it uses this information to calculate joint position and other variables necessary to make the appropriate movement.
4. Postural adjustments. The motor system must constantly produce postural adjustments in order to compensate for changes in the body’s center of mass as we move our limbs, head, and torso. Without these automatic adjustments, the simple act of reaching for a cup would cause us to fall, as the body’s center of mass shifts to a location in front of the body axis.
5. Sensory feedback. In addition to the use of proprioception to sense the position of the body before a movement, the motor system must use other sensory information in order to perform the movement accurately. By comparing desired activity with actual activity, sensory feedback allows for corrections in movements as they take place, and it also allows modifications to motor programs so that future movements are performed more accurately.
6. Compensation for the physical characteristics of the body and muscles. To exert a defined force on an object, it is not sufficient to know only the characteristics of the object (e.g., its mass, size, etc.). The motor system must account for the physical characteristics of the body and muscles themselves. The bones and muscles have mass that must be considered when moving a joint, and the muscles themselves have a certain degree of resistance to movement.
7. Unconscious processing. The motor system must perform many procedures in an automatic fashion, without the need for high-order control. Imagine if walking across the room required thinking about planting the foot at each step, paying attention to the movement of each muscle in the leg and making sure that the appropriate forces and contraction speeds are taking place. It would be hard to do anything else but that one task. Instead, many motor tasks are performed in an automatic fashion that does not require conscious processing. For example, many of the postural adjustments that the body makes during movement are performed without our awareness. These unconscious processes allow higher-order brain areas to concern themselves with broad desires and goals, rather than low-level implementations of movements.
8. Adaptability. The motor system must adapt to changing circumstances. For example, as a child grows and its body changes, different constraints are placed on the motor system in terms of the size and mass of bones and muscles. The motor commands that work to raise the hand of an infant would fail completely to raise the hand of an adult. The system must adapt over time to change its output to accomplish the same goals. Furthermore, if the system were unable to adapt, we would never be able to acquire motor skills, such as playing a piano, hitting a baseball, or performing microsurgery.

These are some of the many components of the motor system that allow us to perform complex movements in a seemingly effortless way. The brain has evolved exceedingly complex and sophisticated mechanisms to perform these tasks, and researchers have only scratched the surface in understanding the principles that underlie the brain’s control of movement.1.3 Motor Control Requires Sensory Input One of the major principles of the motor system is that motor control requires sensory input to accurately plan and execute movements.

This principle applies to low levels of the hierarchy, such as spinal reflexes, and to higher levels. As we shall see throughout this material on the motor system, our abilities to make movements that are accurate, properly timed, and with proper force depend critically on the sensory input that is ubiquitous at all levels of the motor system hierarchy.1.4 Functional Segregation and Hierarchical Organization The ease with which we make most of our movements belies the enormous sophistication and complexity of the motor system.

Engineers have spent decades trying to make machines perform simple tasks that we take for granted, yet the most advanced robotic systems do not come close to emulating the precision and smoothness of movement, under all types of conditions, that we achieve effortlessly and automatically.

• Functional Segregation. The motor system is divided into a number of different areas that control different aspects of movement (a “divide and conquer” strategy). These areas are located throughout the nervous system. One of the key questions of research on motor control is to understand the functional roles played by each area.
• Hierarchical Organization. The different areas of the motor system are organized in a hierarchical fashion. The higher-order areas can concern themselves with more global tasks regarding action, such as deciding when to act, devising an appropriate sequence of actions, and coordinating the activity of many limbs. They do not have to program the exact force and velocity of individual muscles, or coordinate movements with changes in posture; these low-level tasks are performed by the lower levels of the hierarchy.

The motor system hierarchy consists of 4 levels (Figure 1.2): the spinal cord, the brain stem, the motor cortex, and the association cortex. It also contains two side loops: the basal ganglia and the cerebellum, which interact with the hierarchy through connections with the thalamus.

Figure 1.2 Schematic representation of the different levels and interconnections of the motor system hierarchy. The brain figure on the left is a schematic version of an idealized brain section that contains the major structures of the motor system hierarchy for illustrative purposes; no actual brain section would contain all of these structures. Tap on each box on the right to highlight the inputs (blue) and outputs (red) of each region.

1.5 The Spinal Cord: The First Hierarchical Level The spinal cord is the first level of the motor hierarchy. It is the site where motor neurons are located. It is also the site of many interneurons and complex neural circuits that perform the “nuts and bolts” processing of motor control.

These circuits execute the low-level commands that generate the proper forces on individual muscles and muscle groups to enable adaptive movements. The spinal cord also contains complex circuitry for such rhythmic behaviors as walking. Because this low level of the hierarchy takes care of these basic functions, higher levels (such as the motor cortex) can process information related to the planning of movements, the construction of adaptive sequences of movements, and the coordination of whole-body movements, without having to encode the precise details of each muscle contraction.1.6 Motor Neurons Alpha motor neurons (also called lower motor neurons ) innervate skeletal muscle and cause the muscle contractions that generate movement.

Motor neurons release the neurotransmitter acetylcholine at a synapse called the neuromuscular junction. When the acetylcholine binds to acetylcholine receptors on the muscle fiber, an action potential is propagated along the muscle fiber in both directions (see of for review).

The action potential triggers the contraction of the muscle. If the ends of the muscle are fixed, keeping the muscle at the same length, then the contraction results on an increased force on the supports (i sometric contraction ). If the muscle shortens against no resistance, the contraction results in constant force ( isotonic contraction ).

The motor neurons that control limb and body movements are located in the anterior horn of the spinal cord, and the motor neurons that control head and facial movements are located in the motor nuclei of the brainstem. Even though the motor system is composed of many different types of neurons scattered throughout the CNS, the motor neuron is the only way in which the motor system can communicate with the muscles.

Figure 1.3 Spinal cord with motor neuron in anterior horn.

Motor neurons are not merely the conduits of motor commands generated from higher levels of the hierarchy. They are themselves components of complex circuits that perform sophisticated information processing. As shown in Figure 1.3, motor neurons have highly branched, elaborate dendritic trees, enabling them to integrate the inputs from large numbers of other neurons and to calculate proper outputs.

1. Motor neurons are clustered in columnar, spinal nuclei called motor neuron pools (or motor nuclei). All of the motor neurons in a motor neuron pool innervate a single muscle (Figure 1.4), and all motor neurons that innervate a particular muscle are contained in the same motor neuron pool. Thus, there is a one-to-one relationship between a muscle and a motor neuron pool.
2. Each individual muscle fiber in a muscle is innervated by one, and only one, motor neuron (make sure you understand the difference between a muscle and a muscle fiber). A single motor neuron, however, can innervate many muscle fibers. The combination of an individual motor neuron and all of the muscle fibers that it innervates is called a motor unit, The number of fibers innervated by a motor unit is called its innervation ratio,

Figure 1.4 Motor unit and motor neuron pool.

If a muscle is required for fine control or for delicate movements (e.g., movement of the fingers or hands), its motor units will tend to have small innervation ratios. That is, each motor neuron will innervate a small number of muscle fibers (10-100), enabling many nuances of movement of the entire muscle.

If a muscle is required only for coarse movements (e.g., a thigh muscle), its motor units will tend to have a high innervation ratio (i.e., each motor neuron innervating 1000 or more muscle fibers), as there is no necessity for individual muscle fibers to undergo highly coordinated, differential contractions to produce a fine movement.1.7 Control of Muscle Force A motor neuron controls the amount of force that is exerted by muscle fibers.

There are two principles that govern the relationship between motor neuron activity and muscle force: the rate code and the size principle.

1. Rate Code. Motor neurons use a rate code to signal the amount of force to be exerted by a muscle. An increase in the rate of action potentials fired by the motor neuron causes an increase in the amount of force that the motor unit generates. This code is illustrated in Figure 1.5. When the motor neuron fires a single action potential (Play 1), the muscle twitches slightly, and then relaxes back to its resting state. If the motor neuron fires after the muscle has returned to baseline, then the magnitude of the next muscle twitch will be the same as the first twitch. However, if the rate of firing of the motor neuron increases, such that a second action potential occurs before the muscle has relaxed back to baseline, then the second action potential produces a greater amount of force than the first (i.e., the strength of the muscle contraction summates) (Play 2). With increasing firing rates, the summation grows stronger, up to a limit. When the successive action potentials no longer produce a summation of muscle contraction (because the muscle is at its maximum state of contraction), the muscle is in a state called tetanus (Play 3).
   

   Figure 1.5 Rate code for muscle force. The upper trace on the oscilloscope shows the action potentials generated by the alpha motor neuron. The lower trace shows the force generated by the isometrically contracting muscle. PLAY 1: Single spikes by the motor neuron produce small twitches of the muscle. PLAY 2: Multiple spikes in succession summate to produce larger contractions. PLAY 3: Very high rates of spikes produce maximal contraction called tetanus.

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2. Size Principle. When a signal is sent to the motor neurons to execute a movement, motor neurons are not all recruited at the same time or at random. The motor neuron size principle states that, with increasing strength of input onto motor neurons, smaller motor neurons are recruited and fire action potentials before larger motor neurons are recruited. Why does this orderly recruitment occur? Recall the relationship between voltage, current, and resistance ( Ohm’s Law ): V = IR. Because smaller motor neurons have a smaller membrane surface area, they have fewer ion channels, and therefore a larger input resistance. Larger motor neurons have more membrane surface and correspondingly more ion channels; therefore, they have a smaller input resistance. Because of Ohm’s Law, a small amount of synaptic current will be sufficient to cause the membrane potential of a small motor neuron to reach firing threshold, while the large motor neuron stays below threshold. As the amount of current increases, the membrane potential of the larger motor neuron also increases, until it also reaches firing threshold.

Figure 1.6 demonstrates how the size principle governs the amount of force generated by a muscle. Because motor units are recruited in an orderly fashion, weak inputs onto motor neurons will cause only a few motor units to be active, resulting in a small force exerted by the muscle (Play 1).

• With stronger inputs, more motor neurons will be recruited, resulting in more force applied to the muscle (Play 2 and Play 3).
• Moreover, different types of muscle fibers are innervated by small and larger motor neurons.
• Small motor neurons innervate slow-twitch fibers ; intermediate-sized motor neurons innervate fast-twitch, fatigue-resistant fibers ; and large motor neurons innervate fast-twitch, fatigable muscle fibers,

The slow-twitch fibers generate less force than the fast-twitch fibers, but they are able to maintain these levels of force for long periods. These fibers are used for maintaining posture and making other low-force movements. Fast-twitch, fatigue-resistant fibers are recruited when the input onto motor neurons is large enough to recruit intermediate-sized motor neurons.

These fibers generate more force than slow-twitch fibers, but they are not able to maintain the force as long as the slow-twitch fibers. Finally, fast-twitch, fatigable fibers are recruited when the largest motor neurons are activated. These fibers produce large amounts of force, but they fatigue very quickly.

They are used when the organism must generate a burst of large amounts of force, such as in an escape mechanism. Most muscles contain both fast- and slow-twitch fibers, but in different proportions. Thus, the white meat of a chicken, used to control the wings, is composed primarily of fast-twitch fibers, whereas the dark meat, used to maintain balance and posture, is composed primarily of slow-twitch fibers.

Figure 1.6 Size principle of muscle force. Upper trace of oscilloscope represents the action potentials of a descending pathway axon. With low rates of activity of the descending pathway, only small alpha motor neurons are activated, producing small amounts of muscle force (lower trace of oscilloscope). With increasing rates of descending pathway activity, intermediate-size alpha motor neurons are activated in addition to the small neurons. Because more motor units are activated, the muscle produces more force. Finally, with the highest rates of descending activity, the largest alpha motor neurons are recruited, producing maximal muscle force.

1.8 Muscle Receptors and Proprioception The motor system requires sensory input in order to function properly. In addition to sensory information about the external environment, the motor system also requires sensory information about the current state of the muscles and limbs themselves.

Proprioception is the sense of the body’s position in space based on specialized receptors that reside in the muscles and tendons. The muscle spindle signals the length of a muscle and changes in the length of a muscle. The Golgi tendon organ signals the amount of force being applied to a muscle. Muscle Spindles Muscle spindles are collections of 6-8 specialized muscle fibers that are located within the muscle mass itself (Figure 1.7).

These fibers do not contribute significantly to the force generated by the muscle. Rather, they are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle. Because of the fusiform shape of the muscle spindle, these fibers are referred to as intrafusal fibers,

Figure 1.7 Muscle spindle and Golgi tendon organ.

1.9 Types of Muscle Spindle Fibers

Figure 1.8 Muscle spindle.

There are 3 types of muscle spindle fibers, characterized by their shape and the type of information they convey (Figure 1.8).

1. Nuclear Chain fibers. These fibers are so-named because their nuclei are aligned in a single row (chain) in the center of the fiber. They signal information about the static length of the muscle.
2. Static Nuclear Bag fibers. These fibers are so-named because their nuclei are collected in a bundle in the middle of the fiber. Like the nuclear chain fiber, these fibers signal information about the static length of a muscle.
3. Dynamic Nuclear Bag fibers. These fibers are anatomically similar to the static nuclear bag fibers, but they signal primarily information about the rate of change (velocity) of muscle length. A typical muscle spindle is composed of 1 dynamic nuclear bag fiber, 1 static nuclear bag fiber, and ~5 nuclear chain fibers.

1.10 Sensory Innervation of Muscle Spindles Because the muscle spindle is located in parallel with the extrafusal fibers, it will stretch along with the muscle. The muscle spindle signals muscle length and velocity to the CNS through two types of specialized sensory fibers that innervate the intrafusal fibers.

1. Group Ia afferents (also called primary afferents ) wrap around the central portion of all 3 types of intrafusal fibers; these specialized endings are called annulospiral endings, Because they innervate all 3 types of intrafusal fibers, Group Ia afferents provide information about both length and velocity.
2. Group II afferents (also called secondary afferents ) innervate the ends of the nuclear chain fibers and the static nuclear bag fibers at specialized junctions termed flower spray endings, Because they do not innervate the dynamic nuclear bag fibers, Group II afferents signal information about muscle length only.

Because of their patterns of innervation onto the three types of intrafusal fibers, Group Ia and Group II afferents respond differently to different types of muscle movements. Figure 1.9 shows the responses of each type of afferent to a linear stretch of the muscle.

1. Initially, both Group Ia and Group II fibers fire at a certain rate, encoding the current length of the muscle.
2. During the stretch, the two types differ in their responses.
3. The Group Ia afferent fires at a very high rate during the stretch, encoding the velocity of the muscle length; at the end of the stretch, its firing decreases, as the muscle is no longer changing length.

Note, however, that its firing rate is still higher than it was before the stretch, as it is now encoding the new length of the muscle. Compare the response of the Group Ia afferent to the Group II afferent. The Group II afferent increases its firing rate steadily as the muscle is stretched.

Figure 1.9 Responses of muscle spindles. The Group Ia afferent responds at a highest rate when the muscle is actively stretching, but also signals the static length of the muscle because of its innervation of the static nuclear bag fiber and the nuclear chain fiber. The Group II afferent signals only the static length of the muscle, increasing its firing rate linearly as a function of muscle length.

1.11 Gamma Motor Neurons Although intrafusal fibers do not contribute significantly to muscle contraction, they do have contractile elements at their ends that are innervated by motor neurons.

Figure 1.10 Alpha-gamma coactivation. The muscle starts at a certain length, encoded by the firing of a Ia afferent. When the muscle is stretched, the muscle spindle stretches and the Ia afferent fires more strongly. When the muscle is released from the stretch and contracts, the muscle spindle becomes slack, causing the Ia afferent to fall silent. The muscle spindle is rendered insensitive to further stretches of muscle. To restore sensitivity, gamma motor neurons fire and cause the spindle to contract, thereby becoming taut and able to signal the muscle length again.

Motor neurons are divided into two groups. Alpha motor neurons innervate extrafusal fibers, the highly contracting fibers that supply the muscle with its power. Gamma motor neurons innervate intrafusal fibers, which contract only slightly. The function of intrafusal fiber contraction is not to provide force to the muscle; rather, gamma activation of the intrafusal fiber is necessary to keep the muscle spindle taut, and therefore sensitive to stretch, over a wide range of muscle lengths.

1. This concept is illustrated in Figure 1.10.
2. If a resting muscle is stretched, the muscle spindle becomes stretched in parallel, sending signals through the primary and secondary afferents.
3. A subsequent contraction of the muscle, however, removes the pull on the spindle, and it becomes slack, causing the spindle afferents to cease firing.

If the muscle were to be stretched again, the muscle spindle would not be able to signal this stretch. Thus, the spindle is rendered temporarily insensitive to stretch after the muscle has contracted. Activation of gamma motor neurons prevents this temporary insensitivity by causing a weak contraction of the intrafusal fibers, in parallel with the contraction of the muscle.

Figure 1.11 Golgi tendon organ.

The Golgi tendon organ is a specialized receptor that is located between the muscle and the tendon (Figure 1.7). Unlike the muscle spindle, which is located in parallel with extrafusal fibers, the Golgi tendon organ is located in series with the muscle and signals information about the load or force being applied to the muscle.

A Golgi tendon organ is made up of a capsule containing numerous collagen fibers (Figure 1.11). The organ is innervated by primary afferents called Group Ib fibers, which have specialized endings that weave in between the collagen fibers. When force is applied to a muscle, the Golgi tendon organ is stretched, causing the collagen fibers to squeeze and distort the membranes of the primary afferent sensory endings.

As a result, the afferent is depolarized, and it fires action potentials to signal the amount of force. Figure 1.12 illustrates the difference in information conveyed by muscle spindles and Golgi tendon organs. At the resting position, the Ia afferents of spindles in the triceps muscle fire at a steady rate to encode the present length of the muscle, and the Ib afferents of the Golgi tendon organs of the biceps muscle fire at a low rate.

• When a light object (a balloon) is placed in the hand, there is little change in the firing rate of either afferent.
• When the hand starts to rise, however, the triceps muscle is stretched, and the Ia afferent fibers increase their firing rate as a function of muscle length.
• The Ib fibers do not change appreciably, because the balloon does not add much load to the muscle.

What if a heavy object (a bowling ball) were placed in the hand instead? Because a heavy load is now placed on the biceps, the Ib afferents fire vigorously. Note that the Ia afferent is not affected, as the muscle length has not changed. When the arm begins to rise, however, the Ia afferents fire, just as with the balloon.

Figure 1.12 Difference between muscle spindle and Golgi tendon organ.

In summary,

1. Muscle spindles signal information about the length and velocity of a muscle
2. Golgi tendon organs signal information about the load or force applied to a muscle

Test Your Knowledge Types of fibers contained within muscle spindles include.

• A. Dynamic nuclear bag fibers
• B. Dynamic nuclear chain fibers
• C. Group Ib afferent fibers
• D. Extrafusal fibers
• E. Group IV afferent fibers

Types of fibers contained within muscle spindles include.A. Dynamic nuclear bag fibers This answer is CORRECT!

1. B. Dynamic nuclear chain fibers
2. C. Group Ib afferent fibers
3. D. Extrafusal fibers
4. E. Group IV afferent fibers

Types of fibers contained within muscle spindles include.A. Dynamic nuclear bag fibers B. Dynamic nuclear chain fibers This answer is INCORRECT.

• Nuclear chain fibers signal only static muscle length.
• C. Group Ib afferent fibers
• D. Extrafusal fibers
• E. Group IV afferent fibers

Types of fibers contained within muscle spindles include.A. Dynamic nuclear bag fibers B. Dynamic nuclear chain fibers C. Group Ib afferent fibers This answer is INCORRECT.

1. Group Ib afferents are associated with Golgi tendon organs.
2. D. Extrafusal fibers
3. E. Group IV afferent fibers

Types of fibers contained within muscle spindles include.

• A. Dynamic nuclear bag fibers
• B. Dynamic nuclear chain fibers
• C. Group Ib afferent fibers

D. Extrafusal fibers This answer is INCORRECT. Extrafusal fibers are outside the muscle spindle.E. Group IV afferent fibers Types of fibers contained within muscle spindles include.

1. A. Dynamic nuclear bag fibers
2. B. Dynamic nuclear chain fibers
3. C. Group Ib afferent fibers
4. D. Extrafusal fibers

E. Group IV afferent fibers This answer is INCORRECT. Group IV afferent fibers are not part of the muscle spindle. Muscle force is controlled in part by.

• A. Alpha-gamma coactivation
• B. Intrafusal fibers
• C. Rate code
• D. Golgi tendon organs
• E. Gamma motor neurons

Muscle force is controlled in part by.A. Alpha-gamma coactivation This answer is INCORRECT.

1. Alpha-gamma coactivation ensures that muscle spindles maintain sensitivity to stretch over a wide range of muscle lengths.
2. B. Intrafusal fibers
3. C. Rate code
4. D. Golgi tendon organs
5. E. Gamma motor neurons

Muscle force is controlled in part by.A. Alpha-gamma coactivation B. Intrafusal fibers This answer is INCORRECT.

• Intrafusal fibers do not contribute significantly to muscle force.
• C. Rate code
• D. Golgi tendon organs
• E. Gamma motor neurons

Muscle force is controlled in part by.A. Alpha-gamma coactivation B. Intrafusal fibers C. Rate code This answer is CORRECT! D. Golgi tendon organs E. Gamma motor neurons Muscle force is controlled in part by.

1. A. Alpha-gamma coactivation
2. B. Intrafusal fibers
3. C. Rate code

D. Golgi tendon organs This answer is INCORRECT. Golgi tendon organs signal information about muscle force, but do not control that force directly.E. Gamma motor neurons Muscle force is controlled in part by.

• A. Alpha-gamma coactivation
• B. Intrafusal fibers
• C. Rate code
• D. Golgi tendon organs

E. Gamma motor neurons This answer is INCORRECT. Gamma motor neurons innervate intrafusal fibers, which do not contribute significantly to muscle force.

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Motor Units and Muscle Receptors (Section 3, Chapter 1) Neuroscience Online

What stimulates a muscle cell?

2. Skeletal muscle contraction – Skeletal muscles comprise multiple individual muscle fibers that are stimulated by motor neurons stemming from the spinal cord. They are grouped together to form “motor units” and more than one type of muscle fiber can be present within each motor unit.

Muscle fibers can be divided into fast- and slow-twitch muscles. Fast-twitch muscles use glycolytic metabolism and are recruited for phasic activity (an active contraction). Slow-twitch muscles (also known as red muscles) are rich in myoglobin, mitochondria, and oxidative enzymes and specialized for sustained or tonic activity.

See Schiaffino and Reggiani (2011) for a more complete discussion of skeletal muscle types and the types of myosin isoforms that make up fast- and slow-twitch muscles. The neuromuscular junction (NMJ) that connects skeletal muscle with the nerves that innervate them consists of three distinct parts: the distal motor nerve ending, the synaptic cleft, and the postsynaptic region, located on the muscle membrane.

1. Motor neurons branch into multiple termini, which are juxtaposed to motor endplates, specialized regions of muscle where neurotransmitter receptors are concentrated ( Fig.3 A).
2. The transfer of information between the nerve and muscle is mediated by the release of acetylcholine from the motor neuron, which diffuses across the synaptic cleft, and binds to and activates the ligand-gated, nicotinic acetylcholine receptors (nAChRs) on the endplate.

Activation of the nAChR leads to an influx of cations (sodium and calcium) that causes depolarization of the muscle cell membrane. This depolarization in turn activates a high density of voltage-gated sodium channels on the muscle membrane, eliciting an action potential. Skeletal muscle contraction and changes with exercise. ( A ) Neurotransmitter (acetylcholine, ACh) released from nerve endings binds to receptors (AChRs) on the muscle surface. The ensuing depolarization causes sodium channels to open, which elicits an action potential that propagates along the cell.

The action potential invades T-tubules and causes the L-type calcium channels to open, which in turn causes ryanodine receptors (RyRs) in the SR to open and release calcium, which stimulates contraction. Calcium is pumped back into the SR by (SR/ER calcium ATPase SERCA) pumps. The decreasing cytosolic calcium levels cause calcium to disassociate from troponin C and, consequently, tropomyosin reverts to a conformation that covers the myosin-binding sites.

( B ) Signaling in exercised skeletal muscle. Both calcium and calcium-independent signals stimulate the transcriptional coactivator PGC1α. This activates a number of transcription factors that regulate genes associated with mitochondrial biogenesis, glucose, and lipid homeostasis.

The action potential runs along the top of the muscle and invades the T-tubules (specialized invaginations of the membrane containing numerous ion channels). The opening of voltage-gated sodium channels activates L-type voltage-gated calcium channels lining the T-tubule. A conformational change in these enables release of calcium on the closely apposed SR via activation of RyR1.

Calcium then binds to troponin as described above, initiating the contraction process. Calcium-bound CaM also activates MLCK, whose phosphorylation of the MLC changes cross-bridge properties. This modulates the troponin-dependent contraction, although there is no effect on the ATPase activity of MLC.

Why do muscle cells need energy?

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Although muscles and engines work in different ways, they both convert chemical energy into energy of motion. A motorbike engine uses the stored energy of petrol and converts it to heat and energy of motion (kinetic energy). Muscles use the stored chemical energy of food we eat and convert that to heat and energy of motion (kinetic energy). We need energy to enable growth and repair of tissues, to maintain body temperature and to fuel physical activity. Energy comes from foods rich in carbohydrate, protein and fat.

What are functional adaptations?

Functional adaptations are special biological processes that an organism’s body might perform to be well suited to its environment. Behavioral adaptations are specific actions that an organism might perform to make it well suited to its environment.

What are 5 examples of adaptations?

Body Parts – The shape of a beak, the type of feet, the placement of eyes, the presence of whiskers, the shape of the nose or ears, and the sharpness of teeth are all examples of structural adaptations which help different animals to survive. As shown in the picture on the right, different kinds of birds have adapted different kinds of beaks that help them obtain their particular source of food.

Beaks come in all shapes and sizes. For example, a hawk has a sharp, curved beak to tear its food into small pieces. A hummingbird has a long, thin beak to reach into flowers and get nectar. A parrot has a strong, thick beak to help it crack fruits and nuts. A pelican has a long beak with a pouch to help it scoop fish out of water.

All kinds of body parts may be adaptations. Horses and zebras have flat teeth for grinding their food (grass), while lions have sharp teeth for tearing their food (meat.) To escape predators, zebras also have excellent hearing and eyesight and powerful legs for running and kicking.

1. Birds have hollow bones that help them fly.
2. Ducks have oil glands that keep their feathers from becoming water-soaked, and webbed feet that help them to swim.
3. A woodpecker not only has a strong, sharp beak for drilling holes, but it also has a very long barbed tongue to catch insects, two toes that point backward to help with climbing trees, and a stiff tail for support on the tree.

Alligators have eyes and nostrils placed on top of their heads, allowing them to keep most of their body underwater so their prey cannot see them. For river otters, whiskers are an adaptation that help them feel their way through tight spots both on land and in water. Animals in the desert have special adaptations that help them conserve water and survive a habitat with extreme temperatures and lack of shelter. Camels have humps where they can store fat, allowing them to go without food and water for periods of time.

Camels also have two rows of long, thick eyelashes to protect their eyes from blowing sand, and their nostrils can be closed as well. Their broad, leathery hooves act like snowshoes to prevent them from sinking in the sand. Other desert animals have different adaptations. Jackrabbits have large ears that keep them cool by spreading out their body heat.

Fennec foxes have thick fur on the bottoms of their feet so they can walk on the hot desert ground. Learn more about desert adaptations, Adaptation Facts for Kids: Kiddle Encyclopedia In polar habitats, animals also have important adaptations that allow them to keep warm and survive extreme cold. For example, the penguin lives in the Antarctic and swims through icy cold water. Its feathers are tightly packed and layered like roof shingles.

These special feathers keep cold water out and keep body heat in. The penguin’s eyes have special lenses that allow it see both above and below the water. Its powerful wings help it swim through the water, and its feet help it steer as it swims. Being able to stay warm, see well, and swim quickly helps the penguin find food and avoid predators.

In the Arctic, polar bears have webbed front paws that are shaped to propel them through the water. The bottoms of their feet are covered with hairy bumps that grip the ice and keep them from slipping, and a layer of blubber insulates them from the cold. Animals who live in the oceans have unique adaptations that allow them to move through water and defend themselves from marine predators. For example, sharks have streamlined bodies for fast swimming, and noses with special sensors that let them sense electric fields put out by other fish and animals.

Stingrays swim along the ocean floor, with their eyes on top of their bodies and their mouth on the bottom, so they can see while they’re swimming and still take in food they find in the sand. Lobsters use their claws to crush their food and their strong tails to move backward on the ocean floor. Harbor seals have four flippers to help them swim, with hind flippers to propel them forward and forward flippers to help them steer.

Learn more about ocean adaptations, Some physical adaptations have more than one purpose. Horns and antlers may be used by animals to protect themselves, to fight with others for territory, or to attract a mate. A crab’s hard shell protects it from predators, from drying out, and from being crushed by waves.

What is an example of a functional adaptation?

A functional adaptation, also known as a physiological adaptation, is a special function that an organism’s body performs that makes it well suited to its environment. For example, if we get hot, we start to sweat so that when it evaporates, it cools us down. The release of venom, a chemical toxin, is another example.

What do muscle cells contain?

The cell membrane of a muscle cell is known as the sarcolemma and the cytoplasm is called sarcoplasm. The sarcoplasm contains myoglobin, an oxygen storage site, as well as glycogen in the form of granules in the cytosol, which both provide an energy supply.

What are muscle cells called?

Introduction – The muscle cell, also known as the myocyte is the smallest subunit of all muscular tissues and organs throughout the body. It is here in the myocyte, where the physiological steps of muscle contraction and where the pathophysiology of numerous muscular diseases takes place.

• There are three types of muscle cells in the human body: skeletal, smooth, and cardiac muscle.
• The common function of each specialized myocyte is the contraction of their various organs, some essential for life.
• Therefore, dysregulation of these crucial functions can lead to significant morbidity and mortality.

This article examines the role of the muscle myocyte in various systems, the physiology of myocyte contraction and the pathophysiology of diseases involving the myocyte.

What is an example of a muscle adaptability?

Major Properties of the Muscular System – There are 5 major properties to the muscular system

1. Excitable or Irritable: Muscles are Excitable or Irritable. This means that they are capable of receiving stimulation and responding to stimulation from the nerves.
2. Contractible: T hey are contractible. After receiving stimulation, they are capable of contracting, or shortening.
3. Extensible: Being extensible means a muscle can be stretched without damage by the application of force.
4. Elasticity: With elasticity, a muscle is able to return to its original resting shape and length after being extended or contracted.
5. Adaptability: The muscular system is adaptable in that it can be changed in response to how it is used. For example, a muscle will enlarge, or undergo hypertrophy with increased work; but on the other hand it can go in atrophy, or waste away if deprived of work.

Types of Muscle Movements Now, lets look at the 5 types of muscle movements.

1. Adduction,,is the moving of a body part toward the mid-line of the body.
2. Abduction is moving a body part away from the body.
3. Flexion Flexion means bending a joint to decrease the angle between two bones or two body parts.
4. Extension extension is straightening and extending of the joint to increase the angle between two bones or body parts.
5. Rotation and last, rotation involves move a body part around an axis.

3 Types of Muscles The Muscular System is divided into three main types. E ach of these types can be moved 1 of 2 ways. either voluntary, or involuntary.

1. Cardiac Muscle – The cardiac muscle, is an involuntary muscle; meaning it operates without any conscious control.
2. The Visceral or smooth muscles, are also considered involuntary – these muscles are found in organs or organs systems such as the digestive or respiratory system.
3. The third type of muscle is the Skeletal muscle, These are what we would typically think of when talking about muscles. These muscles attach to the skeleton and provide the skeleton with the ability to move. The Skeletal Muscles are classified as voluntary. This is because we have to make a conscious effort or decision to make them move.

What are the adaptation of smooth muscles?

Abstract – Airway and bladder smooth muscles are known to undergo length adaptation under sustained contraction. This adaptation process entails a remodelling of the intracellular actin and myosin filaments which shifts the peak of the active force-length curve towards the current length.

Smooth muscles are therefore able to generate the maximum force over a wide range of lengths. In contrast, length adaptation of vascular smooth muscle has attracted very little attention and only a handful of studies have been reported. Although their results are conflicting on the existence of a length adaptation process in vascular smooth muscle, it seems that, at least, peripheral arteries and arterioles undergo such adaptation.

This is of interest since peripheral vessels are responsible for pressure regulation, and a length adaptation will affect the function of the cardiovascular system. It has, e.g., been suggested that the inward remodelling of resistance vessels associated with hypertension disorders may be related to smooth muscle adaptation.

1. In this study we develop a continuum mechanical model for vascular smooth muscle length adaptation by assuming that the muscle cells remodel the actomyosin network such that the peak of the active stress-stretch curve is shifted towards the operating point.
2. The model is specialised to hamster cheek pouch arterioles and the simulated response to stepwise length changes under contraction.

The results show that the model is able to recover the salient features of length adaptation reported in the literature. Keywords: Artery; Continuum mechanics; Model; Remodelling; Smooth muscle cell. Copyright © 2016 Elsevier Ltd. All rights reserved.

What are the physiological adaptations of muscles?

Physiological muscle adaptations to exercise – Muscle adaptations to exercise include morphofunctional modifications triggered by the repetition of muscular contraction bouts, leading to increased mitochondrial biosynthesis and angiogenesis, fibers hypertrophy and fundamental changes in cell metabolism, including increase lactate tolerance ( Tab.1 ).

These adaptations follow modifications of the expression and the activation a series of subcellular signals and a series, still partially unknown, of pre- and post-transcriptional events. The primitive stimulus (exercise or training) with its quality (strength or endurance) are able to activate a large number of cellular events, in turn responsible for the activation, inhibition or modulation of cross linked signaling routes, implicated in the regulation of transcription and translation.

At the center of these routes mTORC1 and peroxisome PGC1α are cross-linked master regulators of the plastic responses due to strength type and endurance type exercise respectively ( Fig.1 ). Schematic representation of the sub-cellular signals activated by the endurance (EE) and resistance (RE) exercises. In EE, the activation of the downstream pathways foresees modifications of the energetic availability (ATP), oxidative stress with production of reactive oxygen species (ROS), meccanostresses with p38 / MAPK activation or changes in cellular calcium content (ERα = alpha receptor for estrogens; PPARα = peroxisomal proliferator-activated receptor alpha), leading to PGC-1α mediated mitochondriogenesis and mitochondrial β-oxidation.

In RE, Insulin Growth Factor 1 (IGF-1), amino acids, mechanical strain and calcium disposal converge on upstream signals activating mTORC1. Akt = protein kinase B; FAK = Focal Adhesion Kinase; S6K = ribosomal protein 6 kinase; 4E-BP1 = eukaryotic translation initiation factor 4E-binding protein 1. Modified with permission from: Physical Activity.

Giuseppe D’Antona. Poletto publisher 2019 (1 st edition) ( 62 ).