13.2: Video- Anatomy of a Muscle Fiber - Biology

13.2: Video- Anatomy of a Muscle Fiber

13.2: Video- Anatomy of a Muscle Fiber - Biology

The sequence of events that result in the contraction of an individual muscle fiber begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na + ) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca ++ ) from storage in the sarcoplasmic reticulum (SR). The Ca ++ then initiates contraction, which is sustained by ATP (Figure 1). As long as Ca ++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.

Figure 1. Contraction of a Muscle Fiber. A cross-bridge forms between actin and the myosin heads triggering contraction. As long as Ca ++ ions remain in the sarcoplasm to bind to troponin, and as long as ATP is available, the muscle fiber will continue to shorten.

Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma and T-tubules, and closes the voltage-gated calcium channels in the SR. Ca ++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands. A muscle also can stop contracting when it runs out of ATP and becomes fatigued (Figure 2).

Figure 2. Relaxation of a Muscle Fiber. Ca ++ ions are pumped back into the SR, which causes the tropomyosin to reshield the binding sites on the actin strands. A muscle may also stop contracting when it runs out of ATP and becomes fatigued.

The molecular events of muscle fiber shortening occur within the fiber’s sarcomeres (see Figure 3). The contraction of a striated muscle fiber occurs as the sarcomeres, linearly arranged within myofibrils, shorten as myosin heads pull on the actin filaments.

The region where thick and thin filaments overlap has a dense appearance, as there is little space between the filaments. This zone where thin and thick filaments overlap is very important to muscle contraction, as it is the site where filament movement starts. Thin filaments, anchored at their ends by the Z-discs, do not extend completely into the central region that only contains thick filaments, anchored at their bases at a spot called the M-line. A myofibril is composed of many sarcomeres running along its length thus, myofibrils and muscle cells contract as the sarcomeres contract.


Twenty-nine muscles from each of six paired hindlimbs were removed from adult male Sprague-Dawley rats (Rattus norvegicus Harlan Scientific,Indianapolis, IN, USA 323±15 g). One leg was used for analysis of fiber type distribution and the contralateral limb was used for architectural measurements. Animals were sacrificed by intracardiac injection of pentobarbital and immediately skinned and quartered. One limb was placed in 10% buffered formaldehyde within 30 min of sacrifice, with hip and knee held at 90° and ankle in neutral, and fixed overnight. Muscles from the contralateral limb were frozen in liquid nitrogen (–159°C), and stored at –80°C for subsequent fiber type analysis.

Fiber type determination

Myosin heavy chain (MHC) isoforms were defined by SDS-PAGE as previously described (Talmadge and Roy,1993). A myofibril-rich fraction of individual whole muscles(N=3 for each of 29 different muscles) was prepared and the final pellet was resuspended in sample buffer to a concentration of 0.125 mg protein ml –1 (BCA protein assay, Pierce, Rockford, IL, USA). Total acrylamide concentration was 4% and 8% in the stacking and resolving gels,respectively (bis-acrylamide, 1:50). Gels (16×22 cm, 0.75 mm thick) were run at a constant current of 10 mA until voltage rose to 275 V, and thereafter at constant voltage for 21 h at 4–6°C. A volume of 1.25 μg total protein was loaded into a well and gels were stained with Coomassie Brilliant Blue. To ensure that adequate sensitivity was achieved for detecting minor MHC bands, each sample was also run on separate gels that were silver stained(Bio-Rad, Hercules, CA, USA). MHC bands were identified and quantified with densitometry (GS-800, Bio-Rad). The Coomassie and silver-stained gels gave similar results, so quantification results are reported exclusively from Coomassie-stained gels.

Skeletal muscle architecture

Muscle groups

Muscle groups were identified based on their action about each joint. Hip flexors consisted of rectus femoris (RF) and psoas (PS), and hip extensors consisted of gluteus superficialis (GSup), gluteus medius (GMed), biceps femoris (BF), semitendinosus (ST), semimembranosus (SM) and `muscle X'. Muscle X was a previously undescribed muscle for which no reference could be found and no homologous mammalian muscle could be defined. Its origin was the craniolateral pelvis and its insertion was the craniomedial tibia(Fig. 1). Hip adductors included adductor magnus (AddM), adductor longus (AddL), adductor tertius(AddT) and adductor brevis (AddB). Muscles in the knee flexor group were gracilis (cranial and caudal heads GRcr and GRca, respectively), BF, ST, SM,muscle X, gastrocnemius (GLH and GMH lateral and medial heads, respectively)and plantaris (PLA), and knee extensors included vastus intermedius (VI),vastus lateralis (VL), vastus medialis (VM) and RF. Ankle plantarflexors included GLH and GMH, PLA, soleus (SOL), tibialis posterior (TP), flexor digitorum longus (FDL) and flexor hallucis longus (FHL), and the dorsiflexors included tibialis anterior (TA), extensor digitorum longus (EDL) and extensor hallucis longus (EHL). Ankle everters included peroneus longus (PL) and peroneus brevis (PB). These functional groups were defined to compare muscle architectural measures and fiber type distributions across joints.

Comparisons were also made between muscles that served primarily an anti-gravity function and those that did not. The anti-gravity muscles were GSup, GMed, muscle X, VI, VL, VM, RF, GLH, GMH, SOL, PLA, TP, FDL and FHL. Remaining muscles were considered non-anti-gravity muscles.

There are several muscles in the rat hindlimb that are widely studied in laboratories, which we have defined as `typical' muscles. This was important in order to determine whether `typical' muscles really are representative of the entire hindlimb. These muscles included VL, GLH, GMH, SOL, PLA, TA and EDL.

Statistical analysis

All values are reported as mean ± standard error (s.e.m.) unless otherwise noted. Independent sample t-tests were used to compare architectural variables from typical rat muscles to the other muscles in the hindlimb and to make functional group comparisons. One-way repeated measures analyses of variance (ANOVA) was used to test for architectural and fiber type differences among the typically studied rat muscles. Post-hocpairwise comparisons (with Tukey's post-hoc corrections) were made for variables after finding a significant one-way ANOVA.

PCSA was calculated using two measures made directly on the muscles: mass and fiber length. To determine which of these two measures drives the PCSA value, multiple stepwise regression was used to determine the relative contributions of fiber length and mass to PCSA.

Discriminant analysis was performed to investigate differences in architectural and fiber type parameters between functional muscle groups within the rat hindlimb. Grouping variables included joint, anti-gravity versus non-anti-gravity muscles, and functional muscle groups. Architectural data and fiber type data from contralateral limbs were combined based on the assumption that minimal differences should exist between limbs. Discriminant analysis was performed on the rat hindlimb dataset using the following variables: mass, muscle length, fiber length, PCSA, Lf/Lm ratio, fiber type I percentage,type IIA percentage, type IIX percentage and type IIB percentage.

To examine architectural patterns across species, discriminant analysis was also used to predict species or muscle, given either absolute or relative architectural parameters. The species examined were the mouse (N=8)(Burkholder et al., 1994), rat(N=6), cat (N⩽4)(Sacks and Roy, 1982), human(N=19) (Ward et al., in press), and horse (N=7)(Payne et al., 2005). Because complete data sets from the cat and horse were not available, muscle architectural variables were averaged across individual specimens for each species. Absolute architectural variables used were fiber length, mass and PCSA. Relative architectural variables included(Lf/Lm ratio) and PCSA relative to VL mass (PCSA/VLmass).

Lateral view of a rat hindlimb transected above the lumbar spine, with muscle X indicated by the arrow. The origin of the muscle is on the craniolateral pelvis and its insertion on the craniomedial tibia. Scale bar,10 mm.

Lateral view of a rat hindlimb transected above the lumbar spine, with muscle X indicated by the arrow. The origin of the muscle is on the craniolateral pelvis and its insertion on the craniomedial tibia. Scale bar,10 mm.

Scatter plot of fiber length and physiological cross-sectional area (PCSA)in the muscles of the rat hindlimb. Muscles included psoas, gluteus superficialis (GSup), gluteus medius (GMed), adductor brevis (AddB), adductor longus (AddL), adductor magnus (AddM), adductor tertius (AddT), rectus femoris(RF), vastus intermedius (VI), vastus lateralis (VL), vastus medialis (VM),biceps femoris (BF), semitendinosus (ST), semimembranosus (SM), muscle X,cranial head of gracilis (GRcr), caudal head of gracilis (GRca), medial head of gastrocnemius (GMH), lateral head of gastrocnemius (GLH), plantaris (PLA),soleus (SOL), tibialis posterior (TP), flexor digitorum longus (FDL), flexor hallucis longus (FHL), peroneus longus (PL), peroneus brevis (PB), tibialis anterior (TA), extensor digitorum longus (EDL), and extensor hallucis longus(EHL). Typically studied rat muscles are represented by filled triangles all other muscles are represented by open squares.

Scatter plot of fiber length and physiological cross-sectional area (PCSA)in the muscles of the rat hindlimb. Muscles included psoas, gluteus superficialis (GSup), gluteus medius (GMed), adductor brevis (AddB), adductor longus (AddL), adductor magnus (AddM), adductor tertius (AddT), rectus femoris(RF), vastus intermedius (VI), vastus lateralis (VL), vastus medialis (VM),biceps femoris (BF), semitendinosus (ST), semimembranosus (SM), muscle X,cranial head of gracilis (GRcr), caudal head of gracilis (GRca), medial head of gastrocnemius (GMH), lateral head of gastrocnemius (GLH), plantaris (PLA),soleus (SOL), tibialis posterior (TP), flexor digitorum longus (FDL), flexor hallucis longus (FHL), peroneus longus (PL), peroneus brevis (PB), tibialis anterior (TA), extensor digitorum longus (EDL), and extensor hallucis longus(EHL). Typically studied rat muscles are represented by filled triangles all other muscles are represented by open squares.

Scaling of muscle architecture with body mass (M) across species was examined using least squares regression of log-transformed variables. Body mass was treated as the independent variable and the architectural variable was the dependent variable. The coefficient and exponent of the allometric equation, y=aM b (where y is the architectural variable, a is the coefficient, M is body mass, and b is the scaling exponent) were used to compare scaling relationships among hindlimb muscles. Statistical tests were performed using SPSS software (SPSS, Inc., Version 11.5, Chicago, IL, USA). Significance was set at the P<0.05 level.

Initial muscle fibre formation

Initial muscle fibre formation has predominantly been studied in the limb. During initial myogenesis in the embryonic muscle anlagen, precursor cells proliferate to form compact groups, within which individual cells fuse together in longitudinal arrays to form multinucleated fibres (see poster). This occurs in phases, beginning with a synchronous fusion of cells expressing the paired box transcription factors Pax3 and Pax7 across the whole length of the newly emerging muscle anlagen to form primary muscle fibres (Lee et al., 2013), which act as a scaffolding for subsequent rounds of fibre formation. In mice, a second subset of Pax3 + , Pax7 − myogenic cells associate and align with the primary fibres. They fuse sequentially with one another, beginning in the middle of the fibre and progressing towards the two ends, to form secondary fibres (Lee et al., 2013) (see poster). In large mammals, a tertiary and even a quaternary phase of myogenesis may occur, although the evidence is uncertain (Edom-Vovard et al., 1999 Bröhl et al., 2012).

13.2: Video- Anatomy of a Muscle Fiber - Biology

The principal functionality of muscle is rooted in its ability to contract and relax. The foundation for muscle contraction is the sarcomere. Sarcomeres contain a motor protein called myosin, which powers the muscle to contract by “grabbing” onto another protein called actin and “flexing.” When the myosin releases the actin, the muscle relaxes. This process is regulated by another protein called troponin.

Definition of Sarcomere

The sarcomere is a molecular structure found in skeletal and cardiac muscles that allows cardiac myocytes to contract and generate force.

Location of Sarcomere

The heart muscle cells, or cardiac myocytes, have specialized structures that allow them to respond to action potentials and generate the contractile force necessary for pumping blood through the body.

a cylindrical fiber composed of repeating sarcomeres

a molecular structure in myofibrils that allows cardiac myocytes to contract and generate force

Sarcomere Components

The structure of the sarcomere is organized into bands of interdigitating thick filaments and thin filaments. Thick filaments attach to the middle of the sarcomere, or M line, and thin filaments attach to the borders, or Z lines.

Thick and Thin Filaments

1. Thick Filaments
The molecular motors that generate force upon thin filaments. Opposing thick filaments attach to the M line.

2. Thin Filaments
Filaments that are pulled toward the M line by thick filaments to shorten the sarcomere. Adjacent thin filaments attach to Z lines.

Components of Thin Filaments

3. Actin
Actin molecules are the main components of thin filaments and bind to the head domains of myosin.

4. Troponin
A calcium-sensing regulatory protein that shifts the position of tropomyosin to facilitate myosin binding to actin.

5. Tropomyosin
A regulatory polymer that wraps around the actin filament to block or enhance the binding of myosin to actin.

Components of Thick Filaments

6. Myosin
The main component of thick filaments. Myosin molecules have tail, head, and lever arm domains. The tail domain attaches to the M line. The head domain interacts with actin and ATP. The lever arm domain moves the head domain to contract the sarcomere. 1

Molecular Activators

7. Calcium
An ion that releases from the sarcoplasmic reticulum following an action potential. Calcium ions bind to troponin, causing a conformational change in tropomyosin that allows myosin to bind to actin.

8. ATP
ATP hydrolysis drives myosin to generate force upon actin and shorten the sarcomere.

How the Sarcomere Works

The sarcomere generates force when myosin binds with actin and undergoes a “power stroke”. 2,3

Sarcomere Importance

The sarcomere is the core of muscle contractility. Its dysfunction, either in decreased or increased cardiac contractility, is central to heart failure with reduced ejection fraction (HFrEF) and hypertrophic cardiomyopathy (HCM). 4,5

HFrEF and the Sarcomere

Heart failure with reduced ejection fraction (HFrEF) is a chronic, progressive condition in which the left ventricle does not contract effectively during systole. As a result, the heart does not pump enough oxygen-rich blood to meet the body’s needs. 6

In HFrEF, heart muscle has decreased contractility. 4

HFrEF Therapies

Neurohormonal Therapies

The current first line therapy for heart failure is a combination of beta blockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers ( ARBs) or angiotensin receptor–neprilysin inhibitors (ARNIs) , and mineralocorticoid receptor antagonists (MRAs). 7,8

These therapies relieve vasoconstriction, lower blood pressure, reduce biological stress, and improve heart function. 7,8 They indirectly address cardiac contractility. 4

Cardiac Calcitropes

Positive inotropes that increase myocardial contractility by altering intracellular calcium can be classified as cardiac calcitropes. Examples include dobutamine and milrinone. While these medications improve contractility short-term, long-term use can increase risks of arrhythmia and mortality. 9,10

HFrEF Mechanism of Disease

Targeting the sarcomere directly could be a viable area for research in HFrEF. 4,7

HCM and the Sarcomere

In Hypertrophic Cardiomyopathy (HCM), the ventricular myocardium thickens abnormally and has increased contractility. 5,11 HCM often results from pathogenic mutations of the genes that encode sarcomere-associated proteins, such as myosin. 5 HCM mutations appear to increase sarcomere contractility. 5,12


There are currently no approved targeted medications designed specifically to treat HCM. Treatments aim to manage symptoms and reduce complications. 13,14 Treatment options vary depending on the symptoms but can include beta blockers and surgery. 13,15


Targeting the sarcomere directly is a viable area for research in HCM. 14

13.2: Video- Anatomy of a Muscle Fiber - Biology

Article Reviewed:
Charge, S. B. P., and Rudnicki, M.A. (2004). Cellular and molecular regulation of muscle regeneration. Physiological Reviews, Volume 84, 209-238.

Personal trainers and fitness professionals often spend countless hours reading articles and research on new training programs and exercise ideas for developing muscular fitness. However, largely because of its physiological complexity, few fitness professionals are as well informed in how muscles actually adapt and grow to the progressively increasing overload demands of exercise. In fact, skeletal muscle is the most adaptable tissue in the human body and muscle hypertrophy (increase in size) is a vastly researched topic, yet still considered a fertile area of research. This column will provide a brief update on some of the intriguing cellular changes that occur leading to muscle growth, referred to as the satellite cell theory of hypertrophy.

Trauma to the Muscle: Activating The Satellite Cells
When muscles undergo intense exercise, as from a resistance training bout, there is trauma to the muscle fibers that is referred to as muscle injury or damage in scientific investigations. This disruption to muscle cell organelles activates satellite cells, which are located on the outside of the muscle fibers between the basal lamina (basement membrane) and the plasma membrane (sarcolemma) of muscles fibers to proliferate to the injury site (Charge and Rudnicki 2004). In essence, a biological effort to repair or replace damaged muscle fibers begins with the satellite cells fusing together and to the muscles fibers, often leading to increases in muscle fiber cross-sectional area or hypertrophy. The satellite cells have only one nucleus and can replicate by dividing. As the satellite cells multiply, some remain as organelles on the muscle fiber where as the majority differentiate (the process cells undergo as they mature into normal cells) and fuse to muscle fibers to form new muscle protein stands (or myofibrils) and/or repair damaged fibers. Thus, the muscle cells’ myofibrils will increase in thickness and number. After fusion with the muscle fiber, some satellite cells serve as a source of new nuclei to supplement the growing muscle fiber. With these additional nuclei, the muscle fiber can synthesize more proteins and create more contractile myofilaments, known as actin and myosin, in skeletal muscle cells. It is interesting to note that high numbers of satellite cells are found associated within slow-twitch muscle fibers as compared to fast-twitch muscle fibers within the same muscle, as they are regularly going through cell maintenance repair from daily activities.

Growth factors
Growth factors are hormones or hormone-like compounds that stimulate satellite cells to produce the gains in the muscle fiber size. These growth factors have been shown to affect muscle growth by regulating satellite cell activity. Hepatocyte growth factor (HGF) is a key regulator of satellite cell activity. It has been shown to be the active factor in damaged muscle and may also be responsible for causing satellite cells to migrate to the damaged muscle area (Charge and Rudnicki 2004).
Fibroblast growth factor (FGF) is another important growth factor in muscle repair following exercise. The role of FGF may be in the revascularization (forming new blood capillaries) process during muscle regeneration (Charge and Rudnicki 2004).
A great deal of research has been focused on the role of insulin-like growth factor-I and –II (IGFs) in muscle growth. The IGFs play a primary role in regulating the amount of muscle mass growth, promoting changes occurring in the DNA for protein synthesis, and promoting muscle cell repair.
Insulin also stimulates muscle growth by enhancing protein synthesis and facilitating the entry of glucose into cells. The satellite cells use glucose as a fuel substrate, thus enabling their cell growth activities. And, glucose is also used for intramuscular energy needs.

Growth hormone is also highly recognized for its role in muscle growth. Resistance exercise stimulates the release of growth hormone from the anterior pituitary gland, with released levels being very dependent on exercise intensity. Growth hormone helps to trigger fat metabolism for energy use in the muscle growth process. As well, growth hormone stimulates the uptake and incorporation of amino acids into protein in skeletal muscle.
Lastly, testosterone also affects muscle hypertrophy. This hormone can stimulate growth hormone responses in the pituitary, which enhances cellular amino acid uptake and protein synthesis in skeletal muscle. In addition, testosterone can increase the presence of neurotransmitters at the fiber site, which can help to activate tissue growth. As a steroid hormone, testosterone can interact with nuclear receptors on the DNA, resulting in protein synthesis. Testosterone may also have some type of regulatory effect on satellite cells.

Muscle Growth: The ‘Bigger’ Picture
The previous discussion clearly shows that muscle growth is a complex molecular biology cell process involving the interplay of numerous cellular organelles and growth factors, occurring as a result of resistance exercise. However, for client education some important applications need to be summarized. Muscle growth occurs whenever the rate of muscle protein synthesis is greater than the rate of muscle protein breakdown. Both, the synthesis and breakdown of proteins are controlled by complimentary cellular mechanisms. Resistance exercise can profoundly stimulate muscle cell hypertrophy and the resultant gain in strength. However, the time course for this hypertrophy is relatively slow, generally taking several weeks or months to be apparent (Rasmussen and Phillips, 2003). Interestingly, a single bout of exercise stimulates protein synthesis within 2-4 hours after the workout which may remain elevated for up to 24 hours (Rasmussen and Phillips, 2003). Some specific factors that influence these adaptations are helpful to highlight to your clients.

All studies show that men and women respond to a resistance training stimulus very similarly. However, due to gender differences in body size, body composition and hormone levels, gender will have a varying effect on the extent of hypertrophy one may possibly attain. As well, greater changes in muscle mass will occur in individuals with more muscle mass at the start of a training program.

Aging also mediates cellular changes in muscle decreasing the actual muscle mass. This loss of muscle mass is referred to as sarcopenia. Happily, the detrimental effects of aging on muscle have been shown be restrained or even reversed with regular resistance exercise. Importantly, resistance exercise also improves the connective tissue harness surrounding muscle, thus being most beneficial for injury prevention and in physical rehabilitation therapy.

Heredity differentiates the percentage and amount of the two markedly different fiber types. In humans the cardiovascular-type fibers have at different times been called red, tonic, Type I, slow-twitch (ST), or slow-oxidative (SO) fibers. Contrariwise, the anaerobic-type fibers have been called the white, phasic, Type II, fast-twitch (FT), or fast-glycolytic (FG) fibers. A further subdivision of Type II fibers is the IIa (fast-oxidative-glycolytic) and IIb (fast-glycolytic) fibers. It is worthy of note to mention that the soleus, a muscle involved in standing posture and gait, generally contains 25% to 40% more Type I fibers, while the triceps has 10% to 30% more Type II fibers than the other arm muscles (Foss and Ketyian, 1998). The proportions and types of muscle fibers vary greatly between adults. It is suggested that the new, popular periodization models of exercise training, which include light, moderate and high intensity training phases, satisfactorily overload the different muscle fiber types of the body while also providing sufficient rest for protein synthesis to occur.

Muscle Hypertrophy Summary
Resistance training leads to trauma or injury of the cellular proteins in muscle. This prompts cell-signaling messages to activate satellite cells to begin a cascade of events leading to muscle repair and growth. Several growth factors are involved that regulate the mechanisms of change in protein number and size within the muscle. The adaptation of muscle to the overload stress of resistance exercise begins immediately after each exercise bout, but often takes weeks or months for it to physically manifest itself. The most adaptable tissue in the human body is skeletal muscle, and it is remarkably remodeled after continuous, and carefully designed, resistance exercise training programs.

Interactive Link Questions

Watch this video to learn more about macro- and microstructures of skeletal muscles. (a) What are the names of the “junction points” between sarcomeres? (b) What are the names of the “subunits” within the myofibrils that run the length of skeletal muscle fibers? (c) What is the “double strand of pearls” described in the video? (d) What gives a skeletal muscle fiber its striated appearance?

Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video to learn more about what happens at the neuromuscular junction. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? Can you give an example of each? (c) Why is the neurotransmitter acetylcholine degraded after binding to its receptor?

The release of calcium ions initiates muscle contractions. Watch this video to learn more about the role of calcium. (a) What are “T-tubules” and what is their role? (b) Please also describe how actin-binding sites are made available for cross-bridging with myosin heads during contraction.

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    Muscles Labeling

    This activity is aligned to my anatomy and physiology curriculum where students study the structure and function of muscle tissues. This has been a challenging topic to cover remotely because I can’t use traditional models. Typically, I would use straws and rubber bands to model fascicles and myofibrils.

    This year, students get a modified version of the lesson on Google Slides which explains how actin and myosin are organized and how those muscle fibers are grouped into bundles (fascicles) that make up a muscle. You are welcome to make a copy of these slides and modify them for you own class. I use a phenomenon based approach where each unit showcases a particular disorder and how that disorder affects the system. For the muscular system, students learn about a boy with Duchenne Muscular Dystrophy.

    Part 2 of the slides goes into more detail about how this disease affects the dystrophin in the muscles and how it is inherited as a sex-linked disorder.

    The activity linked below is a drag and drop activity for students to practice labeling the muscles, there are 6 slides showing images of muscles and fibers and the connective tissue surrounding the fibers (endomysium, perimysium, epimysium).

    Critical Thinking Questions

    How would muscle contractions be affected if skeletal muscle fibers did not have T-tubules?

    Without T-tubules, action potential conduction into the interior of the cell would happen much more slowly, causing delays between neural stimulation and muscle contraction, resulting in slower, weaker contractions.

    What causes the striated appearance of skeletal muscle tissue?

    Dark A bands and light I bands repeat along myofibrils, and the alignment of myofibrils in the cell cause the entire cell to appear striated.

    How would muscle contractions be affected if ATP was completely depleted in a muscle fiber?

    Without ATP, the myosin heads cannot detach from the actin-binding sites. All of the “stuck” cross-bridges result in muscle stiffness. In a live person, this can cause a condition like “writer’s cramps.” In a recently dead person, it results in rigor mortis.

    Watch the video: Μυϊκή Συστολή (January 2022).