Topic 3: Chapt 12 Flashcards
(115 cards)
1
Q
What functions do muscles serve in the body?
A
Muscles serve two common functions: generating motion and generating force. Additionally, skeletal muscles contribute significantly to the homeostasis of body temperature by generating heat, such as through shivering when cold conditions threaten homeostasis.
2
Q
How many types of muscle tissue are found in the human body, and what are they?
A
The human body has three types of muscle tissue: skeletal muscle, cardiac muscle, and smooth muscle.
3
Q
What distinguishes skeletal muscle from cardiac and smooth muscle in terms of appearance?
A
Skeletal and cardiac muscles are classified as striated muscles due to their alternating light and dark bands seen under the light microscope, while smooth muscle lacks obvious cross-bands.
4
Q
What is the signal to initiate muscle contraction, and what motor protein is involved?
A
The signal to initiate muscle contraction is an intracellular calcium signal, and movement is created when a motor protein called myosin uses energy from adenosine triphosphate (ATP) to change its conformation.
5
Q
Despite differences, what do skeletal, smooth, and cardiac muscles have in common?
A
All three muscle types share certain properties, including the initiation of muscle contraction by an intracellular calcium signal and the involvement of the motor protein myosin using ATP to create movement.
6
Q
What percentage of total body weight do skeletal muscles constitute?
A
Skeletal muscles make up about 40% of total body weight.
7
Q
What are tendons made of?
A
Tendons are made of collagen.
8
Q
What is the origin of a muscle, and what is its insertion?
A
The origin of a muscle is the end of the muscle that is attached closest to the trunk or to the more stationary bone, while the insertion of the muscle is the more distal or more mobile attachment.
9
Q
Define flexor and extensor muscles and their respective movements.
A
A muscle is called a flexor if the centers of the connected bones are brought closer together when the muscle contracts, resulting in flexion. Conversely, a muscle is called an extensor if the bones move away from each other when the muscle contracts, resulting in extension.
10
Q
What are flexor-extensor pairs called, and why?
A
Flexor-extensor pairs are called antagonistic muscle groups because they exert opposite effects.
11
Q
Provide an example of an antagonistic muscle pair in the arm.
A
An example of an antagonistic muscle pair in the arm is the biceps brachii, which acts as the flexor, and the triceps brachii, which acts as the extensor.
12
Q
Describe the movements associated with the contraction of the biceps brachii and the triceps brachii.
A
When the biceps brachii contracts, the hand and forearm move toward the shoulder, resulting in flexion. Conversely, when the triceps brachii contracts, the flexed forearm moves away from the shoulder, resulting in extension.
13
Q
What is the structure of a skeletal muscle fiber?
A
A skeletal muscle fiber is a long, cylindrical cell with up to several hundred nuclei near the surface of the fiber.
14
Q
What are satellite cells, and what is their role?
A
Satellite cells are committed stem cells located just outside the muscle fiber membrane. They become active and differentiate into muscle when needed for muscle growth and repair.
15
Q
Describe the arrangement of muscle fibers within a muscle.
A
The fibers in a given muscle are arranged with their long axes in parallel, bundled together into units called fascicles.
16
Q
What is the connective tissue sheath that encloses the entire muscle?
A
The entire muscle is enclosed in a connective tissue sheath that is continuous with the connective tissue around the muscle fibers and fascicles and with the tendons holding the muscle to underlying bones.
17
Q
What are the main intracellular structures in striated muscles, and what is their function?
A
The main intracellular structures in striated muscles are myofibrils, highly organized bundles of contractile and elastic proteins that carry out the work of contraction.
18
Q
What is the function of the sarcoplasmic reticulum (SR) in muscle fibers?
A
The sarcoplasmic reticulum concentrates and sequesters calcium ions (Ca2+) with the help of a Ca2+ ATPase in the SR membrane. Calcium release from the SR creates calcium signals that play a key role in contraction in all types of muscle.
19
Q
What are t-tubules, and what is their function?
A
T-tubules are a branching network of transverse tubules that are adjacent to and closely associated with the terminal cisternae of the sarcoplasmic reticulum. They allow action potentials to move rapidly from the cell surface into the interior of the fiber, facilitating simultaneous calcium release from the terminal cisternae and muscle contraction.
20
Q
What is the role of glycogen and mitochondria in muscle fibers?
A
Glycogen serves as a reserve source of energy, while mitochondria produce much of the ATP required for muscle contraction through oxidative phosphorylation of glucose and other biomolecules.
21
Q
What are myofibrils, and what is their composition?
A
Myofibrils are contractile structures found within muscle fibers. They are composed of several types of proteins, including myosin, actin, tropomyosin, troponin, titin, and nebulin
22
Q
Describe the structure and function of myosin.
A
Myosin is a motor protein consisting of two identical protein chains, each with one large heavy chain plus two smaller light chains. It forms thick filaments in muscle fibers and contains a motor domain that uses energy from ATP to create movement, as well as binding sites for actin.
23
Q
What is actin, and what role does it play in muscle contraction?
A
Actin is a protein that makes up the thin filaments of muscle fibers. It forms long chains or filaments that, in skeletal muscle, twist together to create the thin filaments. Actin provides binding sites for myosin crossbridges, facilitating muscle contraction.
24
Q
What is the structure and function of a sarcomere?
A
A sarcomere is the functional unit of a myofibril, responsible for muscle contraction. It consists of alternating light and dark bands and includes the following structures:
-Z disks: Zigzag protein structures serving as attachment sites for thin filaments.
-I bands: Light bands occupied only by thin filaments.
-A bands: Dark bands encompassing the entire length of thick filaments.
-H zones: Central regions of A bands occupied by thick filaments only.
-M lines: Bands representing proteins that form attachment sites for thick filaments, dividing A bands in half.
25
What is the role of titin in muscle physiology?
Titin is a large elastic protein that stretches from one Z disk to the neighboring M line, stabilizing the position of contractile filaments and returning stretched muscles to their resting length. It plays a crucial role in muscle elasticity.
26
How does nebulin contribute to muscle function?
Nebulin is an inelastic giant protein found alongside thin filaments, attaching to the Z disk. It helps align actin filaments within the sarcomere, ensuring proper filament alignment during muscle contraction
27
What is muscle tension, and what role does it play in muscle physiology?
Muscle tension is the force created by contracting muscle fibers, enabling movement or resistance against a load. It is a crucial aspect of muscle physiology, allowing for various physical activities.
28
Describe the major steps leading up to skeletal muscle contraction.
The major steps leading up to skeletal muscle contraction are as follows:
1. Events at the neuromuscular junction: This involves the conversion of an acetylcholine signal from a somatic motor neuron into an electrical signal in the muscle fiber. It initiates the process of muscle excitation.
2. Excitation-contraction (E-C) coupling: This process translates muscle action potentials into calcium signals within the muscle fiber. These calcium signals trigger the contraction-relaxation cycle.
3. Contraction-relaxation cycle at the molecular level: The sliding filament theory of contraction explains how actin and myosin filaments interact within the muscle fiber, leading to muscle contraction and relaxation.
29
What is the sliding filament theory of muscle contraction, and how was it developed?
The sliding filament theory of muscle contraction proposes that overlapping actin and myosin filaments of fixed length slide past one another in an energy-requiring process, resulting in muscle contraction. This theory was developed by scientists Andrew Huxley and Rolf Niedergerke in 1954, who discovered that the length of the A band of a myofibril remains constant during contraction, leading them to propose this alternative model.
30
Describe the changes that occur in a sarcomere during muscle contraction according to the sliding filament theory.
During muscle contraction, the Z disks of the sarcomere move closer together as the sarcomere shortens. The I band and H zone, regions where actin and myosin do not overlap in resting muscle, almost disappear. Despite the shortening of the sarcomere, the length of the A band remains constant. These changes are consistent with the sliding of thin actin filaments along the thick myosin filaments as the actin filaments move toward the M line in the center of the sarcomere.
31
How does the sliding filament theory explain muscle contraction without movement?
The sliding filament theory explains how a muscle can contract and create force without necessarily creating movement. For example, when pushing against a wall, tension is generated in the muscles without moving the wall. According to the theory, tension generated in a muscle fiber is directly proportional to the number of high-force crossbridges between the thick and thin filaments, allowing for force generation without movement.
32
How does the movement of myosin crossbridges contribute to muscle contraction?
The movement of myosin crossbridges provides force that pushes the actin filament during contraction. Similar to a competitive sailing team raising a heavy mainsail, myosin heads bind to actin molecules (the "rope"), initiating a power stroke where the myosin crossbridges swivel and push the actin filaments toward the center of the sarcomere. This process repeats many times as the muscle fiber contracts.
33
What initiates the power stroke in muscle contraction?
The power stroke in muscle contraction is initiated by a calcium signal. When calcium ions bind to troponin, it triggers a conformational change in tropomyosin, exposing the myosin-binding sites on actin. This allows myosin crossbridges to bind to actin and initiate the power stroke.
34
How is the energy for the power stroke generated in muscle contraction?
The energy for the power stroke in muscle contraction comes from ATP. Myosin is an ATPase (myosin ATPase) that hydrolyzes ATP to ADP and inorganic phosphate (Pi). The energy released by ATP hydrolysis is stored as potential energy in the angle between the myosin head and the long axis of the myosin filament. This potential energy is then converted into kinetic energy during the power stroke, moving actin filaments.
35
How does a calcium signal initiate muscle contraction?
A calcium signal initiates muscle contraction by binding to troponin C, which is part of the troponin complex. When calcium binds to troponin C, it causes a conformational change in the troponin complex, pulling tropomyosin away from actin's myosin-binding sites. This exposes the binding sites, allowing myosin heads to form strong crossbridges with actin filaments and initiate the power stroke, leading to muscle contraction.
36
What is the role of troponin in muscle contraction?
Troponin is a calcium-binding complex consisting of three proteins. It controls the positioning of tropomyosin, an elongated protein polymer that wraps around actin filaments and partially covers actin's myosin-binding sites in resting muscle. When calcium binds to troponin C, troponin undergoes a conformational change that moves tropomyosin away from actin's myosin-binding sites, allowing muscle contraction to occur
37
How does muscle relaxation occur after contraction?
Muscle relaxation occurs when cytosolic calcium concentrations decrease. As calcium unbinds from troponin, tropomyosin returns to its "off" position, covering most of actin's myosin-binding sites. This prevents myosin heads from forming strong crossbridges with actin filaments. During relaxation, the filaments of the sarcomere slide back to their original positions with the help of titin and elastic connective tissues within the muscle.
38
Describe the molecular events of a contractile cycle in skeletal muscle
the contractile cycle in skeletal muscle starts with the rigor state, where myosin heads are tightly bound to G-actin molecules without ATP or ADP bound to myosin. The cycle proceeds as follows:
1. ATP binds and myosin detaches: An ATP molecule binds to the myosin head, causing myosin to release from actin due to decreased actin-binding affinity.
2. ATP hydrolysis and cocking of myosin head: ATP hydrolysis occurs, providing energy for the myosin head to rotate and reattach to actin. The myosin head forms a 90° angle with the filaments, storing potential energy.
3. Power stroke: Calcium binding to troponin uncovers the myosin-binding sites on actin, allowing the myosin head to swivel and form strong, high-force bonds. The myosin head and hinge region tilt from a 90° angle to a 45° angle, sliding the attached actin filament along with them.
4. Myosin releases ADP: At the end of the power stroke, myosin releases ADP, returning to the rigor state and preparing for the next cycle.
39
What happens in the rigor state of muscle contraction?
In the rigor state, no ATP or ADP is bound to myosin, and myosin heads are tightly bound to G-actin molecules. This state is brief in living muscle fibers, as ATP quickly binds to myosin once ADP is released. However, after death and when ATP supplies are exhausted, muscles remain in the rigor state, leading to rigor mortis where muscles "freeze" due to immovable crossbridges between actin and myosin.
40
What challenges exist in studying muscle contraction at the molecular level?
Studying muscle contraction at the molecular level faces challenges due to the complexity of the process and limitations of research techniques. Techniques such as crystallization of molecules and electron microscopy cannot be used with living tissues. Additionally, the movement of molecules in a myofibril is difficult to observe, and progress in understanding muscle contraction relies on snapshots of the beginning and end stages of contraction. However, ongoing research aims to overcome these challenges, offering the potential for a more comprehensive understanding of muscle contraction in the future.
41
Describe the process of excitation-contraction coupling in skeletal muscle.
Excitation-contraction coupling in skeletal muscle involves the following steps:
1. Release of Acetylcholine (ACh): Acetylcholine is released from the somatic motor neuron and binds to ACh receptor-channels on the motor end plate of the muscle fiber.
2.Generation of Endplate Potential (EPP): ACh-gated channels open, allowing Na+ and K+ to cross the membrane. Na+ influx exceeds K+ efflux, depolarizing the membrane and generating an endplate potential (EPP).
3.Initiation of Muscle Action Potential: The EPP reaches threshold and initiates a muscle action potential, which propagates along the surface of the muscle fiber and into the t-tubules.
4. Calcium Release from Sarcoplasmic Reticulum: The muscle action potential triggers the opening of voltage-gated Na+ channels, leading to Ca2+ release from the sarcoplasmic reticulum.
5. Calcium Binding to Troponin: Elevated cytosolic Ca2+ levels cause Ca2+ to bind to troponin, leading to a conformational change in tropomyosin and exposure of myosin-binding sites on actin.
6. Initiation of Contraction: With the myosin-binding sites exposed, cross-bridge formation occurs between actin and myosin, initiating muscle contraction.
42
How is calcium release triggered in excitation-contraction coupling?
Calcium release is triggered in excitation-contraction coupling when the muscle action potential reaches the t-tubules. Voltage-gated L-type calcium channels (DHP receptors) in the t-tubule membrane change conformation in response to depolarization, leading to the opening of ryanodine receptors (RyR) in the sarcoplasmic reticulum. This allows stored calcium to flow into the cytosol, initiating muscle contraction.
43
What is the role of tropomyosin in muscle contraction?
Tropomyosin plays a crucial role in muscle contraction by regulating the exposure of myosin-binding sites on actin. In the absence of calcium, tropomyosin blocks these binding sites, preventing cross-bridge formation and muscle contraction. When calcium binds to troponin, tropomyosin undergoes a conformational change, allowing myosin to bind to actin and initiate contraction.
44
What is the latent period in excitation-contraction coupling?
The latent period is the short delay between the muscle action potential and the beginning of muscle tension development during excitation-contraction coupling. This delay represents the time required for calcium release from the sarcoplasmic reticulum and its binding to troponin. Once contraction begins, muscle tension increases steadily to a maximum value before decreasing during relaxation.
45
Explain how skeletal muscles obtain ATP for contraction.
Skeletal muscles obtain ATP for contraction through various metabolic pathways and energy sources:
- Phosphocreatine (PCr) System: Muscles store a small amount of ATP, which is quickly used up during contraction. Phosphocreatine, another high-energy molecule stored in muscle cells, can rapidly regenerate ATP from ADP during intense exercise. Creatine kinase catalyzes the transfer of phosphate from phosphocreatine to ADP, forming ATP.
- Glycolysis: Glucose is metabolized through glycolysis to produce ATP. This process occurs both aerobically (in the presence of oxygen) and anaerobically (in the absence of oxygen). Aerobic glycolysis yields more ATP per glucose molecule compared to anaerobic glycolysis. However, during strenuous exercise when oxygen supply is limited, anaerobic glycolysis becomes the primary source of ATP production.
- Oxidative Phosphorylation: Pyruvate, the end product of glycolysis, enters the citric acid cycle (Krebs cycle) in the presence of oxygen. This process, known as oxidative phosphorylation, generates a large amount of ATP from the oxidation of glucose.
- Fatty Acid Oxidation: Skeletal muscles can also utilize fatty acids as an energy source, especially during rest and low-intensity exercise. Fatty acids are oxidized through beta-oxidation to produce acetyl-CoA, which enters the citric acid cycle to generate ATP.
- Protein Metabolism: While proteins are not the primary energy source for muscle contraction, amino acids can be metabolized to produce ATP under certain conditions. However, protein metabolism is generally limited compared to carbohydrate and lipid metabolism.
46
What role does phosphocreatine play in muscle contraction?
Phosphocreatine (PCr) serves as a rapid source of ATP regeneration during intense muscle contraction. Creatine kinase catalyzes the transfer of a phosphate group from phosphocreatine to ADP, forming ATP. This process helps replenish ATP levels quickly, allowing muscles to sustain high-intensity contractions.
47
How does muscle metabolism change during strenuous exercise?
During strenuous exercise, muscle metabolism shifts towards anaerobic glycolysis due to limited oxygen availability. As a result, glucose is metabolized to lactate, yielding a smaller amount of ATP compared to aerobic glycolysis. Fatty acid oxidation cannot provide ATP rapidly enough to meet the increased energy demands during intense exercise. Therefore, muscles primarily rely on glycolysis for ATP production under these conditions.
48
Do muscles ever run out of ATP during exercise?
Despite the perception of fatigue during intense exercise, studies suggest that muscles rarely exhaust their ATP supply completely. Most studies indicate that only about 30% of the ATP in a muscle fiber is utilized during intense exercise. Fatigue during exercise is attributed to factors such as depletion of glycogen stores, accumulation of metabolic byproducts like lactate, and changes in muscle pH and ion concentrations, rather than complete ATP depletion.
49
What is fatigue in the context of muscle physiology?
Fatigue refers to a reversible condition where an exercising muscle is unable to generate or sustain the expected power output. It is influenced by various factors including the intensity and duration of contractile activity, metabolic pathways utilized (aerobic or anaerobic), muscle composition, and individual fitness levels.
50
What are the main categories of factors proposed to contribute to muscle fatigue?
Factors contributing to muscle fatigue are categorized into central fatigue mechanisms, originating in the central nervous system, and peripheral fatigue mechanisms, occurring between the neuromuscular junction and the muscle's contractile elements.
51
How does central fatigue differ from peripheral fatigue?
Central fatigue involves subjective feelings of tiredness and a desire to cease activity, which precede physiological fatigue in the muscles. It is believed to arise from psychological factors and may serve as a protective mechanism. Peripheral fatigue, on the other hand, involves excitation-contraction failure or changes in contraction force within the muscle fiber itself.
52
What are some proposed causes of peripheral fatigue within the muscle fiber?
Peripheral fatigue within the muscle fiber could result from various factors, including depletion of muscle glycogen stores during extended submaximal exertion, increased levels of inorganic phosphate (P i ) during short-duration maximal exertion, alterations in calcium (Ca2+) release from the sarcoplasmic reticulum, and ion imbalances such as elevated potassium (K+) concentrations in the extracellular fluid of the t-tubules.
53
How are skeletal muscle fibers classified, and what are the currently accepted muscle fiber types in humans?
Skeletal muscle fibers are classified based on their speed of contraction and resistance to fatigue. The currently accepted muscle fiber types in humans include slow-twitch fibers (Type I), fast-twitch oxidative-glycolytic fibers (Type IIA), and fast-twitch glycolytic fibers (Type IIB/IIX).
54
What are the main differences between fast-twitch and slow-twitch muscle fibers in terms of contraction speed and fatigue resistance?
Fast-twitch muscle fibers contract two to three times faster than slow-twitch fibers and have quicker twitches. However, they fatigue more easily due to their reliance on anaerobic glycolysis for ATP production. Slow-twitch fibers, on the other hand, contract more slowly but are more resistant to fatigue because they primarily rely on oxidative phosphorylation for ATP production.
55
How does the type of metabolism differ between oxidative and glycolytic muscle fibers, and how does this affect fatigue?
Oxidative fibers primarily rely on oxidative phosphorylation for ATP production and have more mitochondria and blood vessels to support this process. They are more fatigue-resistant because they do not accumulate H+ ions from anaerobic glycolysis, which contributes to fatigue. In contrast, glycolytic fibers rely on anaerobic glycolysis and fatigue more rapidly due to the accumulation of H+ ions.
56
What role does myoglobin play in muscle fibers, and how does its presence differ between oxidative and glycolytic fibers?
Myoglobin is a red oxygen-binding pigment with a high affinity for oxygen, facilitating the diffusion of oxygen into muscle fibers. Oxidative fibers contain more myoglobin, which allows for faster oxygen diffusion and supports oxidative phosphorylation. In contrast, glycolytic fibers have lower myoglobin content, resulting in slower oxygen diffusion and greater reliance on anaerobic glycolysis.
57
How do the characteristics of muscle fibers contribute to their color and fatigue resistance?
Oxidative fibers, which contain more myoglobin and mitochondria, are described as red muscle due to their high myoglobin content. They have better oxygen supply and utilize oxidative phosphorylation, making them more fatigue-resistant. In contrast, glycolytic fibers, with lower myoglobin content and reliance on anaerobic glycolysis, are described as white muscle and fatigue more rapidly.
58
How does the resting length of a muscle fiber affect the tension developed during a twitch?
The tension developed during a twitch in a muscle fiber is directly influenced by the length of individual sarcomeres before contraction begins. Each sarcomere contracts with optimal force if it is at the optimum length, ensuring proper overlap between the thick and thin filaments. If the sarcomere is too long, there is minimal overlap between the filaments, resulting in few crossbridges and minimal force generation. Conversely, if the sarcomere is too short, excessive overlap prevents crossbridge formation, leading to decreased tension development.
59
What is the relationship between sarcomere length and filament overlap, and how does this affect force generation?
Sarcomere length reflects the degree of overlap between the thick and thin filaments. At the optimum sarcomere length, there is optimal filament overlap, allowing for the formation of numerous crossbridges between the thick and thin filaments. This optimal overlap enables the muscle fiber to generate maximum force during contraction. However, if the sarcomere is too long or too short, the degree of filament overlap is suboptimal, resulting in decreased force generation due to fewer crossbridges or interference with crossbridge formation.
60
How does filament overlap and sarcomere length influence tension generation during muscle contraction?
The development of tension during muscle contraction is a passive property dependent on filament overlap and sarcomere length. Optimal sarcomere length ensures proper filament overlap, allowing for the formation of numerous crossbridges and maximum force generation. Deviations from the optimal length result in suboptimal filament overlap, leading to decreased force generation due to reduced crossbridge formation or interference with crossbridge activity.
61
What happens if the sarcomere is too short or too long at the beginning of contraction?
If the sarcomere is too short, excessive filament overlap occurs, preventing proper crossbridge formation and leading to decreased tension development. Conversely, if the sarcomere is too long, there is minimal filament overlap, resulting in fewer crossbridges and minimal force generation. Both scenarios lead to suboptimal force production during muscle contraction
62
What determines the maximum force that a muscle fiber can develop?
The force generated by the contraction of a single muscle fiber can be increased by increasing the rate (frequency) at which muscle action potentials stimulate the muscle fiber.
63
What is the effect of shortening the interval between action potentials on muscle fiber contraction?
Shortening the interval between action potentials results in a more forceful contraction because the muscle fiber does not have time to relax completely between two stimuli.
64
What is the process known as when action potentials stimulate the muscle fiber repeatedly at short intervals?
The process is known as summation, similar to the temporal summation of graded potentials that takes place in neurons.
65
What is tetanus in the context of muscle contraction?
Tetanus is a state of maximal contraction achieved by a muscle fiber when action potentials stimulate it repeatedly at short intervals, resulting in diminished relaxation between contractions. There are two types: incomplete (unfused) tetanus, where the fiber relaxes slightly between stimuli, and complete (fused) tetanus, where the fiber reaches maximum tension and remains there without relaxing.
66
How are muscle action potentials initiated?
Muscle action potentials are initiated by the somatic motor neuron that controls the muscle fiber.
67
What is the basic unit of contraction in an intact skeletal muscle?
The basic unit of contraction in an intact skeletal muscle is a motor unit, composed of a group of muscle fibers that function together and the somatic motor neuron that controls them.
68
How do muscle fibers within a motor unit respond when the somatic motor neuron fires an action potential?
All muscle fibers in the motor unit contract simultaneously.
69
How does the number of muscle fibers in a motor unit vary?
The number of muscle fibers in a motor unit varies depending on the function of the muscle. Muscles used for fine motor actions may contain as few as three to five muscle fibers per motor unit, while muscles used for gross motor actions may contain hundreds or even thousands of muscle fibers per motor unit.
70
What determines the response of a muscle when additional motor units are activated?
When additional motor units are activated, the muscle response increases by small or large increments, depending on the number of muscle fibers in each motor unit. Fine motor muscles show small increments, while gross motor muscles show larger increments.
71
How do muscle fibers within a single motor unit differ?
All muscle fibers within a single motor unit are of the same fiber type, either fast-twitch or slow-twitch.
72
What factors influence the distribution of muscle fiber types in individuals?
Factors such as inheritance and training influence the distribution of muscle fiber types. Endurance athletes tend to have a predominance of slow-twitch fibers, while sprinters and weight lifters tend to have more fast-twitch fibers.
73
How can endurance training affect the fiber composition of muscles?
Endurance training can enhance the aerobic capacity of fast-twitch fibers, making them almost as fatigue-resistant as slow-twitch fibers. This is achieved through increased capillaries and mitochondria in the trained muscles, allowing for better oxygen delivery and utilization.
74
How can muscles create graded contractions of varying force and duration despite the all-or-none manner of motor unit contraction?
Muscles can create graded contractions by changing the types of motor units that are active or by changing the number of motor units that are responding at any one time.
75
How does recruitment of motor units contribute to increasing the force of contraction in a skeletal muscle?
Recruitment of motor units increases the force of contraction by activating additional motor units in a standardized sequence. Initially, low-threshold motor neurons controlling fatigue-resistant slow-twitch fibers are activated, followed by neurons controlling fast-twitch oxidative-glycolytic fibers, and finally, neurons controlling glycolytic fast-twitch fibers. This sequential activation leads to greater force generation as more motor units participate in the contraction.
76
Why do fast-twitch fibers generate more force than slow-twitch fibers?
Fast-twitch fibers generate more force than slow-twitch fibers due to differences in myosin and crossbridge formation. However, fast-twitch fibers fatigue more rapidly than slow-twitch fibers.
77
How does the nervous system avoid fatigue in sustained contractions?
The nervous system avoids fatigue in sustained contractions by asynchronously recruiting motor units, allowing some motor units to rest between contractions. This modulation of firing rates prevents fatigue in submaximal contractions.
78
What is the consequence of sustained, high-tension contractions on motor units?
In sustained, high-tension contractions, individual motor units may reach a state of unfused tetanus, where muscle fibers cycle between contraction and partial relaxation. As different motor units fatigue, the force of the contraction gradually decreases.
79
What is the difference between isotonic and isometric contractions?
Isotonic contractions move loads by creating force and generating movement, while isometric contractions create force without moving a load.
80
How can you demonstrate an isotonic contraction experimentally?
An isotonic contraction can be demonstrated experimentally by hanging a weight (the load) from the muscle and electrically stimulating the muscle. The muscle contracts, lifting the weight.
81
What is an example of a lengthening (eccentric) contraction?
An example of a lengthening (eccentric) contraction is when you slowly extend your arms while holding weights, resisting the gravitational forces pulling the weights down.
82
How do muscles create force in isometric contractions without significantly changing in length?
In isometric contractions, muscles create force without significant shortening because the elastic elements of the muscle, including elastic fibers in tendons and connective tissues, stretch as the sarcomeres shorten in the initial stages of contraction. This stretching allows the muscle fibers to maintain a relatively constant length.
83
What happens once the elastic elements of the muscle have been stretched in an isometric contraction?
Once the elastic elements of the muscle have been stretched, if the sarcomeres generate force equal to the load, the muscle shortens in an isotonic contraction and lifts the load.
84
What is the relationship between the anatomical arrangement of muscles, bones, and joints, and how muscles work?
The body uses its bones and joints as levers and fulcrums, where muscles exert force to move or resist a load. Levers are rigid bars that pivot around a fulcrum, and bones form levers while flexible joints serve as fulcrums. Muscles, attached to bones, create force by contracting, thus facilitating movement or resisting loads.
85
How do lever systems in the body function?
Most lever systems in the body resemble a fishing pole, with the fulcrum at one end, the load at the other, and force applied between them. This arrangement maximizes the distance and speed of movement but requires more force. Lever systems allow for movements like flexion of the forearm, where the elbow joint acts as the fulcrum and the biceps muscle creates an upward force.
86
What determines the force exerted by a muscle in a lever system?
The force exerted by a muscle depends on its contraction and the distance between the fulcrum and the muscle insertion point. For example, if a muscle must hold a forearm stationary at a 90° angle, it must generate enough force to offset the weight of the forearm. Genetic variability in insertion points can significantly affect the force required to move or resist a load.
87
How does the lever-fulcrum system of the arm amplify movement?
Lever-fulcrum systems maximize speed and mobility. A small movement of the muscle insertion point results in a much larger movement at the load end. Additionally, both movements occur at the same time, amplifying the speed of contraction at the insertion point, thus amplifying both the distance and speed of movement.
88
What are some causes of dysfunction in skeletal muscles?
Dysfunction in skeletal muscles can arise from problems with the signal from the nervous system, miscommunication at the neuromuscular junction, or defects in the muscle itself. Muscle disorders can result from hyperexcitability of somatic motor neurons, overuse, disuse, infectious diseases, toxins, or inherited conditions.
89
What is a common muscle disorder, and what causes it?
One common muscle disorder is a "charley horse" or muscle cramp, which involves sustained painful contractions of skeletal muscles. Many muscle cramps are caused by hyperexcitability of somatic motor neurons, leading to painful sustained contractions of muscle fibers within a motor unit.
90
How can muscle cramps be relieved?
Muscle cramps can sometimes be relieved by forcibly stretching the affected muscle. Stretching sends sensory information to the central nervous system, inhibiting the somatic motor neuron and relieving the cramp.
91
What are some acquired disorders that affect the skeletal muscle system?
Acquired disorders affecting the skeletal muscle system include infectious diseases like influenza, poisoning by toxins such as botulinum toxin (Botulism) and tetanus toxin (Tetanus), which decrease acetylcholine release from somatic motor neurons. Botulinum toxin injections are used for conditions like writer's cramp and for cosmetic wrinkle reduction.
92
What are some examples of inherited muscular disorders?
Inherited muscular disorders include various forms of muscular dystrophy, such as Duchenne muscular dystrophy, where the absence of the structural protein dystrophin leads to progressive muscle weakness. Another example is McArdle's disease, where the enzyme myophosphorylase, necessary for converting glycogen to glucose 6-phosphate in muscles, is absent, limiting exercise tolerance due to lack of usable glycogen energy supply.
93
How can smooth muscle be categorized based on location?
Smooth muscle in humans can be divided into six major groups based on location: vascular (blood vessel walls), gastrointestinal (walls of digestive tract and associated organs), urinary (walls of bladder and ureters), respiratory (airway passages), reproductive (uterus in females and other reproductive structures), and ocular (eye).
94
How can smooth muscle be classified based on contraction pattern?
Smooth muscle can be classified based on whether it undergoes periodic contraction and relaxation cycles (phasic smooth muscles) or whether it is continuously contracted (tonic smooth muscles). Phasic smooth muscles contract only when stimulated, such as the lower esophagus during swallowing. Tonic smooth muscles, like the esophageal and urinary bladder sphincters, maintain a constant level of contraction.
95
What is the difference between single-unit smooth muscle and multiunit smooth muscle?
In single-unit smooth muscle, cells are electrically connected by gap junctions and contract as a coordinated unit. This type of smooth muscle is found in organs like the uterus and gastrointestinal tract. In multiunit smooth muscle, cells are not electrically linked, and each cell functions independently. Examples of multiunit smooth muscle include the ciliary muscles of the eye and the piloerector muscles of hair follicles.
96
What is single-unit smooth muscle, and why is it also called visceral smooth muscle?
Single-unit smooth muscle, also known as visceral smooth muscle, forms the walls of internal organs (viscera), such as the intestinal tract. It is called single-unit because its fibers are connected to one another by gap junctions, allowing electrical signals to spread rapidly through the tissue and coordinate contraction.
97
How does contraction occur in single-unit smooth muscle?
In single-unit smooth muscle, all fibers contract simultaneously in response to an electrical signal that spreads through the tissue via gap junctions. The force of contraction is determined by the amount of calcium ions (Ca2+) that enters the cell.
98
What is multiunit smooth muscle, and how does it differ from single-unit smooth muscle?
Multiunit smooth muscle consists of individual muscle cells that are not electrically linked. Each cell must be stimulated independently to contract. This allows for fine control of contractions through selective activation of individual muscle cells. Multiunit smooth muscle is found in structures like the iris and ciliary muscle of the eye and in parts of the male reproductive tract.
99
What are the two principles that apply to all smooth muscle, similar to skeletal muscle?
The two principles that apply to all smooth muscle are:
1. Force is created by actin-myosin crossbridge interaction between sliding filaments.
2. Contraction is initiated by an increase in free cytosolic calcium ion (Ca2+) concentrations.
100
How do the functions of smooth muscle differ from skeletal muscle?
1. Smooth muscles must operate over a range of lengths, unlike skeletal muscles that operate over a narrow range.
2. The layers of smooth muscle within an organ may run in several directions, changing the shape of the organ, while most skeletal muscles contract to shorten.
3. Smooth muscles contract and relax much more slowly than skeletal or cardiac muscle.
4. Smooth muscle uses less energy to generate and maintain force compared to striated muscles.
5. Smooth muscle can sustain contractions for extended periods without fatiguing.
6. Smooth muscles have small, spindle-shaped cells with a single nucleus, unlike the large multinucleated fibers of skeletal muscles.
7. In smooth muscle, the contractile fibers are not arranged in sarcomeres.
8. Contraction in smooth muscle may be initiated by electrical or chemical signals or both, while skeletal muscle contraction always begins with an action potential.
9. Smooth muscle is controlled by the autonomic nervous system, while skeletal muscle is controlled by the somatic motor division.
10. Smooth muscle lacks specialized receptor regions and instead, receptors are found all over the cell surface.
11. In smooth muscle, the calcium for contraction comes from both extracellular fluid and the sarcoplasmic reticulum, while in skeletal muscle, it comes only from the sarcoplasmic reticulum.
12. In smooth muscle, the calcium signal initiates a cascade that ends with phosphorylation of myosin light chains and activation of myosin ATPase, while in skeletal muscle, the calcium signal binds to troponin to initiate contraction.
101
What are some examples of smooth muscle functions at the organ level?
Smooth muscle functions at the organ level include operating over a range of lengths, changing the shape of organs, and sustaining contractions for extended periods without fatiguing. Examples include the distensibility of the bladder and the sequential waves of smooth muscle contraction that move material through the small intestine.
102
How do the structural elements of actin and myosin differ in smooth muscle compared to skeletal muscle?
In smooth muscle, actin is more plentiful than in skeletal muscle, with an actin-to-myosin ratio of 10–15 to 1, compared to 2–4 to 1 in skeletal muscle. Smooth muscle actin is associated with tropomyosin but lacks troponin. Smooth muscles have fewer myosin filaments than skeletal muscle, and these filaments are longer and have myosin heads covering their entire surface. The contractile units in smooth muscle are arranged parallel to the long axis of the cell, allowing for more stretch while maintaining tension. Additionally, smooth muscle cells have an extensive cytoskeleton consisting of intermediate filaments and protein dense bodies, which help hold actin in place and transfer force from contracting cells to their neighbors.
103
How does the sarcoplasmic reticulum (SR) in smooth muscle differ from that in skeletal muscle?
The amount and arrangement of the sarcoplasmic reticulum (SR) in smooth muscle vary among different types of smooth muscle. In smooth muscle, the SR is less organized compared to skeletal muscle and consists of a network of tubules extending from just under the cell membrane into the interior of the cell. Unlike skeletal muscle, smooth muscle lacks t-tubules, but the SR is closely associated with membrane invaginations called caveolae, which are involved in cell signaling.
104
What are the steps involved in smooth muscle contraction, and what are their respective roles?
1. An increase in cytosolic Ca2+ initiates contraction by being released from the sarcoplasmic reticulum and entering from the extracellular fluid.
2. Ca2+ binds to calmodulin, a calcium-binding protein found in the cytosol.
3. Ca2+ binding to calmodulin initiates a cascade that ends in the phosphorylation of myosin light chains.
4. Phosphorylation of myosin light chains enhances myosin ATPase activity, leading to muscle contraction. Additionally, the myosin ATPase isoform in smooth muscle is slower than that in skeletal muscle, resulting in a slower rate of crossbridge cycling.
105
What enzyme is activated by the Ca2+-calmodulin complex during smooth muscle contraction?
Myosin light chain kinase (MLCK).
106
What is the role of myosin light chain kinase (MLCK) in smooth muscle contraction?
MLCK phosphorylates the myosin light protein chains, leading to enhanced myosin ATPase activity and muscle contraction.
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What is the significance of the myosin ATPase isoform in smooth muscle compared to skeletal muscle?
The myosin ATPase isoform in smooth muscle is much slower than that in skeletal muscle, resulting in a slower rate of crossbridge cycling.
108
What is the role of myosin light chain phosphatase (MLCP) in smooth muscle relaxation?
MLCP dephosphorylates myosin, leading to a decrease in myosin ATPase activity and muscle relaxation.
109
What is the "latch state" in smooth muscle contraction?
The latch state is an isometric contraction where dephosphorylated myosin remains in a contracted state, maintaining tension in the muscle fiber while consuming minimal ATP.
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What determines the contraction state of smooth muscle?
The ratio of MLCK to MLCP activity determines the contraction state of smooth muscle, with MLCK activity being dependent on Ca2+-calmodulin.
111
What factors influence the Ca2+ sensitivity in smooth muscle contraction?
MLCP Controls Ca2+ Sensitivity:
- Chemical signals like neurotransmitters, hormones, and paracrine molecules modulate MLCP activity.
- An increase in MLCP activity leads to a decrease in contraction force, even without changes in cytosolic Ca2+ concentration, resulting in desensitization to calcium.
- Conversely, decreased MLCP activity increases sensitivity to Ca2+, enhancing contraction force.
- The ratio of MLCK to MLCP activity determines smooth muscle contraction state.
- MLCP dephosphorylates myosin light chains, leading to muscle relaxation.
112
How does smooth muscle contraction initiate, and what are the sources of Ca2+ for contraction?
Initiation of Smooth Muscle Contraction:
- Contraction can start with electrical signals (electromechanical coupling) or chemical signals (pharmacomechanical coupling).
- Ca2+ initiates contraction by coming from two sources: the sarcoplasmic reticulum (SR) and the extracellular fluid.
Sources of Ca2+ for Contraction:
- Sarcoplasmic Ca2+ Release:
-- Mediated by ryanodine receptor (RyR) and IP3 receptor channels.
-- RyR channel opens due to calcium-induced calcium release (CICR).
-- IP3 channels open when G protein-coupled receptors activate phospholipase C.
- Cell Membrane Ca2+ Entry:
-- Voltage-gated Ca2+ channels open in response to depolarization.
-- Ligand-gated Ca2+ channels open upon ligand binding.
-- Stretch-activated channels open in response to cell membrane distortion, initiating myogenic contractions.
113
How does the role of membrane potentials in smooth muscle contraction differ from skeletal muscle?
In smooth muscle:
-Membrane potentials play a more complex role than in skeletal muscle.
-Smooth muscle can hyperpolarize, decreasing the likelihood of contraction, or depolarize without firing action potentials.
-Contraction may occur after an action potential, subthreshold graded potential, or without any change in membrane potential.
-Resting membrane potentials in smooth muscle vary between -40 and -80 mV.
-Cells with cyclic depolarization and repolarization have slow wave potentials, while those with regular depolarizations that reach threshold are termed pacemaker potentials, creating rhythmic contractions.
-Both slow wave and pacemaker potentials result from ion channels spontaneously opening and closing in the cell membrane.
-In pharmacomechanical coupling, the membrane potential may remain unchanged during contraction.
114
How do chemical signals influence smooth muscle activity?
Chemical signals, including neurotransmitters, hormones, and paracrine signals, can have excitatory or inhibitory effects on smooth muscle contraction. They modulate contraction through second messenger action at the level of myosin and by influencing Ca^2+ signals.
-Autonomic neurotransmitters and hormones, such as epinephrine, can exert antagonistic control over smooth muscles.
-The effects of chemical signals depend on receptor type, with some promoting contraction (e.g., alpha adrenergic receptors) and others promoting relaxation (e.g., beta 2 adrenergic receptors).
-Most smooth muscle neurotransmitters and hormones bind to G protein-linked receptors, which activate second messenger pathways.
-Pathways that increase IP3 trigger contraction by releasing Ca^2+ from the sarcoplasmic reticulum and inhibiting myosin phosphatase activity.
-Signals that cause muscle relaxation decrease cytosolic Ca^2+ concentrations, hyperpolarize the cell, and increase myosin phosphatase activity.
-Paracrine signals, like histamine and nitric oxide, can also alter smooth muscle contraction, with nitric oxide relaxing adjacent smooth muscle in blood vessels.
-Smooth muscle fibers act as integrating centers, coordinating responses to contradictory signals, which can make them difficult to study in the laboratory despite their critical role in body function.
115
What are the features of cardiac muscle?
- Striated and Sarcomere Structure: Like skeletal muscle, cardiac muscle fibers are striated and possess a sarcomere structure.
- Shorter Fibers and Branched: Cardiac muscle fibers are shorter and may be branched compared to skeletal muscle fibers.
- Single Nucleus: Each cardiac muscle fiber has a single nucleus, unlike multinucleate skeletal muscle fibers.
- Electrical Coupling: Similar to single-unit smooth muscle, cardiac muscle fibers are electrically linked to one another via gap junctions, located in specialized cell junctions called intercalated disks.
- Pacemaker Potentials: Some cardiac muscle exhibits pacemaker potentials, akin to certain types of smooth muscle.
- Autonomic and Hormonal Control: Cardiac muscle is under both sympathetic and parasympathetic control, as well as hormonal influence.
