Conception Questions Related to MSK Flashcards
Which of the following best describes the mechanism by which hypercalcemia interferes with action potential production in neurons?
Blockade of voltage-gated sodium channels. This is the correct answer. Voltage-gated sodium and calcium channels are more closely related to one another than they are to potassium channels, and structural similarities exist that allow excess calcium to enter the vestibule of the sodium channel and block it, this interfering with function and APs.
TAKEAWAY: In neurons, hypercalcemia interferes with action potential generation by excess calcium blocking voltage-gated sodium channels. Hypercalcemia also causes muscular problems.
In rapidly contracting muscles, such as the leg muscles in running or the extraocular muscles, most of the energy for contraction is supplied by anaerobic glycolysis of stored glycogen. The buildup of intermediary metabolites from this pathway, particularly lactic acid, can produce an oxygen deficit that causes ischemic pain (cramps) in cases of extreme muscular exertion.
Most of the energy used by muscle recovering from contraction or by resting muscle is derived from oxidative phosphorylation. This process closely follows the β-oxidation of fatty acids in mitochondria that liberates two carbon fragments. The oxygen needed for oxidative phosphorylation and other terminal metabolic reactions is derived from hemoglobin in circulating erythrocytes and from oxygen bound to myoglobin stored in the muscle cells.
Because of its inheritance as an __________ trait, DMD primarily affects boys (an estimated 1 in 3,500 boys worldwide). Onset of DMD is between 3 and 5 years of age and progresses rapidly. Most
X-linked recessive
_____ is similar to DMD except that it progresses at a much slower rate. Symptoms usually appear at about age 12, and the ability to walk is lost at an average age of 25 to 30.
Becker muscular dystrophy (BMD)
When a muscle contracts, each sarcomere _________, but the myofilaments remain the same length.
Shortens
In resting muscle, myosin heads are prevented from binding with actin molecules by tropomyosin, which covers myosin-binding sites on actin molecules
Following nerve stimulation, Ca2+ is released into the sarcoplasm and binds to troponin, which then acts on the tropomyosin to expose the myosin-binding sites on actin molecules (Fig. 11.11b). Once the binding sites are exposed, the myosin heads are able to interact with actin molecules and form cross-bridges, and the two filaments slide over one another.
Shortening of a muscle involves rapid, repeated interactions between actin and myosin molecules that move the ______filaments along the _______ filament.
Thin and thick
Each cross-bridge cycle consists of five stages: attachment, release, bending, force generation, and _______
Reattachment
Attachment is the _______ stage of the cross-bridge cycle; the myosin head is tightly bound to the actin molecule of the thin filament.
Inital
At the beginning of the cross-bridge cycle, the myosin head is strongly bound to the actin molecule of the thin filament, and ATP is absent (Fig. 11.11c). Position of the myosin head in this stage is referred as an original or unbent confirmation. This very short-lived arrangement is known as the rigor configuration. The muscular stiffening and rigidity that begins at the moment of death is caused by lack of ATP and is known as rigor mortis. In an actively contracting muscle, this step ends with the binding of ATP to the myosin head.
A glaucoma patient is prescribed a cholinergic drug to reduce their intraocular pressure.
Which of the following mechanisms explains the effects of acetylcholine at the neuromuscular junction?
Binds to nicotinic receptors and depolarizes myocytes- This is the correct answer. Depolarization of myocytes is the excitation step produced by acetylcholine released from motor neurons to initiate excitation-contraction coupling.
TAKEAWAY – Excitation-contraction coupling is initiated by acetylcholine binding to nicotinic acetylcholine receptors followed by depolarization of myocytes. Excitation-contraction coupling results in the active tension generated by the sliding filament power stroke mechanism within the myocyte sarcomeres that is required for purposeful movement.
50-year-old woman is brought to the emergency department by an ambulance is barely breathing. Her family says that she has no chronic diseases and had been well until a few hours ago when she complained of profound fatigue and weakness after the family returned home from a church picnic. At the picnic, the menu consisted of grilled hot dogs, hamburgers and potato salad
A deficiency in activity of which of the following substances is most likely to explain the woman’s condition?
Acetylcholine - This is the correct answer. Botulinum toxin binds to and inhibits release of acetylcholine from the acetylcholine-storage vesicles at motor neuron terminals, thereby causing generalized muscle weakness that may include the voluntary respiratory muscles.
TAKEAWAY – Botulinum toxin primarily binds to and inhibits the SNARE proteins comprising part of the acetylcholine-containing vesicles at motor neuron terminals. Binding to the SNARE proteins inhibits the release of acetylcholine which, in turn, inhibits muscle contractions; thereby, weakening the skeletal voluntary diaphragm and chest wall respiratory pumping muscle contractions. A church picnic where bacterial growth in uncooked portions of food such as mayonnaise or eggs in the potato salad is generally recognized as a cause of botulism
50-year-old woman presents to her primary care physician for a routine physical. Her medical history is unremarkable. Her only complaint is her appearance. She states concerns about facial wrinkling that she thinks makes her look older than she is. The physician recommends subcutaneous administration of botulinum toxin as a treatment
Which of the following is the primary site of the action of botulinum toxin in this woman?
Vesicular proteins - This is the correct answer. Botulinum toxin binds to and inhibits release of acetylcholine from the acetylcholine-storage vesicles at motor neuron terminals.
TAKEAWAY – Botulinum toxin primarily binds to and inhibits the SNARE proteins comprising part of the acetylcholine-containing vesicles at motor neuron terminals. Binding to the SNARE proteins inhibits the release of acetylcholine which, in turn, inhibits muscle contractions; thereby, decreasing the appearance of facial skin wrinkles. The treatment is commonly referred to as Botox
A 49-year-old man is brought to the ER by ambulance because of repeated convulsions. The patient was a garbage truck driver known to be alcoholic, who fell down and suffered an injury to the left face two days before the onset of the convulsion. The patient refused a tetanus shot. Intravenous administration of anti-seizure and muscle relaxant medications partially relieved the convulsions. Six hours later, the patient became unable to open his mouth.
An abnormality in which of the following cell or cell structure is the likely cause of this man’s condition?
Inhibitory interneuron- This is the correct answer. Inhibitory interneurons are the main source of infection by the Clostridium tetanii toxin resulting in neural disinhibition evidenced by overstimulation of nerves and skeletal muscles. Seizures, convulsions, painful stiff muscles, especially those of the jaw; i.e., lockjaw affecting the muscles of mastication are the signs of bacteriological tetanus.
TAKEAWAY – Bacteriological tetanus and physiological tetanus are high excitability states involving accumulation of Ca2+ in the sarcoplasm of skeletal muscle fibers that increases cross-bridge cycling and muscle force to high levels that make the muscles stiff and painful.
A researcher is performing a neuromuscular junction experiment wherein a specific immunoglobulin G (IgG) is administered to cultures of innervated skeletal myocytes. Administration of antibodies directed against nicotinic acetylcholine receptors demonstrates a significant decrease in the number of receptors following administration of the IgG and an attenuated response of the myocytes to electrical stimulation of the cells innervating the myocytes.
Which of the following physiological mechanisms is likely to improve the response of these myocytes to electrical stimulation?
Inhibiting the activity of acetylcholinesterase- This is the correct answer. Acetylcholinesterase is an enzyme and component of the nicotinic receptor subtype located on the motor endplate which hydrolyzes the neurotransmitter acetylcholine. Acetylcholine breakdown is necessary to maintain skeletal myocyte excitability. Accumulation of acetylcholine at motor endplates increases responsiveness of skeletal myocytes to electrical stimulation, especially in conditions such a myasthenia gravis wherein there is loss of nicotinic acetylcholine receptors due to immunologic attack and destruction. Indeed, acetylcholinesterase inhibitors are given to myasthenia patients as a positive diagnostic test wherein muscle contraction is expected to be improved by acetylcholine buildup overcomes the loss of nicotinic acetylcholine receptors. However, too much inhibition of acetylcholinesterase tends to decrease the responsiveness of myocytes to acetylcholine and electrical stimulation, as occurs in conditions of organophosphate and carbamate insecticide- and nerve gas-induced acetylcholinesterase inhibition which weakens contractions or paralyzes skeletal muscles, especially the respiratory muscles, resulting in respiratory failure.
TAKEAWAY – Destruction of nicotinic acetylcholine receptors on motor endplates at neuromuscular junctions decreases he responsiveness of skeletal myocytes to electrical stimulation and weakens skeletal muscle contractions. Myasthenia gravis is a disease that results from immunologic destruction of such nicotinic acetylcholine receptors which is observed as skeletal muscle weakness as a cardinal sign of the disease. Diagnosis and treatment of myasthenia gravis involves noting a significant improvement in muscle strength after administration of an acetylcholinesterase inhibitor drug.
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A physical trainer tells his client that calcium metabolism is important for building muscle strength because calcium ions provide the “spark” for muscle contractions.
Which of the following best describes the role does calcium ions play in muscle contractions?
More Ca2+ in the sarcoplasm increases the number of cross-bridges and increases twitch and contractile force- This is the correct answer. Ca2+ is the “spark” for contraction. Therefore, more calcium in the sarcomere cytoplasm (sarcoplasm) increases the number of cross-bridges and muscle twitch and contractile force.
TAKEAWAY – The sarcoplasmic reticulum of skeletal muscles is a storage site for Ca2+. Ca2+ is the “spark” for contraction and must be released through the ryanodine receptor Ca2+ release channel. Ca2+ release from the sarcoplasmic reticulum to the sarcoplasm produces the active tension required for purposeful movement by stimulating cross-bridge cycling.
A healthy person is convinced by a TV advertisement to purchase a home kit for genetic testing to trace their ancestry. The results show a mutation in their dystrophin gene which, if passed on to their offspring, could result in a muscular dystrophy.
Stiffens the actin filament, increases the number of cross-bridges cycling and the active force for purposeful movement- This is the correct answer. dystrophin attaches the actin filament to the sarcolemma and functions to stiffen the actin filament. Increased expression/production of dystrophin is an adaptation that could increase contractile force by the mechanism of stiffening the actin filament, thereby increasing the number of cross-bridges cycling.
TAKEAWAY - Deficiency of dystrophin, as observed in muscular dystrophies, results in decreased (weak) contractile force due to lack of stiffness, thereby decreasing the number of cross-bridges cycling.
A 35-year-old male advertising executive is complaining to his physician of severe jaw pain that often awakens him during the night. His dentist notices tooth and gingival changes which suggest that the man is suffering from bruxism associated with jaw clenching that often occurs during sleep, known as temporomandibular joint syndrome.
Which of the following abnormality’s within the myocytes of the masseter, internal lateral pterygoid and temporalis muscles is most likely to create the conditions for high temporomandibular joint contractile force in this patient?
Increased myosin ATPase content- This is the correct answer. Myosin ATPase is responsible for hydrolyzing ATP to ADP + Pi and creating the energy for the actin-myosin cross-bridge power stroke that produces active tension, the force for purposeful movement. When muscles are used excessively (or trained0 to respond to high resistive loads, the fibers hypertrophy by adding sarcomeres. The addition of sarcomeres also increases the diameter of the fibers and often transforms the muscles to express a higher percentage of type I and type IIa fatigue-resistant subtypes.
TAKEAWAY – Knowing how the sarcomere creates high muscle forces for purposeful movement and low muscle forces associated with fatigue, relaxation, rest and recovery from periods of high contractile activity helps one identify the potential mechanisms for muscle disorders. High active tension in the muscles of mastication should occur only when eating and masticating food. Individuals with temporomandibular joint disorders and various mandibular malocclusion disorders have high active tension in their jaw muscles, often throughout the day, at inappropriate times, such as when they are resting or sleeping when low muscle force should predominate. Excessive neuromuscular activity causes the muscle fibers to hypertrophy and transform to the fatigue-resistant subtypes I and IIa.
Which of the following best describes a patient scenario that is most likely to benefit from a drug that blocks smooth muscle inositol triphosphate receptors?
Septic patient with intestinal hypermotility and diarrhea- This is the correct answer. The inositol triphosphate (IP3) receptor is an integral part of the intracellular transduction signaling molecule cascade that results in increases in intracellular release of calcium ions. Sensitization of the intracellular machinery for calcium ions increases contractility in smooth muscles and hypermotility in the smooth muscle of the gastrointestinal tract.
TAKEAWAY –A septic patient with gastrointestinal hypermotility and diarrhea is likely to benefit from blockade of IP3 receptors because blockade of IP3 receptors is expected to decrease gastrointestinal smooth muscle contractility and hypermotility of the gastrointestinal tract.
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A man is reporting to his primary care physician that he is being awakened from sound sleep several times a week by sudden onset of muscle spasms. Physical examination is unremarkable.
Which of the following physiological mechanisms is most likely to be responsible for muscle spasms?
Decreasing permeability of motor endplates to K+- This is the correct answer. Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Decreasing permeability of the motor endplates of skeletal muscles will have a depolarizing effect, thereby contributing to the high excitability state and muscle spasms.
TAKEAWAY –Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Muscle spasms are produced when excitation-contraction coupling mechanisms are upregulated and activated in an uncontrolled manner.
A group of researchers are working on the hypothesis that a mutation in the ryanodine receptor protein is a key factor in epilepsy. They are using cultures of human skeletal myocytes as a control preparation and comparing the effects of various ryanodine receptor agonists and antagonists on functions of myocytes and neurons.
Which of the following best describes the response that is expected from administration of a ryanodine receptor agonist to a culture of skeletal myocytes?
Contraction without depolarization- This is the correct answer. The excitation-contraction coupling mechanism is dependent on Na+ influx and depolarization conducted through T-tubules to the dihydropyridine (DHP) -ryanodine receptor complex for Ca2+ release. The ryanodine receptor is the Ca2+ release channel within the sarcoplasmic reticulum that provides the “spark” for actin-myosin cross-bridge cycling and increases active tension, the contractile force required for purposeful movement. Administration of a ryanodine receptor agonist bypasses the depolarization step, resulting in contractile force in the absence of depolarization.
TAKEAWAY – Ryanodine receptor agonists and gain-in-function ryanodine receptor mutations result in uncontrolled release of Ca2+ from the sarcoplasmic reticulum. Such a skeletal muscle mutation is the cause of malignant hyperthermia wherein uncontrolled release of Ca2+ is stimulated by volatile halogenated anesthetics administered for general surgery, succinylcholine administered for muscle paralysis during endotracheal intubation and in rare cases caffeine.
Which of the following is a uniques feature of cardiac muscles?
Often branched
Which of the following best describes the trigger area for firing an action potential for a Pacinian corpuscle (lamellar corpuscle)?
First node of Ranvier. This is the correct answer. If enough depolarizing signal arrives from the nerve fiber in the lamellar layers of the distal nerve (analogous to a dendrite), then an action potential will fire and travel along the single process to the dorsal horn.
TAKEAWAY: For many sensory neurons, the first node of Ranvier acts as the trigger region for decisions about AP generation, similar to the initial segment in multipolar cells.
An athlete is told by a coach that light stretching before practice improves muscle performance by activating cross-bridges at a low cross-bridge attachment rate, best accomplished with light, not heavy, loads.
Which of the following best explains the effects of increasing the cross-bridge attachment rate of skeletal muscle fibers?
Increased speed of sarcomere shortening and active tension- This is the correct answer. Increasing the cross-bridge attachment rate increases maximum muscle force. This would create faster attachment of the heavy merromyosin subunits (myosin heads) to the thin troponin subunit binding site on the actin filament. The faster rate of attachment results in faster cross-bridge cycling and increased active tension, the force for purposeful movement.
TAKEAWAY - Faster attachment leads to faster cross-bridge cycling and is produced by the fast-twitch (type II glycolytic) muscle fibers. Slower attachment leads to slower cross-bridge cycling and is produced by the slow-twitch (type I oxidative) muscle fibers.
A 78-year-old woman is beginning to become more unstable when she is upright. On her physician’s advice to build-up her muscle mass she decides to join a gym. She employs a trainer to get started on a regular exercise regimen. The trainer advises the woman to increase her dietary intake of protein to build up the amount of actin and myosin proteins in her sarcomeres.
Which of the following statements best describes the state of actin and myosin filaments within skeletal muscles during a normal muscle contraction?
Actin and myosin both have fixed lengths- This is the correct answer. The active tension produced by a normal sarcomere results from actin and myosin microfilaments of a fixed length sliding past each other.
TAKEAWAY - According to the sliding filament model of muscle contraction, binding of actin and myosin filaments produce cross-bridges and cross-bridge cycling results in a power stroke wherein the actin filaments are pulled toward the middle of the sarcomere. This sarcomere movement results in active tension, the main force for purposeful movement.
A researcher is trying to discover a drug to improve muscle contractility by modulating sarcoplasmic calcium.
Which of the following best describes a drug that block a muscle protein that would result in the highest concentration of Ca2+ in the sarcomere?
SERCA- This is the correct answer. SERCA is the Ca2+ pump that transports Ca2+ from sarcoplasm to terminal cisternae of the sarcoplasmic reticulum against a concentration gradient by active transport. Blocking SERCA increases sarcoplasm (cytoplasm) Ca2+.
TAKEAWAY – SERCA blockade or loss-of-function mutation increases sarcoplasm Ca2+ and muscle contractility. This can be the cause of muscle contracture and muscle spasm.
6-year-old girl is brought to the ER by her parents with chief complaint of sudden onset of muscle spasms in the fingers of one hand. Physical examination reveals a mark resembling a spider bite with inflammation in the surrounding area of the same hand.
Which of the following best describes the physiological mechanism that is likely to decrease this girl’s muscle spasms?
Decreasing permeability of motor neurons to Ca2+- This is the correct answer. Muscle spasm is a high excitability state resulting in uncontrolled muscle contractions. Motor neuron terminals release the neurotransmitter acetylcholine in response to action potentials which increase influx of Ca2+ through voltage gated Ca2+ channels. Decreasing permeability of the motor neuron terminal to Ca2+ by blocking the voltage gated Ca2+ channels will decrease acetylcholine release and should relieve the muscle spasms.
TAKEAWAY – Black widow spider bites are common and inject latrotoxins which increase release of acetylcholine from affected motor neurons. Latrotoxins increase excitation and uncontrolled contractions of the affected skeletal muscles. Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Treatment for muscle spasms are based on inhibiting excitation-contraction coupling mechanisms.
A 26-year-old male athlete is awakened from sleep at night because of painful muscle spasms in both legs following a 3-hour workout at the gym.
Which of the following physiological mechanisms is likely to decrease this man’s night-time muscle spasms?
Increasing plasma Ca2+- This is the correct answer. Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Extracellular fluid (plasma) Ca2+ binds to voltage-gated Na+ channels, thereby regulating the speed of Na+ influx, depolarization, action potential (firing) frequency and release of neurotransmitters such as acetylcholine at motor endplates. Decreasing plasma Ca2+ can produce hypocalcemia which increases the rate of Na+ influx whereas increasing plasma Ca2+ decreases the rate of Na+ influx in motor neurons and skeletal muscles. Decreasing the rate of Na+ influx in motor neurons decreases excitability and release of acetylcholine, thereby inhibiting excitation-contraction coupling mechanisms known to relieve muscle spasms.
TAKEAWAY - Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Administration of calcium increases plasma Ca2+ which, in turn, causes more Ca2+ to bind to voltage-gated Na+ channels and decreases neuronal and muscle excitability. Decreased plasma Ca2+ increase neuronal excitability. Increased plasma Ca2+ decreases neuronal excitability which, in turn, decreases release of acetylcholine, muscle excitability and muscle contractions. Paradoxically, Ca2+ administered to neuronal terminals can increase excitability at excitatory synapses by increasing neurotransmitter release. Increased and decreased plasma Mg2+ also decreases and increases neuronal excitability similarly as plasma Ca2+. Paradoxically, administration of Mg2+ directly to neuronal terminals has the opposite effect as Ca2+ because it inhibits Ca2+ induced neurotransmitter release, thereby decreasing excitability at excitatory synapses.
A man is reporting to his primary care physician that he is being awakened from sound sleep several times a week by sudden onset of muscle spasms. Physical examination is unremarkable.
Which of the following physiological mechanisms is most likely to be responsible for muscle spasms?
Decreasing permeability of motor endplates to K+- This is the correct answer. Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Decreasing permeability of the motor endplates of skeletal muscles will have a depolarizing effect, thereby contributing to the high excitability state and muscle spasms.
TAKEAWAY –Muscle spasm is a high excitability state resulting from uncontrolled muscle contractions. Muscle spasms are produced when excitation-contraction coupling mechanisms are upregulated and activated in an uncontrolled manner.
Note in Figure 6-10 that when the muscle is at its normal resting length, which is at a sarcomere length of about 2 micrometers, it contracts on activation with the approximate maximum force of contraction. However, the increase in tension that occurs during contraction, called active tension , decreases as the muscle is stretched beyond its normal length—that is, to a sarcomere length greater than about 2.2 micrometers. This phenomenon is demonstrated by the decreased length of the arrow in the figure at greater than normal muscle length.
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A woman is undergoing bariatric surgery with general anesthesia. The neuromuscular blocking agent succinylcholine is used to facilitate endotracheal intubation and a volatile halogen anesthetic is employed for the anesthesia. During the procedure, the patient’s body temperature is observed to suddenly increase and her muscles are becoming rigid.
Which of the following receptor locations and mechanisms is most likely to explain the increases in body temperature and muscle tone in this woman?
Hypersensitivity of sarcoplasmic reticular receptors- This is the correct answer. Hypersensitivity of skeletal myocyte ryanodine Ca2+ release channels, sarcoplasmic reticular receptors, has the potential to increase both muscle tone by massive release of Ca2+ into the sarcoplasm which increase cross-bridge cycling without relaxation and the high metabolic rate produced by skeletal myocytes throughout the body has the potential to increase body temperature to a very high level. This occurs in malignant hyperthermia induced by the muscle relaxant succinylcholine and volatile general anesthetics such as halothane during surgical procedures in a person with a gain-in-function mutation of their ryanodine receptor.
TAKEAWAY – Persons with a gain-in-function mutation of a ryanodine receptor gene, most commonly RYR1, are susceptible to experiencing muscle rigidity associated with a marked increase in body temperature as a result of accumulation of Ca2+ in the sarcoplasm of skeletal muscles. This condition is known as malignant hyperthermia, most commonly triggered by administration of succinylcholine and/or volatile halogenated general anesthetics during surgical procedures. Affected persons may be otherwise normal and may not be aware of the mutation until they are undergoing surgery with general anesthesia. Malignant hyperthermia is inherited in an autosomal dominant manner; so, if a parent has had such an adverse reaction previously, the probability is relatively high for one of their offspring experiencing muscle rigidity with hyperthermia during surgery when succinylcholine and/or halogenated volatile anesthetics are used. The treatment for malignant hyperthermia is dantrolene, a ryanodine receptor/Ca2+ channel blocking agent.
Passive tension- This is the correct answer. This image shows the most stretched state of the sarcomere, demonstrated by the largest width of the I-band. This state is associated with increased passive tension.
TAKEAWAY - The vignette scenario is referring to fatigue when skeletal muscle force is weakened; therefore active tension is less than the workload and the only answer choice that is consistent with decreased active tension is increased passive tension, thereby matching the electron micrograph that shows the most stretch. Note that the I-band, the area with only actin filaments, is exhibiting the amount of stretch.
100 kg- This is the correct answer. Power = force x velocity. Load and force are equal during a contraction. Minimum isometric load is the point on the graph where the load or force is maximum and velocity of shortening is zero. According to the graph, the maximum power output of a muscle is developed at approximately one-third of the minimum isometric load. Considering that changes in the 1-RM load reflect changes in the minimum isometric load, the 1-RM load is an approximation of the minimum isometric load. Therefore, 35 kg force (load) is closest to one-third (33.3%) of a 100 kg force (load).
TAKEAWAY – Physical therapists use the 1-RM load, an approximation of the minimum isometric, as an index of muscle strength. Therapeutic exercises are often performed using loads that permit maximum power output, about one-third of the 1-RM load because they are adequate for building muscle strength by increasing the density of sarcomeres (hypertrophy) while minimizing the risk of further injury.
B- This is the correct answer. The normal resting muscle length of any muscle is the point on the graph where active tension is maximal. Notice that it corresponds to the point where passive tension is minimal.
TAKEAWAY – The normal resting length of a muscle is that muscle length where the active tension is maximal, and the passive tension is minimal. This is the point at which the muscle’s sarcomeres are arranged with optimal overlap of actin and myosin filaments prior to contraction.
4 - This is the correct answer. The site on the graph numbered 4 is the only muscle-afterloaded site on the graph.
TAKEAWAY – Afterload is an internal or external force operating on muscle fibers that shortens or compresses their sarcomeres at rest; thereby, providing less space for cross-bridge cycling and decreasing the sarcomeres’ ability to produce maximal (tetanic) active tension. The opposite is true for a preloaded muscle produced by stretching muscle fibers and lengthening their sarcomeres. Such sarcomere lengthening above the muscle’s normal resting length decreases the ability of the sarcomere filaments to create cross-bridges; thereby also decreasing cross-bridge cycling and maximal (tetanic) active tension. According to the length-tension relationship, any load that requires a muscle to contract from a resting (relaxed) length lesser or greater than its normal resting length deceases the maximal active tension that can be generated
Passive tension describes what takes place in our connective tissue. The tendon as well as the Epi, peri and endomysium
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