Chapter 12 Muscle Physiology - Important Questions: 6. Mechanism of Muscle Contraction
Chapter 12 Muscle Physiology - Important Questions: 6. Mechanism of Muscle Contraction
Chapter 12 Muscle Physiology - Important Questions: 6. Mechanism of Muscle Contraction
a. Skeletal muscles are multinucleate and have striations (light and dark bands arrangement).
b. Cardiac muscles are uninucleate, have striations, branching and intercalated discs with gap junctions.
c. Smooth muscles are uninucleate, no striations, spindle shaped and may have gap junctions.
a. Thick and thin filaments myofibril muscle fiber = cell (covered by endomysium) fascicle
(covered by perimysium) muscle (covered by epimysium). All connective tissue coverings are
continuous with tendon.
a. In a relaxed muscle it covers the binding sites of actin for cross-bridges of myosin.
a. Troponin has a binding site for Ca2+. When Ca2+ joins troponin undergoes conformational change and
pulls the tropomyosin away and exposes the binding sites.
A motor neuron has many terminal branches ending in knobs. A terminal knob neuron and motor end plate of
sarcolemma lie very close across synaptic cleft and form a neuromuscular junction. Motor end plate has
receptors for acetylcholine secreted by terminal knob.
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9. How does nervous stimulus pass through synaptic cleft? List the main events.
c. Acetylcholine binds to receptors in postsynaptic membrane = motor end plate and opens Na+ channels.
10. How many action potentials of neuron needed to cause action potential of motor end plate?
a. 1 action potential of neuron is sufficient to produce action potential of motor end plate.
11. What breaks the continuity of depolarization once the motor end plate gets depolarized?
a. Acetylcholine detaches from receptors when the motor end plate gets depolarized. Enzyme
cholinesterase present in the synapse breaks acetylcholine acetate + choline. Terminal knob
reabsorbs the choline.
a. Depolarization wave travels from motor end plate to sarcolemma and enters t-tubules = invaginations of
sarcolemma. Depolarization wave travels deep into muscle fiber through t-tubules.
a. Depolarization of t-tubules causes depolarization of terminal cisternae that lie on each side of t-tubule.
The fall in voltage activates Dihydropyridine receptors; that open Ryanodine receptors and Ca2+ ions
move out in cytosol.
14. Explain the 4 steps of cross-bridge cycle. (A = actin, M = myosin, M.ADP = period represents a
bond between myosin and ADP) Also study fig 12.9.
a. Cross bridge binds to actin. In this stage cross bridge is already in cocked up position due to energy
provided by earlier cycle. ADP + Pi are attached to the binding site of cross-bridge.
b. Cross bridge moves to pull actin by using the provided by release of ADP + Pi
c. ATP binds to the cross bridge and provides energy for detachment of cross bridge.
d. ATP breaks into ADP + Pi and cross bridge returns to original cocked up position by using this energy.
i. A + M.ATP A + M.ADP.PI
15. What keeps the muscle contracted continuously and what ends the contraction?
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a. A series of action potentials from neuron keeps the muscle contracted by keeping Ca2+ in cytosol. When
action potentials of neuron stop motor end plate – sarcolemma – t-tubule – terminal cisternae get
repolarized. Ca2+ are actively pumped by Ca2+ ATPase. The fall in Ca2+ in cytosol brings the change in
conformation of troponin-tropomyosin and covers the binding sites of actin.
a. Contraction means turning on of Cross-Bridge-Cycle. It may or may not result in shortening of a muscle.
a. Isometric Contraction – muscle generates tension (force) but maintains length. For example holding a
weight in hand without moving the arm or trying to push immovable weight.
b. Isotonic Contraction – muscle changes length but maintains tension. For example after lifting a weight
in hands, flexing your arm; tension remains same but muscle shortens (a concentric contraction).
c. A lengthening (eccentric) contraction – tension generated by cross bridges of muscle is less than the
load (weight) carried by muscle. It increases the length of muscle though the cross bridge cycle is on. For
example the lengthening of quadriceps muscles in femur allows you to lower yourself to a seat. Fig 9.18
a. When a 2nd stimulus is applied before the completion of 1st twitch, it results in a greater contraction
called summation because it sums the 2 contraction.
a. A fast series of stimulations resulting in a continued contraction at maximum level is called tetanus. It
can by unfused tetanus if you can see individual contractions. A very fast series of stimulations causes a
fused tetanus when we cannot see individual contractions.
21. What is the relationship between length of muscle fiber and isometric tension?
a. Maximum isometric tension is produced at optimal sarcomere length (L0) due to optimal overlap of actin
and myosin filaments. Both increase and decrease in sarcomere length decrease the isometric tension.
c. Power stroke – the bending of cross-bridge to pull actin toward center of sarcomere.
24. Write briefly about 3-ways how ATP can be generated in a muscle fiber?
A muscle is fatigued when it fails to contract in the presence of neural stimulus. Main 3 causes are:
b. Accumulation of inorganic phosphates in cytosol of muscle cell during short term maximal exertion.
Slow Oxidative fibers = Type - 1 Fast Oxidative-Glycolytic = Type 2 Glycolytic Fibers = Type 3
• Many capillaries, many • Many capillaries, many • Few
mitochondria mitochondria capillaries/mitochondria
• High myoglobin – red muscle • High myoglobin – red muscle • Low – white muscle fiber
fiber fiber
• Glycolytic enzyme activity low • intermediate • high
• Fiber diameter and motor unit • Both intermediate • Both large
small
• Contraction velocity slow • fast • fast
a. Muscle fiber and motor units obey all or none principle but muscles do not. CNS can make a muscle
generate greater tension by activating a greater number of motor units.
a. Frequency of action potentials – a minimal fast series of action potentials to generate maximal fused
tetanus contraction.
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b. Length of fiber – optimal length of sarcomeres needed to produce maximum tension
d. Fatigue
29. Why do many poisons like arrowhead poison cause paralysis of muscles?
a. They inhibit neuromuscular junctions by strongly binding to Ach binding sites without opening Na+
channels.
a. Duchenne muscular dystrophy. It is due to a mutation of a gene on X-chromosome which alters the
structure of protein Dystrophin needed for attachment of cytoskeletal muscles to membrane and
integrity of membrane.
31. Name an autoimmune disorder of muscles leading to chronic muscle fatigue and weakness.
32. Name the involuntary contraction of skeletal muscles (may occur due to excessive muscle activity).
a. Muscle Cramps – reasons not fully understood yet but may be due to electrolyte imbalance.
a. Single-unit smooth muscle fibers lie in vessels and hollow organs and multi-unit smooth muscle fibers –
example is hair arrector pili muscles of integument.
34. What is the arrangement of thick and thin filaments in smooth muscle fibers?
a. They do not form striations of dark and light bands. Thin fibers lack troponin. Thin fibers are attached to
either cell membrane or Dense bodies present in cytosol. In function dense bodies are similar to Z-lines.
Contraction is due to sliding of thin filaments over thick filaments.
36. Which muscle fiber is likely to have spontaneously generated action potential s by pace-makers (no impulse
needed from CNS)?
a. Single unit smooth muscle fiber and some cardiac muscle fibers (SA node of heart).
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37. What is the site of Ca2+ regulation in smooth and skeletal muscle fibers?
a. Cytosolic Ca2+ level gets high due to its release by varicosities of SR and its entry through membrane
channels.
d. Myosin-light-chain kinase uses ATP to phosphorylate (add phosphate) to myosin cross bridges.
f. Cross bridge cycle produces tension and shortening. (it operates similar to a skeletal muscle fiber).
Smooth muscle fibers are stimulated by autonomic nerve fibers. Instead of ending into terminal knobs the axon
branch into beaded branches and neurotransmitters are released by beads = varicosities. In addition single unit
smooth muscle fibers have gap junctions over most cells. Therefore if a few cells are depolarized the action
potentials pass through gap junctions to next cells, making all cells in group to contract simultaneously = single
unit.
40. What are pace-maker potentials? How do they change to action potentials?
Smooth muscle fibers of GI tract and some cardiac muscle fibers continuously generate graded potentials less
than threshold stimulus. When an excitatory input, like entry of food to a segment, is added these potentials
cross threshold and change to action potentials. GI tract, heart and some neurons in CNS can contract
rhythmically in absence of neural stimulation.
They are branched and have special end plates = intercalated discs with gap junctions.
a. Both have striations of dark and light bands due to similar arrangement of thin and thick filaments in
sarcomeres.
43. Why are skeletal muscle fibers fast contracting and cardiac smooth muscle fibers slow contractors?
a. Action potential of skeletal muscle fibers is like a spike. It persists only for 1-2 milliseconds. It develops a
faster contraction which also relaxes at a fast rate.
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b. Action potential of cardiac muscle fibers develops rapidly but remains high for about 250milliseconds.
The cardiac muscle contraction develops slowly and starts declining only after about 200milliseconds.
This suits the working of heart because heart muscle needs to pump blood but then relax to allow filling
of the atria and ventricles.