Muscle Force and Mechanisms of Contraction Flashcards Preview

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Flashcards in Muscle Force and Mechanisms of Contraction Deck (26):

What is agonist vs antagonist vs synergist muscle?

agonist - muscles for which contraction leads to motion
antagonist - muscle that moves joint opposite to agonist motion
synergist - muscle that assists another muscle to accomplish a movement


What constitutes the load of skeletal muscle?

1. Skeleton
2. External load
3. Load to overcome passive resistance to contraction of agonist muscle
4. Load to overcome passive resistance to stretch of the antagonist muscle


What is meant by pinnation?

Pennate muscle form a common oblique angle with a tendon, so contraction does not move tendons as far as parallel muscles, but produces a greater physiological cross-sectional area


What is the law of laplace? How is it transformed for hearts?

Tension = Pressure * Radius

Wall stress = (Pressure * radius) / (wall thickness)

Thus, greater wall thickness = reduced stress on vessels


For a pennate muscle contractile force, what two vectors run at 90 degree angles?

Tension runs at a right angle to the targeted force (in the direction of the tendon)


What is the function of tension generated on veins?

Important in maintaining blood flow from feet back to heart


What is muscle hypertrophy?

An increase in the number of sarcomeres (not muscle fibers / myocytes though)


What is the function of cardiac contraction and what happens in response to increased blood pressure?

Contracts longitudinally create tension to counteract wall stress. There are concentric layers of cardiac muscles to create tension. Since blood pressure increases wall stress, cardiac cells hypertrophy to counteract that stress


What is the function of arterial smooth muscle? Why don't capillaries need smooth muscle?

Creates tension to offset wall stress. Capillaries need no smooth muscle because capillaries have a tiny radius and thus require little tension to offset the pressure


What is the function of titin?

Traverses the entire sarcomere to keep the thin and thick filaments aligned


What are the steps of the crossbridge cycle of the actinomyosin ATPase, starting with the actin being exposed by troponin-C binding calcium? What is the power stroke?

Crossbridges form:
1. Activated myosin head binds to actin
2. Power stroke - MYOSIN undergoes conformational change, releasing phosphate and using energy to pull actin backwards

Crossbridges break:
3. ATP binds myosin, causing it to unbind actin
4. ATP is hydrolyzed on myosin, returning to resting state and ADP is released.


What is continued contraction dependent on?

Typically, the amount of calcium available. ATP is generally not limiting.


In excitation-contraction coupling of cardiac muscle, what channels are open during the peak rate of force development and the peak rate of relaxation?

Peak rate of force development - contraction phase - L-type (longlasting) Ca+2 channels on T-tubules, and RyR receptor on SR

Peak rate of relaxation - SERCA - Sarcoplasmic / endoplasmic reticulum ca+2 ATPase, to pump Ca+2 back into the SER


What does the maximum rate of rise of the myocyte twitch depend on?

The isoform of the myosin in the myocyte - fast twitch vs slow twitch


What is the function of the sarcolemma / T-tubules of the sarcolemma for EC coupling?

Voltage gated sodium channels trigger L-type Ca+2 channels, which are longlasting dihydropyridine receptors (DHPR). These serve to cause the influx of "trigger calcium" which binds to Ryanodine receptors (ryanodine-sensitive Ca+2 channel)


What channels exist on the sarcoplasmic reticulum which influence EC coupling? What is spark vs transient?

1. SERCA - priamary control of lowering intracellular Ca+2 by pumping it into the SR
2. RyR - Ca+2 transient release - coordinated Ca+2 release.
Spontaneous = sparks, small increases in intracellular calcium which cause slight depolarization but not a full contraction


What exchangers maintain the ion gradients of muscle cells?

1. Na,K-ATPase
2. Na,Ca-exchanger (NCX), Cannot pump as much Ca out whenever digitalis has destroyed sodium gradient


What is the resting potential of myocytes?

-80-90 mV


What are the different isoforms of the L-type Ca+2 channel in each striated muscle type?

Skeletal muscle - Voltage dependent 1.1 - interacts directly with RyR to make a voltage-induced Calcium release (does not release calcium into the sarcoplasm)

Cardiac muscle - Voltage dependent 1.4 - interacts with RyR via calcium-induced means by producing a transmembrane Ca+2 current.


Why does the max peak of force from EC coupling happen after transient Ca+2 is almost down to rest?

Because calcium remains bound to troponin even after myoplasmic calcium levels have dropped (takes a while for the protein to release calcium)


What isoform of L-type Ca+2 channel is in smooth muscle?

Voltage dependent 1.2 - conducts Ca+2 which activates proteins such as calmodulin, is not dependent on RyR.


How does smooth muscle contract?

Ca+2 regulates the thick filament rather than the thin filamen by binding calmodulin, a protien homologous to troponin. Calmodulin activates myosin light chain kinase.

Phosphylated myosin light chains via MLCK will allow for contraction


What is the latch state of smooth muscle and what stops it?

Latch state is the ability of smooth muscle to be contracting for long periods of time. Inactivated my myosin light chain phosphatase.


What is the cause of malignant hyperthermia?

RyR1 (skeletal muscle) point mutations will lead to leak of Ca+2 into cytoplasm if costimulated by anesthetic agents - important in surgery.

This leads to chronic SERCA activation and overheating


What is the cause of catecholaminergic polymorphic ventricular tachycardia?

Ryr2 (cardiac muscle) point mutation leading to leak of SR Ca+2, especially following co-stimulation by catecholamines.

Important in ventricular arrythmias


What are the two common types of muscular dystrophy and their causes?

X-linked disorder caused by dystrophin / dystroglycan complex mutations, a structure which couples myofilament contraction to cellular contraction.

Duchenne - frameshift causing premature termination in mRNA

Becker - splicing of exons that preserves reading frame so dystrophin is partially functional