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Phys Lect 13
| Question | Answer |
|---|---|
| What determines Contractile force? | Number of Cross-Bridges formed between thick and thin filaments. **Each Cross-Bridge generates 4pN of force** |
| Regulation of Cardiac muscle | All cardiac muscle contracts every beat. Therefore inc/dec for must apply to ALL the myocardia **Tetany IMPOSSIBLE** |
| Regulation of Skeletal muscle | Amount of muscle recruitment varies depending on need. Tetany is possible due to shorter APs. **More fiber recruitment for more force generation |
| Muscle regulation through Ca2+ release. | More regulation with cardiac muscle since Ca2+ release from the SR is based mostly on Ca2+ influx through DHPR. **Skeletal muscle has less regulation through Ca2+ due to the paired DHPR and RyRs. |
| Cardiac muscle: Increased Intracellular Ca2+ | Increases the force of contraction. Greater Ca2+ influx through DHPR, activating more RyRs to release SR Ca2+. This Ca2+ binds to more Troponin C allowing the formation of more cross-bridges -> More force. |
| SR [Ca2+] : Force of contraction | Inc SR [Ca2+], Inc force of contraction. Dec SR [Ca2+], Dec Force of contraction |
| How could the plasma membrane Ca ATPase and Ca-Na Antiporter affect muscle contraction force? | 1.Increased activity: Decrease force due to dec intracellular Ca2+ available to pumped back into the SR for future contractions. 2.Dec Activity: Inc force of contractions due to higher intracellular Ca2+ |
| Increasing SERCA pump activity | 1.Increases the force of contractions via increasing SR [Ca2+]. 2.increases the rate of relaxation b/c of rapid Ca2+ removal |
| Decreasing SERCA pump activity | 1.Dec Force of contraction. 2.Dec rate of relaxation. |
| 4 ways to increase contractile force in cardiac muscle | 1.Dec Ca ATPase, Na-Ca Antiporter activity. 2.Inc SR Ca. 3.Inc SERCA activity. 4.Allow more Ca to enter through the DHPR (phosphorylation by PKA). |
| What type of cardiac receptors does Epi/norepi bind to? | Beta Androgenic receptors. |
| How is PKA activated and how does it influence contractile force in cardiac muscle? | Epi/norepi-bound b-Androgenic receptors activate cAMP which activates PKA. PKA Increases contractile force by phosphorylating: 1.A SERCA pump regulator (preventing inhibition of SERCA pump). 2.DHPR (allows more Ca2+ influx) |
| How is force increased in a skeletal muscle fiber? | summation of twitches. (due to the relative refractory period, an increase in twitchs will build on eachother generating greater force). |
| Ca2+ concentrations during low frequencies of skeletal muscle twitch summation | Ca2+ concentrations increase and decrease with each twitch. |
| Ca2+ concentrations during high frequencies of skeletal muscle twitch summation | TETANY. Ca2+ levels remain elevated |
| Motor unit recruitment in skeletal muscle | 1.Small motor units (slow twitch): recruited first during low force requirements, usually for FINE motor control. 2.Large motor units (Fast Twitch): recruited in during high force demands. |
| Tension | (Force of contraction) The force that can cause a shortening of the muscle. **Bringing two ends closer together |
| Increased ventricular filling/volume | Causes an increased force of contraction generated by the ventricles because they have a greater distance to shorten = greater tension (explained by the length-tension relationship). |
| Isometric contraction | Tension without shortening. **Ex: pushing against a wall. |
| Isotonic contraction | Muscle shortening against a constant load. **Ex: lifting weights |
| Isometric ACTIVE Tension | is the tension generated by the actin-myosin interaction (crossbridges). **Total tension - Passive tension |
| Length-tension relationship: Resting Skeletal versus Cardiac muscle | 1.Skeletal: rests at the optimum length for max cross-bridging (therefore tension will not increase if they are stretched). 2.Cardiac: rests at a shorter length than its optimum length for max cross-bridging (this is why tension inc when stretched) |
| Short Sarcomere length | will not generate a lot of force due to too much actin-myosin overlap (they have no more room to power-stroke and bring the z-lines closer together). |
| Long sarcomere length | Will not generate a lot of force due to the inability of the myosin heads to reach the actin and form cross-bridges. |
| Load-velocity relationship | Inversely related. Smaller load/weight = faster velocity b/c there are more spare cross-bridges available/ not being used to counter the weight. **Max vel = 0 Load (lots of spare cross-bridges). Max Load = 0 vel (no spare cross-brides) |
| Cross-Bridge formation: Tension vs velocity | 1.Tension (NO SHORTENING): depends on the total # of static cross-bridges that can be formed. 2.Velocity (SHORTENING): depends of the total # of spare cross bridges available (the cross-bridges formed to counter the weight are NOT available). |
| Steps of regular muscle contraction | 1.Isometric contraction (forming cross-bridges to counter the wgt). 2.Isotonic contraction (wgt stays same but movement occurs). 3.Isotonic relaxation (muscle returns to originial length). 4.Isometric relaxation (cross-bridges to counter wgt are freed) |
| Skeletal Muscle: Red Fibers | 1.Type 1. 2.Slow Twitch. 3.Oxidative metabolism (Aerobic). 4.NO FATIGUE |
| Skeletal Muscle: White Fibers | 1.Type IIb. 2.Fast-twitch. 3.Glycolytic metabolism (Anaerobic). 4.EASILY FATIGUED (lactic acid build up) |
| How does Myosin ATPase affect the velocity? | Directly related. Inc myosin ATPase activity, Inc velocity of contraction. **Vel is dependent on the available cross-bridges, but those are useless without the ability to rapidly hydrolze ATP so the myosin heads can bind to actin. |
Created by:
WeeG
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