muscle physiology notes

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Muscle physiology: Lab 2 Action Potential: self-propagating electrical impulses produced by muscle and nerve cells. Resulted from the Na and K movement across cell membrane. Resting membrane potential: membrane potential (electrical difference-mV between in-cell and out-of-cell) when muscle and nerve cells are at rest Muscle contraction 1. Nerve action potential reaches the synaptic knob 2. Knob’s membrane becomes more permeable to interstitial calcium ions present in the synaptic cleft. 3. Ions diffuse into the knob and activate the secretory vesicles containing neurotransmitters. 4. Neurotransmitters bind to docking protein of presynaptic membrane and release ACh into the synaptic cleft 5. The sarcolemma at the synaptic cleft is folded into a motor end pate and contains ACh receptor sites. 6. ACh binds to receptor, the muscle fiber responds by producing a muscle action potential which spread across the entire muscle fiber surface and along the T-tubule a. Na flood through Sodium channels in the sarcolemma (muscle fiber cell membrane) into muscle cells, and leads to depolarization (membrane become less negative). b. At the peak of depolarization, sodium channels close and potassium channel open, with K ions exiting the fiber and causing repolarizes to resting potential. 7. The electrical current travels along the sarcolemma and down the transverse tubules inside the muscle fiber. 8. Current stimulates the release stored calcium ions from the cisternae of the sarcoplasmic reticulum. 9. Calcium floods the sarcoplasm inside the muscle fiber, contraction occurs.

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Biology 153 at University of British Columbia

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Muscle physiology: Lab 2Action Potential: self-propagating electrical impulses produced by muscle and nerve cells. Resulted from the Na and K movement across cell membrane. Resting membrane potential: membrane potential (electrical difference-mV between in-cell and out-of-cell) when muscle and nerve cells are at restMuscle contraction1. Nerve action potential reaches the synaptic knob 2. Knobs membrane becomes more permeable to interstitial calcium ions present in the synaptic cleft. 3. Ions diffuse into the knob and activate the secretory vesicles containing neurotransmitters.4. Neurotransmitters bind to docking protein of presynaptic membrane and release ACh into the synaptic cleft 5. The sarcolemma at the synaptic cleft is folded into a motor end pate and contains ACh receptor sites. 6. ACh binds to receptor, the muscle fiber responds by producing a muscle action potential which spread across the entire muscle fiber surface and along the T-tubulea. Na flood through Sodium channels in the sarcolemma (muscle fiber cell membrane) into muscle cells, and leads to depolarization (membrane become less negative). b. At the peak of depolarization, sodium channels close and potassium channel open, with K ions exiting the fiber and causing repolarizes to resting potential. 7. The electrical current travels along the sarcolemma and down the transverse tubules inside the muscle fiber. 8. Current stimulates the release stored calcium ions from the cisternae of the sarcoplasmic reticulum. 9. Calcium floods the sarcoplasm inside the muscle fiber, contraction occurs. 10. Muscle fiber relaxation: Fibers produces AChE (acetylcholinesterase), which deactivates Ach, sarcolemma no longer produces an action potential. Active transport pumps calcium ion in the sarcoplasm back into the sarcoplasmic reticulum. a. Calcium ion unbind troponin and tropomyosin moves into place to block the active sites on actin. This blocks cross-bridge attachment, and thin filaments slide outwards away from the middle of each sarcomere. The sliding filament theory (current muscle contraction model) During muscle contraction, filaments slide past on another, causing the fibers (sarcomere chain) to shorten. Thin filaments (mainly protein actin) are pulled inward by the pivoting of myosin heads of the thick filaments. Zone of overlap increase during muscle contraction. H-Zone: (within A zone) mainly myosin thick filament with no thin filament overlap, shorten during contraction I-Band: mainly actin protein (thin filament with no thick filament overlap) shorten during contraction

Z-Line: boarder of sarcomere. Within I-Band. Z-lines move closer together during contraction. A-Band: entire length of a thick filaments. Remains the same during contraction. The contraction involves 5 chemical steps. 1. Active-site exposure: active site is located on the thin filament where myosin head can bind to an actin molecule. a. At Rest: Troponin holds tropomyosin molecules in pace to cover the active sites on the actin filaments. b. Stimulation: Calcium ions rush into sarcoplasm (passive?), bind to troponin and cause the tropomyosin to roll away, in-turn exposing the active site to myosin heads. Active site remain exposed as long as calcium ions are bound to troponin molecules, so tropomyosin molecules unblock active site. 2. Cross-bridge attachment: actin and myosin have a strong affinity for each other. Once active sites on actin molecule are exposed, the myosin heads chemically bind to the sites. 3. Pivoting: myosin head uses stored energy to pull thin filaments toward the M line of the sarcomere, causing the entire muscle fiber to contract. Myosin are depleted of stored energy and release the ADP and phosphate into sarcoplasm. a. At Rest: myosin heads split ATP and become energized by storing the energy released from the split4. Cross-bridge detachment: ATP molecule binds to each head and cause it to back out of active site. The heads are now ready to be reenergized for another attachment-pivoting sequence.5. Myosin reactivation: myosin heads reenergize by splitting ATP to return to resting position. ATPase is located on the myosin head. a. Attachment, pivoting, detachment, and reactivation sequence repeats until all calcium ions are removed from sarcoplasm and returned to the sarcoplasmic reticulum. Type of Muscle ContractionMotor unit: any group of muscle fibers controlled by the same motor neuron. Contract together when stimulated. One motor neuron can control multiple fibersAll-or-None Principle: muscle fibers are said to be on for contraction or off for relaxation Twitch: Single stimulation-contraction-relaxation event. Single action potential occurs in the neuron, only a small amount of ACh is released.small amount of calcium ions are released. Myogram: recording of muscle contractions for compassion. Fast-> slow twitches: eye, gastrocnemius, and soleus. Each twitch has: Latent Period: Time from initial stimulation to the start of muscle contraction. Muscle fibers are stimulated by ACh -> release calcium ions. Exposes active sites, leads to cross-bridge attachment. Contraction Period: myosin head pivot to shorten fiber and produce muscle tension. Cycles through attach-pivot-detach-return sequence. Increase in calcium ions in sarcoplasm: more cross-bridges are formed and tension increases during contraction. Relaxation phase: ACHe inactivates ACh and calcium ions are actively transported to the sarcoplasmic reticulum. The thin filaments passively slide back to resting position, and muscle tension decreases. Contraction type (doesnt determine the overall tension a muscle produces)Treppe: muscle contraction with complete relaxation between each stimulus. Repeat muscle stimulation, calcium ion accumulate in sarcoplasm, causing the first 30-50 contractions to increase in tension. Wave Summation: Increasing the frequency at which a skeletal muscle is stimulated. If the muscle is stimulated a second time before it has completely relaxed from a first stimulation, then the two contractions are summed. Increase in tension with each summation. Ie. More calcium ions in the sarcoplasm and more cross-bridges. Incomplete tetanus: further increase in frequency of stimulation, to produce peak tension with short cycles of relaxationComplete tetanus: increase frequency of stimulation until relaxation phase is completely eliminated. All muscle work require complete tetanus to do work. Isometric contraction: muscle length is relative constant but muscle tension changes. Ie. Maintain posture Isotonic contraction: constant tension while the length of the muscle changes. Is. Flex arm while holding book. Muscle strength: depends on the number of motor units activated. Recruitment: stimulates more motor units to carry or move a load placed on a muscle. Tension increases as more motor units contract. Fatigue: the force of contraction decreases as fibers lose the ability to maintain complete tetanic contraction. Caused by decrease in cellular energy and oxygen sources in the muscle and an accumulation of waste products. Low ATP levels, build-up of lactic acid (by product of anaerobic respiration).

Cardiovascular physiology Lab 3Cardiac Cycle: one complete heartbeat. Each atrium and ventricle contracts and relaxes once. Systole: the contraction phase of a chamber. Squeezing of chamber walls cause an increase in blood pressure in the heart and arteries Diastole: the relaxation phase of a chamber. Relaxation of chamber wall causes decrease in blood pressure in the heart and arteries. ~75 cardiac cycles/minutePhases of Cardiac Cycle: 8 seconds1. Atrial systole (1 second): atrial systole pumps 30% of blood, fluid pressure and gravity force the remaining 70% of blood into relaxed ventricles. 2. Atrial diastole and Ventricular systole (~4 seconds): Phase I ventricular contraction push atrialventricular valves closed. Semilunar valves are also close. Phase II: Ventricular pressure exceeds pressure in pulmonary artery and aorta, the semilunar valves are open, and blood is ejected.

3. Ventricular diastole (~4 seconds): Early: ventricles relax, pressure in ventricles drops, blood flows back against cusps of semilunar valves and forces them closed. Blood flow into the relaxed atria Late: all chambers relaxed, ventricles fill passively. AV valves are open, blood fill from atrial to ventricle. SL valves are closed to prevent backflow of blood from aorta into the left ventricle (pulmonary valve), and from the pulmonary artery to the right ventricle (aortic valve).

Lab Activity 1: listening to heart soundsAuscultation: listening to internal sounds of the body. Soft bone and tissue overlying heart deflect the cardiac sound waves located lateral to the valves. Auscultation of heart: evaluate valve function, and heart sounds S4: Contraction of atria. Lubb: S1, closure of AV valves during contraction (systole) phase of ventricles. Dupp: S2, closure of SLvalves at the beginning of relaxation (diastole) phase of ventricles. S3: blood flowing into the ventricles from the atrium through the AV in the late phase of ventricle diastole Murmur: holes in chamber walls, as blood pass through. Or turbulent flow in heart chamber. Stethoscope: amplify sounds to an audible level. Bell: flat metal disk placed on skin, contains diaphragm touch skin to amplify sound. Lab Activity 2: determining blood pressure Blood pressure: Measure of the force the blood exerts on the walls of the systemic arteries. 120/80 mm Hg for males, 110/70 mm Hg for females Systolic pressure: left ventricle constrict to pump blood through the semilunar valve into the aorta Diastolic pressure: when the left ventricle relax, and less blood flow into the aorta. Sphygmomanometer: inflatable cuff to measure blood pressure. Pressure gauge to read pressure Rubber bulb to inflate the cuff Valve close/ open to hold/release pressure, respectively. Orientation arrow: line with antecubitis Placed just above elbow, inflated to 160 mm Hg to compress and block blood flow from bronchial artery. Stethoscope is placed on antecubital region, and pressure is gradually vented from cuff. Pressure in cuff is slightly less than pressure in the brachial artery, blood spurts through the artery and the turbulent flow makes korotkoffs sounds. The pressure on the gauge that match the first sound is the systolic pressure As more pressure is relieved from the cuff, blood becomes less turbulent. Pressure at the last faint sound is the diastolic pressure. Hypertension: High salt intake leads to increase in blood volume (osmosis), and high blood pressure.Effect of posture on BPSupine posture (on back): higher BP for both systolic and diastolic Effect of exercise on BP Mean arterial pressure (MAP): First determine pulse pressure: difference between diastolic and systolic pressures. Systolic-diastolic= 1/3 pulse pressure + diastolic pressure= MAP Lab activity 3: measuring the pulse Pulse/pressure waves: determine the heart rate. It is the change in vessel diameter from ventricular systole, bp increase to expand arterial walls, and then ventricular diastole, bp decrease to relax artery diameter. Pulse is felt at various pressure points: Radial artery on the lateral forearm just superior to the thumb. Common carotid artery in the neck Popliteal artery of the posterior knee. Activity 4: Biopac: ElectrocardiographyElectrocardiogram (ECG): a recording of impulses: seconds x-axis, amplitude and intensity (mV) on y axis Isoelectric line: straight baseline P wave: atria depolarize for contraction. Atrial systole occur 0.1 second after depolarization Q-R-S complex: depolarization of the ventricles, repolarization of atria (undetected). Next is ventricle systole T-Wave: ventricle repolarizationIntervals: include wave and return to baseline. P-R interval: includes the start of p wave and the start of Q-R-S complex Q-T interval: start of Q wave to the start of T wave. From ventricular depolarization, to ventricular repolarizationSegment: baseline recording between any two waves P-R segment: time for impulse to travel from AV node to the ventricles. S-T segment: delay between ventricular depolarization and repolarization.Arrhythmias: irregular heartbeat.Activity 5: Biopac: electrocardiography and blood volume Plethysmogram: recording of how the volume of blood at a given pressure point in the body changes as a pressure wave passes through the point. Wave flow along the arteries, the vessel walls will first expand and then rebound to its original size.