Muscular System Flashcards

Question

Requirements for contraction

Answer 1

1. Neuron stimulation of muscle fiber 2. Generation, spread of electrical current (action potential) along muscle fiber sarcolemma 3. Rise in muscle fiber intracellular Ca2+ -triggers contraction Excitation-contraction coupling

Answer 2

• Transmembrane potential: – Uneven (+/-) charges across sarcolemma membrane - negative inside sarcoplasm vs outside – Muscle fiber stimulated by neuron activity: Na+ moves in, K+ moves out = change in transmembrane potential – Excitation (action potential produced)- contraction coupling

Answer 3

• Neural control of skeletal muscle contraction – Axon of somatic motor neuron in brain, spinal cord extends out to skeletal muscle fiber • Action potential (electrical signal) travels along axon of neuron • Converted to chemical signal (ACh) to stimulate muscle fiber • Produces action potential (electrical signal) in muscle fiber which results in contraction – Neuromuscular junction (NMJ): • Communication site between neuron- muscle cell • Neuromuscular junction (NMJ): (type of synapse- communication site between neuron and another cell (ie. muscle fiber, neuron)) 1. Axon terminal (neuron) • Synaptic vesicles with chemical neurotransmitter: acetylcholine (ACh) 2. Synaptic cleft: small liquid-filled space between neuron and muscle fiber 3. Motor end plate (muscle cell sarcolemma) • One muscle fiber controlled by only one motor neuron • Sarcolemma in folds

Answer 4

• Excitation: electrical change (action potential) in the neuron axon leads to action potential in the muscle fiber 1. Neuronal action potential (electrical signal) arrives at neuron’s axon terminal: – Causes Ca2+ entry into terminal 2. Ca2+ entering neuron axon terminal causes release of acetylcholine (chemical signal) from neuron axon terminal into cleft – Electrical signal (AP) has been turned into chemical signal (ACh) – ACh diffuses across synaptic cleft to motor end plate – ACh binds to ACh receptors on protein ion channel in muscle fiber sarcolemma (motor end plate) 3. When Ach binds sarcolemma protein ion channel (type of ligand-gated ion channel) –channel open – A lot of Na+ moves in, some K+ moves out – why? – Extracellular Na+ > intracellular Na+ inside muscle fiber SO............ Na+ rushes into sarcoplasm!! = depolarization (more + charge inside fiber) 4. Na+ entry starts action potential (AP) in sarcolemma – Na+ entry causes more voltage sensitive Na+ channels to open – Forms AP and spreads along sarcolemma (propagation) • Continues in one direction as more voltage sensitive ion channels open – AP spread (excitation) will lead to sliding of actin and myosin filaments (contraction): Excitation- contraction coupling!! (stay tuned)

Answer 5

• Both Ca2+ and energy (ATP) needed for contraction • Calcium in general – Intracellular cytoplasmic [Ca2+] kept low – Stored in sarcoplasmic reticulum (SR)....terminal cisternae – Important for muscle contraction: released from terminal cisternae into sarcoplasm

Answer 6

• AP moves along sarcolemma and down T-tubules – AP causes Ca2+ channels in sarcoplasmic reticulum to open – Ca2+ released from SR terminal cisternae – Large amount of Ca2+ enters sarcoplasm at zones of overlap • Excitation coupled to contraction: effect of Ca2+

Answer 7

• Resting sarcomere before contraction starts – Myosin head energized (cocked position) – Energy stored in head as a result of prior ATP breakdown • Will be used to power contraction – Tropomyosin covers myosin binding sites on actin 1. Contraction cycle start – Ca2+ from SR terminal cisternae released within zone of overlap 2. Active sites exposed – Ca2+ binds troponin • Changes troponin shape • Tropomyosin rolled off myosin binding sites on actin • Allows actin and myosin to interact 3. Cross bridge formation: “attach” – Myosin heads (which were in cocked position from previous cycle) bind to exposed active sites on actin – Form cross-bridges 4. Powerstroke: “pull” – ADP and Pi released – Cocked myosin head pivots – Pulls on actin, slides actin past myosin filaments towards M line 5. Cross bridge detaches: “release” – Another ATP binds to myosin to cause cross- bridge release – Myosin and actin link broken – If active sites on actin still exposed: bind another myosin 6. Myosin reactivation: “reset” – ATP split by ATPase in myosin head →energy used to re-cock myosin

Answer 8

• Neural stimulus ends • AChE breaks down ACh • Membrane returns to normal resting transmembrane potential End of muscle excitation: relaxation

Answer 9

• SR Ca2+ channels close, Ca2+ returns to SR – Ca2+ pumped (requires ATP!) into terminal cisternae – Takes longer than release: relaxation takes longer than contraction • Troponin-tropomyosin return to normal – Active sites covered, no cross bridges • Rigor mortis? • Note: ATP needed for contraction and relaxation!

Answer 10

• Starting sarcomere length affects tension (force of contraction) produced • Affects number of cross bridges that can form • Optimal starting sarcomere length? – 100% resting length and moderate range around (80-120% resting length) -allows optimal overlap of filament • Starting sarcomere length too short or too long? – can not form optimal # of cross bridges, affects filaments sliding/tension

Answer 11

• Understand contraction of muscle fiber to understand contraction of skeletal muscle!! • Muscle twitch: contraction of muscle fiber (or skeletal muscle) – In response to motor neuron stimulation – Produces tension: pulling force • Measure of force of muscle contraction – Single twitch: not enough tension to perform work (ie. move object (load))

Answer 12

• Latent period – No tension yet but excitation! – AP spreads, SR releases Ca2+ • Contraction period – Tension (force of contraction) peaks – Ca2+ binding troponin – Myosin binding sites on actin exposed- cross bridges form – If tension> load, muscle shortens • Relaxation period- longer – Ca2+ pumped into SR – Cross bridges detach, tropomyosin covers active sites – Tension returns to resting

Answer 13

• Amount of tension produced by 1 muscle fiber varies, depends on: – Frequency of stimulation – affects Ca2+ in cytosol – How stretched muscle was before stimulation: length- tension relationship • Resting produces optimal # of x-bridges – Temperature: “warming up” benefits

Answer 14

• Repeated stimulation (frequency of stimulation) of muscle fiber by motor neuron results in twitches with greater tension: Wave summation – Waves of contraction add together – No time to pump all Ca2+ back into SR, Ca2+ increases with each stimulus • Types of wave summation: – Incomplete (unfused) tetanus: lower rate of stimulation, partial relaxation occurs – Complete (fused) tetanus: high rate of stimulation, no relaxation before next stimulation

Answer 15

• Amount of tension in whole muscle, depends on: – Amount of tension in individual fibers (frequency of stimulation) – # of muscle fibers contracting at same time (recruitment)

Answer 16

• Motor unit: Somatic motor neuron + all muscle fibers it controls (more than 1 fiber!) • Fibers not clustered together- spread throughout entire muscle • Motor units differ in # of muscle fibers – Size of motor unit reflects control • Few fibers= precise control, less force (eye) • Many fibers= less control, more force (leg) • In 1 muscle = mixture of motor units

Answer 17

• Motor unit recruitment: increase in # of active motor units – Lifting a feather – few motor units recruited – Lifting a box of books – more motor units stimulated

Answer 18

• Remember what happens at muscle fiber level! • Muscle returns to original length: 1. Elastic forces • Recoiling • Pull of tendons, ligaments 2. Opposing muscle contractions: antagonistic pairs 3. Gravity

Answer 19

• Resting muscle fibers: – Low ATP demand – some ATP storage but not significant (5-6 sec) – Fatty acids used – Some glucose stored as glycogen – ATP used to convert creatine to creatine phosphate: quick “energy” storage

Answer 20

• Glucose = energy source • 5-6 seconds (like 50m dash) – immediate energy needed! – Immediate energy source: ATP and Creatine phosphate (CP) • 50-60 seconds (like 400m run) – short term, quick energy needed! – High demand for ATP, but oxygen diffusion into mitochondria slow – Most from CP and anaerobic glycolysis, little from aerobic metabolism – Drawbacks: ↑ lactic acid produced, pH ↓, inefficient ATP production, rapid fatigue results

Answer 21

• Mins- hrs (moderate pace long run)- long term, continual energy needed – Increased demand for ATP, no excess ATP made – Mitochondria meets demand if O2 supply sufficient – aerobic metabolism of glycogen! – O2 consumption ↑, blood flow to muscles ↑ to meet demand – If glycogen low, other nutrients used – Glycogen, lipids and amino acid depleted? = muscle fatigue

Answer 22

• Muscle contraction can not continue even with nervous stimulation – Not well understood!- CNS or muscle level? – Lactic acid, H+ build up: pH ↓ – Ca2+ release and uptake – Decreased O2 available – Energy sources depleted (CP, glycogen, other substrates) – Hyperthermia – Psychological basis

Answer 23

• Return body to pre-exercise conditions – Lactic acid recycled to pyruvate – make ATP, rebuild glycogen – Excess post-exercise oxygen consumption (EPOC) – “O2 debt” • Increased amount of O2 inhale to help return • The more ATP required for recovery, the more O2 needed • Correct blood pH: lactic acid recycled, CO2 exhaled • Replace O2 on hemoglobin in blood, myoglobin in muscle – Heat elimination • Delayed onset muscle soreness (DOMS) – small muscle tears? Injury to tendons, body adapts after and becomes stronger

Answer 24

• Typed by: – Time to reach peak tension (fast vs. slow) – Major metabolic pathways for forming ATP (glycolytic vs. oxidative) • Types: – Fast glycolytic: (fast fibers) • WHITE muscle fibers – Slow oxidative (slow fibers) • RED (dark) muscle fibers • Red Slow-oxidative – Slow contraction – Small diameter fibers- fewer myofibrils – Less forceful contractions – More mitochondria-red – Extensive blood supply- dark • More O2 - Aerobic metabolism – More myoglobin: red • Red-colored O2-binding/ releasing protein – Slow to fatigue: prolonged sustained contractions for hours= endurance • Maintain posture, marathon running (endurance) • White Fast-glycolytic – Majority in body – Largest diameter, most myofibrils: powerful – Faster contractions – Less myoglobin, fewer blood vessels, few mitochondria – Lots of glycogen for glycolysis: anaerobic – Fatigue easily – Best suited for strong, powerful, short contractions • Anaerobic exercise: weight lifting, sprinting, swing bat

Answer 25

• White muscles: pale – Fast fibers more abundant – Speed – Turkey breast “white meat” • Red muscle: reddish – Slow fibers more abundant – Endurance – Turkey legs “dark meat” • Humans: – One muscle usually mixture – % genetically determined – But fibers in motor unit = SAME!... Refer back to motor unit recruitment – Aerobic physical conditioning can affect muscle fiber performance

Answer 26

• Anaerobic conditioning – Short duration, high intensity, frequent: i.e. weight lifting, sprint training – Promote strength, speed and power – Contraction of fast-glycolytic fibers – Adaptations cause muscles to get bigger (hypertrophy) – due to ↑ # of fiber myofibrils NOT fibers! ? • Aerobic conditioning – Longer activity, moderate intensity, endurance training (ie. marathon) – Must be supported by oxidative phosphorylation (O2, mitochondria) – Adaptations to support metabolism, some fast fibers physiologically be more like slower fibers – No hypertrophy