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Length-tension relationship
During an isometric contraction, at the level of the sarcomere the maximum active force (tension developed) is dependent on the degree of actin and myosin overlap
Understretched
Sarcomere < 2.0 µm, actin and myosin overlap excessively, actin filaments from opposite ends of the sarcomere may even interfere with each other or with the M-line, this limits the effective number of cross-bridges that can form between actin and myosin. Resulting in decreased force production due to inefficient contraction.
Optimal length
Sarcomere is 2.0 - 2.2 µm, actin and myosin filaments have maximum overlap without interference, this allows the maximum number of cross-bridges to form. Resulting in maximal force production — this is the most effective length for contraction.
Overstretched
Sarcomere > 2.2 µm, very little or no overlap between actin and myosin filaments, few or no cross-bridges can form. Resulting in greatly reduced or no force production, because contraction can't effectively occur.
Total tension
Active force + passive force
Muscle has elastic components, active tension is dependent on sarcomere length
Passive force
Increases as the muscle is stretched due to the passive elements
Active force
Developed via cross-bridge cycling and dependent on actin-myosin overlap
Motor-unit
Consists of a motor neuron and all the muscle fibres it innervates
Excitation-contraction coupling
Excitation (7 steps) and contraction (7 steps)
Excitation Step 1
Depolarisation of axon terminal on motor neuron
Excitation Step 2
Causes voltage-gated calcium channels to open, flooding the axon terminal
Excitation Step 3
Synaptic vesicles of acetylcholine are released via exocytosis
Excitation Step 4
Acetylcholine diffuses across synaptic cleft to bind to ACh-gated cation channels which cause a conformational change
Excitation Step 5
ACh-gated cation channels open
Excitation Step 6
A large influx of Na2+ ions and a small efflux of K+ ions into and out of the muscle fibre making muscle cell less negative (End-plate potential/EPP)
Excitation Step 7
Once membrane potential reaches threshold, voltage-gated Na+ channels open and AP is generated along sarcolemma and T-tubule. Acetylcholine unbinds
Clearing of acetylcholine from synaptic cleft
Diffuses out or broken down by acetylcholinesterase into acetic acid and choline, choline is retaken back into the axon terminal for resynthesis of acetylcholine
AP in skeletal muscle
Similar to nerve cell and AP is ~2 ms
Contraction Step 1
AP conducted down T-tubule is in close contact with sarcoplasmic reticulum (SR), forming a triad
Contraction Step 2
Dihydrogen pyridine receptors (DHPRs) sense depolarisation and physically interact with ryanodine receptors (RyR1) on SR, causing them to open
Contraction Step 3
Ca2+ released into the cytosol
Contraction Step 4
Ca2+ binds with troponin when concentrations reach a critical threshold, the myosin binding sites on the actin filaments are exposed
Contraction Step 5
Cross-bridge cycle occurs
Contraction Step 6
Contraction ends with concentration of Ca2+ ions decrease as they are actively pumped back into the SR via Ca2+-ATPase pumps
Contraction Step 7
Tropomyosin moves back covering there myosin binding site
Muscle metabolism
Sources of ATP are creatine phosphate, anaerobic glycolysis, aerobic metabolism
Creatine phosphate
Used at the very start of contractions, creating phosphates acts as ATP store but duration of energy is ~15 seconds, anaerobic
Anaerobic glycolysis
Fast but inefficient, dominant system from about 10 - 30 s of maximal effort, build of metabolites (H+ limits duration to 120s), anaerobic
Aerobic metabolism
Efficient but slow, max 300 W, important for postural muscles and endurance exercise, aerobic
Muscle fibres
Slow twitch fibres (Type 1) and Fast twitch fibres (Type 2)
Slow twitch fibres (Type 1)
Smaller, darker due to more myoglobin, slow oxidative, maintaining posture and walking
Fast twitch fibres (Type 2)
Bigger, fast glycolytic, fatigue rapidly but develop large forces, jumping and weight lifting
Regulation of force
Rate of stimulation of individual motor units and the number of motor units recruited
Unfused (incomplete) tetanus
Low stimulation frequency, temporal summation
Fused (complete) tetanus
High stimulation frequency, temporal summation
Tetanus
Infection causes tetanus of muscle which suppresses inhibition of motor neuron activity = lots of AP