Motor neuron & the muscle fiber it innervates. The smallest amount of muscle that can be activated voluntarily
Graduation of force in skeletal muscle is coordinated largely by the nervous system
Recruitment of motor units is the most important means of controlling muscle tension
All fibers in the motor unit contract simultaneously
Physiological profiles of motor units
All fibers in a motor unit are of the same fiber type, slow with slow, fast with fast...
3 parts of muscle contraction
Sliding filament theory
1. Alpha motor nuerons innervate skeletal muscle fibers at specialized junsctions call "neuromuscular junction" or "myoneural junction"
2. One neuron can innervate multiple fibers: "synaptic bouton"
3. The sarcolemma in the neuromuscular junction is called the "motor end plate"
4. The neurotransmitter released is "Ach" which binds to specialized cholinergic receptors called "nicotinic receptor" that causes an opening of ligand gated Na+ ion channel production of postsynaptic potential - resulting in action potential in muscle fiber.
Acetyl choline metabolism
Acetyl CoA binds with choline acetyl transferase creating Acetyl choline
Add Ca+ and the acetyl choline packages fuse with the membrane, causing the release of the Ach (this is where Clostridium botulinum toxin attacks)
The Ach goes to the Ach receptor, allowing the Na+ to flood into the muscles (this is where Curare M. gravis attacks)
From here the Acetyl choline esterase releases the acetate and choline separate. (Neostigmine (m. gravis) will attack here)
The choline is then absorbed back into the nerve ending where is again binds with Acetyl CoA
Acetyl choline metabolism: disease
Curare: (poison from SA Frogs) Blocks Nicotinic receptors-prevents Ach induced muscle contractions. Curare derivatives - to relax muscles prior to surgery
Clostridium: Toxin prevents Ach release from somatic motor neurons. Death by paralysis of respiratory muscles.
Ach E (Acetylcholine esterase) inhibitors: Myasthenis gravis - autoimmune disease - reduced Ach receptor function - treated with AchE inhibitor Neostigmine
AP travels down T tubule. Ca+ release into sarcoplasm -> Ca+ binds to Troponin - conformation change - active sites of Tropomyosin exposed -> "power stroke" myosin head binds to and pulls actin towards M line (sliding filament theory) -> Myosin head detaches from actin with ATP binding
Factors affecting skeletal muscle contraction
Muscle length and tension
Relationships: length vs tension and force vs velocity
Isometric vs Isotonis
Twitch - Treppe - Wave summation - Tetanus
Skeletal muscle metabolism
Muscle is "plastic"
Muscle "adapts" to meet the habitual level of demand placed on it. This is affected by frequency of recruitment and the load.
Muscle generates force while muscle length remains constant
Postural muscles - maintain constant body position while opposing gravity
Muscle shortens under a constant load. Muscle length changes as force is generated = movement. Common in animal locomotion.
Decrease muscle length (cross bridges formed - thick & thin filaments interdigitate to overcome resistance)
Increase muscle length (tension developed < load on muscles) For example, when an animal walks down a steep incline - animal controls rate of elongation of muscles as the legs stretch to the next location.
Muscle stimulated 2nd time immediately after the relaxation phase of 1st twitch - results in increased tension known as Treppe. This increased tension is due to gradual increase in SR Ca+ between because the Ca+ pumps in SR are unable to sequester all Ca between twitches. If the repetitive stimuli & contractions continue - tension will eventually decrease and fatigue occurs
Summation (wave summation)
2nd stimulation occurs before complete relaxation = 2nd twitch will cause greater tension than original twitch. This occurs at stimulation @ 50/sec and SR can no longer sequester the Ca+ between twitches.
Tetan = Rigid): individual twitches are distinguishable
Individual twitches indistinguishable- because of high frequency of stimulations - no relaxation phase. This is the normal state observed during muscle contraction. Ca+ are released from SR faster than they are pumped back in - Ca+ conc in cytoplasm is above the threshold required for muscle contraction
No relaxation phase
Creatinine Phosphate (anaerobic)
Excess energy stored as Creatine Phosphate - exclusively in muscle: Conc is 3-6 times more than ATP
Creatine Kinase: key enzyme for rapid ATP generation