Muscle Physiology. Introduction. Four Characteristics of Muscle tissue. Skeletal Muscle

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1 Muscle Physiology Introduction Muscle = tissue capable of forceful shortening or contraction Converts chemical energy (ATP) into mechanical energy Important in: Respiration Urine collection & flow Gastrointestinal motility Blood flow: cardiac output & vascular smooth muscle Movement: food gathering & escaping predators Reproduction / Childbirth There are three types based on histology 1) Skeletal, 2) Cardiac & 3) Smooth Four Characteristics of Muscle tissue Skeletal Muscle 1) Irritability and Excitability: responds to chemicals, (neurotransmitters or hormones), stretch or other signals (irritability) with a wave of electricity across the plasma (cell) membrane (excitability). This property is shared with nervous tissue. 2) Contractility undergoes forceful shortens when stimulated. This is a unique property of muscle alone. 3) Extensibility capable of being lengthened 4) Elasticity returns to its original resting length after being stretched Attached to skeleton Exhibits alternating light and dark bands or striations Individual cells or fibers may be as long as 30 cm (~12 in) Mostly voluntary (under conscious control) Except for respiration and swallowing

2 Structure of Skeletal Muscle Fibers (Cells) Sarcolemma (plasma membrane) has unique proteins that are capable of generating waves of electricity called action potentials. The sarcolemma has regularly spaced invaginations called transverse tubules (or t-tubules) that penetrate the cell interior. These carry the electric signals inward to where contractile and regulatory proteins are located. Sarcoplasm (cytoplasm) filled with Two types of contractile proteins 1) Actin = thin filaments 2) Myosin = thick filaments Two types of regulatory proteins 1) Troponin 2) Tropomyosin Glycogen = (glucose polymer) for stored energy Myoglobin = oxygen binding protein that is evolutionarily related to the oxygen carrying protein of blood (hemoglobin) Sarcoplasmic reticulum (specialized endoplasmic reticulum) is series of interconnected, calcium storage sacs called terminal cisternae releases calcium into sarcoplasm to initiate contraction, takes the calcium back up to end contraction (relaxation). Contractile & Regulatory Protein Function Myosin thick filaments have head-like structures that can be energized into an extended state using the chemical energy in ATP Actin thin filaments possess specific sites (called active sites) where energized Myosin head groups can bind or attach and PULL the filaments in opposite directions Tropomyosin & troponin act like a switch that starts & stops contractions. 1) Calcium is released from the sarcoplasmic reticulum into sarcoplasm

3 2) The calcium binds to troponin, which is bound to tropomyosin. 3) Tropomyosin normally blocks the binding of the myosin head to the active site on the actin. The calcium-bound form of troponin moves the tropomysin off the active site on actin and thus allows myosin heads to bind and pull the filaments in opposite directions. (contraction) 4) Once the action potential (electrical wave) across the sarcolemma has stopped the calcium is taken back up by the sarcoplasmic reticulum and the tropomyosin covers the active site. This enables relaxation. Overlap of Thick & Thin Filaments in Striated Muscle The visible striations seen in skeletal and cardiac muscle are produced by a regular repeating pattern of contractile proteins (actin and myosin) Darker A bands alternate with lighter I bands The A band contains light-blocking thick filaments (myosin) with some overlapping thin filaments (actin). The somewhat lighter, central H band region of the A band contains no thin filaments The very light I band on either side of an A band contains only thin filaments (actin). The entire structure is held together by Z discs or Z lines that connect the thin filaments vertically The repeating structure from one Z disc to the next is a sarcomere Sliding filament theory of muscle contraction. Do NOT shorten; 1) actin 2) myosin DO shorten: 1) I band 2) H band 3) A band 4) Z line 3) Sarcomere

4 Sarcomeres shorten or lengthen by increasing or decreasing the overlap between actin thin filaments and myosin thick filaments as the filaments SLIDE past one another (like your fingers). Length-Tension Relationship Amount of tension or force generated by a striated muscle depends on its length before it was stimulated. Overly contracted (weak contraction results) thick filaments are too close to Z discs & can t move Too stretched (weak contraction results) little overlap of thin & thick allows for few cross bridges too form Optimum resting length (usually in the middle of the range of motion) produces greatest force when muscle contracts Nerve-Muscle Relationship Skeletal muscle must be stimulated by a nerve (called motor neuron) or it will not contract (paralyzed) Each motor neuron and all the muscle fibers it innervates are called a motor unit Neuromuscular Junctions The place where nerve fibers (cells) connect with a target cells is a synapse. The neuromuscular junction is a specialized synapse because the target is skeletal muscle exclusively. Components of a neuromuscular junction: synaptic knob = swollen end of the motor neuron contains vesicles that are filled with an extracellular chemical messenger or neurotransmitter called Acetylcholine (Ach) synaptic cleft = tiny gap between nerve and muscle cell contains an enzyme that can destroy Ach and remove it from the synapse called cholinesterase. motor end plate = specialized region of muscle cell surface These are highly enriched with proteins that specifically bind to Ach and becomes activated called acetylcholine receptors

5 Neuromuscular Junction Physiology 1) The CNS initiates wave of electricity (action potential) down a motor neuron. 2) The wave of positive charge triggers calcium entry into the synaptic knob. 3) The presence of calcium ions in the cytoplasm in turn triggers the release (exocytosis) of vesicles containing the neurotransmitter (acetylcholine /ACh) from the nerve terminal. 4) The acetylcholine diffuses across that synaptic cleft and binds to Ach receptors on the motor end plate. 5) The binding of Ach to its receptor activates it (like a lock and key) and initiates a wave of positive charge (a 2nd action potential) in the skeletal muscle fiber. 6) This action potential travels down the sarcolemma, into the t-tubules and triggers the release of calcium from the sarcoplasmic reticulum into the sarcoplasm. (and you know the rest of the story ) 7) Once the CNS stops sending action potentials the Ach stops being released from the synaptic knob and cholinesterase breaks down the remaining ACh in the synaptic cleft & thus enables relaxation Neuromuscular Toxins & Paralysis 1) Curare (from poison arrow frogs) binds to Ach receptors on the motor end plate and does nothing. This prevents Ach from binding to and activating the receptors, causing a limp or flaccid type of paralysis. These drugs are useful in surgery and on death row. 2) Certain pesticides & Sarin nerve gas are cholinesterase inhibitors that bind acetylcholinesterase & prevent it from degrading Ach. Continued stimulation of skeletal muscle by Ach may cause a spastic paralysis & possible tetanic paralysis (sustained contraction) Even a minor startle response can cause affixation and possibly death. Related drugs are used to treat myasthenia gravis. (autoimmune attack on AchR) 3) Botulism toxin (type of food poisoning) contains an agent that interferes with exocytosis of acetylcholine from the neuromuscular junction for 6-8 weeks. This causes a limp or flaccid paralysis. This so-called drug is used to prevent excess sweating, certain types of eye paralyses and wrinkles.