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Movement Facilitation Thermogenesis Postural Support Regulation of Organ Volume Protects Internal Organs Pumps Blood (HEART) The study of muscles Contractility – able to shorten Extensibility (Flexibility) – able to lengthen Elasticity – able to return to original shape Excitability (Irritability) – able to respond to a stimulus Attached to bones Striated appearance under a microscope Voluntary control (conscious control) Multinucleated Myofilaments - contractile elements of each muscle fiber Functions: • • • • movement thermogenesis posture protection of internal organs 1 1 Forms the bulk of heart wall (Myocardium) Striated Involuntary Fibers are quadrangular and branching Cardiac fibers typically have a centrally located nucleus Sarcolemmas connected by intercalated discs • Strengthens cardiac muscle tissue • Propagates an action potential from cell to cell through specialized structures on the intercalated discs called gap junctions Function: contractions of the heart Located in walls of hollow internal surfaces such as: • • • • blood vessels stomach urinary bladder intestines Non-striated in appearance Involuntary (typically) Can be stretched to great lengths Allows for tremendous size variability Functions: • • • controls diameter of blood vessels Peristalsis Muscular contractions to push urine out the urinary bladder 2 2 Myofilaments - structural components of myofibrils • Myosin - thick myofilaments • Actin - thin myofilaments Structure of muscle Thick myofilaments Occupy the A Band of the sarcomere Overlap free ends of the actin myofilament Shaped like a golf club • Long, thick protein molecule (tail) • Globular head at the ends Thin myofilaments Anchored to the Z Line Two stranded protein molecule intertwined around each other Associated with two regulatory proteins • Tropomyosin – • long stranded protein molecule that follows the contour of actin • When the muscle fiber’s sarcomere is relaxed, tropomyosin blocks actin’s active sites preventing cross-bridge formation with myosin • Troponin - protein located at regular interval along the tropomyosin that covers the active sites on actin. Has three subunits, one that binds with actin, another with tropomyosin, and the last bind to Ca++ 3 3 An electrical impulse that originates at the motor end plate, travels along the length of the sarcolemma, down a transverse tubule, and causes the muscle to contract. Due to an action potential, the actin and myosin myofilaments slide past one another shortening the sarcomere No change in length of myofilaments H Zone narrows or disappears I Band narrows or may disappear A Band remains the same length Neuron - nerve cell Axon - long, threadlike process that transmits impulse away from cell body (may be up to 1 meter in length) Motor Unit - motor neuron and all the muscle fibers it innervates Neuromuscular Junction - junction between axon terminal and muscle fiber 4 4 • • • • • • • • • • • • Synaptic Cleft - space between axon terminal and motor end plate Subneural Clefts - folds in sarcolemma along the synaptic gutter Acetylcholine (Ach) - neurotransmitter released from synaptic vesicles that initiates an action potential in a muscle Motor End Plate - location on the muscle fiber at the end of an axon terminal Synaptic End Bulb - distal end of axon terminal Synaptic Vesicles - membrane enclosed sacs within the synaptic end bulbs that store neurotransmitters All or None Principle • Once a threshold stimulus is applied to a motor unit the muscle fibers innervated by that motor unit will contract to their fullest potential Threshold Stimulus - the weakest stimulus from a neuron that will initiate a muscular contraction An action potential travels down the motor neuron. When it arrives at the synaptic knob, the membrane of the nerve at the synaptic cleft is depolarized, thereby increasing the Ca++ permeability of the membrane. Ca++ diffuses from outside of the synaptic knob to inside the synaptic knob. The influx of Ca++ into the nerve causes the release of Ach. Ach is ejected into the synaptic cleft, diffuses across the cleft, and depolarizes the muscle membrane. This increases the permeability of the muscle membrane to Na+. Na+ rushes into the muscle cell, depolarizing the membrane as it travels away from the motor end plate thus initiating an action potential. Ach is quickly broken down in the cleft by Ach-ase so that each action potential arriving from the nerve initiates only one action potential within the muscle. The action potential spreads across the muscle membrane and down the T-tubules deep into the muscle cell. The action potential of the T-tubules depolarizes the membrane of the nearby sarcoplasmic reticulum which results in the release of Ca++ into the sarcoplasm. Ca++ is very quickly removed out of the sarcoplasm by the sarcoplasmic reticulum so the effects of one action potential are very short lived and produce a very small contraction. Many action potentials are necessary to produce enough force to produce a strong or prolonged muscle contraction. The Ca++ released from the sarcoplasmic reticulum binds with troponin and cause troponin to change shape. 5 5 When troponin changes shape, it physically moves the other regulatory protein, tropomyosin, out of the way exposing the active sites on the actin myofilament. Since the heads or cross-bridges of myosin have a very strong affinity for the active sites on actin, they make contact immediately after the active sites have been exposed. The acto-myosin complex has ATPase activity and ATP is split into ADP + P and energy is released. The energy released by the splitting of ATP is used to produce movement of the cross-bridges, sliding the actin and myosin filaments past one another which causes the sarcomere to shorten and the muscle to contract and produce force. The myosin cross-bridge has a low affinity for ADP but a very high affinity for ATP. It discards the ADP and becomes recharged with a new ATP. The myosin then releases its hold on the active sites on actin, swivels back to its original position, and is ready to respond to another action potential. When another action potential comes along the entire process is repeated. It takes many action potentials to produce enough shortening of the sarcomeres to generate enough force to produce movement of a body segment. 6 6 Origin • Body segment with most mass • Usually more proximally located • Usually larger surface area of attachment Insertion • Body segment with least mass • Usually more distally located • Usually smaller surface area of attachment Gaster (Belly) • Fleshy portion of the muscle between the tendons of the origin and insertion Agonist (Prime Mover) • Muscle responsible for the majority of force Antagonist • Performs the opposite movement Synergist • Muscle that assists the agonist • provides additional force • redirects the force of the agonist Pectoralis major Deltoid Biceps brachii Sternocleidomastoid Diaphragm Quadriceps • • • • Fixator (Stabilizer) • Stabilizes a body segment so the prime mover can rectus femoris vastus medialis vastus lateralis vastus intermedius act more effectively Trapezius Triceps brachii Gastrocnemius Latissimus dorsi Hamstring Group • semimembranosus • biceps femoris • semitendinosus Gluteus maximus 7 7 Aponeurosis a strong flat sheet of fibrous connective tissue that serves as a tendon to attach muscles to bone or as fascia to bind muscles together or to other tissues at their origin or insertion Bursa a fluid-filled sac or saclike cavity situated in places in tissues where friction would otherwise occur Flaccid Hypertrophy Atrophy weak, lax, lacking normal muscle tone enlargement or overgrowth of an organ or part due to increase i n size of its constituent cells a wasting away; a diminution in the size of a cell, tissue, organ, or part Painful disorders of muscles, tendons, and surrounding soft tissue Muscle destroying diseases characterized by the degeneration of individual muscle fibers Leads to progressive atrophy of skeletal muscles Due to a genetic defect Autoimmune muscle disease characterized by muscular weakness and chronic fatigue Caused by a lack of Ach Body sends antibodies to destroy Ach The action potential cannot be sent to the skeletal muscles 8 8 Occurs a few hours after death when the skeletal muscles undergo a partial contraction that causes the joints to become fixed Seems to result from an increase in membrane permeability to calcium ions, which promote contraction and decrease in the availability of ATP, which prevents relaxation Approximate times for algor and rigor mortis in temperate regions The actin and the myosin filaments remain linked together until the muscles begin to decompose Body temperature Body stiffness Time since death warm not stiff dead not more than three hours warm stiff dead 3 to 8 hours cold stiff dead 8 to 36 hours cold not stiff dead more than 36 hours SOURCE: Stærkeby, M. "What Happens after Death?" In the University of Oslo Forensic Entomology [web site]. Available from http://folk.uio.no/mostarke/forens_ent/afterdeath.shtml. Connective tissue sheath of the tendon becomes inflamed and swollen following an injury or repeated stress of athletic activity Most commonly affected are those of the shoulder, elbow, and hip This is when the tendinous attachments of muscles to the are torn as a result of strenuous activity The painful injury is accompanied by internal bleeding from damaged blood vessels that supply the muscles A form of food poisoning that results when the bacteria have not been heated high enough to inactivate the toxin Caused by a toxin (made by Clostridium botulinum) that can prevent the release of Ach from the motor nerve fibers at the neuromuscular junctions. When the muscle fibers fail to be stimulated, the body, including the muscles responsible for breathing, may be paralyzed. Without prompt medical attention, death may result. Hypertrophy • • Muscle growth Caused by using the muscle Hypotrophy • • • • Better known as atrophy Decrease in muscle size and strength Caused by NOT using the muscle Muscle wasting 9 9 Pain in the lower leg Tendonitis of the tibialis posterior muscle Inflammation of the periosteum Stress fracture of the tibia Exaggerated enlargement of muscles within the epimysium Pulling away of the periosteum from the underlying bone Treatment: • RICE • strengthen tibialis anterior muscle The forcible wrenching or twisting of a joint with partial or complete rupture or injury to joint attachments without dislocation 1st Degree Sprain = stretching of ligaments 2nd Degree Sprain = partial tearing of ligaments 3rd Degree Sprain = complete tear of ligaments Pulling or overstretching a muscle Soft tissue (muscle) injury 10 10
