Organization and General Functions
"Myo" refers to muscles.
Sarco = "flesh"--some muscle structures such as "sarcomere," "sarcoplasmic reticulum," and "sarcolemma."
Sarcophagus = "flesh eating." Dates back to ancient Egyptians and the belief that stone tombs (typically limestone) ate away at flesh of the dead, leaving behind only bones.
Muscle is a principal tissue type, Specialized for contraction.
Like neurons, muscle is an excitable tissue, in that it can conduct or transmit electrical impulses (respond to stimuli).
3 muscle types: skeletal, cardiac and smooth.
All muscle tissues have 4 characteristics in common:
1) Movement and Regulation.
Examples related to:
2) Posture and Support
3) Body Temperature Regulation.
Heat is a byproduct of metabolism. Since skeletal muscles make up 40% of total mass of body, they play a major role in generating heat. During exercise, a large amount of heat is generated. In cold, muscles will "shiver" to produce heat.
General structure of a skeletal muscle: Tendon ---- Body of Muscle ----- Tendon
Tendon Histology: dense regular connective tissue
Aponeurosis: tendon that is broad or sheet-like. For example, the aponeurosis of Galen and the lumbar aponeurosis that is the origin of the latissimus dorsi.
Levels of Organization of Skeletal Muscle:
Associated Connective Tissue Organizes Muscle Tissue
Bundles of muscle fibers are grouped or bundled together by connective tissue.
Superficial fascia: layer adjacent to hypodermis. Deep fascia: binds muscles together.
Blood and Nerve Supply
Muscles are highly vascular organs -- high rate of metabolic activity.
Nerves control or modify muscle contraction. A "motor" nerve is any nerve that innervates a muscle. Skeletal muscles require input from a nerve in order to contract. Cardiac and smooth muscle can contract on their own (they have an intrinsic spontaneous contraction rate), but the rate is controlled by nerves and hormones.
Sensory nerves are abundant in muscle also--supply nervous system with information on muscle contraction and joint position.
Muscle Spindles: monitor tension/stretch within muscles.
Excitation-Contraction Coupling & Sliding Filament Theory
Mechanism by which excitation of muscle cell membrane stimulates muscle cell contraction.
Neuromuscular Junction--3 components:
1) Terminal of motor axon interfaces with muscle cell.
Motor neuron terminal has synaptic vesicles that contain the neurotransmitter acetylcholine (ACh). ACh is released by nerve stimulation (nerve action potential).
2) Synaptic Cleft: Gap thru which transmitter diffuses.
3) Muscle Endplate: Area specialized for reception of neurotransmitter. Endplate has ACh receptors: ACh binds to receptors -- causes endplate potential (EPP) and then a muscle action potential. ACh-esterase: enzyme on endplate that breaks down ACh -- initiation of muscle impulse ends.
Sequence of Events at Neuromuscular Junction and Excitation-Contraction Coupling.
1. Nerve impulse (action potential) arrives at terminal and induces the entry of calcium into terminal via voltage-gated calcium channels.
2. Calcium entry stimulates exocytosis of ACh filled vesicles.
3. ACh diffuses across synaptic cleft and binds onto ACh receptors on muscle endplate.
4. ACh receptors activate Na/K ion channels. Sodium entry depolarizes endplate --generates endplate potential (EPP).
5. Endplate membrane is brought to threshold voltage and adjacent muscle cell membrane generates an action potential (muscle impulse).
6. Muscle Impulse: travels down sarcolemma and then into myofibrils via the transverse tubules;
7. Transverse tubules transmit signal to Sarcoplasmic Reticulum (S.R.) and S.R. releases calcium to myofibrils (initiates contraction).
8. Actin and myosin filaments interact -- they slide past each other and muscle cell shortens. (Calcium binds to troponin -- pulls tropomyosin away from active site on actin -- myosin can now bind to actin -- myosin head moves actin filaments) This is the sliding filament theory of muscle contraction.
ATP provides energy for strokes. Myosin head is an ATPase in that it cleaves ATP to form ADP and Pi, yielding energy for movement.
Note: myosin is also found in non-muscle cells
ATP is also need to disengage actin from myosin head.
Lack of ATP -- rigor mortis sets in. Muscles are stiff because actin and myosin filaments are cross-linked.
Short term effect.
Muscle Relaxation: "What ends muscle contraction?"
1. ACh is broken down by ACh-esterase. No further stimulation of muscle fiber.
2. S.R. pumps calcium back inside -- this uses ATP!
3. Without calcium present, troponin and tropomyosin block active site on actin prevent
cross-bridge formation between actin and myosin.
4. Actin and myosin filaments return to their original positions.
Other Elements of Muscle Contraction
Length-Tension Relationship: Based on arrangement of muscle filaments. Historical significance.
Isometric Vs Isotonic Muscle contraction
Whole muscle contraction:
Twitch, Summation, and Tetanus (incomplete and complete)
Staircase effect or Treppe
Tonus: Due to baseline activity of motor units.
Series Elastic Component: Total effect of muscle connective tissues.
Resting muscle uses aerobic respiration pathway to supply ATP. Prime energy sources are fatty acids and glucose (from glycogen via glycogenolysis).
Glucose converted to pyruvic acid, which is broken down by citric acid cycle (in mitochondria, aerobic) to produce ATP.
Aerobic and Anaerobic metabolism of glucose
Advantage of Aerobic respiration: Energy efficient
Disadvantage of Aerobic respiration: Exercising muscle uses ATP, but use soon outweighs ATP production. Muscle respires anaerobically (glycolysis -- lactic acid produced). ATP is also generated from creatine phosphate:
Creatine Phosphate + ADP --> ATP + Creatine
Muscle has large stores of creatine phosphate but it is rapidly used up during sustained contraction.
Creatine Supplements: Do they work?
As a result of heavy exercise, lactic acid accumulates from anaerobic respiration. Lactic acid then travels to the liver, which converts it to glucose. Conversion to glucose requires ATP and oxygen. During exercise, available oxygen is used primarily by muscle, so less is available for use by liver.
The "oxygen debt" created is equal to the amount of oxygen needed by liver to convert accumulated lactic acid into glucose, plus the amount needed by muscle for ATP and CP regeneration. Total process may take hours.
(*Note: Exercise physiologists prefer to call oxygen debt "EPOC" for "Excess post-exercise oxygen consumption.")
Accumulation of lactic acid and low ATP results in fatigue (reduction in ability to contract). Other factors include: change in pH, interruption of blood supply, depletion of acetylcholine.
Tolerance to fatigue from athletic training is due to increased muscle blood supply, increased number of mitochondria in muscle fibers.
Energy use of muscles can be modified as a result of exercise.
Effects of Resistance Training: Muscle Hypertrophy and Hyperplasia
Responses of Muscle to Endurance Training: Numerous factors related to aerobic metabolism
Loss of Muscle Mass
Atrophy: wasting away of muscle tissue. E.g., disuse atrophy, in which muscle mass is lost because of inactivity.
Also from loss of motor neurons.
Dystrophy: literally, "defective nutrition." Tissue fails to develop correctly or thrive. Usually congenital or genetic in cause.
Sarcopenia: means "vanishing flesh." Age-related loss of muscle with replacement by fat.
Skeletal Muscle Fiber Types
1) Slow Twitch (Type I)--e.g., soleus. 100 msec for contraction.
2) Intermediate (Type IIA) e.g., gastrocnemius. Fast twitch.
3) Fast Twitch (Fatigable) (Type IIB)--e.g., extraocular muscles. 7.3 msec for contraction.
Fiber type dictated by innervation (experimentally demonstrated) and by genetics.Effect of training? Twitch type (fast or slow) stays the same. Aerobic capacity/fatigue resistance can be increased in fast-twitch muscles. (Fast-twitch fatigable become intermediate).
Fibers also differ in: Myoglobin content (oxygen supply), Vascularization and Myosin ATPase activity.
Ratio of fast to slow fibers varies among individuals.
Gastrocnemius muscles of runners for example: Sprinters have more fast twitch fibers, long distance runners have more slow twitch fibers.
Specialized muscle of the heart.
Structure: Striated, but differs from skeletal muscle in the following ways:
1. Short fibers.
2. Single nucleus usually.
3. Cells connected by arrays of gap junctions called "intercalated discs." These discs allow electric current to spread quickly through all linked cells. The cells then contract as a unit -- a "functional syncytium."
4. Arrangement of sarcoplasmic reticulum and transverse tubules is slightly different.
5. Strictly aerobic.
6. Autorhythmic (has automaticity)
Typically associated with "viscera" and "involuntary" systems (circulatory, respiratory, digestive, urinary, reproductive and integumentary).
1. Group of diseases - not a single disease
2. Progressive skeletal muscle degeneration and increase in fat and connective tissue.
3. Generally begins in childhood.
4. Gene Therapy for some forms of MD has begun recently.
Duchenne M.D. is well characterized. It is a genetic disease (sex-linked) in which a protein called "dystrophin" is either lacking or defective. Dystrophin helps organize the structure of the muscle fiber.
Becker Muscular Dystrophy is a related disease in which dystrophin is present in low amounts.
Botulinum toxin comes from Clostridium botulinum, a soil bacterium. The toxin inhibits the release of ACh from motor nerve terminals, causing flaccid paralysis.
Tetanus or lockjaw
Severe muscle spasms from toxin produced by the bacterium Clostridium tetani. Not a direct muscle effect. The toxin blocks inhibitory neurotransmitters in spinal cord, so motor neurons are inhibited less. Causes spastic paralysis.