(7th edition) LECTURE OUTLINE - UNIT 7 Muscles and Muscle Tissue [*The following lecture outline follows your

textbook very closely; read the outline and the associated sections in Chapter 9 of your textbook] I. Muscle Overview A The main tissue in the heart, skeletal muscles, and the walls of hollow organs B. Makes up nearly half the bodys mass C. Types of Muscle Tissue

1. SKELETAL muscle tissue packaged into skeletal muscles; makes up 40% of body weight 2. CARDIAC muscle tissue occurs only in the walls of the heart 3. SMOOTH muscle tissue occupies the walls of hollow organs and other diverse places in the body D. Functional Features 1. contractility long cells shorten and generate pulling forces 2. excitability electrical nerve impulse stimulates the muscle cell to contract 3. extensibility can be stretched back to its original length by contraction of an opposing muscle (agonist / antagonist relationship) 4. elasticity can recoil after being stretched E. Functions of muscle tissue 1. movement (e.g. skeletal muscle moves body by moving the bones) 2. squeezes fluids and other substances through hollow organs (smooth muscle) 3. maintenance of posture enables the body to remain sitting or standing 4. joint stabilization

(7th edition) 5. heat generation muscle contractions produce heat (shivering) to help maintain normal body temperature

6. allows breathing to occur - e.g. the diaphragm contracts and relaxes to enable air to enter and exit the lungs II. SKELETAL MUSCLE ANATOMY A. Each skeletal muscle is an ORGAN 1. consists mostly of muscle tissue 2. skeletal muscle also contains connective tissue (remember that muscle tissue is not a connective tissue!), blood vessels, nerves B. Macroscopic Anatomy of Skeletal Muscle 1. FASCICLES are bundles of MUSCLE CELLS; muscle cells are also called MUSCLE FIBERS (fig. 9.2) 2. Connective tissue sheaths bind a skeletal muscle and its fibers (cells) together a. EPIMYSIUM dense connective tissue surrounding entire muscle b. PERIMYSIUM surrounds each fascicle (group of muscle fibers) c. ENDOMYSIUM a fine sheath of connective tissue wrapping each muscle cell 3. Muscle attachments a. most skeletal muscles run from one bone to another b. ORIGIN less movable attachment site c. INSERTION more movable attachment site d. one bone will move (it has the insertion), while the other bone remains fixed (it has the origin) -- thus, the insertion moves toward the origin; e.g. the biceps brachii originates (at 2 points) in the scapula and inserts into the radius; the radius (insertion) moves toward the scapula (origin) e. muscles attach to origins and insertions by connective tissue; often the connective tissue is in the form of a TENDON or APONEUROSIS (broad tendon)

(7th edition) f. bone markings are often present where tendons meet bones (e.g. tubercles, trochanters, and crests); that is why you learned the bones before studying the muscles! You will apply the bone marking terms that you learned in Units 4 & 5 when you learn the muscles of the body in the next unit (Unit 8) C. Microscopic Anatomy of Skeletal Muscle 1. Overview of the Muscle Fiber Structure (fig. 9.3 a,b,c) a. composed of MYOFIBRILS b. MYOFIBRILS are composed of MYOFILAMENTS c. MYOFILAMENTS are composed of a THIN FILAMENTS (contain ACTIN) and THICK FILAMENTS (contain MYOSIN)

d. the plasma membrane of the muscle cell is called the SARCOLEMMA e. the cytoplasm of the muscle cell is called the SARCOPLASM 2. SARCOMERE - the basic unit of contraction of skeletal muscle (fig. 9.3 c,d,e) a. Z discs (also called Z lines) the boundaries of each sarcomere b. thin (actin) filaments extend from Z disc toward the center of the sarcomere c. thick (myosin) filaments located in the center of the sarcomere; overlap inner ends of the thin filaments d. A bands full length of the thick filament; includes inner end of thin filaments (thus, there is overlap of thin and thick filaments) e. H zone center part of A band where no thin filaments occur (thus, there is no overlap of thin and thick filaments) f. I band region with only thin filaments (thus, there is no overlap of thin and thick filaments) 3. Ultrastructure and Molecular Composition of the Myofilaments (fig. 9.4) a. MYOSIN molecules contain the MYOSIN HEADS b. ACTIN chains contain TROPONIN, TROPOMYOSIN, and ACTIN molecules

(7th edition) 4. SARCOPLASMIC RETICULUM a specialized smooth ER (fig. 9.5) a. composed of interconnecting tubules surrounding each myofibril b. CISTERNAE occur in pairs on either side of a T TUBULE c. some tubules form cross-channels called TERMINAL CISTERNAE d. the T TUBULE is a deep invagination of the SARCOLEMMA e. a TRIAD is composed of a T TUBULE + 2 TERMINAL CISTERNAE

f. the sarcoplasmic reticulum contains calcium ions; the ions are released when muscle is stimulated to contract; during stimulation calcium ions diffuse through the cytoplasm (sarcoplasm) of the muscle cell and trigger the sliding filament mechanism; when a muscle cell relaxes, calcium is actively pumped back into the sarcoplasmic reticulum III. SKELETAL MUSCLE PHYSIOLOGY A. SLIDING FILAMENT THEORY (of skeletal muscle contraction) - An Overview (fig. 9.6) 1. the myosin heads of the thick filaments attach to the actin in the thin filaments, and then pivot to pull thin filaments inward toward the center of the sarcomere; this leads to the H Zones disappearing, the I bands becoming smaller, and the sarcomere becoming shorter; the A band is unchanged during contraction 2. this is controlled by a nerve-generated ACTION POTENTIAL; the impulse travels along the sarcolemma of the muscle cell, down the T tubules, and into the terminal cisternae -- ultimately releasing the stored calcium, and contracting the muscle B. SLIDING FILAMENT THEORY (of skeletal muscle contraction) - The Details 1. the ACTION POTENTIAL on the somatic motor neuron - we will not cover the details of this step until we get to the nervous system; for now just know that: a. the action potential is conducted along the neuron by traveling along the long, thread-like extension called the AXON, until it reaches the end of the neuron

(7th edition) b. VESICLES containing the neurotransmitter ACETYLCHOLINE (ACh) bind with the plasma membrane at the end of the neuron, and release of ACh (by exocytosis) into the SYNAPTIC CLEFT of the NEUROMUSCULAR JUNCTION (fig 9.7 a,b,c) c. diffusion of ACh across the synaptic cleft to the muscle cell membrane d. binding of ACh to receptors on the muscle cell membrane 2. generation of the Action Potential on the Sarcolemma (muscle cell membrane) a. binding of ACh to receptors on the sarcolemma causes opening of SODIUM/POTASSIUM CHANNELS on the muscle cell membrane (fig. 9.7 c); Sodium (Na+) comes in (influx) / Potassium (K+) goes out (efflux) b. Na+ INFLUX (into cell) is greater than K+ EFFLUX (out of the cell), causing muscle cell membrane DEPOLARIZATION to action potential threshold (fig. 9.8; read through steps a-d of this figure in book) c. the action potential is generated and spreads along the muscle cell membrane (sarcolemma), including down the T-tubules (invaginations in the muscle cell membrane) 3. inside of the muscle cell - EXCITATION-CONTRACTION COUPLING (fig. 9.10): a. action potential travelling down the T-Tubules causes opening of sarcoplasmic reticulum (SR) calcium channels and release of calcium (Ca2+) into the cell from the SR c. causes increase in muscle intracellular calcium concentration d. binding of calcium to troponin of thin filaments, changing its conformation

e. movement of tropomyosin of thin filaments to expose myosin-binding sites on actin f. binding of ACTIVATED MYOSIN to actin (fig. 9.12, step 1) [*previously, binding of ATP to myosin head and hydrolysis of ATP occurred to ACTIVATE (or cock) the MYOSIN; think of this like cocking the gun (see figure 9.12, step 4)]

(7th edition) g. pivoting of the myosin head to slide actin relative to myosin - this uses the energy from ATP hydrolysis that had been stored to activate (or cock) the myosin head to cause POWER STROKE; think of this as pulling the trigger of the gun (see fig. 9.12, step 2) h. each power stroke moves the thin filaments toward each other, as though the process was like a ratchet; thus, the sarcomere gets shorter i. sarcomere shortening results in muscle contractile force (tension) and can result in the whole muscle shortening 4. then, for relaxation to occur: a. the motor neuron no longer stimulates the muscle cell; thus, the motor neuron membrane potential returns to resting value, and no more ACh is released at the neuromuscular junction

b. ACh dissociates from the ACh receptors on the muscle cell membrane and binds to ACETYLCHOLINESTERASE (an enzyme) at the synapse c. acetylcholinesterase breaks down ACh d. there is no more stimulus of receptors on the muscle cell membrane, so the sodium/potassium channels on the muscle cell membrane close e. the muscle cell membrane potential returns to resting value f. the T-tubules are no longer depolarized, so the sarcoplasmic reticulum (SR) calcium channels close g. Ca++ can no longer diffuse from the SR, and SR Ca++ ATPase actively pumps Ca++ back into the SR (against its concentration gradient) h. muscle intracellular calcium concentration returns to resting level i. Ca++ can no longer bind to troponin of the thin filaments, so its conformation and the position of tropomyosin return to the resting state (where myosin-binding sites on actin are blocked) j. also, note that the binding of ATP to the myosin head has occurred to detach the myosin from the actin (fig. 9.12, step 3); without a constant supply of ATP in our bodies, the myosin heads remain attached to the actin in a state of constant contraction, or a rigor complex also known as rigor mortis; when we die we no longer make ATP, so the myosin heads remain attached to the actin (for about 72 hours).

(7th edition) C. Contraction of Skeletal Muscle 1. the force created by the contracting muscle is called the muscle TENSION 2. the LOAD is a weight or force that opposes the contraction of the muscle 3. muscles shorten when they contract

4. events at the neuromuscular junction convert a chemical signal from a somatic motor neuron (the neurotransmitter ACh) into an electrical signal in the muscle fiber 5. a muscle TWITCH is one cycle of contraction followed by relaxation 6. the Motor Unit (fig. 9.13) a. somatic motor neuron axons branch to innervate many skeletal muscle fibers b. MOTOR UNIT a motor neuron and all of the muscle fibers it that innervates (controls) 7. COMPLETE TETANUS (fig. 9.15) - A smooth, sustained muscle contraction plateau resulting from high-frequency stimulation 8. TREPPE (fig. 9.18) The Staircase Effect - treppe describes the staircase pattern of a muscle tracing that begins with smaller, initial contractions (perhaps half as strong), and ends with full contractions 9. ISOTONIC CONTRACTIONS move loads, but ISOMETRIC CONTRACTIONS create force without movement (fig. 9.19) D. Types of Skeletal Muscle Fibers 1. skeletal muscle fibers are categorized according to: a. how they manufacture energy (ATP) - aerobic vs. anaerobic b. how quickly they contract 2. skeletal muscle fibers are divided into three classes (table 9.2): a. SLOW OXIDATIVE fibers b. FAST GLYCOLYTIC fibers

(7th edition) c. FAST OXIDATIVE fibers 3. slow oxidative fibers a. dark red color due to abundant myoglobin b. obtain energy from aerobic metabolic reactions (oxygen dependent) c. contain a large number of mitochondria d. rich supply of capillaries e. contract slowly and resistant to fatigue 4. fast glycolytic fibers a. contain little myoglobin (white in color) and few mitochondria b. about twice the diameter of slow-oxidative fibers c. contain more myofilaments and generate more power d. depend on anaerobic pathways (not oxygen dependent) e. contract rapidly and tire quickly 5. fast oxidative fibers a. have an intermediate diameter b. contract quickly like fast glycolytic fibers c. are oxygen-dependent (aerobic) d. have high myoglobin content (red color) and rich supply of capillaries e. somewhat fatigue-resistant f. more powerful than slow oxidative fibers *skeletal muscles typically have all 3 types of fibers, but vary in the amount of each fiber; athletes can actually alter the composition of their muscles based on the activities that they do; for example, marathon runners develop their slow oxidative fibers, whereas weight lifters develop their fast glycolytic fibers.

(7th edition) E. Muscle Metabolism 1. immediate energy - used in first 10-30 seconds of vigorous exercise; ATP creatine phosphate (ATP-CP) system used; creatine phosphate contributes a phosphate to ADP to make ATP; 1 creatine phosphate (CP) = 1 ATP; all 3 skeletal fiber types use this system

2. short-term energy - used approx. 30 - 90 seconds into vigorous exercise; uses glycolysis to break down glucose to pyruvate to lactate (lactic acid); 1 glucose = 2 ATP; used by fast glycolytic fibers 3. long-term energy - used approx after 2 min of vigorous exercise; uses glycolysis, citric acid cycle (krebs cycle), and electron transport chain to fully oxidize glucose; 1 glucose = 36 ATP (max); used by slow oxidative fibers and fast oxidative fibers IV. Comparison of the 3 Types of Muscle Tissue (Table 9.3) A. SKELETAL MUSCLE characteristics: 1. striated 2. multinucleated 3. under the control of the voluntary (somatic) nervous system 4. contains myofibrils composed of sarcomeres (gives it the striated appearance) 5. contains T tubules 6. no gap junctions 7. well developed sarcoplasmic reticulum 8. fast contracting 9. every fiber is controlled by a nerve B. CARDIAC MUSCLE characteristics: 1. striated and branched 2. uni- or binucleate 3. contains intercalated discs 4. under the control of the involuntary (autonomic) nervous system = ANS 5. contains myofibrils composed of sarcomeres (gives it the striated appearance) 6. contains T tubules 7. presence of gap junctions at the intercalated discs 8. less developed sarcoplasmic reticulum than skeletal muscle 9. found in the wall of the heart only 10. not every fiber is controlled by a nerve; can contract without input from the nervous system

(7th edition) C. SMOOTH MUSCLE characteristics: 1. unstriated and with a fusiform shape 2. uninucleate 3. under the control of the involuntary (autonomic) nervous system = ANS 4. does not contain myofibrils composed of sarcomeres 5. does not contain T tubules 6. presence of gap junctions 7. less developed sarcoplasmic reticulum than skeletal muscle 8. found in the walls of hollow organs 9. not every fiber is controlled by a nerve; can contract without input from the nervous system V. Effects of Exercise on Muscles - Resistance Training (Weights) A. Increase in muscle strength occurs because of neural adaptations and muscle hypertrophy (increase in muscle size) B. Neural Adaptations - occur in the first 4 weeks of weight training; hypertrophy generally does not occur in the first 4 weeks of lifting weights 1. recruitment of more muscle fibers 2. more inhibition of the antagonistic muscles 3. reduced inhibition by the golgi tendon organ - the golgi tendon organ senses tension, and responds by stimulating the relaxation of the muscle to prevent injury; arm wrestlers train themselves in a way that minimizes the effects of the golgi tendon organs C. Muscle Hypertrophy - starts to occur after 4 weeks of training 1. not due to increase in number of muscle fibers (cells) 2. it is due to increase in the number of myofibrils in the muscle cell; muscle cell becomes thicker in diameter

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D. Myth: delayed onset muscle soreness (soreness for the next few days) is due to lactic acid buildup -- FALSE! it is really due to muscle damage (to the sarcolemma and interior of the cell)

(7th edition) E. Flexibility Training 1. flexibility - range of motion around a joint or group of joints 2. flexibility training decreases the risk of injury and can possibly enhance recuperation time and performance 3. Limbering - warming up; not the same as stretching; restores the normal flexibility (what you are presently capable of) of the muscles and tendons; no change in range of motion has been gained; limbering is important prior to exercise for prevention of injuries

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4. Stretching - leads to actual lengthening of the muscle fibers, and likewise, lengthening of proprioceptors (e.g. muscle spindles) which detecting stretch in the muscle or tendon; stretching over long periods of time can lead to a greater range of motion around a joint or group of joints; this often requires assistance from a partner who provides some resistance in order to obtain optimal results VI. More on Exercise and Muscles - Ergogenic (work-producing) Aids *application of nutritional, physical, mechanical, psychological, or pharmacological aids to improve muscular performance: A. Nutritional Supplements 1. protein powers, muscle builders, and bars -- some athletes may require additional protein above their normal diet; however, beware! many supplements may be spiked with ephedrine or anabolic steroids -- the supplement industry is not regulated! (you dont always know exactly what you are taking) 2. gatorade - studies show increased hydration vs. drinking water; because it tastes good, you will drink more of it; however, it contains a lot of sugar and calories! 3. creatine - some athletes take creatine to improve performance; the idea is that the more creatine in the body, the more of the immediate energy source available (recall that creatine phosphate is used during the first 10-30 seconds of vigorous exercise); however, there is little evidence that creatine is beneficial for the average person 4. anabolic steroids - can create increased muscle hypertropy and strength; however, many side effects are associated with steroids; these include small testes (and decreased fertility), increased estrogen (men can develop breasts), prostate gland hypertrophy, increased LDL (bad ones), decreased HDL (good ones), increased heart attack risk, and liver damage

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12 5. caffeine - the most widely consumed drug in the world! it is used to increase mental awareness and decrease fatigue; however, you can build up a tolerance to caffeine if it used too frequently

B. Physical and Mechanical Aids - e.g. use of a weight lifting belt or knee brace; application of massage C. Psychological - e.g. use of visualization; visualizing yourself performing the exercise or event (sports) before it actually occurs; this technique has been shown to be highly effective VII. Disorders of Muscle Tissue - muscle tissues experience few disorders; heart muscle is the exception; skeletal muscle is remarkably resistant to infection A. Muscular Dystrophy a group of inherited muscle destroying diseases; affected muscles enlarge with fat and connective tissue and muscles degenerate B. Strain - tearing of a muscle; also known as a muscle pull (you learned about a sprain in Unit 6; how is a strain different from a sprain?)

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