Chapter 7 The Muscular System Most abundant tissue (600+)
I. Characteristics of Skeletal Muscle 1) Function: motion; posture; body heat Excitable, Contract/Extend, Elastic
2) Structure A. Connective tissue: Epimysium (fascia): wraps whole muscle Perimysium: wrap fasciculi (bundle of cells) Endomysium: wrap muscle cell (fiber)
B. Muscle Cell/Fiber: a) Sarcolemma (cell membrane): long striated cylinder w/nuclei T (transverse) tubules: wrap sarcolemma & connect (pass message-action Potential) to Sacroplasmic Reticulum: Hi Ca ++ conc (conduct (AP) to actin)
b) Sarcoplasm: cytoplasm w/2 myofibril types 1) Actin: thin, beaded Troponin: Ca-binding sites Tropomyosin: regulates myosin binding sites (block w/no AP) 2) Myosin: thick, golf clubs, binds/moves actin
Sarcolemma:
C) Sarcomere: basic repeating myofibril units 1) Z disk: anchors actin; divides sarcomeres 2) I band: light zone: actin only; spans Z disk 3) A band: dark zone; length of myosin (w/actin) 4) H Zone: myosin only; middle 5) M line: anchors myosin; center
3) Nerve/Muscle Membrane Potential (polarized): sends message for action Resting: + out (Na +, K + leak/- in (protns - ) Depolarization: AP-charge reversd; Na + in Repolarization: K+ out Na/K pump returns resting potential
4) Nerve Supply Motor Neurons to Muscles Motor Motor Unit: 1 neuron to all muscle fibers Many units per muscle
Neuromuscular Junction or synapse 1. AP to presynaptic terminal (Ca ++ in) 2. Acetylcholine (Ach): neurotransmitter crosses synaptic cleft (space) open Na + channels 3. Depolarization (postsyn) muscle fiber sarcolemma Na channel closed without Ach Na channel opened with Ach
Acetylcholinesterase: brkdwn Ach Myasthenia Gravis: antibodies destroy Ach receptors (weakness) Curare binds ACH receptors flaccid paralysis
5) Muscle Contraction Sliding Filament Mechanism: Myosin cross-bridges pull actin toward H zone
H/I shorten/a unchanged
1. AP from nerve to muscle 2. Ach released; Na channels open 3. Na in; AP->sarcolemma->T tubls->s. reticlm 4. S. reticulum releases Ca to actin troponin
5. W/Ca ++ Tropomyosin exposes binding sites
6. Myosin form cross-bridge w/actin (rigor) 7. Power stroke moves actin w/adp+p release 8. Cross-bridge broken/head rests w/2 ND ATP Rigor Mortis: No ATP avail for release w/death
9. Contraction continues w/ca and ATP 1. ACH released 2. AP moves along membrane and T-tubules 3. Ca released from SR voltage gated Ca channel opens 4. Ca binds to Troponin-C conformation changes favor tropomyosin opens actin sites 5. myosin cross-bridges attachdetach from actins/pulls filament toward M-line 6. Ca removed (uptake by SR) 7. tropomyosin blocks actin sites relaxation
6) All-or-none contraction: all fibers fully Motor Unit All the muscle fibers (cells) innervated by the same motor neuron All-or-None Principle: All muscle fibers that make up a motor unit contract fully together. This principle holds true at the sarcomere, myofibril, and muscle fiber levels as well. Partial contraction occurs at the muscle level because all motor units are not contracting at the same time. Recruitment: The process by which the number of actively contracting motor units is increased.
7) Summation: increased contraction force w/ stimulation=tetanus: sustained contractn (no relax) Fused or Complete Tetanus: A sustained maximum contraction in which individual contractions are not discernable. In fused tetanus, multiple stimuli are occurring so fast, the muscle does not undergo any relaxation.
8) Recruitment: units over time = smooth strength
9) Energy Requirements: Aerobic Resp: Glucose + O 2 = ATP Anaerobic Resp: Glucose = ATP + lactic acid ATP /Creatine P : rapidly converted to ATP
Food source Creatine level;grams/pound Herring 3.0/lb Pork 2.3/lb Salmon 2.0/lb Beef 2.0/lb Tuna 1.8/lb Cod 1.4/lb Cranberries.0009/lb
10) Types of Muscle Contractions: a) Isometric: no shortg w/ tensn: posture
b) Isotonic: constant tensn w/shortg: movemt Concentric (tension w/shortening) Eccentric (constant tensn w/lengthenin-lower wght)
11) Myofibril Types: a) Slow Twitch: Type I myosin = Aerobic Dark w/bld (myoglobin O 2 ): duck breast/chickn leg b) Fast Twitch: Type II myosin = Anaerobic Quick contract/fatigue: chicken breast
c) Humans Ave adult: equal I/II Sprinters: 80% more II/leg Distance: 95% I/leg Athletes: balanced I/II # muscle cells somewhat constant after birthundifferentiated Satellite cells = new w/injury Hypertrophy: cell size w/exer- mito; myofilmts Relative Distributions of Slow Twitch & Fact Twitch Myosin Isoforms (Type I & Type II) Type I (slow) Type II (fast) Type IIa Type IIx Average person 50% 50% 40% 10% spinal injury 4% 96% 48% 48% sprinter 20% 80% 45% 35% couch potato 40% 60% 30% 30% marathoner 80% 20% 20% 0% These myosin isoforms are conserved evolutionarily: Comparing myosin isoforms from different mammals reveals remarkably little variation species to species. Rat type I is more similar to human type I myosins, than it is to rat type II's. Thus selective evolution has maintained a functional difference between type I's & type II's over eons of evolution.
II. Smooth Muscle: Unstriated, tapered, 1 nucleus, invol (dig) Slow twitch Hormones regulate (autorhythmicity)
III. Cardiac Muscle: Striated, branched, 1 nucleus/cell, invol Slow twitch Hormones regulate Intercalated disks pass AP
Aging on Skeletal Muscle Decreased muscle mass Increased contraction response time Decreased stamina Increased recovery time Affects of aging slowed/reversed w/exercise
Disorders: Muscular Dystrophy; Duchenne MD; Myotonic MD; Myasthenia Gravis; Tendinitis (p189) A patient with this disease produces autoantibodies to the acetylcholine receptors MUSCLE WEAKNESS CAUSED BY MUSCULAR DYSTROPHY Duchenne muscular dystrophy is inherited in an X-linked recessive pattern
Types Skeletal: 40% wt, voluntary Smooth: involuntary Cardiac: involuntary