Muscle Tissue Chapter 9 Biology 2121

Muscle Functions (1). Maintaining posture (2). Stabilizing joints (3). Generating heat (4). Storing and Moving Smooth muscle (peristalsis)

Functional Characteristics of Muscle (1). Excitability and Irritability (2). Contractility Ability to shorten (3). Extensibility Ability to be stretched (4). Elasticity Ability to recoil and resume original shape

Skeletal Muscle Tissue Function Voluntary Large Cells 10 to 100 um diameter 30 cm length Multinucleated Striated Functional Syncyntium

Smooth Muscle Tissue Functions Locations Uninucleated Non-striated Hollow organs “Visceral” Uninucleated Spindle-shaped cells Non-striated Involuntary Peristalsis

Cardiac Muscle Tissue Function – Location Involuntary Striated Intercalated discs Specialized gap junctions

Skeletal Muscle Gross Anatomy (1). Each skeletal muscle is a discrete organ (2). Each muscle is supplied with Nerve and Blood tissue. (3). Organizational levels of skeletal muscles page 282

Organization Level – Muscles

Connective Tissue Sheaths Endomysium Areolar CT fibers Perimysium Dense irregular fiberous CT Epimysium Dense irregular CT CT sheaths Connective Tissue Sheaths

Attachments – Skeletal Muscle Attach to Bones Tendons Aponeurosis Direct or Indirect Attachments

Fascia Superficial- Hypodermis Deep Epimysium Endomysium Perimysium

Blood and Nerve Supply Veins Muscle Contraction Artery Arterioles Somatic Motor Neurons -part of Peripheral Nervous System motor division Muscle Contraction Artery Arterioles Capillaries Venuoles Blood Returns to the Heart Veins

Microscopic Anatomy – Skeletal Muscle (1). Skeletal Muscle fiber Size: multiple nuclei; 10-100 um diameter; some 30 cm long Syncytium Sarcolemma Sarcoplasma (2). Myofibrils 1-2 um diameter; mitochondria and other organelles; densely packed Contractile elements: striations, sarcomeres, and myofilaments

Myofilaments - Striations Sarcomeres Area between two Z discs Smallest contractile unit (functional unit) Myofilaments - Striations Thick: span the entire A band myosin Thin: across I band and partly across (A) Actin

Muscle Proteins Titin,Nebulin,Myomesin Actin, Myosin Structural Contractile Regulatory Titin,Nebulin,Myomesin Actin, Myosin Tropomyosin, Troponin

Ultrastructure of Myofilaments Myosin (protein) Two globular heads Tail two interwoven polypeptide chains (heavy) Thin filaments (Actin protein) Tropomyosin Troponin: 3-polypeptides TnI ; TnT ; TnC Elastic filaments Titin

Microscopic Structure- Actin and Myosin

Sarcoplasmic Reticulum regulates intracellular levels of calcium ions T Tubules Triads: terminal cisterna, T tubule, terminal cisterna Triad Relationship –integral proteins T tubule proteins SR proteins (foot proteins)

How muscles contract Sliding Filament Model Exitation-Coupling Link (ch.7-myofilament and sarcomere contraction)

Sliding Filament Model of Contraction Relaxed Fully Contracted

What Causes a Muscle Contraction to Occur? Muscle Contractions – Nerve Stimulation Neuromuscular Junction Nerves contain Neurotransmitters Muscle contraction – Acetylcholine (ACh) NT bind to sarcolemma of muscle (Receptor Sites) Causes a nerve impulse (Action Potential) Stimulates the Sarcoplasmic Reticulum to release Ca++ Stimulates the muscles to contract

Neuromuscular Junction

Neuromuscular Junction - Steps 1. Nerve impulse reaches axonal end 2. Voltage-gated channels open- Ca 2+ ions flow in 3. Synaptic vesicles fuse with axonal membrane 4. NT (ACh) released via exocytosis 5. ACh diffuses across the synaptic cleft and fuses with sarcolemma ACh receptors ACh is the NT 6. Causes an electrical event stimulates muscle contraction Action Potential 7. ACh is degraded by acetylcholinerasterase Link (ch. 7 neuromuscular junction)

Generation of an Action Potential (a) Polarized membrane -70 mV (resting membrane potential) (+) outside; (-) inside (b) Depolarization (c) Propagation (d) Repolarization

Generation of action potential across sarcolemma 1. SODIUM (OUTSIDE) MORE + ; POTASSIUM (INSIDE) MORE – 2. When ACh binds to receptors, ion channels open. 3. More Na goes into the cell than K moving out. 4. Cell becomes less negative. “Depolarized” 5. This begins the Action Potential II. Steps in the Action Potential 1. Currents spread to adjacent areas along the membrane, become depolarized and gates open and Na diffuses in. 2. Propagation of AP: moves along the length of the Sarcolemma; gates continued to be opened and the AP spreads. 3. Repolarization: Follows behind the depolarization wave; Na gates close and K opens and K diffuses out rapidly down concentration gradient. 4. Refractory period: until repolarization is complete, muscle cannot be stimulated again; original membrane potential is restored.

Excitation-Contraction Coupling – Sequence of Events by which transmission of an Action Potential leads to sliding of the filaments (contraction) Steps in Excitation and Contraction 1. AP propagates down sarcolemma to T tubules. 2. At the triad the AP causes the SR to release Ca ions into the sarcoplasm. 3. Some Ca binds to troponin and it changes shape and removes the blockade of tropomyosin. 4. Myosin heads attach and pull the thin filaments to center of sarcomere. 5. Ca disapates, and the AP is over; Ca moved back into the SR via Ca pump (ATP driven) (page 293) 6. When Ca drops very low the tropomyosin again blocks the myosin binding sites.

Excitation-Contraction Coupling 1. AP propagates along sarcolemma and down T-Tubule 2. AP transmission past triads --- terminal cisternae of SR --- releases calcium ions Becomes available to the myofilaments 3. Calcium binds to troponin -- changes shape- removes blocking action of tropomyosin 4. If Ca levels (10-5 M) myosin heads attach and pull thin filaments toward center of sarcomere Cross-bridge formation 5. Ca signal ends (30ms)-- Ca levels fall (ATP calcium pump-back into SR) 6. Tropomyosin blocks binding site ending cross-bridge activity

Role of Ionic Calcium in Contraction 1. Tropomyosin blocks binding site (low Ca levels) 2. As Ca levels rise, binds to TnC of troponin 3. Troponin undergoes a transformation change- moves tropomyosin away from binding site 4. Attachment of myosin head Notes on the Slide TnT, TnC and Tnl are regulatory proteins in troponin. Ca binds to the TnC which makes the troponin change shape and allow for exposure of the binding sites.

Events in Muscle Fiber Contraction 1. Cross-bridge is formed 2. Power Stroke 3. Cross-bridge detachment 4. Cocking of myosin head Rigor Mortis

Events in the Sliding of Thin Filaments During Contraction Notes on this Slide Formation of the Cross-Bridge Heads are fully attached to the tropomyosin on actin Power Stroke Head pivots changing from high energy configuration to low energy config (bent); this pulls on the actin sliding it towards the center of the sarcomere. ADP And Pi are released from the head Detachment ATP binds to head, myosin loosens hold on actin and CB detachment occurs Cocking ATPase hydrolyses ATP; energy is released and the head returns to pre-stroke cocked position. Ready for another CB formation.

Links for Action Potential and Coupling Link (ch. 7 – action potential) NHC (sliding filament)

Each axon divides and serves muscle fibers Each muscle is served by one motor nerve or neuron which contains axons of hundreds of motor neurons (may serve many muscle fibers or a few) Cell body of neuron Contained within the spinal cord ‘grey matter’ Each axon divides and serves muscle fibers All muscle fibers contract when the motor neuron sends impulses Muscle control – fine vs weight bearing

Graded Muscle responses Myogram Response of motor unit to a single action potential of its motor neuron is called a muscle twitch Latent period Contraction Relaxation Graded Muscle responses Muscle Twitch Myogram: Produced when a muscle is attached to an apparatus Twitch: response of a motor unit to a single action potential; involves a contraction and relaxation. 3. Parts of a myogram Latent period Ms following stimulation; excitation and coupling is occuring but cannot see on the myogram Contraction CB are activated 10-100 ms Relaxation Ca reenters the SR; CB broken 4. Graded Responses Healthy muscle contractions are smooth unlike the muscle twitch Graded responses are control mechanisms for smooth contractions Changes in Stimulation Frequency Two identical stimuli are applied to a muscle in succession, second twitch is always stronger (wave summation) Occurs before the muscle has relaxed. Why? More Ca is released, muscle tension during the second contraction caused more shortening than the first Summation of contractions (refractory period is always honored) Sustained stimulation at faster rates causes the summation to be greater, quivering (incomplete tetanus) If all relaxation disappears complete tetanus occurs Response to strong stimuli Force of contraction is controlled by motor unit summation Called recruitment (many muscle fibers are called into play) First contraction occurs- threshold Max stimulus- strongest stimulus that produces a contractile force. Increasing the stimulus beyond this point will not make the muscle contract stronger. Recruitment accounts for a smooth touch or pat and the same hand can deliever a blow. Treppe When the same stimulus is applied the contractions get more strong Due to increase in Ca ions opening up more binding sites. As the muscle works harder it produces heat which makes it more pliable.

Twitches and Wave Summations

Treppe: Initial contractions are not as strong as later contractions caused by the same amount of stimulus. Why? Increasing availability of Ca in the SR; Increasing Ca increase the number of troponin binding sites open; muscles warm up and liberate heat making them more pliable