The Muscular System Chapter 7

There are four characteristics associated with muscle tissue: Excitability Contractility Extensibility Elasticity - Tissue can receive & respond to stimulation - Tissue can shorten & thicken - Tissue can lengthen - After contracting or lengthening, tissue always wants to return to its resting state

The characteristics of muscle tissue enable it to perform some important functions, including: Movement – both voluntary & involuntary Maintaining posture Supporting soft tissues within body cavities Guarding entrances & exits of the body Maintaining body temperature

Types of muscle tissue: Skeletal muscle tissue Associated with & attached to the skeleton Under our conscious (voluntary) control Microscopically the tissue appears striated Cells are long, cylindrical & multinucleate -c Rapid onset, rapid fatigue

Slower onset, fatigue resistant, can’t tetanize Cardiac muscle tissue Makes up myocardium of heart Unconsciously (involuntarily) controlled Microscopically appears striated Cells are short, branching & have a single nucleus Cells connect to each other at intercalated discs Slower onset, fatigue resistant, can’t tetanize

Slow onset, fatigue resistant Smooth (visceral) muscle tissue Makes up walls of organs & blood vessels Tissue is non-striated & involuntary Cells are short, spindle-shaped & have a single nucleus Tissue is extremely extensible, while still retaining ability to contract Slow onset, fatigue resistant

Anatomy of a Skeletal Muscle Entire muscle is surrounded by epimysium (fibrous ct)—at the end forms a tendon Contains blood vessels and nerves Made up of fascicles (bundles of muscle fibers) surrounded by perimysium Fascicles made up of muscle fibers surrounded by endomysium Fibers are the cells-made of myofibrils

Sarcolemma—muscle cell membrane Sarcoplasm—cytoplasm-many mitochondria, many nuclei

Myofibrils are surrounded by sarcoplasmic reticulum which stores Ca needed for contraction Myofibrils are bundles of thick filaments (myosin) and thin filaments (actin) Repeating units of these filaments form a sarcomere Interactions between the myosin and actin filaments produce contraction

Organization of Skeletal Muscles

Anatomy of skeletal muscles epimysium tendon perimysium Muscle Fascicle Surrounded by perimysium endomysium Skeletal muscle Skeletal muscle fiber (cell) Surrounded by epimysium Surrounded by endomysium Play IP Anatomy of Skeletal muscles (IP p. 4-6)

Microanatomy of a Muscle Fiber

transverse (T) tubules sarcoplasmic reticulum Microanatomy of a Muscle Fiber (Cell) transverse (T) tubules sarcoplasmic reticulum sarcolemma terminal cisternae mitochondria myoglobin thick myofilament thin myofilament myofibril triad nuclei

myofibril Muscle fiber sarcomere Z-line Thin filaments Thick filaments Myosin molecule of thick myofilament Thin myofilament

Myofilaments of sarcomere Z line M line Z line Thin myofilaments Thick myofilaments

Muscle contraction Under control of nervous system Nerves and skeletal muscle fiber connect at neuromuscular junctions Neuron branches out and ends in expanded knobs-synaptic knobs which contain a neurotransmitter Acetylcholine (Ach) that changes the sarcolemma and triggers contraction

Neuromuscular junction telodendria Synaptic terminal (end bulb) Synaptic vessicles containing Ach Synaptic cleft Neuromuscular junction Motor end plate of sarcolemma

Muscle contraction 1. electrical impulse from brain 2. release of Ach 3. triggers Ca ions to be released from SR into sarcoplasm 4. linkages (cross bridges) form between the actin and myosin filaments –requires ATP 5. actin filaments slide inward along myosin filaments 6.muscle fiber shortens (contraction)

Sliding Filament Theory Myosin heads attach to actin molecules (at binding (active) site) Myosin “pulls” on actin, causing thin myofilaments to slide across thick myofilaments, towards the center of the sarcomere Sarcomere shortens, I bands get smaller, H zone gets smaller, & zone of overlap increases

relaxation 1. cholinesterase is secreted and causes ACh to decompose 2. Ca are pumped back into SR 3. linkages between actin and myosin broken 4. actin and myosin slide apart 5. muscle relaxes

Muscle mechanics All or none response A muscle fiber contracts or doesn’t The amount of tension produced by a whole muscle is determined by the frequency of stimulation and the # of fibers stimulated

Twitch—single stimulus contraction relaxation sequence Latent period-getting ready Contraction-tension rises to a peak Relaxation-tension falls to resting lines contraction latent relaxation

Summation-(sustained contraction)-stimuli arrive before relaxation complete Complete tetanus-(sustained powerful contraction)-frequency of stimulation so high-relaxation eliminated Motor unit- all muscle fibers controlled by a single neuron (finer control, fewer muscle fibers)

small motor units  precise control (e.g. eye muscles The size of the motor unit determines how fine the control of movement can be – small motor units  precise control (e.g. eye muscles large motor units gross control (e.g. leg muscles) Recruitment is the ability to activate more motor units as more force (tension) needs to be generated There are always some motor units active, even when at rest. This creates a resting tension known as muscle tone, which helps stabilize bones & joints, & prevents atrophy PLAY Play IP Contraction of motor units p. 3-7

Recruitment- increased tension produced by increase in the number of motor units muscle tone-resting tension Isotonic contraction-increased tension to move resistance (lifting, walking, running) Isometric contraction-resistance doesn’t move (pushing against wall, maintaining posture)

Muscle fatigue-muscles cannot contract due to: Exhaustion of ATP Damage to SR Decrease in oxygen Decreased blood flow

Recovery period-return to preexertion levels Oxygen debt-breathing rate increases until homeostasis is reached (preexertion level) Hypertrophy Increased muscle size due to increased numbers of mitochondria, myofibrils, and glycogen reserves Due to repeated exhaustive stimulation

Atrophy Muscle not stimulated on a regular basis Loss of muscle tone and mass

Muscle performance Types of Fibers 1. fast- contract .01 seconds or less, large, powerful contractions, fatigue rapidly, “white color” 2. Slow- ½ size of fast, takes 3 times longer to contract, increased endurance, increased blood flow, red pigment (myoglobin) carries oxygen darker in color 3. intermediate- pale, more capillaries than fast fibers, resistant to fatigue Humans are a mixture of types. Fast & intermediate in eyes & hand Slow in legs

Physical Conditioning Increased blood flow improves oxygen and nutrient availability Anaerobic endurance-fast fibers, brief intensive workouts that stimulate hypertrophy Aerobic endurance-sustained low level workouts, jogging, distance swimming, warm up to increase blood flow & treppe

Hormones for muscles 1. growth hormone & testosterone Increase synthesis of proteins and enlargement of muscles 2. thyroid hormone Increases the rate of energy consumption 3. Adrenaline Stimulates muscle metabolism and increases the duration of stimulation and force of contraction

Aging Muscle fibers decrease in diameter due to a decrease in myofibrils Decrease in ATP, strength and endurance Increased fibrous connective tissue-less flexible Rapid fatigue, may overheat Decreased healing, increased scar tissue

Thin Myofilament (myosin binding site)

Thick myofilament (has ATP & actin binding site) *Play IP sliding filament theory p.5-14 for overview of thin & thick filaments

Sarcomere A band Z line Z line I band Zone of overlap M line H zone I band Zone of overlap Zone of overlap M line Thin myofilaments Thick myofilaments

As sarcomeres shorten, myofibril shortens As sarcomeres shorten, myofibril shortens. As myofibrils shorten, so does muscle fiber Once a muscle fiber begins to contract, it will contract maximally This is known as the “all or none” principle

Physiology of skeletal muscle contraction Skeletal muscles require stimulation from the nervous system in order to contract Motor neurons are the cells that cause muscle fibers to contract cell body dendrites Synaptic terminals (synaptic end bulbs) axon telodendria (motor neuron)

Overview of Events at the neuromuscular junction An action potential (AP), an electrical impulse, travels down the axon of the motor neuron to the end bulbs (synaptic terminals) Release of Acetylcholine (Ach) into the synaptic cleft Ach diffuses across the synaptic cleft & binds to Ach receptors on the motor end plate The binding of Ach to its receptors causes a new AP to be generated along the muscle cell membrane Immediately after it binds to its receptors, Ach will be broken down by Acetylcholinesterase (AchE) – an enzyme present in the synaptic cleft

Action potential Arrival of an action potential at the synaptic terminal Axon Arriving action potential Synaptic terminal Sarcolemma Vesicles ACh Synaptic cleft AChE molecules ACh receptor site Muscle fiber Sarcolemma of motor end plate An action potential (AP), an electrical impulse, travels down the axon of the motor neuron to the end bulbs (synaptic terminals) Figure 7-4(b-c) 2 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Release of Acetylcholine (Ach) into the synaptic cleft Action potential Arrival of an action potential at the synaptic terminal Axon Arriving action potential Synaptic terminal Sarcolemma Vesicles ACh Synaptic cleft AChE molecules ACh receptor site Muscle fiber Sarcolemma of motor end plate Release of acetylcholine Vesicles in the synaptic terminal fuse with the neuronal membrane and dump their contents into the synaptic cleft. Release of Acetylcholine (Ach) into the synaptic cleft Figure 7-4(b-c) 3 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Action potential Arrival of an action potential at the synaptic terminal Axon Arriving action potential Synaptic terminal Sarcolemma Vesicles ACh Synaptic cleft AChE molecules ACh receptor site Muscle fiber Sarcolemma of motor end plate ACh binding at the motor and plate Ach diffuses across the synaptic cleft & binds to Ach receptors on the motor end plate Release of acetylcholine Vesicles in the synaptic terminal fuse with the neuronal membrane and dump their contents into the synaptic cleft. The binding of ACh to the receptors increases the membrane permeability to sodium ions. Sodium ions then rush into the cell. Na+ Na+ Na+ Figure 7-4(b-c) 4 of 5 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

The binding of Ach to its receptors causes a new AP to be generated along the muscle cell membrane Immediately after it binds to its receptors, Ach will be broken down by Acetylcholinesterase (AchE) – an enzyme present in the synaptic cleft

Play IP neuromuscular junction p. 14 Action potential Arrival of an action potential at the synaptic terminal Axon Arriving action potential Synaptic terminal Sarcolemma Vesicles ACh Synaptic cleft AChE molecules ACh receptor site Muscle fiber Sarcolemma of motor end plate ACh binding at the motor and plate Appearance of an action potential in the sarcolemma Release of acetylcholine Vesicles in the synaptic terminal fuse with the neuronal membrane and dump their contents into the synaptic cleft. The binding of ACh to the receptors increases the membrane permeability to sodium ions. Sodium ions then rush into the cell. An action potential spreads across the surface of the sarcolemma. While this occurs, AChE removes the ACh. Action potential Na+ Na+ Na+ Play IP neuromuscular junction p. 14

Physiology of Skeletal Muscle Contraction Once an action potential (AP) is generated at the motor end plate it will spread like an electrical current along the sarcolemma of the muscle fiber The AP will also spread into the T-tubules, exciting the terminal cisternae of the sarcoplasmic reticula This will cause Calcium (Ca+2 ) gates in the SR to open, allowing Ca+2 to diffuse into the sarcoplasm Calcium will bind to troponin (on the thin myofilament), causing it to change its shape. This then pulls tropomyosin away from the active sites of actin molecules. The exposure of the active sites allow the sliding of the filaments Table 7-1

Physiology of skeletal muscle contraction – events at the myofilaments Resting sarcomere Active-site exposure Cross-bridge formation ADP Myosin head ADP + P + Sarcoplasm P Troponin ADP + P Ca2+ Ca2+ Ca2+ ADP Active site Ca2+ Tropomyosin Actin + ADP ADP P P + P + Myosin reactivation Cross bridge detachment Pivoting of myosin head ADP ATP ADP + P + P Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ ADP P + ATP ADP + P Figure 7-5 1 of 7 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Resting sarcomere Active-site exposure ADP Myosin head ADP + P + Sarcoplasm P Troponin Ca2+ Ca2+ Tropomyosin Actin Active site ADP ADP P + P + Calcium (Ca+2 ) gates in the SR open, allowing Ca+2 to diffuse into the sarcoplasm Calcium will bind to troponin (on the thin myofilament), causing it to change its shape. This then pulls tropomyosin away from the active sites of actin molecules. Figure 7-5 3 of 7 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Resting sarcomere Active-site exposure Cross-bridge formation ADP Myosin head ADP + P + Sarcoplasm P Troponin ADP + P Ca2+ Ca2+ Ca2+ ADP Tropomyosin Actin Active site Ca2+ + ADP ADP P P + P + Myosin heads are “energized” by the presence of ADP + PO43- at the ATP binding site (energy is released as phosphate bond of ATP breaks) Once the active sites are exposed, the energized myosin heads hook into actin molecules forming cross-bridges Figure 7-5 4 of 7 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

The ADP & phosphate group are released from the myosin head Resting sarcomere Active-site exposure Cross-bridge formation ADP Myosin head ADP + P + Sarcoplasm P Troponin ADP + P Ca2+ Ca2+ Ca2+ ADP Ca2+ Tropomyosin Actin Active site + ADP ADP P P + P + Pivoting of myosin head Using the stored energy, the attached myosin heads pivot toward the center of the sarcomere The ADP & phosphate group are released from the myosin head ADP + P Ca2+ Ca2+ ADP + P Figure 7-5 5 of 7 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Resting sarcomere Active-site exposure Cross-bridge formation ADP Myosin head ADP + + Sarcoplasm P P Troponin ADP + P Ca2+ Ca2+ Ca2+ ADP Active site Ca2+ Tropomyosin Actin + ADP ADP P P + P + A new molecule of ATP binds to the myosin head, causing the cross bridge to detach from the actin strand The myosin head will get re-energized as the ATP  ADP+P Cross bridge detachment Pivoting of myosin head ATP ADP + P Ca2+ Ca2+ Ca2+ Ca2+ ATP ADP + P As long as the active sites are still exposed, the myosin head can bind again to the next active site

Resting sarcomere Active-site exposure Cross-bridge formation ADP Myosin head ADP + Sarcoplasm P + P Troponin ADP + P Ca2+ Ca2+ Ca2+ ADP Tropomyosin Actin Active site Ca2+ + ADP ADP P P + P + Myosin reactivation Cross bridge detachment Pivoting of myosin head ADP ATP ADP + P + P Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ Ca2+ ADP P + ATP ADP + P IP Sliding filament theory – p. 17-24 single cross bridge; p. 27 multiple cross bridges PLAY Figure 7-5 7 of 7 Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

Physiology of Skeletal Muscle Contraction If there are no longer APs generated on the motor neuron, no more Ach will be released AchE will remove Ach from the motor end plate, and AP transmission on the muscle fiber will end Ca+2 gates in the SR will close & Ca+2 will be actively transported back into the SR With Ca+2 removed from the sarcoplasm (& from troponin), tropomyosin will re-cover the active sites of actin No more cross-bridge interactions can form Thin myofilaments slide back to their resting state Table 7-1

Key Note Skeletal muscle fibers shorten as thin filaments interact with thick filaments and sliding occurs. The trigger for contraction is the calcium ions released by the SR when the muscle fiber is stimulated by its motor neuron. Contraction is an active process; relaxation and the return to resting length is entirely passive.

These physiological processes describe what happen at the cellular level – how skeletal muscle fibers contract But what about at the organ level? How do skeletal muscles (like your biceps brachii) contract to create useful movement?

Skeletal muscles are made up of thousands of muscle fibers A single motor neuron may directly control a few fibers within a muscle, or hundreds to thousands of muscle fibers All of the muscle fibers controlled by a single motor neuron constitute a motor unit

When skeletal muscles contract, they may produce two types of contractions: Isotonic contraction Isometric contraction

Isotonic contraction – as tension increases (more motor units recruited), length of muscle changes usually resulting in movement of a joint. The tension (load) on a muscle stays constant (iso = same, tonic = tension) during a movement. (Example: lifting a baby, picking up object, walking, etc. )

Isometric contraction – no change in length of muscle even as tension increases. The length of a muscle stays constant (iso = same, metric = length) during a “contraction” (Example: holding a baby at arms length, pushing against a closed door.) Necessary in everyday life to counteract effects of gravity (e.g. postural muscles keeping head up)

Anatomy of the Muscular System Origin Muscle attachment that remains fixed Insertion Muscle attachment that moves Action What joint movement a muscle produces i.e. flexion, extension, abduction, etc.

For muscles to create a movement, they can only pull, not push Muscles in the body rarely work alone, & are usually arranged in groups surrounding a joint A muscle that contracts to create the desired action is known as an agonist or prime mover A muscle that helps the agonist is a synergist A muscle that opposes the action of the agonist, therefore undoing the desired action is an antagonist

Skeletal muscle movements Flexion/extension Abduction/adduction Rotation – left/right; internal(medial)/external(lateral) pronation/supination Elevation/depression Protraction/retraction Dorsiflexion/plantarflexion Inversion/eversion

An Overview of the Major Skeletal Muscles Figure 7-11(a)

An Overview of the Major Skeletal Muscles Figure 7-11(b)

Anatomy of the Muscular System Muscles of the Head and Neck Figure 7-12(a)

Anatomy of the Muscular System Muscles of the Head and Neck Figure 7-12(b)

Anatomy of the Muscular System Muscles of the Head and Neck Figure 7-12(c)

Anatomy of the Muscular System Muscles of the Anterior Neck Figure 7-13

Anatomy of the Muscular System Muscles of the Spine Figure 7-14

Anatomy of the Muscular System Oblique and Rectus Muscles and the Diaphragm Figure 7-15(a)

Anatomy of the Muscular System Oblique and Rectus Muscles and the Diaphragm Figure 7-15(b)

Anatomy of the Muscular System Oblique and Rectus Muscles and the Diaphragm Figure 7-15(c)

Anatomy of the Muscular System Muscles of the Shoulder Figure 7-17(a)

Anatomy of the Muscular System Muscles of the Shoulder Figure 7-17(b)

Anatomy of the Muscular System Muscles that Move the Arm Figure 7-18(a)

Anatomy of the Muscular System Muscles that Move the Arm Figure 7-18(b)

Anatomy of the Muscular System Muscles That Move the Forearm and Wrist Figure 7-19

Anatomy of the Muscular System Muscles That Move the Thigh Figure 7-20(a)

Anatomy of the Muscular System Muscles That Move the Thigh Figure 7-20(b)

Anatomy of the Muscular System Muscles That Move the Leg Figure 7-21

Anatomy of the Muscular System Muscles That Move the Foot and Toes Figure 7-22(a)

Anatomy of the Muscular System Muscles That Move the Foot and Toes Figure 7-22(b)

Anatomy of the Muscular System Muscles That Move the Foot and Toes Figure 7-22(c)

Anatomy of the Muscular System Muscles That Move the Foot and Toes Figure 7-22(d)