Anatomy

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Muscle Tissue

Objectives • Describe the organization of muscle and the characteristics of skeletal muscle cells. • Identify the structural components of the sarcomere. • Summarize the events at the neuromuscular junction. • Explain the key concepts involved in skeletal muscle contraction. • Describe how muscle fibers obtain energy for contraction. • Distinguish between aerobic and anaerobic contraction, muscle fiber types, and muscle

performance. • Identify the differences between skeletal, cardiac, and smooth muscle.

Three types of muscle • Skeletal—attached to bone • Cardiac—found in the heart • Smooth—lines hollow organs Characteristics of muscle

Excitability Receive & respond to stimuli. Nervous impulse

Contractility Actively generate force to shorten. Passively lengthens

Extensibility Ability to be stretched by antagonist or gravity.

Elasticity Ability to return to originial shape after stretch/contraction

Skeletal muscle functions • Produce skeletal movement • Maintain posture and body position • Support soft tissues • Guard entrances and exits • Maintain body temperature

Organization of connective tissues • Epimysium surrounds muscle • Perimysium sheathes bundles of muscle fibers • Endomysium covers individual muscle fibers • Tendons or aponeuroses attach muscle to bone or muscle

Skeletal Muscle Histology

Skeletal muscle fibers • Sarcolemma - cell membrane • Sarcoplasm - muscle cell cytoplasm

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• Sarcoplasmic reticulum (modified ER) – sequester Ca++ and form Terminal Cisternae • T-tubules – invaginations of Sarcolemma, and form Triads with Terminal Cisternae • Sarcomeres—regular arrangement of myofibrils – BE ABLE TO DRAW! • Mitochondria – generate ATP

Myofibrils • Comprised of thick and thin filaments Thin filaments • Actin – active site for binding with myosin (thick filament) • Tropomyosin - covers active sites on actin • Troponin - binds to Ca++ during contraction to expose active sites • Other thin filaments: Nebulin

Thick filaments • Bundles of myosin fibers around titan core • Myosin molecule heads form cross-bridges with actin during contraction

Sliding filament theory • Begins at the Neuromuscular Junction:

• Action potential along motor neuron reaches the synaptic terminal (end bulb) • Influx of Ca++ into neuron causes release of ACh into synaptic cleft • ACh binds to receptors in the motor end plate – action potential propagates

along sarcolemma • AChE removes ACh

• Action potential propagates along sarcolemma and dips into cell interior vi T-tubles • Action potential reaches triad, and causes terminal cisternae of SR to relase Ca++ into

sarcoplasm • Calcium binds to troponin of thin filament • Troponin moves, moving tropomyosin and exposing actin active site • Myosin head forms cross bridge and bends toward H zone via energy from ATP • Sarcomere shortens – muscle contracts • New ATP allows release of cross bridge • Cross bridge cycling continues as long as there is action potential, Ca++, ACh, and ATP • Relaxation normally occurs due to lack of action potential, so Ca++ is uptaken by SR,

and troponin/tropomyosin cover binding sites

Tension production by muscle fibers • All or none principle • Amount of tension depends on number of cross bridges formed

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• Twitch • Cycle of contraction, relaxation produced by a single stimulus

• Treppe • Repeated stimulation after relaxation phase has been completed

Summation • Repeated stimulation before relaxation phase has been completed

• Wave summation = one twitch is added to another • Incomplete tetanus = muscle never relaxes completely • Complete tetanus = relaxation phase is eliminated

• Motor units • All the muscle fibers innervated by one motor neuron • Precise control of movement determined by number and size of motor unit • Motor units are progressively recruited to gradually increase tension.

Contractions • Isometric

• Tension rises, length of muscle remains constant = no change in joint angle • Isotonic

• Tension rises, length of muscle changes = change in joint angle • Concentric contractions = muscle shortening – overcoming gravity • Eccentric contractions = muscle lengthening – lowering to ground

Muscle Contraction requires large amounts of energy • Creatine phosphate (CP) releases stored energy to convert ADP to ATP • Aerobic metabolism provides most ATP needed for contraction • At peak activity, anaerobic glycolysis needed to generate ATP

Energy use and level of muscular activity • Energy production and use patterns mirror muscle activity • Fatigued muscle no longer contracts

• Build up of lactic acid • Exhaustion of energy resources

Recovery period • Begins immediately after activity ends • Oxygen debt (excess post-exercise oxygen consumption)

• Amount of oxygen required during resting period to restore muscle to normal conditions

Types of skeletal muscle fibers • Fast fibers • Slow fibers • Intermediate fibers

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Slow Fibers - Type I - Red • Half the diameter of fast fibers • Take three times as long to contract after stimulation • Abundant mitochondria • Extensive capillary supply • High concentrations of myoglobin resulting in red appearance • Can contract for long periods of time- fatigue resistant

Fast fibers – Type II - White • Large in diameter • Contain densely packed myofibrils • Large glycogen reserves • Relatively few mitochondria • Produce rapid, powerful contractions of short duration – fatigue quickly

Intermediate fibers • Similar to fast fibers, yet somewhat greater resistance to fatigue

Fiber type varies between muscles and vary from person to person Consider sprinters vs. marathoners, domestic fowl vs. migratory fowl

Muscles contain a mixture of fiber types: Soleus (postural) 87% slow Orbicularis Oculi 15% slow

All fibers w/n a motor unit (motor neuron & fibers it serves) are the same

Great variability through genetics. Athletes made or born? Leg muscles: Avg. adult = 45% slow Distance runner = 80% slow Sprinters = 23% slow

Muscle performance and the distribution of muscle fibers • Pale muscles dominated by fast fibers are called white muscles • Dark muscles dominated by slow fibers and myoglobin are called red muscles • Training can lead to hypertrophy of stimulated muscle

Physical conditioning • Anaerobic endurance

• Time over which muscular contractions are sustained by glycolysis and ATP/CP reserves

• Aerobic endurance • Time over which muscle can continue to contract while supported by mitochondrial

activities

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Changes in Muscular Size Muscular Atrophy

Decrease in number of myofibrils & overall diameter form disuse Disuse Atrophy cast, bedridden, sedentary Denervation Atrophy cut nerve supply

1/4 original size from 6 mos to 2 yrs Fibers replaced w/ fibrous tissue Irreversible

Muscular Hypertrophy Increase in muscle size from increase in number of myofibrils Not from increase in cell number. This is fixed genetically. More forceful contractions Controlled by genetics & hGH (childhood/puberty), testosterone,

& training (weight lifting)

Cardiac Muscle Tissue Structural characteristics of cardiac muscle • Located only in heart • Cardiac muscle cells are small

• One centrally located nucleus • Short broad T-tubules • Dependent on aerobic metabolism • Intercalated discs where membranes contact one another

Functional characteristics of cardiac muscle tissue • Automaticity • Contractions last longer than skeletal muscle • No tetanic contractions possible

Smooth Muscle Tissue Structural characteristics of smooth muscle • Nonstriated

• Lack sarcomeres • Thin filaments anchored to dense bodies

• Involuntary

Functional characteristics of smooth muscle • Contract when calcium ions interact with calmodulin

• Activates myosin light chain kinase • Functions over a wide range of lengths

• Plasticity • Multi-unit smooth muscle cells are innervated by more than one motor neuron • Visceral smooth muscle cells are not always innervated by motor neurons • Neurons that innervate smooth muscle are not under voluntary control