Lecture Exam 3 Notecards

Muscle and Nervous Systems - focus on physiology

Primary functions of the muscle

voluntary and involuntary movement, posture and body position, joint stabilization, glycemic control, heat generation

How do the muscles warm you up?

Only so much energy is useful, the rest is given off as heat to our body

How does the body prevent dangerous levels of heat during exercise?

body radiation, conduction, and evaporation

Skeletal muscle tissue

attached to bones and skin, striated, voluntary

cardiac muscle tissue

only in the heart, striated and intercalated disks, involuntary movement regulated by the nervous and endocrine systems

Smooth muscle tissue

in the walls of hollow organs (stomach bladder, uterus), not striated, and involuntary movement

Special characteristics or muscle cells

contractility (can shorten; sliding filament theory), excitability (neuromuscular junction), extensibility (can extend), elasticity

what is excitability in terms of muscle cells?

transduces chemical signal to electrical signals (neurons also do this)

What composes the muscle organ?

muscle tissues (cells + areolar CT), fibrous CT (DRCT and DICT) and they are vascularized/innervated (one major artery, nerve, and one or more veins)

How do adult skeletal muscles grow?

by cellular hypertrophy (grow in volume, not quantity/number)

Epimysium

wraps a muscle organ, made of DICT

perimysium

wraps a fascicle, made of areolar and DICT

endomysium

wraps each myofiber (areolar CT ONLY)

what is a myofiber?

one singular muscle cell, multinucleated (many cells fused) that grow by hypertrophy

what is a myofibril?

protein complexes inside the myofiber, contains MANY myofilaments

fascicle (muscle tissue)

a small bundle of myofibers (cells) grouped together inside a muscle

Prefixes - endo, peri, and epi

endo → deepest, peri → middle, epi → epi

Muscle shape and muscle function

the shape and orientation of fascicles in the muscle impacts the force, direction, speed, and precious of the muscle, often trading more force for less overall contraction

What are fasciae?

Fibrous CT that determine compartments, which group functionally related muscles together

Why are fasciae useful?

avoids friction between the muscles, and limits the spread of infections between muscles as well

Satellite cells

grow by hyperplasia, replace the nuclei in the muscle cells since the muscle cells cannot undergo mitosis

myofilaments

thin and thick (myosin) → interconnect with one another within the myofibril

thin filaments

actin + tropomyosin + troponin

Composition of myofibers and myofibrils

One myofiber (cell) has many myofibrils, which is then composed of many myofilaments (thick and thin)

Z disks

marks the limit of the sarcomere, contains the I band (light color), which is made of thin actin filaments

A band

has the thick filaments (dark), contains the H zone and M line

H zone

It sits in the middle of the A band, bisected down the center by a dark vertical line called the M line

M line

straight middle line of the sacromere in the A band

Titin (elastic filament)

connects myosin (thick filament) to the Z disc and the M line → crucial in allow the muscle to contract and relax.

Sarcomere

made of proteins, transcription and translation control (from nucleus), growth by hypertrophy (volume inc., functional unit of the myofibril).

Structural proteins of the sarcomere

maintain its structure (M line, Z disc, and titin)

Contractile proteins of the sarcomere

perform activity of shrinking the sarcomere; actin (thin) and myosin (thick)

Regulatory proteins of the sarcomere

regular the activity of the sarcomere - allow/ don’t allow muscle contraction

Myosin

Head + tail, where the head binds to actin at the binding site alongside ATP at the ATP binding site, makes up the A band of the sarcomere (specifically the tail) → THICK filament

Actin binding sites (thing filament for skeletal and cardiac muscles)

myosin binding site (masked by tropomyosin when relaxed), tropomyosin binding site, and troponin binding site

tropomyosin binding sites

actin binding sites and troponin binding sites

what does troponin bind?

Ca2+, tropomyosin and actin

How is smooth muscle differ in its thin filaments?

Does NOT have troponin, instead has calmodulin, which is a thick filament

Interactions of Ca2+ in muscle fibers

Ca2+ binds troponin → troponin confirmation change → tropomyosin conformation change → unmask the myosin binding site on actin → myosin binds to actin

Organization of the sarcomere mnumonic

Ziggy is an honorable man (Z disc, I band, A band, H zone, M line)

Organization of muscle cells (big to small)

muscle organ → fascicle → myofiber (cell)→ myofibril (proteins) → sarcomere

What can we see when the sarcomere shortens during contraction?

I band shrinks (titin), A band doesn’t change, H zone also shrinks

When both calcium AND ATP are present in the muscle fibrils….

Calcium frees the myosin binding sites on actin, ATP binds to the myosin head and tilts it forward, releasing energy (ADP + pi), causing the sliding filament theory and cross-bridge cycle (IN ALL SARCOMERES)

Steps to the cross-bridge cycle in muscle movement?

1. Myosin heads tilt (ATP)

2. Myosin heads bind to actin (crossbridge)

3. Myosin heads release ADP and Pi (power stroke, sliding filament)

4. Myosin heads bind new ATP, which releases the actin

When is ATP required for muscle contraction?

to release the myosin from the actin (detach the crossbridge), and to activate (tilt) the myosin head prior to crossbridge attachment (ALSO in transporting Ca2+ ions back into the SER)

Sources of ATP - stored

used in the first few seconds of intense exercise

Sources of ATP -Creatine Phosphate (CP)

under 15 seconds of activity, ATP produced from direct phosphorylation of ADP by CP using Creatine Kinase

Sources of ATP - Anaerobic (no O2) respiration

Fermentation → glycolysis + lactate formation (a minute of activity); relatively low ATP yield, changes the pH of our cells, which is bad

Sources of ATP - aerobic (W/ o2) respiration

glycolysis + Krebs cycle (TCA) - (hours of activity), produces most ATP, waste products are water and carbon dioxide, which the body can easily expel

Ideal sarcomere length prior to contraction

relaxed skeletal muscle is at optimal resting length, myosin heads pulling actin inward 20/20, force is 100% (100% of myosin heads overlap thin filament)

Sarcomere length during contraction

Increasing physical hinderance (crossbridges, thin and thick filaments bumping into one another), force decreases → decreasing length (cannot contract anymore)

Sarcomere length during relaxation

Increased length, decreasing overlap (crossbridges), decreasing forces (cannot relax anymore)

How does tension of skeletal muscle relate to crossbridges?

Tension generated by a skeletal muscle fiber is directly proportional to the number of crossbridges formed between thick and thin filaments

When is the sarcomere at its optimum length?

when contraction begins

What type of transport occurs when Ca2+ enters the SR from the cytoplasm?

Primary active transport (requires ATP)

Sarcolemma

directly inside the endomysium; cell membrane of the muscle cells for skeletal muscle

Muscle cell triad

made of T-tubule (sarcolemma invagination), terminal cisternae of the sarcoplasmic reticulum (SR) which stores calcium

Sarcoplasmic Reticulum (SR)

Smooth ER of the myofiber (muscle cell), stores calcium in the cell, has terminal cisternae which enclose the T tubules

Where does calcium bind to the sarcomere’s proteins (thin filaments)

At the I-Band and A-band junction (function of thin and thick filaments, where the actin binds to the myosin after its active site has been opened by the confirmation change of troponin).

Neuromuscular junction

Axon of the neuron releases an action potential via synapse to the axon terminal of the neuromuscular function at the sarcolemma of the muscle fiber, causing the muscle fiber to excite

Excitation of muscle: EC Coupling

Resting membrane potential at -70mV, slight depolarization with action potential, then depolarization as Na+ channels open, polarization happens as charge is +30mV with opening K+ channels, then hyper polarization and back to resting value

Where does the axon potential travel through?

The sarcoplasm - wave of depolarization travels through the t-tubule, which opens up the terminal cisternae and causes a ca2+ influx into the sacroplasm from the SR

Voltage sensitive receptor + mechanically-gated Ca2+ channels on SR

Receptors come from the wave of depolarization from the action potential, which triggers the mechanically-gated Ca2+ channels to open, allowing Ca2+ to bind to troponin

First step in muscle contraction

Nerve impulses stimulates release of the neurotransmitter acetylcholine (Ach) at NMJ

Second step in muscle contraction

Acetylcholine (ACh) diffuses across synaptic cleft and binds to ACh receptors on sarcolemma

Third step in muscle contraction

Ach receptors are Na+/K+ channels → ligan-gated ion channels open

Fourth step in muscle contraction

When enough receptors have been stimulated, the sarcolemma exhibits electrical changes (from negative to neutral charges: depolarization)

Fifth step in muscle contraction

The elect5rical changes spread along the sarcolemma to T-tubule containing voltage-sensitive receptors bound to mechanically-gated Ca2+ channels of the sarcoplasmic reticulum (stores calcium)

Last step in muscle contraction

Ca2+ released in the sarcoplasm → sliding filament occurs → sarcomere shortens → muscle contracts

How does the muscle relax?

Stop axon release of ACh, degrade ACh with AChEsterase→ close ligand-gated ion channels on post-synaptic membrane → sequester Ca2+ back in SR, tropomyosin on myosin-binding sites of actin → elastic structural (titin) proteins of sarcomere reshape

Rigor mortis

Using up all the ATP to contract the muscles, but do not have ATP to relax the muscle (release the myosin heads from the actin)

Motor unit

The motor neuron and all the skeletal muscle fibers (cells) it innervates

Caveat to muscle innervation

one motor neuron innervates many muscle fibers, but each muscle fiber is innervated by only only motor neuron

Small motor units

Fine movements (fingers, eye muscles), small muscle fibers/neuron ratio

Large motor units

large weight-bearing muscles, and gross movements (thighs, hips, back), 1000s of muscle fibers/neurons

What is the force of contraction affected by?

Number of muscle fibers stimulated, relative size of the fibers, frequency of stimulation, and sarcomere length

Force of contraction: number of muscle fibers stimulated

small/large motor unit and recruitment (from small to larger motor neurons) → influences contraction force

Force of contraction: relative size of the fibers

hypertrophy of organs and cells increases strength (myofibrils, glycogen stock, and mitochondria)

Force of contraction: frequency of stimulation

temporal summation → if the simulation is rapid, before the muscle relaxed, the contraction adds on prior contraction

Speed of contraction

depends on how fast the ATPase hydrolyses ATP, which depends on HOW the ATP is being made (aerobic or anaerobic)

Aerobic respiration- fibers and speed of ATP hydrolysis

oxidative fibers, increasing myoglobin, increasing mitochondria, slow ATPases, have resistance to fatigue

Anaerobic respiration- fibers and speed of ATP hydrolysis

Glycolytic fibers → glycogen stores, fast ATPase, more easily fatigues

3 types of skeletal muscle fibers

1. slow oxidative fibers (marathon)

2. fast oxidative-glycolytic fibers (sprinter)

3. Fast glycolytic fibers (quick reflexes)

Aerobic exercise (endurance)

Increases the number of SO fibers (red muscle) → leads to increases muscle capillaries, number of mitochondria, myoglobin synthesis, and may convert some fast glycolytic fibers into fast oxidative fibers

Overall impact of endurance exercises

leads to increase in stamina and delays muscle fatigue

Resistance Exercise/Strength training (typically anaerobic)

FG fibers (white fibers) inc., result in muscle hypertrophy (# of myofibrils/fiber inc.), inc. glycogen stores, easily fatigues

Overall impact of anaerobic activity

bulky muscles generate more force = inc. in muscle strength

Force

Tension exerted by a contracting muscle

Load

opposing force exerted on the muscle by weight of the object to be moved

What is actually contraction?

shortening of the sarcomere, that occurs when tension generated by cross bridges on the thin filament exceeds forces opposes shortening

Isometric contraction

muscle develops tension but does not shorten (just holding an object out ) →load is greater than the tension the muscle is able to develop (increases muscle capacity, but the muscle itself doesn’t change length)

Isotonic concentric contraction

muscle shortens, tension remains constant (upward movement) → only one explained by the sliding filament theory (muscle shortens and does work IE moves the load tension > load)

Isotonic eccentric contraction

muscle lengths while maintaining tension (downward movement) → muscle contracts as it lengthens

What is the neurotransmitter that binds to the ligand-dependent ion channels at the neuromuscular junctions?

ACh

What is important to remember about motor units?

all muscle fibers of a motor unit are of the same type, whereas a muscle organ contains all types of muscle fibers

Two layers of the smooth muscle

longitudinal and circular

What is important to note about smooth muscle cells?

small, spindle-shaped cells, unnucleated and have a high capacity for repair and regeneration

Speed of muscle contraction for smooth muscle

slower contraction (myosin ATPase is 10-100x slower than skeletal muscle), more energy efficient, more aerobic respiration →

Latch phenomenon in smooth muscle contraction

muscle remains contracted without further use of ATP

Smooth vs. Skeletal muscle - myofilaments

Oriented diagonally to the cell, and attached to the membrane via dense bodies and intermediate filaments which anchor thin filaments to the membrane (developing tension)