Chapter 11: Muscle Tissue

Excitability (responsiveness)

to chemical signals, stretch, and electrical changes across the plasma membrane

Conductivity

local electrical excitation sets off a wave of excitation that travels along the muscle fiber

All muscle cells have the following 5 characteristics:

Excitability (responsiveness)—to chemical signals, stretch, and electrical changes across the plasma membrane
Conductivity—local electrical excitation sets off a wave of excitation that travels along the muscle fiber
Contractility—shortens when stimulated
Extensibility—capable of being stretched between contractions
Elasticity—returns to its original rest length after being stretched.

Skeletal muscle

AKA muscle fibers, AKA myofibers.

Voluntary, striated muscle usually attached to bones
• Striations—alternating light and dark transverse bands; results from arrangement of internal contractile proteins
• Voluntary—usually subject to conscious control (the other muscle types are involuntary)

What is the average diameter and length of a myofiber?

Avg 100 μm in diameter and 3 cm (30,000 μm) long, but
can be much thicker (500 μm) and as long as 30 cm

Endomysium

Fibrous connective tissue that surrounds each muscle fiber

Perimysium

Fibrous connective tissue that bundles muscle fibers into fascicles

Epimysium

Fibrous connective tissue that surrounds entire muscle

What are some of the characteristics (4) of collegen that make it well suited for muscle tissue fibrous connective tissue?

Collagen is somewhat extensible and elastic
• Stretches slightly under tension and recoils when released
• Resists excessive stretching, protects muscle from injury
• Returns muscle to its resting length
• Contributes to power output and muscle efficienc

Sarcolemma

plasma membrane of a muscle fiber

Sarcoplasm

cytoplasm of a muscle fiber

Myofibrils

long protein cords occupying most of sarcoplasm

Myoglobin

Red pigment; provides some oxygen needed for muscle activity

Sarcoplasmic reticulum and terminal cisterns

smooth ER that forms a network around each myofibril: contains terminal cisterns,

Terminal cisterns—dilated end-sacs of SR which cross the muscle fiber from one side to the other
• Acts as a calcium reservoir; it releases calcium through channels to
activate contraction
• Within cisterns, calcium is bound to a protein called calsequestrin

Calsequestrin

Binds calcium within the temrinal cisterns of the sarplacmisc reticulum

Transverse (T) tubules

tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side
• Each T tubule has two terminal cisterns associated with it on either
side.

Function: carry electrical signal rapidly from the surface mebrane deep into the core of the muscle celltriggering the relase of calcium ions form the adjacent sarplasmic reticulums that sandwhich the Transverse tubules in what is known as a tirad in skeletal muscle.

What is a triad?

Terminal cisterns—dilated end-sacs of SR which cross
the muscle fiber from one side to the other
• Acts as a calcium reservoir; it releases calcium through channels to
activate contraction
• Within cisterns, calcium is bound to a protein called calsequestrin
• Transverse (T) tubules—tubular infoldings of the
sarcolemma which penetrate through the cell and emerge
on the other side
• Each T tubule has two terminal cisterns associated with it on either
side.

Myoblast

stem cells that fused to form each muscle fiber early in development, each contributing one nucleus

Satellite cells

unspecialized myoblasts remaining between the muscle fiber and endomysium
• Play a role in regeneration of damaged skeletal muscle tissue.

Draw out and list all of the compontents of a skeletal muscle fiber.

Sarcolemma, sarcoplasm, myofibrils, glycogen, myoglobin, sarcoplasmic reticulum, terminal cicsterns, and transverse tubules, myoblast, satellite cells, I-band, A-band, Z-disc, nuclei, mitochondria, and opening into transverse tubules.

Thick filament (myosin)

Made of several hundred myosin molecules (myosin is a motor protein)
• Each molecule shaped like a golf club: two chains intertwined to form a shaft-like tail and a double globular head
• Heads directed outward in a helical array around the bundle
• Heads on one half of the thick filament angle to the left, while heads on other half angle to the right
• Bare zone with no heads in the middle.

Fibrous actin

Two intertwined strands of globular (G) actin subunits, each with an active site that can bind to head of myosin molecule

Tropomyosin

each blocks six or seven active sites on G actin subunits

Troponin

small, calcium-binding protein on each tropomyosin molecule that when not bound to moleule binds tropomyosin in confirmation that blocks the activation of myosin/ the attachment of myosin ot the actin filament. When bound by Ca it binds tropomyosin a way that removes it from blocking the active G actin subiunit’s active site. .

Describe what preotein types make up thin filaments

Composed of three different protein types
• Fibrous (F) actin—two intertwined strands of globular (G) actin subunits, each with an active site that can bind to head of myosin molecule
• Tropomyosin—each blocks six or seven active sites on G actin subunits
• Troponin—small, calcium-binding protein on each tropomyosin molecule.

Elastic filaments

Elastic filaments—made of a huge, springy protein called titin
• Run through core of thin filament and anchor it to Z disc and M line
• Help stabilize and position the thick filament
• Prevent overstretching and provide recoil.

Describe the architecture of Myofibrils

Composed of thre kinds of muscle filaments, or myofilaments

Thick filaments, Thin Filaments, and Elastic filaments

Elastic filaments—made of a huge, springy protein called titin
• Run through core of thin filament and anchor it to Z disc and M line
• Help stabilize and position the thick filament
• Prevent overstretching and provide recoil.

What is the bare zone

Of the three filaments what filamnets of contractile proteins?

Myosin and actin. Of the myofilaments, myosin and actin are the contractile proteins—they do the work of contraction

Describe the regulatory functions of tropomyosin and troponin.

Tropomyosin and troponin act as regulatory proteins
• Act like a switch that determines when fiber can (and cannot) contract
• Contraction activated by release of calcium into sarcoplasm and its binding to troponin
• Troponin changes shape and moves tropomyosin off the active sites on actin.

Dystrophin

links actin in outermost myofilaments to
membrane proteins that link to endomysium
• Transfers forces of muscle contraction to connective tissue
ultimately leading to tendon
• Genetic defects in dystrophin produce disabling disease muscular
dystrophy.

A-band, H-band, and M-line

Anisotropic band = A-band= dark band. Darkest part is where thick filaments overlap a hexagonal array of thin filaments
• H band—not as dark; middle of A band; thick filaments only
• M line—dark, transverse protein in middle of H band

I-band

I band—light band
• Z disc (Z line)—protein complex that provides anchorage for thin
filaments and elastic filaments.

What accounts for the striations of muscle fibers?

In cardiac and skeletal muscle cells, myosin and actin are organized in a precise array that accounts for striations.

Striations are alternating A-bands (dark) and I-bands (light)
• A band—dark band
• Darkest part is where thick filaments overlap a hexagonal array of
thin filaments
• H band—not as dark; middle of A band; thick filaments only
• M line—dark, transverse protein in middle of H band
• I band—light band
• Z disc (Z line)—protein complex that provides anchorage for thin
filaments and elastic filaments.

Sarcomere: anatomy and physiology

segment from Z disc to Z disc; functional contractile unit of muscle fiber
• Muscle cells shorten because their individual sarcomeres shorten
• Z disc (Z lines) are pulled closer together as thick and thin filaments slide past each other
• Neither thick nor thin filaments change length during shortening, only the amount of overlap changes
• During shortening, dystrophin and linking proteins also pull on extracellular proteins
• Transfers pull to extracellular tissue.

Denervation atrophy

Skeletal muscle cannot contract unless stimulated by a nerve.
If nerve connections are severed or poisoned, a muscle is
paralyzed
• Denervation atrophy: shrinkage of paralyzed muscle when
nerve remains disconnected.

If nerve connections are severed or poisoned, a muscle is
paralyzed and may waste away (denervation atrophy)

Describe the anatomy and physiology of a somatic motor neuron

Anatomy: Nerve cells whose cell bodies are in the brainstem and
spinal cord that serve skeletal muscles. Their axons, called somatic motor fibers, lead to the skeletal muscle. Each nerve fiber branches out to a number of muscle fibers. Each muscle fiber is supplied by only one motor neuron.

Physiology: excites skeletal muscle causing it to contract based on concious effort.

Motor unit

One nerve fiber and all the muscle fibers innervated by it; they behave as a functional unit
• Muscle fibers of one motor unit:
• Are dispersed throughout muscle
• Contract in unison
• Produce weak contraction over wide area
• Provide ability to sustain long-term contraction as motor units take turns contracting
• Effective contraction usually requires contraction of several motor units at once.

what is the number of muscle fibers and facicles in the average motor unit?

Average motor unit contains 200 muscle fibers distributed across as many as 100 fascicles

What is a small motor unit? (Provide example)

Small motor units provide a fine degree of control
• Example: eye and hand muscles controlled by motor units with only
3 to 5 muscle fibers each

What is a large motor unit?

Large motor units provide more strength than control
• Powerful contractions supplied by large motor units with hundreds of fibers
• Example: quadriceps femoris and gastrocnemius controlled by motor units that may have 1,000 muscle fibers.

Synapse

Is a point where a nerve fiber meets its target cell

ACh receptors and postynaptic membrane fold (junctional folds)

Muscle cell sarcolemma has millions of ACh receptors—proteins that respond to ACh.

Postsynaptic membrane folds (junctional folds) of sarcolemma
increase surface area, maximize number of ACh receptors

Myasthenia gravis

Lack of receptors causes weakness in the disease myasthenia
gravis

Basal lamina and Acetylcholineesterase

Entire NMJ enclosed in a basal lamina—thin layer of
collagen and glycoprotein separating muscle fiber and nerve ending from surrounding connective tissue
• Passes through synaptic cleft and nearly fills it
• Sarcolemma and lamina with synaptic cleft contain acetylcholinesterase (AChE)—enzyme that breaks down ACh, allowing for relaxation.

Desrcibe the structure and function of the neuromusclar junction (what is it? Describe the structures associated with like Axon terminal, vesciles, ACh, the synaptic cleft, ACh receptors, etc)

A synapse between a nerve fiber and its target muscle cell called a neuromuscular junction (NMJ) or motor end plate.

Each terminal branch of the nerve fiber within the NMJ forms a separate synapse with the muscle fiber consisting of:
• Axon terminal—swollen end of nerve fiber. Contains synaptic vesicles with neurotransmitter called acetylcholine (ACh). Nerve impulse causes synaptic vesicles to undergo exocytosis releasing ACh into synaptic cleft
• Synaptic cleft—narrow gap between axon terminal and sarcolemma.

Muscle cell sarcolemma has millions of ACh receptors— proteins that respond to ACh
• Postsynaptic membrane folds (junctional folds) of sarcolemma increase surface area, maximize number of ACh receptors.
• Entire NMJ enclosed in a basal lamina—thin layer of collagen and glycoprotein separating muscle fiber and nerve ending from surrounding connective tissue. Passes through synaptic cleft and nearly fills it.

Sarcolemma and lamina with synaptic cleft contain acetylcholinesterase (AChE)—enzyme that breaks down ACh, allowing for relaxation.

Electrically excitable cells

Muscle fibers and nerve cells are electrically excitable cells
• Their membranes exhibit voltage changes in response to
stimulation

Electrophysiology ( and electricall excitable cells)

the study of the electrical activity of cells.

Electrical activity. What does the electrical activity depend on? What is the membrane potential of the cell?

Electrical activity depends on concentration differences in ions in the intracellular fluid (ICF) vs extracellular fluid (ECF)
• ICF contains greater concentration of negative anions (negatively charged proteins, nucleic acids, phosphates) than ECF; trapped within cell
• Membrane is polarized—contains a net negative charge
• Also, ICF has more potassium ions+ (K ) than ECF, and ECF has
more sodium ions+ (Na ) than the ICF.

Electrical potential or voltage

Any difference in charge between two points is called an electrical potential, or voltage

In an unstimulated (resting) cell: Testing membrane potential

The plasma membrane is electrically polarized (charged) with a
negative resting membrane potential (RMP)

In a stimulated cell:

• Ion channels in membrane open, allowing +Na to flow into cell (down its electrochemical gradient); causes depolarization of the membrane.

• Then, additional ion channels allow+K to flow out of cell; causes repolarization of the membrane.

• The up-and-down voltage shift is called an action potential.

What are the two types of paralysis that Neuromuscular toxins can inflict upon NMJ?

Spastic paralysis and Flaccid paralysis

• Spastic paralysis: a state of continual contraction of the muscles; possible suffocation

  • Some pesticides contain cholinesterase inhibitors which bind to acetylcholinesterase and prevent it from degrading ACh

• Flaccid paralysis: a state in which the muscles are limp and
  cannot contract

  • Curare: competes with ACh for receptor sites, but does not
    stimulate the muscles. Plant poison used by South American natives to poison blowgun darts

Spastic paralysis

A state of continual contraction of the muscles; possible suffocation.

Tetanus (lockjaw) is a form of spastic paralysis caused by toxin
Clostridium tetani

cholinesterase inhibitors

Bind to acetylcholinesterase and prevent it from degrading ACh cuasing spastic paralysis

Tetanus (lock jaw)

Tetanus (lockjaw) is a form of spastic paralysis caused by toxin Clostridium tetani
• Glycine in the spinal cord normally stops motor neurons from producing unwanted muscle contractions
• Tetanus toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles.

Flaccid paralysis and Curare

a state in which the muscles are limp and cannot contract.

Curare: competes with ACh for receptor sites, but does not stimulate the muscles. Plant poison used by South American natives to poison blowgun darts

Curare

Competes with ACh for receptor sites, but does not stimulate the muscles. Plant poison used by South American natives to poison blowgun darts

Botulism

type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum
• Blocks release of ACh causing flaccid paralysis
• Botox cosmetic injections used for wrinkle removal.

What are the 4 major phases of contraction and relaxation?

Excitation: action potentials in motor nerve fiber lead to
action potentials in the muscle fiber
Excitation–contraction coupling: events that link the
action potentials on the sarcolemma to activation of the
myofilaments, thereby preparing them to contract
Contraction: the step in which the muscle fiber develops
tension and may shorten
Relaxation: when stimulation ends, a muscle fiber relaxes
and returns to its resting length.

What are the 5 steps of the excitation of a muscle fiber? (steps 1-5)

1. Arrival of nerve signal

2. Acetylcholine (ACh) release

3. Binding of ACh to receptor

4. Opening of ligand (ACh)-regulated ion gate: creation of end plate ptoential

5. Opening of voltage-regulated ion gates; creation of action potentials

What are the 4 steps of excitation-contraction coupling (steaps 6-9)

1. Action potential propragated down T tubules

2. calcium released from teminal cisterns

3. binding of calcium to troponin

4. shifting of tropomyosin; exporse of active sites on active sites on actin.

What is the 4 step cycle of contraction phase (10-13)

1. Hydrolysis of ATP to ADP + Pi, activation and cocking of myosin head (recovery stroke).

2. Formation of myosin-actin cross-bridge

3. Power stroke; sliding of thin filament over thick filement.

4. Binding of new ATP; breaking of cross-bridge.

What are the 5 steps of relaxation phase? (steps 14-18)

1. cessation of nervous stimulation and ACh release.

2. ACh breakdown by acetylecholinesterase (AChE)

3. reabsorption of calcium ion by sarcoplasmic reticulum.

4. Loss of calcium ions from troponin cause alt conformation of of tropomyosin.

5. Return of tropomyosin to positon blocking active site of actin.

Length-tension relationship

The amount of tension generated by a muscle depends on how stretched or shortened it was before it was stimulated
• If overly shortened before stimulated, contraction is weak. Thick filaments butt up against Z discs
• If too stretched before stimulated, contraction is weak. Minimal overlap between thick and thin filaments results in minimal cross-bridge formation
• Optimum resting length produces greatest force when
muscle contracts. Nervous system maintains muscle tone (partial contraction) to ensure that resting muscles are near this length.

Rigor mortis

hardening of muscles and stiffening of body beginning 3–4 hours after death
• Deteriorating sarcoplasmic reticulum releases 2+ Ca and deteriorating sarcolemma allows C2+ to enter cytosol. Ca2+ activates myosin–actin cross-bridge formation and muscle contraction
• Muscle relaxation requires ATP, and ATP production is no longer produced after death. Fibers remain contracted until myofilaments begin to decay
• Rigor mortis peaks about 12 hours after death, then diminishes over the next 48–60 hours.

Muscle Twitch

quick cycle of contraction and relaxation when a muscle is directly stimulated with an electrode

What is a Myogram? What are the 3 phases?

Graph measuring twitch; shows three phases:

Latent period—delay just after stimulation of muscle; time required for excitation-contraction coupling and tensing elastic components. Generates internal tension, not visible in myogram
Contraction phase—external tension is generated and a load is moved as the muscle fiber shortens
Relaxation phase—sarcoplasmic calcium levels fall as calcium is reabsorbed into sarcoplasmic reticulum; tension declines.

Voltage Threshold

It is minimum voltage that causes a muscle twitch.

Other than voltage what factor influence the stength of a twitch?

Even if the same voltage is delivered, different stimuli cause twitches varying in strength, because:
• The muscle’s starting length influences tension generation
• Muscles fatigue after continual use
• Warmer muscles’ enzymes work more quickly
• Muscle cell’s hydration level influences cross-bridge
formation
• Increasing the frequency of stimulus delivery increases
tension output.

How does voltage affect contractions?

Stimulating the nerve with higher voltages produces stronger
contractions
• Higher voltages excite more nerve fibers which stimulate
more motor units to contract
• Occurs according to the size principle—weak stimuli (low
voltage) recruit small units, while strong stimuli recruit small and large units for powerful movements.

recruitment or multiple motor unit (MMU) summation

Recruitment or multiple motor unit (MMU) summation—the process of bringing more motor units into play with stronger stimuli.

Size principal

Weak stimuli (low voltage) recruit small units, while strong stimuli recruit small and large units for powerful movements.

Incomplete tetanus

Patial relaxation between stimuli resulting in fluttering. Each new twitch “rides piggyback” on the previous one, generating higher tension. Caused by tempora wave summation which caused by higher frerquency stimuli.

complete (fused) Tetanus

steady contraction caused by unnaturally high stimulus frequencies in lab experiments.

How does frequency of stimulation affect twitch stength?

Low frequency stimuli produce identical twitches

Higher frequency stimuli (for example, 20 stimuli/s) produce temporal (wave) summation. Each new twitch “rides piggyback” on the previous one, generating higher tension. Only partial relaxation between stimuli resulting in fluttering, incomplete tetanus

Unnaturally high stimulus frequencies (in lab experiments) cause a steady, contraction called complete (fused) tetanus.

Isometric contraction

Contraction without a change in length
• Muscle produces internal tension but external resistance causes it to stay the same length
• Can be a prelude to movement when tension is absorbed by elastic component of muscle
• Important in postural muscle function and antagonistic muscle joint
stabilization.

Concentric contraction

One of two forms of isotonic contraction, muscle shortens as it maintains tension (example: lifting weight)

Eccentric contraction

one of two forms of isotonic contraction, muscle lengthens as it maintains tension (example: slowly lowering weight).

Isotonic contraction

contraction with a change in length but no change in tension
• Muscle changes in length with no change in tension

Two forms of isotonic contraction:
• Concentric contraction: muscle shortens as it maintains tension (example:ifting weight)
• Eccentric contraction: muscle lengthens as it maintains tension (example: slowly lowering weight).

Isometric contraction versus isotonic contraction

Isometric contraction: contraction without a change in length

Isotonic contraction: contraction with a change in length but no chang in tension

What are the two main forms of metabolism for muscles/ ways of forming ATP?

ATP supply depends on availability of oxygen and organic energy sources (for example, glucose and fatty acids)
Two main pathways of ATP synthesis:
• Anaerobic fermentation—enables cells to produce ATP in the absence of oxygen; yields little ATP and lactate, which needs to be disposed of by the liver
• Aerobic respiration—produces far more ATP; does not generate lactate; requires a continual supply of oxygen and take more time.

Phosphagen system: ATP, myokinase, and creatine kinase

For short, intense exercise (example: 100 m dash) Oxygen is briefly supplied by myoglobin but is rapidly depleted.

Phosphagen system—the combination of ATP and CP which provides nearly all energy for short bursts of activity (~6 s of sprinting).

Muscles meet most ATP demand by borrowing phosphate groups (Pi) from other molecules and transferring them to ADP.

Two enzyme systems control these phosphate transfers:
• Myokinase—transfers Pi from one ADP to another, converting the latter to ATP
• Creatine kinase—obtains Pi from a phosphate-storage molecule creatine phosphate (CP) and gives it to ADP.

What modes of ATP syntehsis are utilized during the duration of an muscle use

First ATP in teh cell at that time made by aerobic respiration will be used up.

Then the phosphagen system will temporarly provide more ATP to the system.

Then Depending on whihc muscle fiber cell (glycolitc fiber or aerobic fiber) they will kick in the glycogen-lactate (anaerobic fermentation) system or teh aerobic respiration subbported by the cardiopulmonary function with oxygen.

Anaerobic fermentation in terms of muscle metabolism.

Short-term energy
• As the phosphagen system is exhausted, muscles shift to
anaerobic fermentation
• Muscles obtain glucose from blood and their own stored glycogen
• In the absence of oxygen, glycolysis can generate a net gain of 2
ATP for every glucose molecule consumed
• Converts glucose to lactate

Anaerobic threshold

Anaerobic threshold (lactate threshold)—point at which
lactate becomes detectable in the blood

Glycogen-lactate system

Glycogen–lactate system—the pathway from glycogen
to lactate
• Produces enough ATP for 30–40 s of maximum activity

Aerobic respiration in terms of muscle metabolism

After about 40 s, the respiratory and cardiovascular
systems start to deliver oxygen fast enough for aerobic
respiration to meet most of muscle’s ATP demand
• Aerobic respiration produces more ATP per glucose than glycolysis
does (another 30 ATP per glucose)
• Efficient means of meeting the ATP demands of prolonged exercise
• After 3–4 min, the rate of oxygen consumption levels off to a steady
state where aerobic ATP production keeps pace with demand.

How long into the excersize does it take for fatty acids to become the more signficant fuel?

For 30 min energy comes equally from glucose and fatty acids

Beyond 30 min, depletion of glucose causes fatty acids to become
the more significant fuel.

Muscle fatigue

progressive weakness from prolonged use of muscles

Fatigue in high-intensity exercise is thought to result from:

Potassium accumulation in the T tubules reduces excitability.

ADP andiP accumulation—slows cross-bridge movements, inhibit calcium release and decrease force production in myofibrils

Fatigue in low-intensity (long duration) exercise is thought
to result from:

Fuel depletion as glycogen and glucose levels decline.

Electrolyte loss through sweat can decrease muscle excitability.

Central fatigue when less motor signals are issued from brain; brain cells inhibited by exercising muscles’ release of ammonia.

Maximum oxygen uptake (VO2max)

the point at which the rate of oxygen consumption plateaus and does not increase further with added workload.

• Major determinant of one’s ability to maintain high-intensity exercise for more than 4–5 min
• Proportional to body size and peaks at around age 20
• Usually greater in males than females
• Can be twice as great in trained endurance athlete as in untrained person.

What is Excess postexcersize oxygen consumption (EPOC) or Oxygen debt? What is its purpose? How long can it last?

elevated rate of oxygen consumption following exercise

Purpose:
• Aerobically replenish ATP (some of which helps regenerate CP stores)
• Replace oxygen reserves on myoglobin
• Provide oxygen to liver that is busy disposing of lactate
• Provide oxygen to many cells that have elevated metabolic rates after exercise.

EPOC can be six times basal consumption and last an
hour.

Slow-twitch, slow oxidative (SO), red fibers, or type I fibers

One of two major physiological classes of muscle fibers.

Well adapted for endurance; resist fatigue by oxidative (aerobic)
ATP production
• Important for muscles that maintain posture (e.g., erector spinae of
the back, soleus of calf)
• Thin cells with abundant mitochondria, capillaries, myoglobin (deep
red color) and contain a form of myosin with slow ATPase, and a SR that releases calcium slowly
• Grouped in small motor units controlled by small, easily excited motor neurons allowing for precise movements.

Fast-twitch, fast glycolytic (FG), white fibers, or type II fibers

Fibers well adapted for quick responses; utilize glycolysis and
anaerobic fermentation for energy
• Abundant in quick and powerful muscles: eye and hand muscles,
gastrocnemius of calf and biceps brachii
• Contain a form of myosin with fast ATPase and a large SR that
releases calcium quickly
• Fibers are thick and strong; low myoglobin gives them pale color
• Grouped in large motor units controlled by larger, less excitable
neurons allowing for powerful movements

Intermediate or fast oxidative (FO) fiber

type is known mainly in other mammals but relatively rare in humans.

Fast glycolytic fibers versus slow-oxidative fibers in muscle.

Every muscle contains a mix of fiber types, but one type predominates depending on muscle function
• Fiber type within a muscle differs across individuals
• Some individuals seem genetically predisposed to be
sprinters, while others more suited for endurance

SO= dark becuase a lot of mitochondira

FG= light becuase not a lot of mitochondria.

What factors affect musclar stength? (7 factors)

1. Muscle size—thicker muscle forms more cross-bridges; a muscle can exert a tension of 3 or 4 kg/cm² of cross-sectional area.

2. Fascicle arrangement—pennate are stronger than parallel, and parallel stronger than circular.

3. Size of active motor units—the larger the motor unit, the stronger the contraction.

4. Multiple motor unit summation—simultaneous activation of more units increases tension.

5. Temporal summation—the greater the frequency of stimulation, the stronger the muscle contraction.

6. The length–tension relationship—a muscle resting at
   optimal length is prepared to contract more forcefully than a
   muscle that is excessively contracted or stretched

7. Fatigue—fatigued muscles contract more weakly than rested
   muscles

Resistance exercises

contraction of a muscle against a load that resists movement; example: weightlifting
• Growth is from cellular enlargement
• Muscle fibers synthesize more myofilaments and myofibrils and
grow thicker