A&P Test 3 (Muscles and Joints) Flashcards
5 characteristics of Muscles
responsiveness, conductibility, contractibility, extensibility, elasticity
responsiveness
(excitability) capable of responses to chemical signals and stretch
conductibility
local electrical charges trigger a wave of excitation
contractibility
shortens when stimulated
extensibility
capable of being stretched
elasticity
returns to its original resting length after its stretched.
Skeletal Muscles
usually attached to 1 or more bones, myofibrils as long as 30 cm, give us striations, under conscious control
striations
light and ark transverse bands, due to the overlapping of contractile filaments
Connective Tissue
surrounds the muscle and holds it together but does not have same characteristics as muscle tissue; not excitable, not contractile, little elasticity. Main function is to give us a place for blood vessels and nerves
tendon
attaches muscle to bone
ligament
attaches bone to bone
fascia
connective tissue that covers the outside of a muslce
epimysium
thin layer of connective tissue around entire muscle
perimysium
wraps each bundle of fibers w/in the epimysium (wraps a fascicle)
endomysium
wraps each cell or fiber
Muscle Fibers
has many structures including a membrane around it like any cell
Sarcolemma
plasma membrane around the outside of a muscle cell
sarcoplasm
cytoplasm of muscle cell (contains ska organelles as a normal cell), holds glycogen for energy, holds myoglobin for binding oxygen
sarcoplasmic reticulum
smooth ER of muscle cell (stores calcium ions)
triad
2 terminal cistern and a T-tubule (located btwn the SR)
terminal cisternae
lager than tubes of SR, perpendicular to normal SR direction
T-tubule
connects to sarcolemma, has multiple nuclei due to fusion of myoblasts
myoblasts
each has 1 nucleus, fuse to form myotubes, they fuse due to internal membranes disappearing, now multi nucleic
satellite cells
(muscle stem cells) we don’t make more muscle, they just grow from use (hypertrophy). Only produce more muscle cells if injured.
myofilaments
bindles of parallel proteins
filaments
some thick and some thin, Z-line, M-line, striations
Z-line
goes all the way through the myofibril, like a protein pancake, thin filament are attached to to z-line, runs the length of the sarcomere
M-line
middle of the sarcomere where thick filaments are connected
striations
mixture of thick and thin filaments
titin
run through core of each thick filaments and connects to the z-line…helps keep sarcomere aligned.
thick filaments
made of myosin, have knobs that interact with thin filaments, a few hundred myosin molecules, globular heads and are hooked up shaft to shaft
thin filaments
made of actin, create strands that twist, have tropomyosin and troponin, each has an active site
tropomyosin
attached to actin and splits into 8 little proteins
troponin
protein thats attached to tropomyosin
motor neurons
skeletal muscle has to be stimulated to contract
neuron
individual nerve cells, each can go to a few different muscle cells (located in brain and spinal cord)
axons
long extensions of motor neurons that go to each muscle cell, about 200 terminal branches that supply 1 cell each.
motor unit
each neuron and cells that it connects. over 1000 muscle cells total, some need multiple neurons to contract. don’t all contract at once, more units involved, more control we have
postural control
motor units taking turns flexing and resting
fine control
smaller motor units so control is quick and accurate, we have fewer fibers per nerve
strength control
larger units w/ 1000 fibers/nerve. More broad and brute strength (big contractions)
Neuro Muscular Junctions
NMJ - synapse is region where nerve fibers make functional contact w. target cell
Neurotransmitters
ACh gets released from nerve fiber which causes the muscle cell to be stimulated
synaptic terminal
swollen end of the nerve (has vesicles of ACh)
motor end plate
region of muscle cell surface (has ACh receptors that bind to ACh released by the nerve, then AChE is enzyme that comes in to break down the ACh)
Shwann cells
envelopes and isolates the NMJ
Action potential
branch from neuron to axon muscle cells where signals are sent
Neuromuscular toxins
AChE breaks down ACh
cholinesterase inhibitor
keeps ACh from being broken down so muscles must stay contracted (seen in pesticides, kills insects)
botulism
(bacterial) prevents synaptic vesicle release of ACh, muscles cannot contract
curare
causes muscle paralysis, binds to receptors so ACh cant
tetrodotoxin
comes from animals and blocks sodium channels, this stops action potential from flowing.
plasma membrane
polarized, resting potential due to sodium built up on outside and potassium built up on inside. Gives us a membrane potential around -90mV. When stimulated, gates open so Na rushes in and K rushes out, now potential is different. (more positive)
Muscle Contraction 1st
gets electrical signal from action potential, when the signal reaches the synaptic knob, the voltage gated calcium channel is opened and calcium rushes in. this stimulates synaptic vesicles with ACh to be exocytised.
Muscle Contraction 2nd
ACh gets exocytosized and binds to receptors on end plate potential. Now channels get opened so Na can rush in, K can leave, and the membrane potential shifts to more positive
Muscle Contraction 3rd
voltage change gives us the action potential so we have reaction (must reach -55mV). action potential moves across sarcolemma and reaches T-tubule. No voltage gated calcium channels open so calcium can get into SR where its stored.
Muscle Contraction 4th
Calcium is released, binds to troponin, which stimulates tropomyosin to slide down into actin ditch, now myosin can bind to actin’s active site.
Muscle Contraction 5th
myosin head has ATP and forms a cross bridge (this cocks the myosin head for power stroke) thin filaments gets pulled towards M-line
Muscle Relaxation 1st
AChE comes in and removes the ACh from the receptor so muscle is no longer contracted. This kills the action potential, no more calcium
Muscle Relaxation 2nd
calcium gets reabsorbed into terminal cisternae, now it returns back to calsequestrin which holds it until its released. No calcium = no tension in filaments.
Rigor Mortis
stiffening of the body after death, begins 3-4 hours after you die, peaks at 12 hours, stops about 48 hours later. SR releases all of its calcium so myosin is activated and all muscle contract. We need ATP to relax our muscles and since we are dead, theres no ATP so we stay flexed until myofilaments break down
Muscle Recruitment
little stimulation = little contraction, big stimulation = big contraction. When you start exercising you use stored myoglobin, then take in glucose through glycolosis which can make 36 ATP. Next up is phosphogen system, takes in creatine phosphate and makes 1 ATP. Next is anaerobic fermentation (produces lactic acid and 2 ATP)
Immediate energy
oxygen supply runs out, myoglobin provides oxygen for a short burst, most ATP is gained from stealing a phosphate from another molecule. (Phosphagen system) myokinase and creatine kinase…
myokinase
transfers the phosphate from 1 ADP to another which makes it an ATP
creatine kinase
obtains phosphate from creatine phosphate and gives it to ADP so it becomes ATP
Short-term energy
once phopshagen system is out, glycogen-lactic acid system kicks in. Muscles obtain glucose from blood and stored glycogen…gives us anaerobic fermintation
Long-term energy
high levels of long term muscle use, we must have oxygen to our muscles (aerobic respiration) this gives us 36 ATP per 1 glucose. Hard to get to but if you do, its most efficient.
Phosphagen system
quick bursts (sprints, jumping, diving, weight lifting)
Phosphagen and Glycogen-Lactic Acid
basketball, hockey, 200 m dash
Glycogen-Lactic Acid
100 m swim, 400 m dash, tennis, soccer
GLA and aerobic
boxing, 1 mile run, rowing, long swim
Aerobic respiration
marathon, jogging, cross country skiing
Fatigue
progressive weakness and loss of contractibility. Caused by: ATP synthesis declining as glycogen is used, ATP shortage causes sodium potassium pumps to fail, lactic acid lowers pH of sarcoplasm so enzymes aren’t as efficient, motor nerve fibers use up ACh, depletion of creatine phosphate.
Endurance
we need oxygen intake to get most out of our muscles, VO2 max is proportional to body size and peaks at 20. carb loading gives us excess glycogen so muscles and liver can get more energy as needed.
Muscle Recovery
Cori cycle and Oxygen Debt, when muscles are fatigued they have to recover.
Cori cycle
removal and recycling or lactic acid, liver converts lactic acid into pyruvic acid, pyruvic acid used in aerobic resp. to make ATP, which makes glucose and is then stored in glyocgen
Oxygen debt
occurs when you try to catch your breath, O2 is replaced by myoglobin and hemoglobin from your lungs. Thus replenishes your phosphogen system and reconverts lactic acid to glucose.
Slow twitch muscle fibers
(red) more mitochondria, myoglobin, and capillaries
fast twitch muscle fibers
(white) rich in enzymes for phosphagen and glycogen-lactic acids systems. large in diameter, lots of myofibrils, and more glycogen for our smaller quick muscles.
Muscle conditioning
resistance training and endurance training
resistance training
(anaerobic exercise) stimulates cell enlargement (hypertrophy) due to synthesis of more myofilaments
endurance training
(aerobic exercise) produces an increase in mitochondria, glycogen, and density of the capillaries
Cardiac muscles
shorter than skeletal muscles, thicker, branched and linked at intercalated disks. Less SR but larger T-tubules to get Ca+ from ECF. its auto rhythmic so it beats on its own. Uses aerobic reap exclusively
smooth muscle
fuseifrom cells with 1 nucleus, no striations, sarcomeres, or z-discs. thin filaments attach to dense bodies scattered throughout sarcoplasm and on sarcolemma. Nerve supply is autonomic, involuntary control. Could contract due to hormones, CO2, low pH, stretch, O2 defiance.
multi-unit smooth
in larger arteries, iris, pulmonary air passages, arrestor pili muscles. terminal nerve branches synapse on individual monocytes of motor units. independent contraction.
single-unit smooth
in most blood vessels and viscera as both circular and longitudinal muscle layers. electrically couples by gap junctions. large # of cells contract as a single unit.
Smooth muscle contraction and relaxation
calcium form extracellular fluid enter cells through channels. calmoudin activates the myosin light-chain kinase and allows the myosin to bind with actin. Thin filaments pull on intermediate ones that makes the cell twist. slow contraction and relaxation. Uses 10-300 times less ATP (latch-bridge mechanism)
vascular tone
partial contraction
joints
made of fibrous material and cartilage that joins two bones.
cartilage in joints
collagen fibers, hyaline cartilage, fibrocartilage
collagen fibers
connects radius to ulna, and tibia to fibula
hyaline cartilage
synovial joints (highly movable, most common)
fibrocartilage
in spine and pubic symphysis
Types of joints
sutures, gomphosis, syndesmosis, synchondrois, symphysis, synostosis
sutures
fibrous joints of skull bones
gomphosis
tooth in a socket
syndesmosis
two parallel bones
synchondrosis
hyaline cartilage
symphysis
fibrocartilage
synostosis
bone fusion
Synovial Joints
most common (knee, shoulder, elbow)
fiborous capsule
connective tissue that goes from 1 bone to another and encloses the joint space
joint cavity
holds synovial fluid
articular cartilage
hyaline cartilage around ends of the bones
synovial membrane
produces synovial fluid (allows cartilage to slide past each other)
meniscus
pad of fibrocartilage in wrist, knee, jaw
tendons
attach muscle to bone
ligaments
attach bone to bone
bursa
saclike extension of joint capsule that extends btwn structures for lubrication
tendon sheath
elongated cylinders of connective tissue lined with synovial membrane and wrapped around a tendon
humeroscapular joint
most mobile due to shallow glenoid cavity
rotator cuff
subscapularis, supraspinatus, infraspinatus, teres minor
Knee Joint
4 tendons: medial collateral, lateral collateral, posterior cruciate, anterior cruciate. 2 menisii: lateral and medial
arthritis
broad term for pain and inflammation
osteoarthritis
normal wear and tear, cartilage softens and desengrates
crepitus
noise of bones rubbing against things
bone spurs
calcification of bone fragments, leads to extra growth
rheumatoid arthritis
autoimmune disease, antibodies attack synovial membrane and cartilage disentigrates
gout
metabolic disorder, build up of uric acid (big toe)
bursitis
inflammation of bursa
bunion
bursitis of big toe, metatarsal joint leads to big toe turning in
tendonitis/tenosynovitis
inflammation of a tendon and its sheath
ganglion cyst
gelatinous swelling, extension of joint capsule
