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involuntary movement - esophagus walls, stomach, intestines, bronchi, uterus, urethra, blaqdder, blood vessels, etc
longer or even near permanent muscle contractions
peristalsis - rhythmic, wave-like contractions of longitudinal and circular muscle fibers within digestive tract
involuntary and heart only
attach to bones via tendons (a few places by aponeurosis) and allow voluntary movement of body, 15% denser than fat
striated in regular paralell bundles of sarcomeres
exercise prioritizes one type over the other depending on the activity
type I fibers, long contraction duration, assoc with endurance
rely on glycolosys to fuel contractions and include fast twitch fibers - fast muscle contractions and short duration
ATP for muscle contraction from three ways - creatinine phosphate, glycogen, ATP direct from cellular respiration
nervous fatigue: decline in nerve stim (esp strong contractions at upper limit of ability to gen force/ nerve sustain high freq stim)
or physical activity with a low availability of oxygen, involves high intensity muscle contractions for short periods of time, utilizing primarily Type II muscle fibers. short, high intesnsity bouts (more lactic acid levels)
age related skeletal muscle loss - often with osteoporosis
due to eccentric and concentric muscle loading often resulting in delayed onset muscle soreness (which is a result of damage to muscle sarcomeres during contractions), acute and delayed nature of luscle soreness indicates inflammatory immune response
stiffening of all muscles in body after death (3-4hrs after death, max stiff at 12hrs)
supplementation: can mitigate negative effects of exercise - increase energy available to muscles. phosphocreatinine pool for ATP for type II muscles. coaches cant provide but players legally can take it
strength is primarily anaerobic (weight lifting and sprinting - type II, fast twitch fibers),
aerobic usually activities using endurance and sustained muscle contractions (mostly type I, slow twitch muscles). can contract and develop tension at 2-3 times the rate of slow twitch fibers. These fibers are quicker to fatigue.
hyper- less able to stretch (can be upper motor neuron lesion), hypo - chronic reduced muscle tension (can be disruption of afferent input from stretch receptors &/o lack of efferet influence on fusimotor system).
testosterone and things related - increases protein synthesis in cells. neg effects known plus increases ldl and decreases hdl, acne, HTN, lv damage
non-functional muscle proteins that impair proper function - dystrophin protein and protein complexes are altered and unable to join with actin filaments. causes disruption mech stabilization and calcium concentration within sarcomeres altering binding and contraction of fillaments. as it progresses causes death of muscle tissue
form, support, protection, stability, body movement
skeleton, muscles, cartilege, tendons, ligaments
axial skeleton: skull, vertebral column, thoracic cage
skull: divided into cranial (8) and facial bones (14 - provides cavaties for sense organs)
Appendicular skeleton: limbs, pectoral and pelvic girdles
any of central canals and surrounding bony layers found in compact bone
small mineralized spicule that forms network in spongey bone
osteoblast (synth and secrete collagen matrix and calcium salts),
osteoclast (cells break down and reabsorb bone, stem from monocytes and macrophages)
osteoprogenitor (stem cell precursor to osteoblast)
membranous vascular layer of cells which line medullary cavity of bone
blasts and clasts dont have mitotic action = osteogenitc cells are key
stems from ossification from fibrous membranes in flat bones
osteoids form spongey bone around blood vessels which is later remodeled into a thin layer of compact bone tissue
ossification begins when embryo is 6weeks, before this all fibrous membrane and cartilege . bone growth until about age 25
: long bones lengthen at epiphyseal plare with addition of bone tissue and increase in girth. old bone lining medulliary cavity is reabsorbed and new bone tissue is grown under periosteum - increasing bone girth
cartilege formed on epipheseal side, ossified on diapheseal side to lengthen bone. 4 growth zones for reserve (condrocytes connect epypheseal plate to bone) proliferation (larger chondrocytes, make more chondrocytes), maturaltion (older and longer chondrocytes, matrix calcifies), calficiation (chondrocytes are dead bc bone is calcified)
central shaft of long bone
: 1) hematoma forms at break,
2) formation of fibrocartiledgeinous callus,
3) formation of bony callus,
4) remodeling of compact bone
synarthrosis: fibrous connective tissue and cannot move, inc sutures, syndesmoses, and gomphoses
amphiarthrosis: contain cartiledge and allow very little movement, sychondroses and sympheses
sl rounded into sl hollow, one remains stationart other like a door
rounded end of one bone fitting into ring of another - good for rotation
oval end fit into oval hallow. angular movement on two axes
concave and convex fit together for angular movement
allows greatest range of motion
tropomyosin (covers actin binding sites) and troponin change shape and remove tropomyosin from binding sites) prevent myosin from binding to actin while muscle is in resting state
arcoplasmic reticulum: smooth ER found in smooth and striated muscle - contrains lots of calcium which it sequesters and releases when muscle cell is stimulates
connection between action potenital and mechanical muscle contraction
motor neuron connecs to muscle at neuromuscular junction where synaptic terminal forms synaptic cleft with motor plate end - nueral signals triggers Ca release from sarcoplasmic reticulum into sarcoplasm (ACH is the usual signal)
post junctional folds which increase the surface area of the membrane (and ACH receptors) exposed to synaptic cleft
about 30%. up to 95% and will for sure cause damage to body
most abundant and typical. fasicles are parallel
Synergist muscles acts around a moveable joint to produce motion similar to, or in concert with, agonist muscles. They often act to reduce excessive force generated by the agonist muscle, and are referred to as neutralizers.
Agonist muscles are those we typically associate with the movement itself, and are sometimes referred to as prime movers; contracts while another muscle relaxes.
collagen protein of tendons is composed of fibers that run parallel, but have a wave-like appearance due to crimps in the fibers.
bundle of skeletal muscle fibers surrounded by connective tissue
surrounds individual muscle fibers
inflammation os synovium (fluid filled sheath) that surrounds. reduces ability to slide through shealth. can cause finger to LOCK. Sx: labored movement, swelling, periarticularpain, tendernes, rubor. cause: infection, injury, overuse and/or strain. Tx: rest/ immobilize
often deltoid, vastus lateralis, ventrogluteal, dorsogluteal muscles. often vaccines this way. more in than subcutaneous, less chance of irritation faster absorption and greater blood supply
before exercise may reduce injury and increase performance, can increase range of motion. overstretching can lead to instability and pain.
facial paralysis from dysfunction of VII cranial nerve. idiopathic. corticosteroids can help
eyes not properly aligned. can be lack muscle coordination, adversely effects depth perception.
Strabismus can be caused when the cranial nerves III (oculomotor), IV (trochlear), or VI (abducens) have a lesion.
eyepatch unlikely to help
protrusion of abdominal cavity contents through lower abdominal wall (esp inguinal canal). arise from weak abdominal nerve. usually painless buldge in grain area, may be worse with cough, strain or stand
identifying features of cardiac muscle; these connect individual heart muscle cells to work as a single functional organ
A globular structural protein that polymerizes in a helical fashion to form an actin filament (or microfilament).
thin fil. 2 chains wrapped - like the train tracks for myosin, myosin controls the action
the contractile unit of the myofibril of a striated muscle
In the sliding filament model, the thick and thin filaments past each other, shortening the sarcomere.
are composed of thick (myosin) and thin (actin) filaments, which interact to cause muscle contractions.
cylindrical organelles, found within muscle cells, that are the contractile unit of muscles
contains the entire length of a single thick filament
the zone of thin filaments that is not superimposed by thick filaments
the bond between the globular head of a myosin molecule and the actin filament, repeatedly formed during muscle contraction to draw it into the A band of a sarcomere
disc in the middle of the sarcomere, inside the H-zone
ATP prepares myosin for binding with actin by moving it to a "cocked" position.
ATP must bind to myosin to break the cross-bridge and enable the myosin to rebind to actin at the next muscle contraction.
a class of enzymes that catalyze the decomposition of ATP into ADP and a free phosphate ion, releasing energy that is often harnessed to drive other chemical reactions
more cross-bridges, the more tension
amount of tension depends on the cross-sectional area of the muscle fiber and the frequency of neural stimulation.
Maximal tension occurs when thick & thin overlap to the greatest degree in sarcomere;
more motor neurons stim, more myofibers contract, and greater tension in muscle.
let action potential spread over muscle
largest body protein.
elastic. helps return stretched muscle to resting length. interacts with myosin
start and stop actin/myosin muscle contraction.
tropomyosin covers site on actin that myosin binds to.
troponin mediates responsiveness of other to signal (ca release)
more actin, less myosin, no troponin, no sarcomere, (longer and whole thing covered in heads, vs end in skeletal)
sarcoplasmic reticulum is less organized
no t-tubules, caveolae instead - indentations that work similarly - spread action potenital
no sarcomeres - just filament associations
lots of cytoskeleton - dense bodies and intermediate finalemtns - position stuff
calmodulin, complex activates myosin light chain kinase (kinase phosphoralates) here ph myosin light chain, stim ATPase and initate power stroke, cause sliding/tension
CNS integrate sensory info into involuntary response. some born in, some learned. amny negative feedback, some feed worward (anticipate something going to happen)
integrated at spinal cord: monosynaptic reflex - one neuron onto motor neuron, polysynaptic neuron: inter neuron in there
most initated by proprioceptors - inside skeletal muscle, joint capsule and ligaments (balance, etc)
some by nociceptors (hot stove)
: doesnt contract - involved in proprioception (muscle spindles) - degree of stretch. middle of cell no myofibriles, ends of cell do stretch. golgi tendon organ does this between muscle/ tendon - detect the amount and rate of change in length of a muscle.
innervated by two axons, one sensory and one motor.
reflex: simple, integrates in spine
voluntary: cerebral cortex integration (inc muscle memory - can improve, become involuntary)
rhythmic movement - combo reflex/ voluntary. central pattern generators maintain. started cerebellum but spinal cord continues the movement
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