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- Internal organs, blood vessels, eye. Produce movements in internal organs.
- involuntary, single nuclei, non-striated, spindle-shaped
- nerve supply to visceral modifies, nerve supply to MULTIUNIT is necessary
- Heart. Pumps blood.
- Single nuclei, striated, branched, involuntary
- nerve supply not necessary for function--modifies
- skeletal muscles. Moves bones, generates heat.
- Voluntary. Multi-nuclei, striated, long, thin fibers.
- Nerve supply necessary for movement
connective tissue that encircles all fascicles to form a complete muscle
connective tissue that encircles a group of muscle fibers forming a fascicle
a group of muscle fibers (held together by a perimysium)
connective tissue that surrounds each muscle fiber or cell.
where epimysium, perimysium and endomysium come together to attach to a bone
- muscle endoplasmic reticulum
- surrounds each myofibril. Inside, lots of CALCIUM
plasma membrane of a muscle cell
- invaginations of the sarcolemma into the inside of the muscle at a right angle.
- Action potential travels inside of them to stimulate SR and release calcium for contraction
- thin filament in muscles. In I-band (across Z-line) in a sarcomere. Double helix made of F-actin (string) and G-actin molecules (pearls).
- Tropomyosin and troponin attached. Moved by myosin
- thick filament. Tail, hinge and head. Head has ATP/ADP and phosphate to help move actin filament.
- Makes up H-zone in sarcomere.
- All heads in the same direction (on each side). Tails point towards the H-zone
Organization of skeletal muscles
- Muscle bundle
- muscle fiber
- (myofilaments) actin and myosin filaments
boundaries of a single sarcomere. Includes actin and myosin filaments (half I-band, A-band, H-zone)
section of a sarcomere containing myosin. Some actin is inside too
section in sarcomere that contains only actin, spans the Z-line so half is in each sarcomere. Disappears as muscle contracts
portion of sarcomere that contains only myosin, in the middle. Disappears as muscle contracts.
string part of double helix that makes up actin filament
pearls of actin filament
A T-tubule and two terminal cisternaes (part of sarcoplasmic reticulum)
DHP, on T-tubule. Receptor that depolarizes to signal the Ryanodine (RyR) receptor and allow calcium out of the sarcoplasmic reticulum
on sarcoplasmic reticulum, receptor that opens when DHP is depolarized to release calcium into the cell and cause muscle contraction
evil stepmother that covers myosin binding sites on the actin filament until distracted by a calcium-troponin bond.
Tiny bubbles on tropomyosin with three sub-units (bond to G-actin, Calcium or Tropomyosin)
when myosin filaments move actin filaments toward the H-zone, contracting the muscle.
Actin and myosin contraction
action potential goes through DHP, RyR releases calcium, calcium binds to Troponin, Troponin-Ca moves Tropomyosin, Myosin binds to Actin, Myosin hinges move actin towards the H-zone (due to release of ADP and P), causing the power-stroke that contracts the muscle, ATP phosphorylates, re-cocking the hinge
Termination of muscle contraction
energy (ATP) is required to pump Ca2+ back into sarcoplasmic reticulum. Everything releases back into its original form.
Action potential from cardiac muscle is different because:
it contains a plateau instead of a spike, caused by opening of voltage-gated calcium channels (slower). Slower depolarization, extends before repolarization. Longer absolute refractory period creates a forced pause between beats for the ventricles to fill (no tetany)
Strength of muscle tension is dependant on
length of sarcomere pre-contraction. Maximum number of cross bridges is ideal--should be overlap but still contain an h-zone and I-zones.
Twitch (3, last one has 3)
- single instant reaction of muscle, 20-200 milliseconds, goes through phases one time.
- Neuro action potential (spike)
- Muscle action potential (wider, a little less spike)
- Muscle contraction (Latent, contraction, relaxation)
phases of muscle contraction
- latent (action potential to calcium release)
- contraction (calcium release to power stroke)
- Relaxation (calcium pumped back into SR, ADP/ATP released to recock myosin head)
A gain of muscle twitch (more forceful but not longer) caused by a second stimulation shortly AFTER the relaxation phase of the first twitch. Not all calcium was pumped back into SR so there is more force/tension.
- gain of muscle reaction (stronger AND longer) caused by second stimulation DURING relaxation phase. Makes for a graded or sustained contraction, smoother response.
- Can result in FUSED tetanus, for smooth contraction
during wave summation when so many impulses are coming so fast that reactions become constant and smooth. A contraction. Graded, smooth, continuous.
stimuli coming quickly, twitch goes through fused summation for a prolonged contraction. (Normal)
- Greater force of muscle contraction by INCREASING the number of motor units that fire at one time. (more motor units will cause a contraction to get stronger/longer)
- AKA multiple motor unit summation or recruitment summation
Multiple motor unit summation
Greater force of muscle contraction by INCREASING the number of motor units that fire at one time. (more motor units will cause a contraction to get stronger/longer)AKA spatial summation or recruitment summation
Greater force of muscle contraction by INCREASING the number of motor units that fire at one time. (more motor units will cause a contraction to get stronger/longer)AKA multiple motor unit summation or spatial summation
Delicacy of muscle motion
- is dependant on number of fibers controlled by a single motor unit--less is more.
- Smaller motor muscle unit=more delicate movement
- larger muscle motor unit=less precise movement
- storage for ATP in muscle. Short-term, so more needs to be made constantly. Stored during rest.
- phosphocreatine + ADP --(creatine kinase)--> creatine + ATP
Ways for muscle to get ATP
- creatine-phosphate (into creatine, into ATP)
- Anaerobic (glycogen by glycolosis into lactic acid into ATP)
- Aerobic (Most, cellular respiration, electron transport chain)
How can you interefere with muscle synapse?
- Block release of ACH
- too much ACH
- No breakdown of ACH
What was wrong with Maggie? Wound, flaccid paralysis, weak tongue, eyelid tone, difficulty chewing and swallowing.
Botulism. Food poisoning, wound poisoning in horses. Toxin interrupts nerve transmission--prevents release of ACH. Acute symptoms. treated with antitoxin and antibiotics.
What was wrong with Fifi? Fatigue and exercise-induced weakness, change in voice, vomiting.
Myasthenia Gravis. antibodies attacking nicotinic receptors, blocking action potential. Can cause megaesophagus. Often in dogs, rarely in cats. Give tensulin--quick easy test that exposes nicotinic sites and temporarily cures symptoms
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