human physiology - chapter 12 lecture

skeletal muscle

attached to the bone

- striated, voluntary [somatic]

smooth muscle

in organs & skin

- non-striated, involuntary

cardiac muscle

in heart

- striated, involuntary

muscle cells

elongated shapes —> muscle fibers

what do fascicles contain?

many muscle fibers

what do muscle fibers contain?

myofibrils

what do myofibrils contain?

myofilaments

how do multiple nuclei occur in a muscle fiber?

resulting from fusion of multiple cells during development

where does a striated appearance in skeletal muscle come from?

alternating dark A bands & light I bands

where do muscle fibers & neurons meet?

neuromuscular junction

motor unit

one motor neuron innervating many muscle fibers

recruitment

process of increasing the number of motor units that are active in a muscle at any given time, as needed, to increase muscle tension

summation

increases muscle tension; stimulation of motor units at different times, resulting in summation of contraction

myofibril

cylindrical bundle of myofilaments, 1-22mm in diameter

skeletal muscle fiber

fiber [packed with myofibrils] —>

myofibrils [packed with myofilaments [actin/myosin]

- contraction = myofilaments interacting

myosin

thick filaments [dark]: two globular heads that form cross-bridges with actin during muscle contraction

actin

thin filaments [light]: regulatory proteins [regulate contractions]

- troponin C & tropomyosin

troponin C

binds calcium

troponin T

binds tropomyosin

troponin I

binds actin

tropomyosin

blocks myosin binding site on actin

sarcomeres

basic contractile unit in striated muscle [sections of myofibrils]

sarcomere structure

- Z lines at each end

- actin [thin] anchored to Z lines

- myosin anchored by titin

subunits of troponin

C [calcium], T [tropomyosin], I [actin]

cross bridges

forms between myosin & actin during muscle contraction

what is myosin anchored in place by?

titin

what is actin anchored to?

Z lines

what are thick & dark filaments?

myosin

what are thin & light filaments?

actin

where is the H band in a sarcomere?

in the middle of a sarcomere

contraction

activation of the force-generating sites in muscle fibers to generate tension

sliding filament mechanism

when overlapping thick & thin filaments in a sarcomere move past each other to contract a muscle fiber

how does contraction occur?

cross-bridges in myosin binds to actin

why doesn't contraction occur in a relaxed muscle?

binding site in actin is blocked by tropomyosin [thin] from globular head of myosin

what does troponin do to tropomyosin?

holds tropomyosin in a blocking position

troponin subunits

heterotrimer [molecule with 3 subunits]: CTI

CTI

C: binds Ca2+

T: binds tropomyosin

I: binds actin

contraction polarization

muscle fiber is depolarized

- AP travels down transverse tubules in fiber = release of Ca2+ from SR in fiber

- the Ca2+ binds to troponin C

- troponin T undergoes conformational change

- troponin T moves tropomyosin out of the away

- myosin allowed to cross-bridge bind with actin

activation of the myosin head

1] ATP binds to the myosin head, serving as an ATPase

- ATPase splits ATP into ADP & Pi

2] myosin binds to actin, & cross-bridge becomes "cocked"

cross-bridge power stroke

after myosin head binds to actin, forming a cross-bridge

1] Pi is released

2] cross-bridge produces a power stroke [conformational change] to move actin filament [sliding filament mechanism]

excitation-contracion coupling

coupling of AP [excitation] with muscle contraction

- opens voltage-gated DHP receptors

- couples with Ca2+ release channels, ryanodine receptors [on SR]

what do transverse tubules do?

brings action potentials into muscle fibers

- causes SR to release Ca2+ into sarcoplasm

- Ca2+ binds to troponin C, stimulating contraction

latent perioid

period between action potential & contraction [delay]

how long do APs last in latent periods?

1-2 ms + ends before contraction

what does the calcium-troponin complex do?

"pulls" tropomyosin off the myosin-binding site of actin

- allows cross-bridge binding

- afterwards flexing to slide actin filament

when does muscle relaxtion occur?

after contraction when force-generating mechanisms ceases and tension reduces

how does muscle relaxation occur?

muscle cell membrane repolarizes causing calcium moving back into SR

- with Ca2+ gone, tropomyosin blocks binding

- actin & myosin doesn't interact

- myofibrils relaxes

mechanics of contraction

tension, load, twitch, summation, recruitment, tetanus/tetany

tension

force exerted on an object by a contracting muscle

load

force exerted on a muscle by an object

twitch

mechanical response [contraction] of a muscle fiber to a single AP/stimulus

summation

increase in muscle tension from successive APs [or stimuli] occurring during a contraction

recruitment

activation of more motor units or due to increased stimulation

- more activity in muscle fibers

- increased tension

tetanus/tetany

sustained maximal contraction due to repetitive stimulation

unfused/incomplete tetanus

partial dissipation of tension between subsequent stimuli

fused/complete tetanus

no time for dissipation of tension between rapidly recurring stimuli

fent

needdd

isotonic contraction

same tension & constant while muscle length changes

- muscle contraction with shortening of muscle fibers

isometric contraction

same size & develops tension, no length change

- muscle is contracting without change in muscle fiber length

short sarcomere

actin filaments lack room to slide, so little tension can be developed

optimal-length sarcomere

lots of actin-myosin overlap & plenty of room to slide; maximum tension

long sarcomere

actin & myosin do not overlap much, so little tension can be developed

slow-twitch fibers [type I]

- slower contraction, reach maximum tension, to fatigue

- rich blood supply

- responsive to repetitive stimulation

- postural muscles

fast-twitch fibers [type IIX]

- faster contraction, reach maximum tension, to fatigue

- less blood supply, less mitochondria

- stronger, heavily utilized muscles to jump/run

intermediate fibers [type IIA]

- like fast twitch, more mitochondria

- immediate contraction & fatigue

- responsive to repetitive stimulation [walking]

muscle fatigue

decrease in muscle tension due to previous contractile activity

proposed causes for muscle fatigue

- conduction failure due to increased extracellular [K+] after many APs

- lactic acid buildup due to acidification of muscle tissue [denatures contractile proteins]

- reduced ability of SR to release Ca2+ [prevents excitation-contraction coupling]

- depletion of fuel [glycogen] during low-intensity, long duration muscle activity

where are striations found in?

skeletal muscle & cardiac muscle

what are the proteins active in contraction?

tropomyosin, troponin, actin, myosin

cardiac muscle

only in the heart

- involuntary, spontaneous contraction [pacemaker cells]

- striated

- small cells, single nucleus

- intercalated discs

cardiac muscle contraction

AP propagates through T tubules —>

- depolarization: Na+ & Ca2+ influx through voltage-gated channels —>

- entering Ca2+ depolarizes membrane; increases Ca2+ —>

- triggers release of more Ca2+ from SR [positive feedback] —>

- thin filament, cross-bridge activation, force generation

excitation-contraction coupling [cardiac muscle]

1. Na+ & Ca2+ channels open

2. Ca2+ release from SR

3. Ca2+ binds to troponin C stimulating contraction

smooth muscle

- lacks striations, myofibrils. sarcomeres

- involuntary

- small, single nucleus

- blood vessel walls, bronchioles, digestive organs, urinary/reproductive tracts

-layers

cross bridge activation [smooth muscle]

1. Ca2+ mediated changes in thick filaments activate cross-bridges

- no troponin C; tropomyosin doesn't block

2. Ca2+ from internal SR & externally [ECF]

- binds to calmodulin

3. cross bridges form between actin & myosin