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ATP's Role in Myosin Power Stroke

1. Muscle contraction occurs via the sliding filament model, where myosin heads bind to actin and pull it inward, shortening the sarcomere. 2. Relaxation happens when calcium levels fall, causing tropomyosin to block actin binding sites and myosin heads to detach. 3. The force a muscle generates depends on its resting length - an optimal length allows maximum overlap and force, while overstretching reduces force.

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0% found this document useful (0 votes)
126 views5 pages

ATP's Role in Myosin Power Stroke

1. Muscle contraction occurs via the sliding filament model, where myosin heads bind to actin and pull it inward, shortening the sarcomere. 2. Relaxation happens when calcium levels fall, causing tropomyosin to block actin binding sites and myosin heads to detach. 3. The force a muscle generates depends on its resting length - an optimal length allows maximum overlap and force, while overstretching reduces force.

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xcupcakex122006
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Week 13 Learning Guide: Muscles (cont.

 Muscle Contraction

o Contraction: muscle fiber shortens; sliding filament model (thin slide over thick)

o Steps of Contraction:

1. ATP is hydrolyzed to ADP + Phosphate and the myosin head is in active


conformation

2. Myosin binds to the active site on actin forming a cross bridge

3. ADP and Phosphate are release and myosin head bends, pulling actin inwards
towards middle of sarcomere (power-stroke)

4. Head remains bound (rigor mortis) until a new ATP binds, weakening and
eventually breaking the cross bridge (myosin head detaches)
 Cause of rigor mortis: when dead you no longer produce ATP and the
myosin cannot dissociate from actin without ATP

5. ATP is hydrolyzed to ADP + Phosphate and the myosin head returns to active
conformation once again

o Cross Bridges:
- single cross bridge creates v. little movement
- all cross bridges in once cycle only shortens 1% percent of resting length; cycle
must be repeated many times (muscles can contract to 60% muscle length)
- only portion of cross bridges form at a given time; they are asynchronous
- when load is heavier you need more cross bridges

 Relaxation:

o What happens to ACh?


- motor neuron stops firing
- ACH release is stopped
- Remaining ACH in cleft broken down by acetylcholinesterase
- Muscle fiber no longer stimulates

o What happens to Calcium?


- calcium is pumped back in SR by an active transporter
- calcium levels fall and troponin C releases calcium
- tropomyosin moves back into inhibitory position

 Length Tension Relationship:


- Amount of tension generated depends on the resting length of the muscle; if muscle is
already overly contracted or over stimulated at rest, less force is generated

1
o Optimal Resting Length:
- allows maximal cross bridge formation (stronger force); better interaction
between actin and myosin
- muscle produces greatest force
- CNS monitors and adjusts resting length (maintains muscle tone)
- if muscles stretched further than optimal length the force of contraction
decreases; when muscle not stretched out enough it had less cross bridge
because actin filament are overlapping and less active sites; if muscle is
overstretched the myosin and actin no longer overlap and cross bridges cannot
form (ex. lifting something when bent over)

* skeletal muscles are kept at their optimal length (muscle tone); optimal length
most important in cardiac muscle

 Behavior of Whole Muscles:

o Threshold:
- muscle will not fire if stimulus is too weak; threshold is the minimal voltage for
action potential to generate and contraction to occur; single threshold stimulus
results in a muscle twitch (quick cycle of contraction and relaxation); all or none
principle all of none for single muscle fiber not for entire muscle in general

 Latent Period:
- delay between stimulus and onset of twitch (contraction); time
required for excitation contraction coupling to occur; stimulating muscle
directly also has a latent period although shorter

o Adjusting Contraction Strength: CNS calculates how many motor neurons


needed to lift something; recruits more muscles for heavier items

1. Multiple Motor Unit Summation: recruit more units and muscle fibers to
generate more force

 Recruitment: stimulation of nerve with higher voltage results in


more motor units being activated (recruitment) resulting in
stronger contraction; nerves have several neurons organized in
motor units; these motor units have varying thresholds;
increasing the stimulus voltage increases the amount of muscle
units and muscle fibers that are activated; one all muscle fibers
have been recruited a stronger force cannot be generated.

2
2. Temporal Summation: increased stimulus frequency results in stronger
contraction; repetitive stimulation; increase calcium level in cell,
increasing cross bridges formed and increases force of contraction

 Treppe:
 Incomplete Tetanus: one wave of contraction adds to the next

 Complete Tetanus: twitches fuse; providing 4x force of single


twitch, eventually resulting in fatigue

 Isometric and Isotonic Contraction:

o Isometric: no muscle shortening; change in tension but not length (ex. holding a
weight but not moving it; muscle develops tension) ex. planking

o Isotonic: change in length of muscle but not tension (ex. moving a weight causes
muscle to shorten, but tension stays constant)

* heavier loads cause decrease in contraction velocity

 Muscle Metabolism:

o ATP Relies on: available oxygen and organic energy sources such as glucose and
fatty acids

o ATP Synthesis Pathways:

 Anaerobic Fermentation:

- produces ATP in the absence of oxygen


- ATP yield is very low
- produces lactic acid (toxic and is factor in muscle fatigue)

 Aerobic Respiration:

- produces a lot of ATP


- less toxic products are formed (carbon dioxide and water)
- requires continual supply of oxygen
* muscles primarily use aerobic respiration; however they use different
mechanisms depending on duration of use

3
1. Immediate Energy
- short intense energy (1 min brisk walk or 6 sec sprint)
- ATP because lungs and heart cant deliver oxygen quickly enough
- Myokinase transfers phosphate from one ADP molecule to another to form ATP
- Creatine Kinase obtains/donates phosphate from creatine phosphate to ADP
- ADP + Creatine Phosphate = ATP + Creatine

2. Short-Term Energy
- muscles switch to anaerobic respiration (no O2) until cardiopulmonary system
can catch up with demand.
- Converts glucose into lactic acid (muscle fatigue)
- produces enough ATP for 30 sec on max activity

3. Long-Term Energy
- cardiopulmonary system takes over after 40 seconds
- O2 delivery to muscles is fast enough to meet demands
- >90% of ATP produced aerobically in exercising lasting longer than 10 min

 Cardiac Muscle:

o Location: heart

o Description:
- involuntary, striated, branched, centrally located nuclei
- contains intercalated discs that allow electrical continuity (allow cells to
communicate with each other (contains gap junctions within intercalated discs)
- contract automatically (w/out NS stimulation); NS modulates can continue to
contract outside body f in a dish and nourished with saline fluid

 Smooth Muscle:

o Location: blood vessels and bronchioles (circular smooth muscle);


hollow organs (circular and longitudinal smooth muscle);

o Description: smooth muscle is not striated; no sarcomeres; no striations;


contains actin and some myosin (16:1); thin filaments are long and attached
plasma membrane or dense bodies (protein structures); long filaments are
vertically stacked; cross bridges form along entire thick filament length.

o Function: contracts muscles evenly; even when stretched (ex. bladder and
uterus); striated muscle eventually loses ability to contract properly when
overstretched. (ex. bladder still needs to be able to contract even when
maximally distended) smooth muscle is not striated

4
o Excitation Contraction Coupling:
- Calcium is a trigger: calcium is sustained for contraction from the ECF via
voltage gated calcium channels; graded by depolarization because some calcium
comes from outside of the SR, it does not to be as well developed

- NO troponin involved; instead, calcium binds to calmodulin (similar in


structure to troponin) which activates myosin light chain kinase (MLCK)

- Myosin light chain kinase: phosphorylates myosin light chains so that myosin
can bind to actin and make contraction occur; more calcium = more MLCK
activity = graded depolarization.

- Contraction can occur with small amount of calcium entry only (does not
require action potentials); contractions are slow and sustained (energy
efficient)

- relaxation via myosin phosphatase and Ca2+ ATPase pump

Calcium Channel Blockers:


- Dilates blood vessels; useful for hypertension and coronary artery vasospasm

o Smooth Muscle Units:

 Multi-Unit:
- few if any gap junctions
- ex. arrector pili and lens ciliary muscles, bronchioles

 Single-Unit:
- numerous gap junctions; functional syncytium
- ex. digestive tract and uterus
- ANS modulates only
- myogenic activity: contract in response to stretch

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