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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

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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.

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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

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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

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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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