1. Maintain body posture
2. Stabalize joints
3. Produce movement
4. Generate Heat

Myofibril: 1500 myosin, 3000 actin filaments

Myosin filament: 200 myosin molecules.

Bring action potential into the interior of the muscle fiber.

A cytoskeletal protein that helps align actin

Cytoskeletal protein binds the cell to it's membrane.

Sex linked: Passed on X cromosome from mother

Could be spontaneous mutation on X chromosome before or during conception.

Both lead to defective or absent dystrophin protein.

• prograssive muscle weakness
• Skeletal deformity
• Mental retardation
• Respitory infections and heart failure.
• Death with 20 years

• No cure
• Experimental studies of gene therapy and inhibition of myostatin pathway.

The greater the amount of work by muscle, the greater amount of ATP cleaved.

• Inability to remove Ca: promotes binding of myosin cross bridges.
• No ATP available to bind myosin to release cross bridge

• Action potential peaks. When its near it's end, the [Ca] starts to rise.
• [Ca] peaks. When its near it's end, tension starts to rise.
• Tension peaks and falls.

• Object is too heavy to lift.
• Tension builds to peak values but muscle is not allowed to contract.
• Cross-bridges form but no sliding
• Active, Passive, total tension

• Muscle shortens
• Load remains constant(after load)
• Tension rises until it exceeds the amount of resistance

Passive: develops by stretching mucle to different lengths.

Active: force applied when muscle contracts.

Total: active + passive

Preload: resting length of the muscle.

Afterload: constant load (that a muscle is pulling up)

Muscle fiber is stimulated so rapidly that it doesn't have a chance to relax between stimuli.

A maximal sustained contraction occurs.(Plateu)

Rapid action potentials cause a large summation of tension.

The long duration of the action potential leads to a long refractory period.

Unfused Tetanus

Hills leading up to a Tetanus.

• Maximal strength of contraction
• Minimal increment of tension contributed by unit

Type II

Large, Fast, Glycolytic

 Type I

Slow, smaller, oxidative

• refers to a localized state or condition (of muscle in this case)
• Smaller motor units are recruited alot and are frequently active
• Larger motor units are infrequently recruited

also called Myogloburia

• large amount of protein(myglobin) in the urine
• Caused after major muscle trauma
• May cause renal failure if myoglobin is trapped in renal capillaries/tubules.

• Number of fibers contracting
• Tension developed by each contracting fiber.

• # of motor units recruited
• # of muscle fibers per unit
• # of muscle fibers available to contract.

-Size of muscle(muscle fibers in muscle)

-Presence of disease

-Extent of recovery from traumatic loss

• Frequency of stimulation(twitch summation and tetnus)
• Length of fiber at onset of contraction (length-tension relationship)
• Extent of fatigue (extent of activity. How in synch the recruitment is.
• Type of fiber
• Thickness of fiber (testosterone makes them bigger)

1. ATP and Creatine-P: Immediate source. Transfer of hi-energy P from creatine-P to ADP.
2. Anaerobic metabolism-glycolysis: Main source when O₂ is NOT present. glycogen→ pyruvate→ lactic acid. During heavy exercise.
3. Aerobic Metabolism- Oxidative Phosphorylation: Main source when O₂ is present. Fueled by glucose/fatty acids/amino acids from food. Becomes dominant with long exercise.

Increased oxygen intake following strenuous activity.

• Alactate debt: 3.5L (1.5 ATP system)
• Lactase debt: 8L Glycogen system

Typical: external stimulus. (electrical, hormones, stretch, or spontaneous)

Self excitatory: Slow waves(pacemaker waves) ossilate near the threshold. NOT and action potential

Plateau: repolarization delayed up to 1sec due to Ca²⁺ channels. Uterus and Ureter

Interstitial cells of Cajal

Pacemaker for electrical and contractile activity

NO Troponin

• Ca²⁺ binds to Calmodulin(controls actin myosin binding)
• Ca-Calmodulin complex binds and activates myosin kinase.
• That complex uses ATP to phosphorylate and activate myosin. Which can then bind actin.

from the ECF

Enters via voltage channels. Or neurotransmitter or hormone channels.

Phasic: Brief stimulaiton. Twitch-like

Tonic: Force is sustained for long periods of time. Ca levels dont drop all the way down which allows the muscle to remain tense with decreased number of activated corssbridges(myosin) and less ATP used.

• Voltage gated
• Ligand gated
• Leak channels
• IP₃ gated: second messenger system that goes to the SR and gets it to release Ca

• Ca²⁺/Na⁺ exchange
• Ca ATPase

• Abnormal spasms in vascular smooth muscle leads to deminished blood supply to digits.
• Discoloration
• Pain/Tingling/Numbness
• Ulcers
• Gangrene

0- Depolarization/upstroke (Na²⁺ intake)

1- 1st piece of repolarization (K⁺ out Cl^- in)

2- Plateau: L-type channels(long lasting) allow Ca²⁺ in

3- Repolarization (K⁺ in)

4- Baseline resting potential

Atrial phase is similiar except part 2 is shorter because it has fewer Ca²⁺ channels.

0- Upstroke (Ca²⁺ intake)

3- Repolarization (K⁺ out)

4- Spontaneous Depolarization (Na⁺ in) allows for pacemaker potential.

Near the very end of the action potential.

Cell more xcitable than usually.

Easier to start another one.

Cell can get depolarized but there is no action potential.

Right after Absolute

• It occurs when Ca²⁺ enters a Cardiac muscle cell and induces the sarcoplasmic reticulum to release Ca²⁺ into the cell.

Period where heart is filling up with blood after contracting

• Left vetricular end diastolic volume
• Length of muscle at the end of diastole right before contraction.
• Same length tension relationship as skeletal muscle.

The greater the end-diastolic volume(preload), the greater the ventricular pressure that can be developed.

Contraction of heart

If diastol increase too much systol will decrease because overlap will not be optimal.

Intrinsic ability of myocardial cells to develop force at a given muscle length. Correlates directly with [Ca] inside

How do you change the [Ca]?

• Neurohumoral factors like norepinepherin increase sarcolemma permeability to Ca²⁺
• Increase fequency of contraction (treppe)

Ventricular: 250

Atrial and SA node: 150

Purkinje: 300msec