ATP binds a myosin head that is complexed and release it from actin.  

ATP is then hydrolyzed which allows myosin to recomplex with actin at a different site.  

Once the phosphate is complete released and only ADP is attached to myosin, myosin lurches the entire actin filament forward creating a power stroke.  

ADP is released and another binding of ATP will result in another power stroke.

***the binding of a of myosin to an actin binding site is modulated by the conc. of Ca2+.  The binding of Ca2+ to two low affinity Ca binding site causes a comformational chain on actin which exposes a binding site for myosin and "cross-bridgeing" become possible

*** because many myosin heads are in different stages on binding of actin, actin cannot slips back along myosin

phosphocreatine (creatine phosphotransferase transfers a P to ADP) and glycogen (glycolysis)

rigor mortis happens because the sliding of filaments is dependant on ATP

the number of cross-bridges that are active.  If a muscle is stretched beyond its resting length, then the cross-bridges are destroyed and it is less capable of mounting a strong contractile response.

If the filaments are already too contracted, then there is crowding of myosin/actin cross bridge complexes and they begin to interfere with each other

the sarcoplasmic reticulum contains large stores of Ca2+ and span A and I bands.  They open to terminal cisternae (lateral sacs) which are connected by T(transverse)-tubules

T-tubules contain cytosol in their lumens and open to the cytosol of the skeletal muscle cells at the point of the A band and I band

ONE t-tubule and TWO terminal cisternae = triad

ACh is released as a neurotransmitter from the from a neuron's synaptic jxn and signals the opening of nicotinic ACh receptors.

An influx of Na+ ions will occur and depolarize the muscle cell and creates an action potential.

THis action potential is what opens up Ca2+ channels which open up into terminal cisternae and ultimately T-tubules

acetylcholinesterase removes ACh by hydrolysis

the sarcoplasmic reticulum Ca pumps and ATPases will shut down, lowering the intracellular conc. of Ca and the troponin-tropomyosin blocking complexes are able to reform allowing for relaxation

contractions from impulses are additive because there is a delay from impulse to contraction, and all the Ca2+ that was released may not be cleared before a muscle fiber receives a second impulse

muscle fibers are capable of being restimulated repeatedly

trepe is quickly spaced stimuli resulting in contractions that are each of increasing magnitude than the previous; this is also called incomplete tetanus

when the impulses are so frequent that the magnitude of the contraction is constant and becomes one fused contraction, this is known as complete tetanus

*** cardiac contractions are usually only just as long as the impulses, so the same effect doesn't happen with them

isometric = muscle remains the same length (static contraction); the lifting of an immovable object

isotonic = changes in muscle length

two types: concentric (muscle shortens) and eccentric (muscle lengthens)

the sum of the active and passive tension

passive comes from the weight of a load on a muscle while active is the result of an action potential impulse.

maximum active tension depends on the optimum length of the overlap of myosin and actin

slow-oxidative (type 1)

fast-oxidative (type 2a)

fast-glycolytic (type 2b)

the oxidatives are red, have extensive vascularity, lots of myosin and abundant mitochondria

the fast glycolytic has few myoglobin, can perform rapid contractions, has lower endurance

the efficacy of the myosin used is determined by different isoforms of myosin which each have different ATPase activies

high frequency stimulation fatigue:  stimulation of tetanus, Ca+ is depleted because it can't be pumped in fast enough

intrafusal fibers connect at two points to a muscle and are connected to afferent (sensory neurons) which connect to spinal cord

they exist in either nuclear bag or nuclear chains along skeletal muscles

the primary end of the intrafusal fiber detects the rate of muscle tension change while the secondary end detects the length change of a muscle

the result is a motor signalling of an inhibitory response meant to return the muscle back to a state of rest

ex.  knee jerk response, golgi tendon reflex

Improvement in oxidative capacity

increases the number of capillaries in the exercising muscles and the number of mitochondria within the muscle fibers. These changes enable the muscle to use oxygen more efficiently and to improve its oxidative capacity.

Inter-conversion between fast-twitch fiber types

Endurance training, such as long distance running, converts fast-glycolytic (Type IIb) fibers into fast-oxidative (Type IIa) fibers. In contrast, stress training, such as weight lifting, converts fast- oxidative fibers into fast-glycolytic fibers. Notice, slow-oxidative (Type I) fibers cannot be converted to any type of fast fibers.

Muscle Hypertrophy

increasing muscle mass by increasing the number of actin and myosin fibers; weight lifting.

Muscle Atrophy

atrophy; confined to a hospital bed for a long period of time

Sarcopenia

A decrease in the number of muscle fibers with advanced age is called sarcopenia. 

Muscle Regeneration

can happen if not too much muscle is lost post injury thanks to undifferentiated muscle progenitor cells (satellite cells) associated with the damaged fibers are transformed to mononuclear myoblasts.  cannot if damage it too extensive, will be filled by fibrous tissue and fat

allelic refers to different mutations at a single/same gene

locus refers to the production of a like phenotype but through multiple sites and genes (limb girldle MD)

exhibits pleitropy meaning variations in the organ systems affected

tall, thin, lanky, myopia, detached lens, mitral valve defects, dialation of aorta, pectus excavatum (the dent in the sternum)

it's a fibrillin gene defects

XLR, mutations of the dystrophin glycoprotein complex (the complex connecting F-actin to sarcomere)

duchennes is more severe due to larger deletions/mutations in the gene, beckers is milder

patients develop large calf because the muscle gets replaced by fatty, fibrous tissue

limb-girdle MD

fascioscapulohumeral MD

it's a trinucleotide repeat disease (others include fragile X, friedrich ataxia, huntington disease)

-these triplets occur in the DMPK gene which is a protein kinase

exhibits anticipation (worsening phenotypes though generations)

degree of affect is often determined by length of repeat sequence

in EDS what is Kyphoscoliotic caused by?

what is FOP Fibrodysplasia Ossificans Progressiva

connective tissue ossifies and becomes continous with skeleton

mutation is in ACVR1 gene (receptor for bone morphogenetic protein) leading to Uncontrolled Bone Growth

EDS Types

Classic - type I

Hypermobility - least severe

vascular - type III, AD

Type I collagen is made from two alpha 1 chains and one Alpha 2 chain.

Type II collagen is made from three alpha 1 chains.

where are prepro alpha chains synthesized?

low hydroxylation resulting in poor

assembly and crosslinking of collagen as in scurvy, causing weak blood

vessels and poor wound healing