Bio exam 3 part 3

unfused tetanus

Additional stimuli while muscle fibers are partially relaxing, sustained but wavering contraction

Refractory periods

After a muscle fiber has been stimulated and a contraction has occurred, the muscle fiber loses excitability and cannot respond to additional stimulus

Motor units

Axon of a somatic motor neuron branches out, forms NMJ with many separate muscle fibers

Latent period

Brief delay between stimulants and beginning of contraction

Twitch contraction

Contraction of muscle fibers in motor unit in response to a single nerve action potential

Inadequate Ca2+ released from SR and decline of Ca2+ in sarcoplasm, depletion of creatine phosphate, insufficient O2, depletion of glycogen and other nutrients, buildup of lactic acid and ADP, failure of motor neuron to release enough ACh

Contributing factors to muscle fatigue

Flaccid

Damaged motor neurons, loss of tone

Muscle tone

Degree of muscle tension during rest or in response to stretching, important for maintaining posture and balance, functioning of digestive organs, maintaining blood pressure

Red muscle fibers

High myoglobin content, more mitochondria, more blood capillaries

Wave summation

If muscle fibers are stimulated while previous twitch is still occurring then second contraction is stronger, second stimulus triggers release of more Ca2+ activating additional sarcomeres while muscle is still contracting

Slow oxidative fibers

Large amounts of myoglobin and many capillaries, generate ATP by aerobic respiration (many mitochondria), myosin head ATPase hydrolysis ATP slowly, resistant to fatigue, maintaining posture and aerobic

Isometric contraction

Length of muscle does not change during contraction, used for maintaining posture and holding objects in fixed positions

White muscle fibers

Low myoglobin content

motor unit recruitment

Number of active motor units increases, weakest produced first with progressively stronger added if needed, produces smooth movements, delays fatigue, allows contraction for longer periods

Contraction period

Peak tension in muscle fiber, Ca2+ binds to troponin, myosin binding sites on actin are exposed and cross bridges form

slow oxidative, fast oxidative-glycolytic, fast glycolytic

Recruitment order of fibers

Relaxation period

Tension in muscle fiber decreases, Ca2+ transported back into SR, myosin binding sites are covered by tropomyosin, myosin heads detach from actin

Isotonic contraction

Tension remains constant while muscle changes length, used for body movements and moving objects

muscle metabolism

very high amounts of ATP needed during muscle contraction

myosin head

binds ATP and actin

anaerobic glycolysis

catabolism of glucose to generate ATP when creatine phosphate depleted, glucose enters muscle fibers via facilitated diffusion or breakdown of glycogen

3 ways to produce ATP in muscle fibers

creatine phosphate, anaerobic glycolysis, aerobic respiration

junctional folds

deep groves in motor end plate provide surface area

Sources of oxygen in muscular tissue

diffusion from blood, from myoglobin within muscle fibers

axon terminal

end of motor neuron and divides into synaptic end bulbs

Contraction cycle 2: Attachment of Myosin to Actin

energized myosin head attaches to myosin-binding site on actin, phosphate group released from myosin head

synaptic cleft

gap between cells in synapse

aerobic respiration

glycolysis forms pyruvic acid from glucose, much slower but produces more ATP

as long as ATP and Ca2+ are available

how does the contraction cycle repeat?

Muscle fatigue

inability of muscle to maintain force of contraction after prolonged activity

Fast Oxidative-Glycolytic Fibers

largest fibers, large amounts of myoglobin and many blood capillaries, generate ATP by aerobic respiration and anaerobic glycolysis, myosin head ATPase hydrolyze ATP quickly (faster contraction cycle), high resistance to fatigue

acetylcholine receptors

ligand-gated ion channels found in motor end plate

Fast Glycolytic Fibers

low myoglobin, fewer blood capillaries, few mitochondria, generate ATP by anaerobic glycolysis, high glycogen level, hydrolyze ATP quickly (strong and quick contractions, fatigue quickly, intense anaerobic movements

actin

molecules twist together to form helix-shaped filament, myosin-binding sites to bind myosin heads

Myosin

motor protein in all 3 types of muscle tissue, converts ATP chemical energy to mechanical energy

excitation

muscle action potential

Contraction Cycle 1: ATP hydolysis

myosin head binds ATP, ATP hydrolyzed into ADP energy to myosin, energized myosin head moves perpendicular to filaments

Contraction Cycle 4: Detachment of Myosin from Actin

myosin head detaches from actin when ATP binds to myosin

Contraction Cycle 3: Power Stroke

myosin head pivots, think filament pulled along thick filament toward center of sarcomere, generates muscle tension, at the end ADP is released from myosin head

sliding filament mechanism of contraction

myosin heads pull thin filaments inward, total length of sarcomere shortens, distance between Z discs shortens, I band and H zone narrow and eventually disappear, no change in width of A band

motor end plate

part of muscle opposite synaptic end bulbs

myosin tail

points toward M line in center of sarcomere

creatine phosphate

relaxed muscle fibers produce more ATP than needed, creatine kinase catalyzes transfer of high-energy phosphate groups

initiation of contraction cycle

sarcoplasmic reticulum releases calcium ions into sarcoplasm, released Ca2+ bind to troponin, troponin moves tropomyosin away from myosin-binding site on actin, binding sites are free and contraction cycle begins

glycolysis

series of chemical reactions that break down glucose into pyruvic acid

Neuromuscular junction

synapse between somatic moto neuron and skeletal muscle

concentric isotonic contraction

Muscle shortens during contraction

fused tetanus

No muscle relaxation between stimuli, sustained contraction

Concentric isotonic contraction and eccentric isotonic contraction

Two types of isotonic contraction

sense voltage

What do voltage-gated Ca2+ channels do?

Stops muscle contraction

What does a decrease of Ca2+ in sarcoplasm do?

starts muscle contraction

What does an increase of Ca2+ concentration in the sarcoplasm do?

lactic acid

What does pyruvic acid convert to when there is no oxygen?

synaptic end bulbs, synaptic cleft, motor end plate

What does the neuromuscular junction include?

at triad

Where does excitation-contraction happen?

Eccentric isotonic contraction

Muscle lengthens during contraction

nerve impulse arrives at synaptic end bulb, Ca2+ flows through open channels, ACh diffuses across synaptic cleft, ACh binds to ACh receptors, change in membrane potential triggers muscle potential, ACh broken down by acetylcholinesterase

Steps of nerve impulse generating muscle action potential