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