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tension “pulling strength”
sliding of actin and myosin filaments causes sarcomere shortening
in a muscle cell, all sarcomeres shorten causing the muscle cell to shorted
tension in a muscle depends on:
tension that develops in individual muscle cells during contraction
number of muscle cells that contract
amount of shortening depends on tension and resistance
fiber shortening
as sarcomeres shorten, muscle cell shortens, producing tension
pulls on connective tissue and bone to which it is attached
tension produced in individual muscle fibers
can vary due to:
length-tension relationship (how stretch/compressing is for a muscle)
frequency of stimulation by motor neuron
tension produced by entire muscle
can vary due to:
number of muscle cells receiving nerve stimulation, commanding them to contract
muscle cells are grouped in motor units
group of muscle cells all told to contract simultaneously
length-tension relationships
amount of tension depends on number of cross bridges formed
depends on degree of overlap of actin and myosin filaments
skeletal muscle contracts most forcefully over a narrow range of resting lengths
page 8
page 8
twitch
cycle of contraction, relaxation produced by a single action potential in a muscle cell
not typical of most normal skeletal muscle activity
twitch latent phase
action potential occurs
no contraction until Ca+2 is released from SR
twitch contraction phase
tension rises to peak
Ca+2 moves tropomyosin off actin active sites
myosin cross bridges form, actin is pulled
twitch relaxation phase
tension falls to resting levels
Ca+2 is pumped back into SR
actin sites covered by tropomyosin
no cross bridges remain
frequency of stimulation
most muscular activities involve sustained muscular contractions
produced by high frequency of action potentials in muscle cell
produced in response to high frequency of action potentials in motor neuron (high frequency of stimulation)
summation of tension produces greater tension due to more available calcium
twitch
summation
repeated stimulation produced before relaxation phase has been completed
summation of tension caused by build up of calcium ions in sarcoplasm
complete tetanus
sustained contraction
maximum tension production in a muscle cell - maximum cross bridge formation
tetanus disease
caused by clostridium tetani bacteria
bacterial toxin causes high frequency of action potentials in motor neurons
treppe
an increase in peak tension with each successive stimulus delivered shortly after the completion of the relaxation phase of the preceding twitch
the fiber’s maximum potential tension is not reached until tetanus
wave summation
occurs when successive stimuli arrive before the relaxation phase has been completed
action potentials are happening faster, nerve still hasn’t been released
incomplete tetanus
occurs if the stimulus frequency increases further. tension production rises to a peak and the periods of relaxation are very brief
sustaining tension but not to the maximum
complete tetanus
during complete tetanus, the stimulus frequency is so high that the relaxation phase is eliminated. tension plateaus at a maximum level
tension
produced in individuals muscle fibers (cells) can vary due to
length-tension relationship
frequency of stimulation
produced by entire muscle can vary even more widely due to
number of muscle cells receiving nerve stimulation, commanding them to contract
muscle cells are grouped in motor units
motor units
all the muscle fibers innervated by one motor neuron
amount of tension produced in a muscle determined by number of motor units activated
asynchronous motor unit summation for sustained contractions
differences in number and size of motor units in different muscles determines precision of control and movements
small motor unit
precise control
one motor neuron innervates a small number of muscle fibers
large motor unit
gross movement control
one motor neuron innervates a large number of muscle fibers
muscle tone
resting tension in a skeletal muscle
in any muscle, some motor units are always active; tense and firm the muscle
which motor units are active is constantly changing, muscle tone is not produced by a specific subset of motor units
stabilizes bones and joints
greater resting muscle tone causes higher resting rate of metabolism
isotonic
tension rises, length of muscle changes
concentric and eccentric
concentric
muscle tension exceeds resistance and muscle shortens
eccentric
peak tension developed is less than the resistance, muscle elongates
isotonic concentric contraction
a musle is attached to a weight that is ½ its maximum potential tension. when stimulated, it develops enough tension to lift the weight. the tension remains constant, but the muscle shortens
isotonic eccentric contraction
the tension remains constant, but the muscle lengthens
when the eccentric contraction ends, the unopposed load stretches the muscle until either the muscle tears, a tendon breaks, or the elastic recoil of the skeletal muscle is sufficient to oppose the load
isometric (iso- same, metric- measurement/length)
tension rises, length of muscle remains constant
tension produced never exceeds resistance
muscle as a whole does not shorten but individual muscle fibers shorten until internal connective tissues and tendons are taut
cannot shorten further because tension does not exceed resistance
isometric contraction
when stimulated, the tension rises, but the muscle length stays the same
lengthening a muscle
no active mechanism for muscle fiber elongation
a muscle cell does not cause itself to lengthen after contraction process ends
returns to resting length due to
recoil in elastic components in connective tissue
contraction of opposing muscle groups
gravity
when you stop producing tension, the muscle will rebound
energy use and muscle contraction
muscle contraction requires large amounts of ATP
muscle cells stores only enough high energy molecules to sustain contraction until additional ATP can be generated
ATP and creatine phosphate (CP) reserves last ~ 15 seconds once contraction begins
muscle cell must generate ATP at approx. the same rate as it is used for remainder of contraction
creatine phosphate reserves
ATP not used for long term storage of energy
at rest, muscle cell makes more ATP than needed; extra ATP transfers high energy phosphate to creatine for storage
CP reserves released stored energy to convert ADP to ATP when ATP is needed at start of contraction
ATP generation
aerobic cellular respiration: most ATP needed for resting muscle and for moderate levels of muscle activity
aerobic AND anaerobic glycolysis pathways needed to generate additional ATP for PEAK PERFORMANCE (will produce lactic acid)
aerobic metabolism
aerobic cellular respiration
uses O2 - releases CO2
occurs in mitochondria
citric acid cycle
CO2 is produced
electron transport chain
ATP synthesis
O2 is used
muscle cell ATP generation
resting muscle fiber surely on aerobic metabolism of fatty acids to generate ATP
FA absorbed from circulation
broken down to 2-carbon units of acetyl CoA which enter DIRECTLY into the Citric Acid Cycle
excess ATP used to store glucose into glycogen, create creatine phosphate
muscle metabolism in a resting muscle fiber
the demand for ATP is low and sufficient oxygen is available for mitochondria to meet that demand
fatty acids are absorbed and broken down in the mitochondria creating surplus of ATP
some mitochondrial ATP is used to convert absorbed glucose to glycogen
mitochondrial ATP is also used to convert creatine to creatine phosphate (CP)
this results in the buildup of energy reserves (glycogen and CP) in the muscle
muscle cell ATP generation
contracting muscle fibers rely on aerobic AND anaerobic metabolism of glucose
amount of aerobic vs. anaerobic metabolism depends on intensity of muscle contraction
moderate vs peak
glucose comes from circulation and breakdown of glycogen reserves within muscle cell
muscle metabolism during moderate activity
the demand for ATP increases
there is still enough oxygen for the mitochondria to meet the increased demand, but no excess ATP is produced
ATP is generated primarily by aerobic metabolism of glucose from stored glycogen
if the glycogen reserves are low, the muscle fiber can also break down other substrates, such as fatty acids
all of the ATP being generated is used to power muscle contraction
pyruvate metabolism
anaerobic
if oxygen supply to cells is too slow to allow all of pyruvate to be metabolized aerobically by cellular respiration, rest of pyruvate converted to lactic acid
conversion of pyruvate to lactic acid recycles cofactors needed by glycolysis enzymes
muscle metabolism during peak activity
the demand for ATP is enormous. oxygen cannot diffuse into the fiber fast enough for the mitochondria to meet that demand. only a third of the cell’s ATP needs can be met by the mitochondria (not shown)
the rest of the ATP comes from glycolysis, and when this produces pyruvate faster than the mitochondria can utilize it, it pyruvate builds up in the cytosol
the pyruvate is converted to lactate. hydrogen ions from ATP hydrolysis are not absorbed by the mitochondria
the buildup of hydrogen ions increases cytosol acidity, which inhibits muscle contraction, leading to rapid fatigue
aerobic and anaerobic at peak activity, 2/3rds of activity done by glycolysis
anaerobic metabolism
produces ATP rapidly
allows muscle cell to generate additional ATP when mitochondrial cellular respiration pathway is unable to meet cell’s energy demands
anaerobic metabolism disadvantages
inefficient use of glucose
lactic acid lowers intracellular pH
recovery period
begins immediately after activity ends
oxygen debt (excess post-exercise oxygen consumption)
amount of oxygen required during resting period to make enough ATP to restore muscle to normal conditions
rebuilds ATP and creatine phosphate levels
recycle lactic acid to make pyruvate
rebuild glycogen reserves
muscle fatigue
a muscle that can no longer perform at required level of activity
possible causes of fatigue
exhaustion of energy resources
build up of lactic acid and lowering of pH
psychological fatigue