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126 Cards in this Set
- Front
- Back
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What are the functions of the nervous system?
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1. Control of the internal environment (along with the endocrine system)
2. Voluntary control of movement (with muscular system) 3. Programming spinal cord reflexes 4. Assimilation of experiences necessary for memory and learning (& motor control, not discussed in this class) |
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What is in the category of the PNS?
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Everything but brain and spinal cord (CNS)
Neurons outside the CNS Sensory/afferent division - afferent fibers transmit impulses from receptors to CNS Motor/efferent division - efferent fibers transmit impulses from CNS to effector organs |
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What are the subcategories within the afferent division of the PNS?
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Somatosensory
Visceral sensory Special sensory |
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What are the subcategories within the efferent division of the PNS?
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Somatic motor
Autonomic motor - Sympathetic - parasympathetic - Enteric |
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What is innervated by fibers from the autonomic nervous system?
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Smooth muscle, cardiac muscle, and glands
The involuntary tissues SNS innervates skeletal muscle |
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Is a neural cell membrane more permeable to sodium or potassium?
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Potassium!
Need pump to maintain resting membrane potential |
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What properties make neurons excitable tissue?
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Irritability - ability to respond to a stimulus and convert it to a neural impulse
Conductivity - transmission of an impulse along the axon |
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What is the resting membrane potential of a neuron?
Determined by... Maintained by... |
-40 to -75 mV (-5 to -100 mV in other cells)
Determined by permeability of plasma membrane to ions Difference in ion concentrations across membrane (Na+, K+, Cl-, Ca++) Maintained by Sodium-Potassium pump - potassium tends to diffuse out of cell, pump moves 2 K+ in and 3 Na out |
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What's the difference between an electrical current and an action potential?
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An electrical current is electrons moving
Action potential is ions moving |
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When and how does an action potential occur?
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When a stimulus of sufficient strength depolarizes the cell
Opens Na channels and sodium diffuses into the cell, inside becomes more positive |
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How quickly is a neuron's resting potential reversed and how does repolarization occur?
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Potential reversed in about 1 ms (see graph of membrane potential and time)
During repolarization, potassium leaves the cell rapidly (channels open) and sodium channels close |
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Where is a neuron's signal transfered from electrical to chemical? how?
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At a synapse!
Depolarization at terminal causes neurotransmitter (chemical messenger) to be released from presynaptic membrane Binds to receptor on postsynaptic membrane Causes depolarization of psm, or hyperpolarization depending on NT |
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Temporal summation
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summing several EPSP's from one presynaptic neuron
1. two firings with a pause inbetween causes no action potential 2. three firings in rapid succession cause the neuron to reach the threshold of excitation |
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Spatial summation
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summing from several different presynaptic neurons (can be onto postynaptic neuron or several motor end plates on a muscle)
Each firing at different places isn't enough for AP But, all three simultaneously causes AP |
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Receptors located in joints and muscles that provide CNS with information about body position are
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proprioceptors
allow for conscious recognitions of the position of body parts Limb movement rates (kinesthesia) |
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Types of joint proprioceptors
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Free nerve endings - sensitive to touch and pressure, initially strongly stimulated, then adapt
Golgi-type receptors - found in ligaments around joints, similar to free nerve endings Pacinian corpuscles - in tissues around joints, detect rate of joint rotation |
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Types of muscle proprioceptors
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Provide sensory feedback to nervous system - tension developed by muscle, account of muscle length
Muscle spindle (relative muscle length) - detect stretch Golgi Tendon Organ (tension development, inhibits force) |
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Muscle spindle consists of
Process: |
intrafusal fibers - run parallel to extrafusal fibers
Gamma motor neurons - stimulate intrafusal fibers to contract with extrafusal fibers (by alpha motor neuron) 1. muscle spindles detect stretch of the muscle (1a afferents wrapped around fibers deform) 2. Sensory neurons (1a) conduct action potentials to the spinal cord 3. sensory neurons synapse with alpha motor neurons 4. Stimulation of alpha motor neurons causes the muscle to contract and resist being stretched Stretch reflex. Emergency response occurs at the level of the spinal cord |
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What do golgi tendon organs do?
Can they be stopped? |
Monitor muscle tension and prevent muscle damage during excessive force generation
1. Golgi tendon organs detect tension applied to a tendon 2. sensory neurons conduct action potential to the spinal cord 3. they synapse with inhibitory interneurons that synapse with alpha motor neurons 4. inhibition of the alpha motor neurons causes muscle relaxation, relieving the tension applied to the tendon Also excites antagonist muscle With training, you can "accomodate" response, and pay less attention to golgi so you can lift more force |
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Muscle chemoreceptors are often made of ____, which are sensitive to changes in
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in the chemical environment surrounding a muscle - H+ ions, CO2, K+
Provide CNS with information about metabolic rate of muscular activity important in regulation of cardiovascular and pulmonary responses |
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What are reflexes? order of events?
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Rapid, unconscious means of reacting to stimuli
1. Sensory nerve sends impulse to spinal column 2. Interneurons activate motor neurons (if they exist, not in 2-neuronal reflex) 3. Motor neurons control movement of muscles |
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What's reciprocal inhibition?
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EPSPs to muscles to withdraw from stimulus along with
IPSPs to antagonistic muscles (opposite of GTOs) Make movement faster if you touch something hot! |
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What's the crossed-extensor reflex?
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Opposite limb supports body during withdrawal of injured limb
like if you step on a tack - put limb out to catch yourself |
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What is responsible for carrying neural messages from spinal cord to skeletal muscles?
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Somatic motor neurons of the PNS
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motor unit size, i.e. Motor neuron innervation ratios
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low ratio of muscle fibers per motor neuron in muscles that require fine motor control. 23/1 in extraoccular muscles
Higher in others. 1,000/1 or greater in large muscles |
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How are motor units recruited?
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Smaller units with slow-twitch fibers recruited first
Recruitment is additive, smaller units don't stop firing |
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Vestibular apparatus is responsible for
sensitive to changes in |
maintaining general equilibrium and balance - maintains head position
Linear and angular acceleration - stimulated by head movement. Direction, speed, and acceleration Also controls head and eye movement during exercise |
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Pathways of information involving the vestibular apparatus
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sends information to cerebellum and vestibular nuclei (in brain stem)
Vestibular nuclei also receive input from eyes and joint/tendon/muscle receptors and send information to occulomotor center, cerebellum, and spinal cord, which sends output to skeletal muscles |
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ANS is responsible for
How do the two divisions send messages? |
maintaining internal environment
- effector organs not under voluntary control PNS releases acetylcholine, inhibits effector organ (mostly), after stimulation, ACh is degraded by acetylcholinesterase SNS releases norepinephrine (NE), tends to excite effector organs, NE removed from synapse or inactivated after stimulation |
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How many skeletal muscles are in the human body? % body weight?
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over 400... up to 650?
40-50% of total body weight |
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Functions of skeletal muscle
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1. force production for locomotion and breathing
(flexors decrease joint angle, extensors increase) 2. force production for postural support 3. heat production during cold stress (not emphasized here) |
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Why type of muscle action is an isotonic one where the muscle produces force but length increases
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eccentric (type of dynamic/isotonic)
more efficient, but associated with muscle fiber injury and soreness |
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Why does delayed onset muscle soreness occur?
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proposed explanation is 1. structural damage to muscle fibers 2. membrane damage (sarcolemma), 3. calcium leaks out of SR 4. protease activation results in breakdown of cellular proteins, 5. inflammatory response, 6. edema and pain
Appears 24-48 hours after strenuous (or new) exercise Due to microscopic tears in muscle fibers or connective tissue and SR - cellular degradation and inflammatory response (not lactic acid) Eccentric causes more than con slowly begin exercise over 5-10 sessions to avoid DOMS |
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How come you are sore after every workout when you've been working for a while?
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"repeated bout effect"
initial bout -> damage or injury -> adaptation in three possible ways: neural theory (changes in nervous system), Connective tissue theory (increased intramuscular connective tissue), Cellular theory (cellular changes that strengthen and protect muscle fibers) -> repeated bout of exercise -> less muscle damage |
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Describe the layers of connective tissue surrounding skeletal muscle
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Epimysium - around entire muscle
Perimysium - surrounds facicles (bundles of fibers) Endomysuim - surrounds individual muscle fibers Basement membrane - just below endomysium Sarcolemma - muscle cell membrane |
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Myofibrils contain:
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Proteins!
Contractile - actin and myosin Regulatory - troponin and tropomyosin |
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What's up with the sarcoplamic reticulum
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it's a storage site for calcium (also for release and re-uptake)
Sarcoplasm is separate from SR Network/scaffolding (on picture) has terminal cisternae |
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What are the transverse tubules?
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"little yellow tubes" on the picture,
extend from sarcolemma to sarcoplamic reticulum Carries deep within muscle tissue Lateral sacs (terminal cisternae) and T-tubles = triad |
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What does tropomyosin do?
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Fits in grove between helical chains of actin
Covers binding sites for myosin on actin Is pulled out of the way by troponin when calcium is present |
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What does troponin do?
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There's one about every seven actin
Calcium attaches to it and creates a conformational change which makes it bond more strongly with troponin, pulling it out of the way of actin binding sites |
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What's an EPP?
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An action potential at the motor end plate when acetylcholine is released from the motor neuron
Causes depolarization of muscle fiber |
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What is the structure of a sarcomere?
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A band is myosin
H zone is the central portion where there's no overlap with actin M line bisects the H zone Actin attaches to other actin at the Z line I band is where there's only actin (lighter) |
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Why/how does muscle shortening occur?
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sliding filament theory of contraction explains it as the movement of the actin filament over the myosin filament
Formation of cross-bridges between filaments and power stroke brings them closer together creating reduction in the distance between Z lines of the sarcomere (and shortening of I band and H zone) |
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What are the sources of ATP for muscle contraction?
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Phosphocreatine
Glycolysis Oxidative phosphorylation depends on intensity: fast-glycolysis or slow-glycolysis Requires the enzyme myosin ATPase |
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What enzyme allows for muscle relaxation?
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Ca+2 ATPase
removes Ca from cell, leading to relaxation |
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How is depolarization of motor end plate (excitation) coupled to muscular contraction?
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Action potential travels down transverse tubules (which are continuous with outside) and causes release of Ca from SR
Ca binds to troponin and causes position change in tropomyosin, exposing active sites on actin Strong binding state formed between actin and myosin Contraction occurs (look at pictures!) |
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Step-by-step process of excitation
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1. AP in motor neuron causes release of acetylcholine into synaptic cleft
2. Ach binds to receptors on motor end plate, leads to depolarization that is conducted down TTs, which causes release of CA from SR |
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Step-by-step process of contraction
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1. At rest, myosin cross-bridges in weak binding state
2. Ca++ binds to troponin, causing shift in tropomyosin to uncover sites and let cross-bridge form strong binding state 3. P released from myosin, cross bridge movement occurs 4. ADP released from myosin 5. ATP attaches to myosin, breaking the cross bridge and forming weak binding state. Then bound ATP is broken down to ADP+P, which energizes myosin. Continues as long as Ca+2 and ATP are present |
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Steps leading to muscular contraction
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1. ATP bound to myosin is hydrolyzed (partially, sorta broken down), "cocking" the cross bridge
2. Cross bridge binds to actin and P is released, causing conformational change in myosin 3. power stroke causes filaments to slide, ADP is released? 4. New ATP binds to myosin head, allowing it to release from actin |
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How long does muscle contraction continue, and how long does each contraction take?
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continues as long as action potential create calcium and ATP is around
About 5 ms latent period, 40ms contraction and 50ms relaxation for a single twitch |
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Have you drawn out the stages of muscular contraction (including excitation and contraction) yet?
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No
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What are contributing factors to fatigue (reduced ability to perform work, decrease in muscle force production and shortening velocity)
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High-intensity exercise ~60 seconds: accumulation of lactate, H+, ADP, Pi, and free radicals, and decreased cross bridge formation
Long-duration exercise (2-4 hours) Muscle factors - glycogen depletion, accumulation of free radicals, electrolyte imbalance Central fatigue - reduced motor drive to muscle from CNS |
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What are the types of muscle fibers? (include multiple names)
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Type I - slow-twitch, slow-oxidative fibers (SO)
Type IIa - intermediate fibers, fast-oxidative glycolytic fibers (FOG Type IIx - fast-twitch fibers, fast-glycolytic (FG) (IIb are found in rodents) Fibers are determined by biopsy and staining, can be estimated with dynamometer test |
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How are muscle fiber types characterized?
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By biochemical properties (oxidative capacity - capilaries, mitochondria, and myoglobin, and type of myosin ATPase - speed of ATP degradation)
and by contractile properties (maximal force production - force per unit of c-s area, Speed of contraction (Vmax, myosin ATPase activity), and muscle fiber efficiency) |
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Describe the characteristics of the three main skeletal muscle fiber types
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Fiber: Type IIx (fast), Type IIa (fast), Type I (slow)
# of Mitochondria: low, high/med, high Resistance to fatigue: low, high, very high Predominant energy system: anaerobic, both, aerobic ATPase: highest, high, low Vmax (speed of shortening): highest, high, low Efficiency: low, moderate, most Specific tension: high, high, moderate |
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How does max force/tension per cross-sectional area compare across the fiber types?
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1. 10-20% higher in fast fibers (IIa and IIx) compared to slow
2. Fast fibers contain more cross bridges per cross-sectional area |
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What are the typical muscle fiber compositions in elite
distance runners, track sprinters and non athletes? |
Runners: 70-80% slow, 20-30% fast fibers
Track sprinters: 25-30% slow Non athletes: 47-53% slow power athletes have a higher percentage of fast, endurance slow, and non about 50/50. Note the large variation within athletes... not the only thing determining performance |
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Why is the speed of shortening greater in fast fibers?
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SR releases Ca+2 at a faster rate
Higher myosin ATPase activity |
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Force generation in muscle depends on what three factors?
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1. Nature of the neural stimulation of motor units: frequency (simple twitch, summation, tetanus)
2. Types and number of motor units recruited: Fast motor units = greater force, more motor units = greater force 3. Initial muscle length: "ideal" length for force generation based on increased cross-bridge formation |
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How often does tetanus of muscles occur?
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Most movements are tetanic! Allow for smooth motions by having alternating muscles
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What is the range for optimal length of a muscle fiber?
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between 80-100% of resting length
otherwise large overlap causes fewer cross-bridge interactions or not enough overlap and tension can't be developed |
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Where is the maximum velocity of shortening greatest for a slow-twitch fibers?
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At the lowest force production, also true for fast-twitch
But, at any absolute force, the speed of movement is greater in muscle with higher percent of fast-twitch fibers (see graphs) With training, force-velocity line shifts up, more fast twitch I guess |
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What is the relationship between velocity of movement and power output in a muscle?
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Peak power increases with velocity, up to a movement speed of 200-300 degrees per second
Power decreases beyond this velocity because force decreases with increasing movement speed. power = (force x dist)/time Power is greater with more fast-twitch fibers, at any velocity |
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Muscular strength is
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the maximal force a muscle or muscle group can generate
1 rep max |
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Muscular endurance is
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Ability to make repeated contractions against a submaximal load
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Why should you be critical of the results of studies claiming increases in strength with a certain product/technique, especially if the studies are less than 20 weeks long?
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Neural adaptations are most important in the initial 4-20 weeks
improved ability to recruit motor units learning coordination Lead to increases in strength without changes in muscle |
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What occurs during long-term training (20+ weeks)
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hypertrophy
high intensity training can result in hypertrophy with 10 sessions |
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How is muscle mass increased?
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Hypertrophy - increased muscle fiber diameter (more actin & myosin in the 3D structure), responsible for most increase in muscle size
Hyperplasia - increased number of muscle fibers, limited evidence that this occurs in humans, but may account for 5% of increase |
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Are muscle fibers converted with training?
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Yes, some. IIx -> IIa, no matter what type of training (endurance, strength, power...)
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What central nervous system changes occur with training?
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increased motor unit recruitment (spacial summation)
altered motor neuron firing rates (temporal summation) enhanced motor unit synchronization (learning/coordination) Removal of neural inhibition (GTOs) |
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How do endurance training and strength training induce changes in skeletal muscles?
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endurance - increases oxidative capacity
strength - increase in muscle fiber size (hypertrophy) and fiber number (hyperplasia- limited evidence in humans) Type II adds more protein, less hypertrophy in Type I Fast-to-slow shift - type IIx -> IIa - type IIa -> with further training (?) - seen with endurance and resistance training |
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"If you want to become a world-class athlete, you must...
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choose your parents wisely"
genetics plays an important role in how an individual responds to training |
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Is aerobic or anaerobic capacity more genetically determined?
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Anaerobic is more genetically determined
can only improve anaerobic performance to a small degree with training Depending largely on fast IIx fibers, which are determined early in development |
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How does strength compare in males and females?
How about with training? |
Untrained males have greater absolute strength than untrained females - 50% stronger in upper body, 30% in lower
Strength as a function of muscle cross-sectional area is similar - 3-4 kg of force per cm2 of muscle in males and females Training-induced strength changes are the same. Change in strength is proportional to muscle area. Same % strength improvement, in initial weeks of training at least. Men exhibit greater hypertrophy as a result of long-term training, due to higher testosterone levels |
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What happens to strength with detraining and retraining?
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more resistant than aerobic training
slow decrease in strength: 31% decrease following 30 weeks detraining, associated with small changes in fiber size. type one: -2%, Type IIa: -10%, Type IIx: -14%, due primarily to nervous system changes Retraining results in rapid regain of strength and muscle size, within 6 weeks, can maintain strength with reduced training for up to 12 weeks |
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What are the initial causes of muscle atrophy? further? is it permanent?
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Initial (2 days) - due to decreased protein synthesis
Further atrophy - due to increased muscle protein breakdown Atrophy can be reversed by resistance training. During spaceflight, atrophy can be prevented by resistance exercise. Besides space flight, loss of muscle mass and strength can be cause by prolonged bed rest, limb immobilization... |
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How much loss of muscle mass is associated with aging?
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10% muscle mass lost between age 25-50 years
Additional 40% lost between 50-80 years Also a loss of fast fibers and gain in slow Also due to reduced physical activity Though you cannot completely eliminate the age-related loss in muscle mass, regular exercise training can improve strength and endurance and slow the percent loss |
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What is neuroendocrineology?
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Study of the coordination between nervous system (using neurotransmitters) and endocrine system (using hormones directly into the blood)
norepinephrine can have a local effect, or a more generalized effect by being released as a hormone |
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How do hormones have affects on specific tissues if they travel through all the blood?
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Organs have special receptors to which the hormone can bind
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What are the classes of hormones?
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Several classes based on chemical makeup
Amino acid derivative Peptides/protein Steroids (from cholesterol) |
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What is the effectiveness of a hormone determined by?
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The plasma concentration, which is determined by
1. rate of secretion from gland (magnitude of input, stimulatory vs. inhibitory input) 2. rate of metabolism or excretion (at receptor and by the liver and kidneys) 3. quantity of transport protein & affinity (not active when bound to transporters) (steroid hormones) 4. Changes in plasma volume (affect concentration) Magnitude of effect depends on concentration of the hormone, number of receptors on the cell, affinity of the receptor for the hormone |
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What's downregulation?
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High concentration of hormone causes decrease in receptor number
cell with diabetes may respond to high concentration of insulin |
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What's upregulation?
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Low concentration of hormone leads to increase in receptor number to make it more sensitive
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What are the mechanisms of hormone action?
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altering membrane transport (insulin)
Altering activity of DNA to modify protein synthesis (steroid hormones and slow hormones) Activating second messengers via G protein (cyclic AMP, Ca++, inositol triphosphate, diacylglycerol) Tyrosine Kinase (insulin and growth hormone) |
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Why study neuroendocrinology and exercise?
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to understand the factors that control the mixture of fuels used during different exercise intensities and durations,
what stimulates the releases of more Free Fatty Acids from adipose tissue, how the liver is stimulated to restore blood glucose during exercise, and how blood pressure, pH, and ions (Na, Ca, K, H2O) are controlled with exercise |
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Which hormones can diffuse through the cell membrane, and which need receptors on the surface to trigger 2nd messengers/etc?
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Amino acids and peptides have receptors, steroids can diffuse
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What aspects of hormonal control of substrate mobilization during exercise did we talk about?
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1. control of muscle glycogen utilization
2. control of glucose mobilization from liver and FFA from adipose tissue |
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How is glycogenolysis related to exercise intensity?
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High-intensity exercise results in greater and more rapid glycogen depletion (As in graphs we looked at a while ago)
High-I results in greater increases in plasma epinephrine, which is a powerful stimulator of glycogenolysis (but, not only factor in rate of glycogenolysis) |
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Breakdown of muscle glycogen is under dual control, activated by what 2nd messengers
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Epinephrine-cyclic AMP - via B-adrenergic receptors
Calcium-calmodulin - enhanced during exercise due to Ca++ release from SR, delivery of glucose is concurrent with activation of muscle contraction Rate of breakdown of glycogen is similar to the rate of energy (ATP) utilization |
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Cyclic AMP and Ca++-Calmodulin affect what in order to stimulate glycogenolysis?
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phosphorylase b, which (becomes?) phosphorylase a, and makes glycogen become Glucose-1-PO4 and then go into glycolysis
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How is cyclic AMP activated? what happens?
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When a hormone (epinephrine?) binds to a receptor in the cell membrane, a G protein is activated. It activates adenylate cyclase which breaks down ATP into Cyclic AMP -> 5' AMP
Unclear on this but I think caffine inhibits phosphodiesterase which allows conversion of cyclic AMP to 5' AMP Cyclic AMP turns inactive protein kinase into active protein kinase and an inhibitory subunit. Activated protein kinase causes a cellular response So, caffine creates prolonged/more intense response? |
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How does calcium activate a second messenger (acting as a hormone?) and what happens?
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Something about calcium channels and phospholipase C
... |
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What is normal plasma glucose and why must it be maintained?
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Normal - 80-120 mg/deciliter. 1g/liter, so about 5 grams total, 1 tsp, 20kcal... so replenishment is important!
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General mechanisms for maintaining blood glucose homeostasis during exercise:
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Mobilization of glucose from liver glycogen stores (can store about 5g/100g liver, once stores are full, makes acetyleCoA, which forms FFA and is stored in adipose)
Mobilazation of FFA from adipose tissue - spares blood glucose, becomes more efficient with training Gluconeogenesis (in liver?) from amino acids, lactic acid (from glycolysis), and glycerol Blocking the entry of glucose into cells (stays in plasma) Forces use of FFA as a fuel Each process is controlled by more than one hormone |
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What's the handy acronym about blood glucose?
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Blood Glucose Must Last Forever
B - block the entry of glucose into cells (use FFA) G - Gluconeogenesis from amino acids, lactic acid, and glycerol M - mobilize glucose from Liver glycogen stores (glycogenolysis) FFa from adipose tissue (spares blood glucose) |
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What hormones control blood glucose homeostasis during exercise?
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Permissive or slow-acting: act in a permissive manner to support actions of other hormones (thyroid hormone, cortisol, growth hormone)
Fast-acting: epinephrine and norepinephrine, insulin and glucagon |
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What is the mechanism for steroid hormone action?
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Travels to cell membrane on carrier protein,
travels across membrane, Picked up by receptor protein Translocation across nuclear membrane to alter activity of DNA to modify protein synthesis Changes mRNA, affecting protein synthesis and creating steroid hormone response |
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What does thyroid hormone do and how?
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Establishes and maintains overall metabolic rate
Acts in a permissive manner to allow other hormones to exert their full effect - influences the number of receptors for other hormones on the surface of the cell - influences the affinity of a receptor for its hormone (e.g. epinephrine relies upon T3 to affect breakdown of FFA in adipose cells) T3 affects cAMP levels |
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How does concentration of T3 and T4 change during exercise?
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No real change in those thyroid hormones because the turnover rate is greater so even though more is released, the concentration doesn't change because of greater uptake/use
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What is cortisol from and how is it affected?
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from adrenal gland
Levels can be affected by stress, injury, effect of exercise is difficult to isolate (prolonged or intense exercise results in protein breakdown) Cortisol promotes protein breakdown (in high levels) for gluconeogenesis, and protein synthesis for tissue repair when in smaller amounts |
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What is cortisol's mechanism of action?
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Alter gene expression and protein synthesis
Maintains plasma glucose during exercise and long-term fasting 1. blocks entry of glucose into cells 2. Mobilizes amino acids for gluconeogenesis 3. Stimulates FFA mobilization from adipose tissue |
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What tissues does cortisol target?
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Muscle - breaksdown proteins into amino acids tor gluconeogenesis to create glucose
Adipose - break down triglycerides into FFA and glycerol, FFA into blood and glycerol to gluconeogenesis in liver Other tissues - increased FFA oxidation (blocks entry of glucose) |
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How do cortisol levels change with exercise?
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At low intensity, plasma cortisol decreases (removal exceeds secretion, removed at a faster rate)
At high intensity - plasma cortisol increases (for repair of tissue damage?). Above 60% VO2 max, increase in secretion and broken down at a slower rate Repair of tissue damage happens over a period of days (slow-acting hormone) |
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Where is growth hormone from and what does it do?
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Secreted by Anterior pituitary
Affects tissues via insulin-like growth factors (IGF's) IGF-1 in muscle is responsible for muscle growth Essential for normal growth - stimulates protein synthesis and long bone growth |
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How does growth hormone concentration change during exercise?
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Increases during exercise
opposes insulin - important effects on protein, carb, and fat metabolism - mobilizes fatty acids from adipose tissue - aids in the maintenance (sparing) of blood glucose |
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How does growth hormone work?
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Blocks glucose uptake
increases FFA mobilization Enhances gluconeogenesis Important in the maintenance of plasma glucose (net effect of those three actions is preservation of blood glucose) Same effects as cortisol? |
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What is the effect of exercise intensity, duration, and training on growth hormone?
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Increases dramatically with increase in percent VO2 max
(% change of 1,000 by 60% max, 2,000 by 90%) Increases over duration Greater response in trained runners |
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What are the fast-acting hormones that affect plasma lucose?
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norepinephrine and epinephrine
insulin and glucagon |
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How do the fast-acting hormones maintain plasma glucose
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Block glucose uptake
increase gluconeogenesis mobilize - liver (and muscle) glycogenolysis, FFA from adipose cells |
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What are the catecholamines and how do they act?
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Epinephrine and Norepinephrine from adrenal gland
Act via 2nd messengers Adrenergic receptor type dictates tissue response B1: increased HR, glycogenolysis, lipolysis B2: increased bronchodilation, vasodilation a1: increased phosphodiesterase, vasoconstriction a2: opposes B1 and B2 (decreased HR, etc.) |
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What are beta-blockers prescribed for and why?
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for coronary heart disease and hypertension
Because they block beta adrenergic receptors which increase HR, glycogenolysis, lipolysis, brochodilation, vasodilaiton |
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How does plasma epinephrine and norepinephrine change during exercise?
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increases linearly with exercise time, also related to increased HR and BP during exercise - SNS control
Favor the mobilization of FFA and maintenance of plasma glucose |
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How do plasma catecholemines respond to exercise?
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plasma E and NE at same absolute workload decrease with weeks of training (but at high intensity, trained athletes have very high response, relative workload)
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What does the pancreas secrete?
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Exocrine - digestive enzymes and bicarbonate into small intestine
Endocrine - Insulin (beta cells), glucagon (alpha), somatostatin (delta cells) |
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What are the effects of the hormones secreted by the pancreas?
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Insulin is anabolic - promotes the storage of glucose, amino acids, and fats in whole body
Glucagon is catabolic - promotes the mobilization of fatty acids from adipose tissue and glucose from liver Somatostatin - controls the rate of entry of nutrients from digestive system into the circulation |
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What do insulin and glucagon respond to and what are their effects?
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Respond to same stimulus (increased SNS stimulation)
Cause opposite actions regarding mobilization of liver glucose and FFA from adipose tissue Their relative ratio determines net effect Insulin - uptake and storage of glucose and FFA Glucagon - mobilization of glucose and FFA fuels (triglyceride synthesis) |
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What is the receptor for insulin and how does it act?
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Alters membrane transport
Tyrosine kinase receptor on surface of membrane receives insulin, triggers signaling proteins which activate GLUT 4 vesicles and move them to surface (and T-tubules) where they can transport glucose across the membrane Stimulate glycogen synthesis from glucose The 2nd messengers are active with exercise, so you can bypass need for insulin (read the book!) |
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Which tissues have GLUT 4 receptors and what do they trigger?
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skeletal muscle and adipose
When insulin binds to GLUT4, triggers events to transport and trap glucose |
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How does insulin change with exercise?
With training? |
Might think it would increase to bring glucose into muscle, but actually decreases during exercise while glucagon increases
Plasma insulin decreases with exercise intensity up until 80%, when it increases With training, decreased insulin response (keep more of it) |
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How does glucose change with exercise? with training?
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Plasma concentration increases during exercise
Decreased response following training With training: 1. increase in glucagon sensitivity in liver 2. decrease in glucose uptake by muscle 3. increase in fat usage as a fuel by muscle |
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Plasma insulin decreases during exercise, which disallows (blocks) rapid uptake of plasma glucose into all tissues, thus preventing
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hypoglycemia
increases mobilization of liver glucose and FFA |
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Exercising muscles still increase their uptake of glucose by 7-20x during exercise (even with decreased insulin). How?
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increased muscle blood flow during exercise => more glucose available
Ca++-calmodulin 2nd messenger system -provides immediate increase in glucose transporters -helps to explain why insulin resistance decreases with exercise |
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How do E and NE influence insulin and glucagon secretion
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Maintain blood glucose by
1. increasing glycogen mobilization 2. increasing liver glucose mobilization 3. increasing FFA mob 4. interfere with glucose uptake |
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What happens to hormones overall during exercise?
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decrease in insulin and increase in all other hormones
for, the mobilzation of glucose from the liver mobilization of FFA from adipose tissue gluconeogenesis in liver effects are tempered with training with training, low intensity/long term exercise has dampened response, while high intensity has increased response (absolute workload has decreased response) |
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How is there redundancy in the hormone systems?
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many hormones use the same pathway
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Paradox: FFA mobilization decreases during heavy exercise (use more carbs instead of fats) in spite of persisting hormonal stimulation of FFAs
How?? |
may be due to:
high levels of lactic acid - promotes resynthesis of triglycerides elevated H+ concentration inhibits HSL (hormone sensitive lipase, which is necessary for FFA mobilization) Inadequate blood flow to adipose tissue and/or insufficient albumin to transport FFA in plasma the activated form of glycerol is needed to make triglycerides from FFA and is activated with lactic acid... so FFA are recycled as quickly as they are generated *no just slower |
