Test2 Exphys I Flashcards
5 gen f(c) of NS
control of internal environment along with the endocrine sys
voluntary ctrl of movement
involuntary ctrl of movement over vital life functions
programming spinal cord reflexes
assimilation of experiences necessary for memory and learning
CNS
brain and spinal cord
PNS
consists of neurons located outside CNS
What does the archeitecture of the bones in the body tell us about the CNS?
Body will work to preserve NS since it has most protection
Afferent divison of PNS consists of what 3 components?
somatic sensory
visceral sensory
special sensory
Efferent division PNS consist of what?
somatic motor and automatic motor
3 division of automotic motor
sympathetic, parasympathetic, and enteric
SNS controls
skel muscle
ANS controls
smooth, cardiac muscles and glands
cell body
center of operation also called soma or perikaryon
cell contains blank that does is the site of
cell body contains the nucleus, site of protein synthesis that produces neurotransmitters
Nerves have more blank so these use this substrate and why?
nerves have more mitochondria but uses more glucose and heart uses fats so the two main systems are not in competition for fuel
dendrites conduct
impulses toward cell body from the receptor
axon carries
electrical impulse away from cell body
axon may be coverd by
Schwann cells and forms discontinouous myelin sheath along length of axon
gaps of mylein sheath
Nodes of Ranvier
biggest nerve
sciatic nerve
synapse
contact points btwn axon of one neuron an dendrtite of another neuron, goes from electrical to chemical
The mitochondria in the neuron go through what energy system?
aerobic glycolysis
Multiple Sclerosis
neurological disease that destroys myelin sheaths of axons that has a genetic component and is due to an immune attack on the CNS myelin (autoimmune)
MS results in
progressive loss of NS f(x) causing fatigue, muscle weakness, poor motor ctrl, loss of balance, and mental depression
Exs can improve f(c)nal capacity of what disease?
MS
exercise for MS leads to
improved QOL
exercise can do what kind of harm if not controlled
can overheat nerves resulting in necrosis
neurons are what kind of tissue
excitable tissue (conducts stimulus)
Irritability in neurons
ability to respond to a stimulus and convert it to a neural impulse (dendrites and cell body) Once threshold reached,, impulse is processed throughout body
conductivity
transmission of the impulse along the axon
why is resting membrane potential negative?
because of protein anions that are stationary in the cell
synapse
small btwn presynaptic neuron and postsynaptic neuron
Neurotransmitter
chemical jumps synapse
chemical messenger released from presynaptic membrane for communication
Where does neurotransmitter bind to?
binds to receptor on postsynaptic membrane
neurotransmitter can cause
depolarization (EPSP) or hyperpolarization (IPSP) of the postsynaptic membrane
EPSP causes
depolarization
depolarization
Na+ influx into the cell, making the cell more positive and less negative, once threshold is reached
temporal summation
summing several EPSPs from presynaptic neuron
spatial summation
summing from several different presynaptic neurons
two types of EPSP
temporal and spatial
IPSP
cause hyperpolarization
hyperpolarization
make cell more negative
proprioceptors
receptors that provide CNS with information about body position in space ortientation
where are proprioceptors located?
located in joint and muscles
proprioceptors prevent
falls by forming a plan that tuned by the spine
kinesthesia
kinestic awareness
kinesthesia is
consciuous recognition of position of body parts and limb movement rates
free nerve endings are sensitive to
touch and pressure
free nerve endings are initially strongly
stimulated, then they adapt
Golgi-type receptors are found in
ligments and around joints and are diff from gto’s
golgi-type receptors are similar to what
free nerve endings in that they are pressure and touch sensitive
Pacinian corpuscles location
in tissues around joints
pacinian corpuscles detect what
rate of joint rotation
Muscle proprioceptors provide
sensory feedback to nervous system
muscle proprioceptors sensory feedback is from what 2 things
tension development by muscle and account of muscle length
2 types of muscle proprioceptors
muscle spindle
Golgi tendon organ
muscle spindle responds to
changes in muscle length
how long muscle is and joint location
muscle spindle consists of what 2 things
intrafusal fibers and gamma motor neurons
intrafusal fibers of muscle spindles are what
run parallel to normal muscle fibers (extrafusal fibers) to avoid injury
gamma motor neurons stimulate
intrafusal fibers to contract with extrafusal fibers by alpha motor neurons to contract
Stretch reflex
stretch on muscle causes reflex contraction such as knee-jerk and protective mech
How do muscle spindles work (4 steps)?
1) Muscle spindles (intrafusal) detect stretch of the muscle
2) Sensory neurons conduct AP to the spinal cord, exciting muscle and shortening (concentric)
3) Sensory neurons synapse with alpha motor neurons
4) Stimulation of the alpha motor neuron causes the muscle to contract and resist being stretched
GTO
inhibit muscle contraction, receives pull of muscle, so elongation
GTO monitor and this prevents what?
tension developed in the muscle, this prevents muscle damage during excessive force generation (inhibits the contracting muscle)
GTO stimulation results in
reflex relaxation of muscle
GTO have what kind of neurons that do what?
Inhibitory neurons send IPSPs to muscle fibers, thus, inhbiting max force of muscle
Ability to voluntarily oppose GTO
inhibition may be related to gains in strength
GTO MOA
1) GTO detect tension applied to a tendon
2) Sensory neurons conduct AP to the spinal cord, inhibiting the muscle and lengthening (eccentric)
3) Sensory neurons synaspe with inhibitory interneurons that synapse with alpha motor neurons
4) Inhibition of alpha motor neurons causes muscle relaxation, relieving the tension to the tendon, this is the only differnce from muscle spindle MOA
Muscle chemoreceptors are sensitive to
changes in the chemical environment surronding a muscle
3 major chemicals detected by muscle chemoreceptors
H+ ions, co2, and K+
Muscle chemoreceptors provide and why?
CNS with info about metabolic rate of muscular actvitiy, and it is vital for regulation of cardiovascular and pulmonary responses
Withdrawal Reflex
touch hot stuff
Withdrawal reflex contraction of
skel muscle occurs in response to sensory input, and not dependent on higher brain centers
Withdrawal reflex pathways of neural reflex include 3
sensory nerve sends impulse to spinal column, interneurons activate motor neurons, and motor neurons control movement of muscles
Reciprocal Inhibition
When EPSPs to agonist muscles to withdraw from stimulus, and IPSPs to antagonistic muscles
Example of reciprocal inhibition (flexors and extensors of elbow)
biceps brachii flexion receives EPSPs, and triceps extension is inhibited
Cross-extensor reflex
Opposite limb supports body during withdrawal of injured contralateral limb via extension reflex
example cross extensor reflex in elbow flexion and exten
The finger of the right arm touches a nail, this causes the flexor (biceps brachii) to be stimulated by pulling away and the extensor tricep is inhibited to allow the movement. The left arm, contralateral arm, does the opposite since the extensor in the left arm will stimulated (tricep) and the flexor (biceps) will be inhibited allow the left arm to hold down, thus, supporting the body.
Somatic Motor neurons of PNS are responsible for
somatic motor f(x)
carrying neural messages from spinal cord to the skeletal muscles, typically alpha nerves that are myleinated, rapid speed
Motor unit (somatic motor function)
motor neuron and all the muscle fibers it innervates
Innervation ratio (somatic motor function)
number of muscle fibers per motor neuron (extrafusal)
What does a low innervation ratio denote in muscles?
Low ratio in muscles that require fine motor control such as the eye muscles
what does a higher innervation ratio mean?
large muscles such as the quads and multipennate muscle
Motor unit recruitment
recruitment of more muscle fibers through motor unit activation
Size principle
smallest motor units recruited first, and produce larger EPSP and result in action potential sooner because it can achieve threshold since it is smaller
Types of motor units
Type S
Type FR or FF
Type S motor units
Type S is the smallest motor unit, slow, type I fibers and turn on first, utilize FFA and are oxidative, aerobic (red= gets lots of blood supply).
Type FR motor units
Fast, fatigue resistant, Very trainable, type IIa fibers, intermediate fibers, pink= have decent blood supply, oxidative but more glycolytic, turn on second
Type FF
Fast, fatigable, type IIx fibers, largest, and are powerful white fibers not big blood supply, like white meat on a chicken breast, turns on last
Recruitment pattern during incremental exercise turning on
type S –> type FR –> FF
Recruitment pattern during incremental exercise turning iff
FF–> FR – > S
Where is vestibular apparatus located?
in the inner ear
what is the vestibular apparatus similar to in construction?
a level’s bubble bar
Vestibular apparatus is responsible for what?
maintaining general equilibrium and balance such as maintaining head position
Vestibular apparatus is sensitive to
changes in linear and angular acceleration, that is stimulated by head movement (static and dynamic movement)
Vestibular apparatus controls
head and eye movement during physical activity/motion
Brain stem responsible for what?
Many metabolic f(c)
cardiorespiratory cntrl
complex reflexes
Major structures in brain stem
Medulla oblongatta
Pons
Midbrain
reticular formation
2 parts of brain that make up cerebrum
Cerebral cortex
motor cortex
Cerebral cortex three functions
organizations of complex movement
storage of learned experiences (memory)
reception of sensory information
2 fnctions of motor cortex
motor control and voluntary movement
recieves info from other brain regions (cerebellum) in order to formulate, initiate, and perpetuate movement
Cerebellum main f(x)
coordinates and monitors complex movement by incorporating feedback from proprioceptors
Cerebellum has connection to what 4 areas?
Motor cortex
mid brain
brain stem
spinal cord
What may cerebellum initiate ?
fast, ballistic movements
concussion
brain injury resulting from traumatic force
What four things may result from concussions?
Permanent brain damage or death from delayed brain swelling
Second-impact syndrome
same season repeat concssion
late-life consequences of repeated concussions such as AD
Central Fatigue by brain role during exercise induced fatique what are involed
Higher brain centers and/or motor neurons
Central fatigue what gets depleted?
excitatory neurotransmitters in the motor cortex
cental fatigue results in what
reduced motor output to muscle
Central govenor theory regulates
central control center regulates exercise performance by reducing motor output to exercising muscle
central governor theory protects
against catastrophic disruptions of homeostasis
3 motor functions of the spinal cord
Withdrawal reflex, others, and spinal tuning
other reflexes vital for
control of voluntary movement
spinal tuning is
voluntary movement translated into an appropriate muscle action.
higher brain centers do what in spinal tuning
high brain centers concerned w/ general parameters of movement
spinal tuning does what w/ movement
details of movement refined in spinal cord
subcortical and cortical movement areas send
a “rough draft” of the movement to association cortex
Cerebellum and basal ganglia convert
“rough draft” into movement plan
cerebellum is responsible for what movement of rough draft?
fast movements
Basal ganglia is responsible for what kind of movements?
slow, deliberate movements in rough draft
Rough draft from thalamus to motor cortex (motor cortex through thalamus)
Fowards message sent down spinal neurons for “spinal tuning” and onto the muscles
motor cortex through thalamus feedback from
muscle receptors and proprioceptors allows fine tuning of motor program
First structure in process of voluntary movement and what it does
Subcortical and cortical areas, is the intial drive to move sending rough draft
Second structure of voluntary movement is blank and what it does as well
Association cortex Move design of “rough draft”
Third structures’ involved in voluntary movement and action
Basal ganglia and cerebellum (fast) refine movement design
Four structure in voluntary movemnt and action
Thalamus = relay station for spinal tuning
5th structure in voluntary movement and action
motor cortex final executor of motor plan
last structure in voluntary movement and what it does
motor units execution of desired movement
What motivates voluntary movement?
limbic and reticualr formation
ANS responsibility
for maintaining internal environ by effector organs not under voluntary control such as smooth and cardiac muscle, and glands
Sympatheic division of ANS releases and this causes
NE that primarily excites an effector organ, and after stimulation, NE is removed from synapse or inactivated
Parasym division releases and this causes
ACh, primarily inhibits effector organ, and after stimulation, ACh is degraded by acetylcholinesterase
5 ways exs enhances brain health
Enhances learning and memory
Stimulates formation of new neurons
Improves brain vascular function and blood flow
Attenuates mechanisms driving depression
Reduces peripheral factors for cognitive decline such as inflamation, HTN, and insulin resistnace
regular exs can protect brain against
disease and certain types of brain injury (stroke)
exercise improves
brain function and reduces the risk of cognitive impairment associated with aging
Regular exercise increases
brain growth factors
increased brain growth factors cause brain health to get better in three meaans
cognition
neurogenesis
vascular function
Human body contains over how many skel muscles?
600
what percentage of total body weight is skel muscles?
40-50%
4 functions of skel muscle
force production for locomotion and breathing
force production for postural support
protection
heat production during cold stress
Flexor muscle actions
decreases jt angle
extensors muscle actions
increases joint angle
epimysium
surrounds entire muscle, outside layer
perimysium surronds
bundles of muscle fibers, fascicles
Endomysium surrounds
individual muscle fibers
basement membrane of muscle
just below endomysium, is eplithelial tissue
sarcolemma
muscle cell plasma membrane
Satellite cells
undifferentiated cells
undifferentiated cells
immature
satellite cells reside in
basement membrane between sarcolemma and endomysium
satellite cells play a role in
muscle growth and repair when stimulated by physical stress such as exercise, and they increase the number of nuclei so they are multinucleated
Myonuclear domain
cytoplasm surrounding each nucleus, and each nucleus can support a limited myonuclear domainq
More nuclei potentially allow for what?
greater protein synthesis of actin and myosin via DNA in nucleus
what adaptations are satellite cells vital for?
strength training adapts
Myofibrils contain
contractile proteins; actin and myosin
actin
thin
myosin
thick filament, heads bind to actin
Sarcomere includes
Z line, M line, H zone, A band, and I band
SR
storage sites for Ca2+
Terminal cisternae
NMJ
Junction btwn motor neuron and muscle fiber
motor unit
motor neuron and all fibers it innervates
Motor End Plate
Pocket formed around motor neuron by sarcolemma
Neuromuscular celft
short gap between neuron and muscle fiber
ACh is released from
the motor neuron
When ACh is released from motor neuron, it causes an
EPP (end plate potential)
EPP
depolarization of muscle fiber as sarcolemma becomes permeable to a Na+ if threshold value achieved
Sliding filament model aka
swinging lever-arm model
Muscle shortening occurs due to the movement of the actin filament over the
myosin filament
Formation of
cross-bridges btween actin and myosin filaments
power stroke
cross bridging
Reduction in dist btw Z lines of the sarcomere
contraction
Actin Has 2 vital proteins called
tropmyosin and troponin
Myosin filaments have tiny what
protein projections on each end that extend towards the actin filaments; crossbridges
5 steps in sliding filament theory
Rest Excitation-coupling contraction recharging relaxation
Write out how muscle contracts
do it guy
In the center of the sarcomere, the thick filaments lack what?
myosin heads
WHere are myosin heads present?
They are only present in areas of myosin-actin overlap.
Myosin thick filament
Each thick filament consists of many myesin molecules whose heads protrude at opposite ends of the filament
Actin thin filament consists of
2 strands of actin subunits twisted into a helix plus 2 types of regulatory proteins (troponin and tropomyosin)
What happens at resting step of sliding filament theory?
Troponin and tropomyosin prevent actin/myosin crossbridging
What is required for a muscle contraction ?
ATP
What breaks down ATP for muscle contraction?
myosin ATPase
ATP–> ADP + Pi
3 sources of ATP
PC
Glycolysis
Oxidative phosphorylation
During excitiation-contraction coupling phase what is being depolarized?
Depolarization of motor end plate (excitation) is coupled to muscular contraction
excitation-contraction coupling AP travels down
Transverse Tubules and causes release of Ca++ from SR
Once AP travels down T tubules to cause Ca++ release from SR what does Ca2+ bind to? To do what/why is this necessary?
troponin and causes position change in tropomyosin, and exposing active sites on actin
What kind of state is formed between actin and myosin and what does this cause?
a strong binding state and this causes a contraction to occur if ATP is present
First step in excitation of contraction
AP in motor neuron causes release of ACh into synaptic cleft
Second Step in excitation phase of contraction
ACh binds to receptors on motor end plate, leads to depolarization that is conducted down T tubules, which causes release of Ca2+ from the SR
First step in contraction phase of excitation-contraction coupling
At rest, myosin crossbridges in weak binding state
2nd step in contraction phase of excitation-contraction coupling
Ca++ binds to troponin, causes shift in tropomyosin to uncover active sites, and cross bridges forms strong binding state
3rd step in contraction phase of excitation-contraction coupling
Pi released from myosin, crossbridge movement occurs as per a pivoting action of the myosin heads referred to as a power stroke
4th step in contraction phase of excitation-contraction coupling
ADP released from myosin
5th step in contraction phase of excitation-contraction coupling
ATP attaches to myosin, breaking the crossbridge and forming weak binding state. Then ATP binds to myosin, broken down to ADP+Pi, which energizes myosin and continues as long as Ca++ and ATP are present
pivoting action of the myosin heads referred to as a
power stroke
Muscle Fatigue definition
decline in muscle power output due to decrease in force generation and in shortening velocity
Muscle fatigue two characteriscs
force generation and shortening velocity
During muscle fatigue in high intenisty exs what acculmates and what does that cause?
Acculmuation of lactate, H+, ADP, Pi, and free radicals. This causes/ diminishes cross bridges bound to actin
Long duration of high intensity exercise is due to?
Muscle factors that include acculmation of free radicals, electrolyte imbalance, and glycogen depletion
Muscle cramp def
spasmodic, involuntary muscle contractions
Muscle cramp cause theories (2)
Electrolyte depletion and dehydration theory
Altered Neuromuscular control theory
Electrolyte depletion and dehydration theory for muscle cramps
Water and Na+ loss via sweating causes spontaneous muscle contractions
Altered Neuromuscular control theory
Muscle fatigue causes abnormal activity in muscle spindle and GTOs, which leads to increased firing off of motor neurons resulting in a muscle cramp
Biochem props of muscle fibers
Oxidative capacity and type of myosin ATPase
oxidative capacity
of capillaries, mitochondria, and amount of myoglobin
type of myosin ATPase
speed of ATP degradtion
Contractile properties of muscle fiber types
maximal force production, speed of contraction (Vmax), and muscle fiber efficiency
Maximal force production
force per unit of cross-sectional area
speed of contraction (Vmax)
myosin ATPase activtiy
Type I fibers appear
darkest stains of myosin ATPase
Type IIa fibers appear
lightest staining of myosin ATPase
Type IIx fibers appear
inbtwn light and dark stains of myosin ATPase
Immunohistochemical stainining
selective antibody binds to unique myosin proteins, and fiber types differentiated by color diff
Gel Elctrophoresis
ID myosin isoforms specific to different fiber types
Nonathletes have how much of percent of each fiber?
50% slow and 50% fast
Power athletes such as sprinters have higher percentage of what fibers?
fast fibers
Endurance athletes have higher percentage of
slow fibers
Isometric muscle action
muscle exerts force without changing length
pulling against moving object is what kind of muscle action?
isometric
Postural muscles are what kind of muscle action?
isometric
dynamic muscle action is also known as
isotonic
2 types of isotonic/dynamic muscle actions
concentric/shortening-contraction
eccentric
concentric muscle contraction
muscle shortens during force production
Eccenctric
muscle produces force but length increases
What muscle contraction is assoicated with fiber injury and soreness? why?
eccentric
Myosin heads are ripped out of actin binding site, causes pain and the inflamation
Muscle twitch
contraction as the result of a single stimulus
Latent period of muscle contraction
5 ms
Contraction aspect of muscle twitch is when what is developed?
tension for 40 ms
relaxation in muscle twitch
50 ms
Speed of shortening is greater in .. . ? Why?
fast fibers
SR releases Ca++ @ faster rate and higher ATPase activity
Force regulation of muscle 3 factors
Types and numbers of motor units recruited
Initial muscle length
Nature of the neural stimulation of motor units
Types and number of motor units recruited depends on 2 thing for greater force production
more motor units= greater force
Fast motor units = greater force
Initial muscle length
“Ideal” length for force generation (perpendicular jt angle)
Increased cross-bridge formation
Nature of neural stimulation of motor units depends on
frequency of stimulation
3 aspects of frequency of stimulation
Simple twitch
Summation
Tetanus
Less than optimal length for length tension relationship in skel muscles
fewer cross-bridge interactions = reduced tension development
optimal length for length-tension relationship in skel muscle
Maximal cross-bridge interaction = maximal tension dvp
Greater than optimal length for length-tension relationship
No cross-bridge interxn = no tension dvpment
Force-velocity relationship
At any absolute force, the speed of movement is greater in muscle with higher percent of fast-twitch muscle fibers. (faster contraction with fast fibers)
According to the force-velocity relationship, the maxima velocity of shortening is
greatest at the lowest force and is true for both fibers
Force-power relationship
At any given velocity of movement, the power generated is greater in a muscle with a higher percent of fast twitch fibers, and peak power increases with velocity up to movement speed of 200-300 degrees/sec. Power decreases beyond this velocity cuz force decreases with increasing movement speed.
Sarcopenia
loss of muscle mass with aging
With aging there is loss of ______ fibers and a gain of _____
fast fibers and gain in slow fibers
What can delay age-related muscle mass?
resistance training
Diabetes associated with
progressive loss of muscle mass
Diabetes combined with
age-related loss
What can protect people with diabetes
aerobic and resistive training
Cancer causes
cachexia
cachexia
rapid loss of muscle mass
Cachexia from cancer results in
weakness, accounts for 20% deaths in cancer patients
Regular exercise and nutrition therapy may counteract what
cachexia
regular exercise stimulates
protein synthesis
Muscular dystrophy
hereditary defects in muscle protein
MD results in
loss of muscle fibers and weakness
Duchene muscular dystrophy is most common in
childhood
DMD progression
varies based on specific disease type
The circulatory works with the
pulmonary/ respiratory sys
Purposes of the cardiorespiratory sys
Transport O2 and nutrients to tissues
Removal of CO2 wastes from tissues
Regulation of body temperature
2 major adjustments of blood flow during exercise
Increased CO/Q
Redistribution of blood flow
Heart creates (its job)
pressure to pump blood
Arteries and arterioles carry blood
away from the heart
capillaries job
exchange of o2, co2, wastes, and nutrients with tissues
Veins and venules carry blood
toward the heart
______
Pulmonary circuit is what side of the heart?
right side of the heart
Pulmonary circuit pumps what kind of blood to where via what?
Pulmonary pumps deoxygenated blood to the lungs via the pulmonary arteries*
Pulm circuit returns
oxygenated blood to the left side of the heart via pulmonary veins*
Pulmonary veins and pulm arteries
go in same direction just carry different carries different blood
Veins usually carry deoxygenated, but pulm veins oxygenated, while arteries usually carry oxygenated blood, but pulm arteries carry deoxygenated blood
systemic circuit is what side of heart
left side of heart
systemic circuit pumps
oxygenated blood to the whole body via arteries
systemic circuit returns
deoxygenated blood to the right side of the heart via veins
Heart wall consists of these 3 layers
epicardium
myocardium
endocardium
Wall of heart receives blood supply via ____ and has high demand for _____ and ______
coronary arteries
high demand for o2 and nurtrients
Myocardial infarction is what?
MI is a blockage in coronary blood flow results in cell damage
Exercise training does what for MI?
EXs training protects against heart damage during MI
How does exercise training protect heart during MI?
Angiogenesis
Epicardium is what anatomical landmark as well
visceral pericardium
Epicardium characteristics
serous membrane including blood capillaries, lymph capillaires, and nerve fibers
Function of Epicardium
serve as lubricative outer covering
Myocardium characteristics
cardiac muscle tissue seperated by connective tissues and including blood capillaires, lymph capillaries, and nerve fibers
Myocardium F(x)
provides muscular contractions that eject blood from the heart chambers
endocardium characteristics
endothelial tissue and a thick subendothelial layer of elastic and collagenous fibers
endocardium f(c)
serves as protective inner lining of the chambers and valves
Are contractile proteins: actin and myosin found in both the heart and skeletal muscles? Yes or no, eh
Yes
How is the shape of skel and heart muscle differ?
The heart muscle is shorter than skeletal muscle fibers and branching, while skel muscle is elongated with no branching
What is the difference between skel and heart muscle amount of nuclei?
Heart muscle : single nuclei
Skel muscle: multinucleated
Do both heart and skel muscles have Z discs? yes
yes
are both heart and skel muscle striated?
yes
Do heart and skel muscle both have cellular junctions? What is the differnce if there is one?
Only heart does. The heart mucle has intercalated discs while the skel muscle has no junctional complexes.
Do both heart and skel muscle have connective tissue? Any differences?
Both have connective tissue.
Heart muscle has endomysium for conenctive tissue.
Skel muscle has epimysium, perimysium, and endomysium with connective tissue.
HEART muscle energy production
aerobic primarily
skel muscle energy production both
aerobic and anerobic
Ca2+ source for contraction for both muscles and any diff?
both have SR, but heart also gets extracellular Ca++
Neural control of the heart muscle is
nonvoluntary
Neural control of the skel muscle is
voluntary
Regeneration potential in heart muscle?
None- no satellite cells present
Regeneration potential in skel muscle?
Some possibiliteis via satellite cells
Why is regular exercise cardio protective?
reduce incidence of MI
Improves survival from MI
Exercise reduces amount of what?
myocardial damage from MI
Exercise reduces amount of myocardial damage from MI causes 2 improvements:
Improvements in heart’s antioxidant capacity
Improved function of ATP-sensitive K+ channels
Cardiac cycle
systole and diastole
systole is what phase and what happens
contraction phase
Ejection of blood, 2/3 blood is ejected from ventricles per beat
diastole what phase and what happens?
relaxation phase
filling w/ blood
At rest, what happens in cardiac cycle?
At rest, diastole is longer than systole
During exs, cardiac cycle
During Exercise, both systole and diastole are shorter
Diastole pressure changes in ventricles
During diastole, pressure in ventricles is low
Diastole and atria
During diastole, the atria are filling with blood
diastole and valves
AV valves open when ventricular P is less than atrial pressure
systole pressure in ventricles does what
pressure increases/rises
systole blood is
ejected in pulmonary and systemic circulation
systole and valves
semilunar valves open when ventricular pressure is greater aortic presure
Heart first sound lub is what?
closing of AV valves
heart second sound dub is what?
closing of aortic and pulmonary valves (semilunar)
Arterial blood pressure is expressed as
systolic over diastolic
systolic pressure
pressure generatered during ventricular contraction/ systole
Diastolic presure in the
arteries during cardiac relaxation
Pulse pressure is the
difference btween systolic and diastolic
MAP
average pressure n the arteries during cardiac cycle
MAP = eqn
DBP + .33x (SBP-DBP)
Korotkoff sounds first phase
a clear tapping sound, onset of the sound for 2 consecutive beats is considered systolic
Korotkoff sounds second phase
the tapping sound followed by a murmur
Korotkoff sounds 3rd phase
a loud crisp tapping sound
Korotkoff sounds 4th phase
abrupt, distinct muffling sound, gradually decreasing intensity (pre diastolic)
Korotkoff sounds 5th phase
The disapperance of sound, is considere diastolic BP- 2 points below last sound heard
Normal BP
<80
Pre HTN
120-139/80-89
Stage 1 HTN
140-159/90-99
Stage 2 HTN
> /= 160/ >/= 100
Stage 3 HTN
180/110 to 215/125
hypotension
</= 90/60
HTN bp = to or above
140/90 mm Hg
Primary/essential HTN cuase
etiology unkown
primary/essential HTN % of HTN
90% of HTN
Secondary HTN result of some other
disease process
HTN is risk factor for:
LVH
Atherosclerosis and MI
Kideny Damage
stroke
Factors that influence ABP
MAP determinatns, short and long term regulation
Determinants of MAP
Q
TVR
MAP = formula
Q x TVR
Short term regulation is what NS
SNS
Short term regulation happens with what
baroreceptors in aorta and carotid arteries
Increase BP causes baroreceptors to do what?
decrease SNS activity
Decrease BP causes baroreceptors to ?
increase SNS activity
Long term regualtion of BP is by what organ
kidney and either direct or indirect mech
How down kidney regulate long term bp?
via control of blood volume (renin-angiotensin-aldosterone/ diuretics)
Renin-angiotensin-aldoseterone is what mechanims?
longterm indirect mechanism
Decreased arterial bp causes release of
renin
Renin does what
catalyzes conversion of angiotensinogen from Liver to angiotensin I
ACE from lungs and endothelial converts
angiotensin I to angiotensin II
angiotensin II increases
blood volume
How does angiotensin II increase blood volume?
stimulates aldosterone secretion from renal cortex
promotes ADH release
triggers hypothalamic thirst center
Angiotensin II directly increases BP how , and most potent one of these
vasoconstriction
5 factors increasing BP
blood volume increases HR increases SV increases (Q increases) Blood viscosity increases Peripheral resistance increase (TVR )
Contraction of heart depends on
electrical stimulation of the myocardium
Components of conduction system
SA node AV node AV bundle bundle branches purkinje fibers
SA node is located over what and does what?
right atrium
pacemaker, initiates depolarization
AV node is located where and does what
floor of atria
pass depolarization to ventricles
why brief delay at AV node?
Breif delay at AV node allows for ventricular filling
Bundle branches where located
to left and right ventricle
purkinje fibers located
throughout ventricles
First step in conduction system of heart
AP originates in SA node and travel across the wall of the atrium from SA node to the AV node
2nd step in conduction system of heart
AP pass through AV node and along AV bundle, which extends from the AV node, through the fibrous skeleton, into the interventricular septum
3rd step in conduction system of heart
The AV bundle divides into right and left bundle branches, and AP descend to the apex of each ventricle along the bundle branches
4th step in conduction system of heart
AP are carrried by the Purkinje fibers from the bundle branches to the ventricular walls
EKG
records the electrical activity of the heart
P wave
artrial depolarization
QRS complex time afer the P wave
0.10 second after P
QRS complex whats really happening hot stuff
Ventricular depolarixation and atrial repolarization
T wave is what
ventricular repolarization
ECG abnormalities may indicate
coronary heart disease
ST-segment depression can indicate what
myocardial ischemia
ECG during GXT used to eval
cardiac function
GXT and EKG allows person to
observe EKG during exs and changes in BP
Atherosclerosis
fatty plaque that narrows coronary arteries
atherosclerosis reduces
blood flow to myocardium resulting in myocardial ischemia
S-T segment depression suggests
myocardial ischemia
1) Growth hormone supports/decreases the action of cortisol during exercise. GH will increase/decrease with exercise intensity, and well-trained athletes will have a greater/lesser GH response than untrained individuals.
supports
increase
2) Epinephrine/norepinephrine are ___________- acting hormones and will provide glucose in the liver through ____________________ breakdown, instead of gluconeogenesis.
fast-acting
glycogen breakdown
3) Epinephrine and norepinephrine will increase/during as exercise duration increases. As a person becomes more trained, he will secrete more/less hormone during exercise compared to a lesser-trained individual.
increase
less
4) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause glucagon release.
Beta-adrenergic
Alpha pancreatic cell
5) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause insulin suppression.
alpha-adrenergic
beta
6) The result of both of the above actions will be an increase in plasma __________________, a decrease in plasma ___________________, and the breakdown of liver ___________________.
glucagon
insulin
glycogen
7) For most exercise intensities, plasma insulin will increase/decrease compared to rest. However, at very high intensity, plasma insulin may slightly increase/decrease in order to allow _____________________ into the cell as an energy source.
decrease
increase
glucose
8) Because trained individuals are more/less sensitive to hormones levels, glucagon levels will change little/greatly in trained people during exercise.
more
little
9) What are the two primary results of epi/norepi (and therefore insulin and glucagon) response during exercise ?
TG breakdown in FFA, thus increasing plasma FFA
GLycogen breakdown into glucose to maintain blood glucose levels
10) Fatigue can be defined as the inability to maintain _____________________ or ________________________ during repeated muscular contractions.
power output or force
Fitness is what ? 2 parts
General health promotion
stresses moderation of activity
Performance is what sports?
competitive sports
Does performance or fitness require higher dose needed for success?
Performance
Fitness is what to performance
Fitness is a secondary benefit of activity
performance has many factors affected by what?
fatigue
6 sites of fatigue
CNS Function Diet Strength and Skill Environment Energy Production Anaerobic Aerobic Energy Production
Fatigue
Inability to maintain power output or force during repeated muscle contractions
Central fatigue
Central nervous system
Peripheral fatigue
Neural factors
Mechanical factors
Energetics of contraction
Reduction in motor units activated is what kind of fatigue?
central fatigue
Reduction in motor unit firing frequency is what kind of fatigue?
central fatigue
Central nervous system arousal can alter the state of fatigue what kind of fatigue By facilitating motor unit recruitment
Increasing motivation
Physical or mental diversion is this?
central fatigue
Serotonin linked to what 3 things?
relaxation, euphoria, arousal suppression
Amino acid tryptophan (Trp) is precursor to
serotonin
Free (unbound) Trp (f-Trp) shares carrier across
BBB into brain with BCAA
Prolonged exercise:
↑ lipolysis; FFAs compete with Trp in binding to albumin; more f-Trp available for transport to brain
Hypothesis for prolonged exercise : more BCAA will compete with
f-Trp for transport across BBB; less serotonin synth; less fatigue
Peripheral Fatigue: Neural Factors site
Sarcolemma and transverse tubules
Sarcolemma and transverse tubules is the ability of muscle
membrane to conduct an action potential
Peripheral Fatigue neural factor inability of what pump to do what
Inability of Na+/K+ pump to maintain action potential amplitude and frequency
Neural factor for peripheral fatique can be improved by
Can be improved by training
An action potential block in the T-tubules
Reduction in Ca+2 release from sarcoplasmic reticulum
neural factor
Peripheral Fatigue: Mechanical Factors (3)
Cross-bridge cycling and tension development
High H+ concentration may contribute to fatigu e
Longer “relaxation time” is a sign of fatigue
Cross-bridge cycling and tension development depends on:
Arrangement of actin and myosin
Ca+2 binding to troponin
ATP availability
High H+ concentration may contribute to fatigue due to:
Reduce the force per cross-bridge
Reduce the force generated at a given Ca+2 conc.
Inhibit Ca+2 release from SR
Longer “relaxation time” is a sign of fatigue Due to
slower cross-bridge cycling
Peripheral Fatigue: Energetics of Contraction
Imbalance in ATP requirements and ATP generating capacity
Imbalance in ATP requirements and ATP generating capacity due to
Accumulation of Pi
Inhibits maximal force
Reduces cross-bridge binding to actin
Inhibits Ca+2 release from SR
Rate of ATP utilization is slowed faster than rate of ATP generation due to
Maintains ATP conc. – protective effect – minimize change in homeostasis!
Muscle fiber recruitment in increasing intensities of exercise
Type I Type IIa Type IIx
Slow oxidative fast oxidative glycolytic fast glycolytic
Up to 40% VO2 max: type I fibers recruited
40–75% VO2 max: Type IIa fibers recruited
Exercise >75% VO2 max: requires IIx fibers
Results in increased lactate, H+ production
The Energy Continuum
Energy systems do not “turn on/turn off”
Ultra Short-Term Performances duration
Events lasting <10 seconds
Ultra Short-Term Performances Dependent on recruitment of Type II muscle fibers why?
Generate great forces that are needed
Ultra Short-Term Performances what is important?
Motivation, skill, and arousal are important
Ultra Short-Term Performances what is energy source?
Primary energy source is anaerobic
ATP-PC system and glycolysis
Creatine supplementation may improve performance
Short-Term Performances duration
Events lasting 10–180 seconds
Short-Term Performances shift from type of metabolism
Shift from anaerobic to aerobic metabolism
70% energy supplied anaerobically at 10s
60% supplied aerobically at 180s
Primary energy source for short term performances and resultins in and intereferes with?
Anaerobic glycolysis is primary energy source
Results in elevated lactate and H+ levels
Interferes with Ca+2 binding with troponin
Intermediate-Length Performances duration
Events lasting 21–60 minutes
Intermediate-Length Performances energy system
Predominantly aerobic
Usually conducted at <90% VO2 max
High VO2 max is important
Intermediate-Length Performances Other important factors
Running economy High percentage of type I muscle fibers Environmental factors Heat Humidity State of hydration
Long-Term Performances duration
Events lasting 1–4 hours
Long-Term Performances energy system
Clearly aerobic
Long-Term Performances and VO2max
High VO2max not as important
what is is vital for long-term performances?
Environmental factors more important
Influences on long term performances?
Maintaining rate of carbohydrate utilization
Muscle and liver glycogen stores decline
Ingestion of carbohydrate
Maintain carbohydrate oxidation by the muscle
Consumption of fluids and electrolytes
Diet also influences performance
Is VO2max Important in Distance Running Performance?
VO2 max sets the upper limit for ATP production in endurance events
Even though race is not run at 100% VO2 max
long term Performance also determined by:
%VO2 max at which runner can perform
Estimated by the lactate threshold
Running economy
Training program should match the
anaerobic and aerobic demands of the sport
Overload
Increased capacity of a system in response to training above the level to which it is accustomed
Specificity
Specific muscles involved
Specific energy systems that are utilized
Reversibility
When training is stopped, the training effect is quickly lost
Men and women respond
similarly to training programs
Exercise prescriptions should be
individualized
Training improvement is always greater in individuals
with lower initial fitness
50% increase in VO2 max in
sedentary adults
10–15% improvement in
normal, active subjects
3–5% improvement in
trained athletes
1-2% improvement in
elite athletes
Genetics plays an important role in
how an individual responds to training
Åstrand and Rodahl: quote
“If you want to become a world-class athlete, you must choose your parents wisely.”
Anaerobic capacity is more genetically determined
than aerobic capacity
Training can only improve anaerobic performance to
a small degree
Training can only improve anaerobic performance to a small degree dependent on and determined in
Dependent largely on fast (IIx) fibers
Determined early in development
Warm-up
Increases cardiac output and blood flow to muscles
Increases muscle temperature and enzyme activity
Opportunity for stretching exercises
Believed to reduce risk of muscle injury
Workout
Training session
Cool-down
Return blood “pooled” in muscles to central circulation
Reduce hypotensive response
Aerobic power: measure determined by
VO2max
Determined by max cardiac output, a-v O2 diff
Training to Improve Aerobic Power
Long, slow distance
High-intensity, continuous exercise
High-intensity interval training (HIIT, which includes supramaximal sprint interval training (SIT)
Aerobic power should be geared toward improving:
VO2 max
Lactate threshold
Running economy
Long, Slow Distance benefits
economy, VO2max
Long, Slow Distance intensity
Low-intensity exercise
50-60% VO2 max or 70% HRmax
Long, Slow Distance duration
Duration greater than would be expected in competition
Long, Slow Distance is Based on the idea that , but?
training improvements are based on volume of training
However, more is not always better
1.5 hours/day training may result in better performance than 3 hours/day
High-Intensity, Continuous Exercise appears to be what?
Appears to be the best method of increasing VO2 max and lactate threshold
High-intensity exercise
At or slightly above lactate threshold
80–90% HRmax
≥90% HRmax or 95% HRR also suggested
High-Intensity, Continuous Exercise duration
Duration of 25–50 min
Depending on individual fitness level
High-Intensity Interval Training Benefits
Benefit: lactate and H+ clearance
High-Intensity Interval Training are
Repeated exercise bouts
Separated by brief recovery periods
High-Intensity Interval Training Work effort
(repetition)
Distance to be covered
Intensity: 85–100% HRmax
Duration: >60 seconds to improve VO2 max
High-Intensity Interval Training Rest interval
Light activity such as walking
1:1 ratio of work to rest; can be up to 1:3
High-Intensity Interval Training Number of interval sets and repetitions depends on
Depends on purpose of training and fitness level
Supramaximal Sprint Repeats are % vo2max
100-150% VO2max
Supramaximal Sprint Repeats is performed on and how
Performed on cycle ergometer
Sprint as hard as possible against high resistance
Brief work effort: 20-30 s
Supramaximal Sprint Repeats Benefits:
Increased oxidative/endurance capacity
PFK, LDH, PDH, citrate synthase, cytochrome oxidase, MCT, ↑ lipid oxidation, ↓ glycogenolysis, ↓ lactate accumulation
But, no increase in VO2max
Benefits come in form of increased lactate threshold
Altitude Training Improves Exercise Performance at Sea Level
Altitude training may not always improve performance at sea level
Lower training intensity at altitude may result in de-training
Live-High, Train-Low
Spend sleeping and resting time at altitude
Increases red blood cell volume and oxygen transport capacity of blood
Train at lower altitude
Better performance gains compared to living and training at sea level
Historically, training to improve maximal aerobic power has used three methods: and one new method
(1) interval training, (2) long, slow-distance, and (3) high-intensity, continuous exercise. Supramaximal sprint training enhances endurance capacity via lactate threshold, but not VO2max
Although controversy exists as to which of the training methods results in the greatest improvement in VO2 max, there is growing evidence that it is
intensity and not duration that is the most important factor in improving VO2 max.
The “Live-High, Train-Low” altitude training program provides significant
endurance performance gains compared to training and living at sea level.
Most injuries are a result
of overtraining
Short-term, high-intensity exercise
Prolonged, low-intensity exercise
The “ten percent rule” for increasing training load
Increase intensity or duration ≤10% per week
Other injury risk factors
Strength and flexibility imbalance Footwear problems Malalignment Poor running surface Disease (arthritis)
ATP-PC system
Short (5–10 seconds), high-intensity work repeats
30-yard dashes for football players
30- to 60-second rest intervals
Little lactate + H+ is produced, so recovery is rapid
Glycolytic system
Short (20–60 seconds), high-intensity work repeats
Very demanding training
May alternate hard and light training days
Remember supramaximal sprint training? Good for all energy systems
Strength Training Adaptations
Increased muscle mass
Hypertrophy
Increased muscle fiber diameter
Responsible for most of the increase in muscle size
Hyperplasia
Increased number of muscle fibers
Central nervous system changes for strength training adaptations
Increased motor unit recruitment Altered motor neuron firing rates Enhanced motor unit synchronization Removal of neural inhibition “motor morons become motor geniuses”
Delayed onset muscle soreness (DOMS) occurs
Appears 24–48 hours after strenuous exercise
How does DOMS occur?
Due to microscopic tears in muscle fibers or connective tissue
Results in cellular degradation and inflammatory response
Not due to lactic acid
What type of exercise/ contraction causes DOMS?
Eccentric exercise causes more damage than concentric exercise
How to avoid DOMS?
Slowly begin a specific exercise over 5–10 training sessions to avoid DOMS
Why more damage with eccentric exercise?
More force production
Due to LESS cross bridge detachment throughout the contraction
More attachment = more force production
Steps Leading to DOMS
Strenuous muscle contraction results in muscle damage
Membrane damage occurs
Including sarcoplasmic reticulum
Calcium leaks out of SR and collects in mitochondria
Inhibits ATP production
Activates proteases which degrade contractile proteins
Results in inflammatory process
Increase in prostaglandins/histamines
Edema and histamines stimulate pain receptors
A bout of unfamiliar exercise results
in DOMS
Following recovery, another bout of same exercise results
in minimal injury
Theories for the repeated bout effect
Neural theory
Neural Theory
Recruitment of larger number of muscle fibers
Connective tissue theory
Increased connective tissue to protect muscle
Cellular theory
Synthesis of protective proteins within muscle fiber
Overtraining not overload
Workouts that are too long or too strenuous
Greater problem than undertraining
Performing non-specific exercises do not
enhance energy capacities used in competition
Failure to schedule a long-term training plan results in
Misuse of training time
Failure to taper before a performance results in
Inadequate rest; compromises performance
Common Training Mistakes
Overtraining Undertraining Performing non-specific exercises Failure to schedule a long-term training plan Failure to taper before a performance
Overtraining SX
Decrease in performance loss of BW Chronic fatigue increased number of infections psychological staleness Elevated HR and blood lactate levels during EXS
Tapering
Short-term reduction in training load prior to competition
Tapering allows what?
Allows muscles to resynthesizes glycogen and heal from training-induced damage
Tapering Improves performance in both
strength and endurance events
Athletes can reduce training load by 60% without a reduction in performance
