Test2 Exphys I Flashcards

(500 cards)

1
Q

5 gen f(c) of NS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CNS

A

brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PNS

A

consists of neurons located outside CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the archeitecture of the bones in the body tell us about the CNS?

A

Body will work to preserve NS since it has most protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Afferent divison of PNS consists of what 3 components?

A

somatic sensory
visceral sensory
special sensory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Efferent division PNS consist of what?

A

somatic motor and automatic motor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3 division of automotic motor

A

sympathetic, parasympathetic, and enteric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

SNS controls

A

skel muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ANS controls

A

smooth, cardiac muscles and glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cell body

A

center of operation also called soma or perikaryon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cell contains blank that does is the site of

A

cell body contains the nucleus, site of protein synthesis that produces neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nerves have more blank so these use this substrate and why?

A

nerves have more mitochondria but uses more glucose and heart uses fats so the two main systems are not in competition for fuel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

dendrites conduct

A

impulses toward cell body from the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

axon carries

A

electrical impulse away from cell body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

axon may be coverd by

A

Schwann cells and forms discontinouous myelin sheath along length of axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

gaps of mylein sheath

A

Nodes of Ranvier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

biggest nerve

A

sciatic nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

synapse

A

contact points btwn axon of one neuron an dendrtite of another neuron, goes from electrical to chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The mitochondria in the neuron go through what energy system?

A

aerobic glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Multiple Sclerosis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MS results in

A

progressive loss of NS f(x) causing fatigue, muscle weakness, poor motor ctrl, loss of balance, and mental depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Exs can improve f(c)nal capacity of what disease?

A

MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

exercise for MS leads to

A

improved QOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

exercise can do what kind of harm if not controlled

A

can overheat nerves resulting in necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
neurons are what kind of tissue
excitable tissue (conducts stimulus)
26
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
27
conductivity
transmission of the impulse along the axon
28
why is resting membrane potential negative?
because of protein anions that are stationary in the cell
29
synapse
small btwn presynaptic neuron and postsynaptic neuron
30
Neurotransmitter
chemical jumps synapse | chemical messenger released from presynaptic membrane for communication
31
Where does neurotransmitter bind to?
binds to receptor on postsynaptic membrane
32
neurotransmitter can cause
depolarization (EPSP) or hyperpolarization (IPSP) of the postsynaptic membrane
33
EPSP causes
depolarization
34
depolarization
Na+ influx into the cell, making the cell more positive and less negative, once threshold is reached
35
temporal summation
summing several EPSPs from presynaptic neuron
36
spatial summation
summing from several different presynaptic neurons
37
two types of EPSP
temporal and spatial
38
IPSP
cause hyperpolarization
39
hyperpolarization
make cell more negative
40
proprioceptors
receptors that provide CNS with information about body position in space ortientation
41
where are proprioceptors located?
located in joint and muscles
42
proprioceptors prevent
falls by forming a plan that tuned by the spine
43
kinesthesia
kinestic awareness
44
kinesthesia is
consciuous recognition of position of body parts and limb movement rates
45
free nerve endings are sensitive to
touch and pressure
46
free nerve endings are initially strongly
stimulated, then they adapt
47
Golgi-type receptors are found in
ligments and around joints and are diff from gto's
48
golgi-type receptors are similar to what
free nerve endings in that they are pressure and touch sensitive
49
Pacinian corpuscles location
in tissues around joints
50
pacinian corpuscles detect what
rate of joint rotation
51
Muscle proprioceptors provide
sensory feedback to nervous system
52
muscle proprioceptors sensory feedback is from what 2 things
tension development by muscle and account of muscle length
53
2 types of muscle proprioceptors
muscle spindle | Golgi tendon organ
54
muscle spindle responds to
changes in muscle length | how long muscle is and joint location
55
muscle spindle consists of what 2 things
intrafusal fibers and gamma motor neurons
56
intrafusal fibers of muscle spindles are what
run parallel to normal muscle fibers (extrafusal fibers) to avoid injury
57
gamma motor neurons stimulate
intrafusal fibers to contract with extrafusal fibers by alpha motor neurons to contract
58
Stretch reflex
stretch on muscle causes reflex contraction such as knee-jerk and protective mech
59
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
60
GTO
inhibit muscle contraction, receives pull of muscle, so elongation
61
GTO monitor and this prevents what?
tension developed in the muscle, this prevents muscle damage during excessive force generation (inhibits the contracting muscle)
62
GTO stimulation results in
reflex relaxation of muscle
63
GTO have what kind of neurons that do what?
Inhibitory neurons send IPSPs to muscle fibers, thus, inhbiting max force of muscle
64
Ability to voluntarily oppose GTO
inhibition may be related to gains in strength
65
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
66
Muscle chemoreceptors are sensitive to
changes in the chemical environment surronding a muscle
67
3 major chemicals detected by muscle chemoreceptors
H+ ions, co2, and K+
68
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
69
Withdrawal Reflex
touch hot stuff
70
Withdrawal reflex contraction of
skel muscle occurs in response to sensory input, and not dependent on higher brain centers
71
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
72
Reciprocal Inhibition
When EPSPs to agonist muscles to withdraw from stimulus, and IPSPs to antagonistic muscles
73
Example of reciprocal inhibition (flexors and extensors of elbow)
biceps brachii flexion receives EPSPs, and triceps extension is inhibited
74
Cross-extensor reflex
Opposite limb supports body during withdrawal of injured contralateral limb via extension reflex
75
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.
76
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
77
Motor unit (somatic motor function)
motor neuron and all the muscle fibers it innervates
78
Innervation ratio (somatic motor function)
number of muscle fibers per motor neuron (extrafusal)
79
What does a low innervation ratio denote in muscles?
Low ratio in muscles that require fine motor control such as the eye muscles
80
what does a higher innervation ratio mean?
large muscles such as the quads and multipennate muscle
81
Motor unit recruitment
recruitment of more muscle fibers through motor unit activation
82
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
83
Types of motor units
Type S | Type FR or FF
84
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).
85
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
86
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
87
Recruitment pattern during incremental exercise turning on
type S --> type FR --> FF
88
Recruitment pattern during incremental exercise turning iff
FF--> FR -- > S
89
Where is vestibular apparatus located?
in the inner ear
90
what is the vestibular apparatus similar to in construction?
a level's bubble bar
91
Vestibular apparatus is responsible for what?
maintaining general equilibrium and balance such as maintaining head position
92
Vestibular apparatus is sensitive to
changes in linear and angular acceleration, that is stimulated by head movement (static and dynamic movement)
93
Vestibular apparatus controls
head and eye movement during physical activity/motion
94
Brain stem responsible for what?
Many metabolic f(c) cardiorespiratory cntrl complex reflexes
95
Major structures in brain stem
Medulla oblongatta Pons Midbrain reticular formation
96
2 parts of brain that make up cerebrum
Cerebral cortex | motor cortex
97
Cerebral cortex three functions
organizations of complex movement storage of learned experiences (memory) reception of sensory information
98
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
99
Cerebellum main f(x)
coordinates and monitors complex movement by incorporating feedback from proprioceptors
100
Cerebellum has connection to what 4 areas?
Motor cortex mid brain brain stem spinal cord
101
What may cerebellum initiate ?
fast, ballistic movements
102
concussion
brain injury resulting from traumatic force
103
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
104
Central Fatigue by brain role during exercise induced fatique what are involed
Higher brain centers and/or motor neurons
105
Central fatigue what gets depleted?
excitatory neurotransmitters in the motor cortex
106
cental fatigue results in what
reduced motor output to muscle
107
Central govenor theory regulates
central control center regulates exercise performance by reducing motor output to exercising muscle
108
central governor theory protects
against catastrophic disruptions of homeostasis
109
3 motor functions of the spinal cord
Withdrawal reflex, others, and spinal tuning
110
other reflexes vital for
control of voluntary movement
111
spinal tuning is
voluntary movement translated into an appropriate muscle action.
112
higher brain centers do what in spinal tuning
high brain centers concerned w/ general parameters of movement
113
spinal tuning does what w/ movement
details of movement refined in spinal cord
114
subcortical and cortical movement areas send
a "rough draft" of the movement to association cortex
115
Cerebellum and basal ganglia convert
"rough draft" into movement plan
116
cerebellum is responsible for what movement of rough draft?
fast movements
117
Basal ganglia is responsible for what kind of movements?
slow, deliberate movements in rough draft
118
Rough draft from thalamus to motor cortex (motor cortex through thalamus)
Fowards message sent down spinal neurons for "spinal tuning" and onto the muscles
119
motor cortex through thalamus feedback from
muscle receptors and proprioceptors allows fine tuning of motor program
120
First structure in process of voluntary movement and what it does
Subcortical and cortical areas, is the intial drive to move sending rough draft
121
Second structure of voluntary movement is blank and what it does as well
Association cortex Move design of "rough draft"
122
Third structures' involved in voluntary movement and action
Basal ganglia and cerebellum (fast) refine movement design
123
Four structure in voluntary movemnt and action
Thalamus = relay station for spinal tuning
124
5th structure in voluntary movement and action
motor cortex final executor of motor plan
125
last structure in voluntary movement and what it does
motor units execution of desired movement
126
What motivates voluntary movement?
limbic and reticualr formation
127
ANS responsibility
for maintaining internal environ by effector organs not under voluntary control such as smooth and cardiac muscle, and glands
128
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
129
Parasym division releases and this causes
ACh, primarily inhibits effector organ, and after stimulation, ACh is degraded by acetylcholinesterase
130
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
131
regular exs can protect brain against
disease and certain types of brain injury (stroke)
132
exercise improves
brain function and reduces the risk of cognitive impairment associated with aging
133
Regular exercise increases
brain growth factors
134
increased brain growth factors cause brain health to get better in three meaans
cognition neurogenesis vascular function
135
Human body contains over how many skel muscles?
600
136
what percentage of total body weight is skel muscles?
40-50%
137
4 functions of skel muscle
force production for locomotion and breathing force production for postural support protection heat production during cold stress
138
Flexor muscle actions
decreases jt angle
139
extensors muscle actions
increases joint angle
140
epimysium
surrounds entire muscle, outside layer
141
perimysium surronds
bundles of muscle fibers, fascicles
142
Endomysium surrounds
individual muscle fibers
143
basement membrane of muscle
just below endomysium, is eplithelial tissue
144
sarcolemma
muscle cell plasma membrane
145
Satellite cells
undifferentiated cells
146
undifferentiated cells
immature
147
satellite cells reside in
basement membrane between sarcolemma and endomysium
148
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
149
Myonuclear domain
cytoplasm surrounding each nucleus, and each nucleus can support a limited myonuclear domainq
150
More nuclei potentially allow for what?
greater protein synthesis of actin and myosin via DNA in nucleus
151
what adaptations are satellite cells vital for?
strength training adapts
152
Myofibrils contain
contractile proteins; actin and myosin
153
actin
thin
154
myosin
thick filament, heads bind to actin
155
Sarcomere includes
Z line, M line, H zone, A band, and I band
156
SR
storage sites for Ca2+ | Terminal cisternae
157
NMJ
Junction btwn motor neuron and muscle fiber
158
motor unit
motor neuron and all fibers it innervates
159
Motor End Plate
Pocket formed around motor neuron by sarcolemma
160
Neuromuscular celft
short gap between neuron and muscle fiber
161
ACh is released from
the motor neuron
162
When ACh is released from motor neuron, it causes an
EPP (end plate potential)
163
EPP
depolarization of muscle fiber as sarcolemma becomes permeable to a Na+ if threshold value achieved
164
Sliding filament model aka
swinging lever-arm model
165
Muscle shortening occurs due to the movement of the actin filament over the
myosin filament
166
Formation of
cross-bridges btween actin and myosin filaments
167
power stroke
cross bridging
168
Reduction in dist btw Z lines of the sarcomere
contraction
169
Actin Has 2 vital proteins called
tropmyosin and troponin
170
Myosin filaments have tiny what
protein projections on each end that extend towards the actin filaments; crossbridges
171
5 steps in sliding filament theory
``` Rest Excitation-coupling contraction recharging relaxation ```
172
Write out how muscle contracts
do it guy
173
In the center of the sarcomere, the thick filaments lack what?
myosin heads
174
WHere are myosin heads present?
They are only present in areas of myosin-actin overlap.
175
Myosin thick filament
Each thick filament consists of many myesin molecules whose heads protrude at opposite ends of the filament
176
Actin thin filament consists of
2 strands of actin subunits twisted into a helix plus 2 types of regulatory proteins (troponin and tropomyosin)
177
What happens at resting step of sliding filament theory?
Troponin and tropomyosin prevent actin/myosin crossbridging
178
What is required for a muscle contraction ?
ATP
179
What breaks down ATP for muscle contraction?
myosin ATPase | ATP--> ADP + Pi
180
3 sources of ATP
PC Glycolysis Oxidative phosphorylation
181
During excitiation-contraction coupling phase what is being depolarized?
Depolarization of motor end plate (excitation) is coupled to muscular contraction
182
excitation-contraction coupling AP travels down
Transverse Tubules and causes release of Ca++ from SR
183
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
184
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
185
First step in excitation of contraction
AP in motor neuron causes release of ACh into synaptic cleft
186
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
187
First step in contraction phase of excitation-contraction coupling
At rest, myosin crossbridges in weak binding state
188
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
189
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
190
4th step in contraction phase of excitation-contraction coupling
ADP released from myosin
191
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
192
pivoting action of the myosin heads referred to as a
power stroke
193
Muscle Fatigue definition
decline in muscle power output due to decrease in force generation and in shortening velocity
194
Muscle fatigue two characteriscs
force generation and shortening velocity
195
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
196
Long duration of high intensity exercise is due to?
Muscle factors that include acculmation of free radicals, electrolyte imbalance, and glycogen depletion
197
Muscle cramp def
spasmodic, involuntary muscle contractions
198
Muscle cramp cause theories (2)
Electrolyte depletion and dehydration theory | Altered Neuromuscular control theory
199
Electrolyte depletion and dehydration theory for muscle cramps
Water and Na+ loss via sweating causes spontaneous muscle contractions
200
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
201
Biochem props of muscle fibers
Oxidative capacity and type of myosin ATPase
202
oxidative capacity
of capillaries, mitochondria, and amount of myoglobin
203
type of myosin ATPase
speed of ATP degradtion
204
Contractile properties of muscle fiber types
maximal force production, speed of contraction (Vmax), and muscle fiber efficiency
205
Maximal force production
force per unit of cross-sectional area
206
speed of contraction (Vmax)
myosin ATPase activtiy
207
Type I fibers appear
darkest stains of myosin ATPase
208
Type IIa fibers appear
lightest staining of myosin ATPase
209
Type IIx fibers appear
inbtwn light and dark stains of myosin ATPase
210
Immunohistochemical stainining
selective antibody binds to unique myosin proteins, and fiber types differentiated by color diff
211
Gel Elctrophoresis
ID myosin isoforms specific to different fiber types
212
Nonathletes have how much of percent of each fiber?
50% slow and 50% fast
213
Power athletes such as sprinters have higher percentage of what fibers?
fast fibers
214
Endurance athletes have higher percentage of
slow fibers
215
Isometric muscle action
muscle exerts force without changing length
216
pulling against moving object is what kind of muscle action?
isometric
217
Postural muscles are what kind of muscle action?
isometric
218
dynamic muscle action is also known as
isotonic
219
2 types of isotonic/dynamic muscle actions
concentric/shortening-contraction | eccentric
220
concentric muscle contraction
muscle shortens during force production
221
Eccenctric
muscle produces force but length increases
222
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
223
Muscle twitch
contraction as the result of a single stimulus
224
Latent period of muscle contraction
5 ms
225
Contraction aspect of muscle twitch is when what is developed?
tension for 40 ms
226
relaxation in muscle twitch
50 ms
227
Speed of shortening is greater in .. . ? Why?
fast fibers | SR releases Ca++ @ faster rate and higher ATPase activity
228
Force regulation of muscle 3 factors
Types and numbers of motor units recruited Initial muscle length Nature of the neural stimulation of motor units
229
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
230
Initial muscle length
"Ideal" length for force generation (perpendicular jt angle) | Increased cross-bridge formation
231
Nature of neural stimulation of motor units depends on
frequency of stimulation
232
3 aspects of frequency of stimulation
Simple twitch Summation Tetanus
233
Less than optimal length for length tension relationship in skel muscles
fewer cross-bridge interactions = reduced tension development
234
optimal length for length-tension relationship in skel muscle
Maximal cross-bridge interaction = maximal tension dvp
235
Greater than optimal length for length-tension relationship
No cross-bridge interxn = no tension dvpment
236
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)
237
According to the force-velocity relationship, the maxima velocity of shortening is
greatest at the lowest force and is true for both fibers
238
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.
239
Sarcopenia
loss of muscle mass with aging
240
With aging there is loss of ______ fibers and a gain of _____
fast fibers and gain in slow fibers
241
What can delay age-related muscle mass?
resistance training
242
Diabetes associated with
progressive loss of muscle mass
243
Diabetes combined with
age-related loss
244
What can protect people with diabetes
aerobic and resistive training
245
Cancer causes
cachexia
246
cachexia
rapid loss of muscle mass
247
Cachexia from cancer results in
weakness, accounts for 20% deaths in cancer patients
248
Regular exercise and nutrition therapy may counteract what
cachexia
249
regular exercise stimulates
protein synthesis
250
Muscular dystrophy
hereditary defects in muscle protein
251
MD results in
loss of muscle fibers and weakness
252
Duchene muscular dystrophy is most common in
childhood
253
DMD progression
varies based on specific disease type
254
The circulatory works with the
pulmonary/ respiratory sys
255
Purposes of the cardiorespiratory sys
Transport O2 and nutrients to tissues Removal of CO2 wastes from tissues Regulation of body temperature
256
2 major adjustments of blood flow during exercise
Increased CO/Q | Redistribution of blood flow
257
Heart creates (its job)
pressure to pump blood
258
Arteries and arterioles carry blood
away from the heart
259
capillaries job
exchange of o2, co2, wastes, and nutrients with tissues
260
Veins and venules carry blood
toward the heart | ______
261
Pulmonary circuit is what side of the heart?
right side of the heart
262
Pulmonary circuit pumps what kind of blood to where via what?
Pulmonary pumps deoxygenated blood to the lungs via the pulmonary arteries*
263
Pulm circuit returns
oxygenated blood to the left side of the heart via pulmonary veins*
264
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
265
systemic circuit is what side of heart
left side of heart
266
systemic circuit pumps
oxygenated blood to the whole body via arteries
267
systemic circuit returns
deoxygenated blood to the right side of the heart via veins
268
Heart wall consists of these 3 layers
epicardium myocardium endocardium
269
Wall of heart receives blood supply via ____ and has high demand for _____ and ______
coronary arteries | high demand for o2 and nurtrients
270
Myocardial infarction is what?
MI is a blockage in coronary blood flow results in cell damage
271
Exercise training does what for MI?
EXs training protects against heart damage during MI
272
How does exercise training protect heart during MI?
Angiogenesis
273
Epicardium is what anatomical landmark as well
visceral pericardium
274
Epicardium characteristics
serous membrane including blood capillaries, lymph capillaires, and nerve fibers
275
Function of Epicardium
serve as lubricative outer covering
276
Myocardium characteristics
cardiac muscle tissue seperated by connective tissues and including blood capillaires, lymph capillaries, and nerve fibers
277
Myocardium F(x)
provides muscular contractions that eject blood from the heart chambers
278
endocardium characteristics
endothelial tissue and a thick subendothelial layer of elastic and collagenous fibers
279
endocardium f(c)
serves as protective inner lining of the chambers and valves
280
Are contractile proteins: actin and myosin found in both the heart and skeletal muscles? Yes or no, eh
Yes
281
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
282
What is the difference between skel and heart muscle amount of nuclei?
Heart muscle : single nuclei | Skel muscle: multinucleated
283
Do both heart and skel muscles have Z discs? yes
yes
284
are both heart and skel muscle striated?
yes
285
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.
286
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.
287
HEART muscle energy production
aerobic primarily
288
skel muscle energy production both
aerobic and anerobic
289
Ca2+ source for contraction for both muscles and any diff?
both have SR, but heart also gets extracellular Ca++
290
Neural control of the heart muscle is
nonvoluntary
291
Neural control of the skel muscle is
voluntary
292
Regeneration potential in heart muscle?
None- no satellite cells present
293
Regeneration potential in skel muscle?
Some possibiliteis via satellite cells
294
Why is regular exercise cardio protective?
reduce incidence of MI | Improves survival from MI
295
Exercise reduces amount of what?
myocardial damage from MI
296
Exercise reduces amount of myocardial damage from MI causes 2 improvements:
Improvements in heart's antioxidant capacity | Improved function of ATP-sensitive K+ channels
297
Cardiac cycle
systole and diastole
298
systole is what phase and what happens
contraction phase | Ejection of blood, 2/3 blood is ejected from ventricles per beat
299
diastole what phase and what happens?
relaxation phase | filling w/ blood
300
At rest, what happens in cardiac cycle?
At rest, diastole is longer than systole
301
During exs, cardiac cycle
During Exercise, both systole and diastole are shorter
302
Diastole pressure changes in ventricles
During diastole, pressure in ventricles is low
303
Diastole and atria
During diastole, the atria are filling with blood
304
diastole and valves
AV valves open when ventricular P is less than atrial pressure
305
systole pressure in ventricles does what
pressure increases/rises
306
systole blood is
ejected in pulmonary and systemic circulation
307
systole and valves
semilunar valves open when ventricular pressure is greater aortic presure
308
Heart first sound lub is what?
closing of AV valves
309
heart second sound dub is what?
closing of aortic and pulmonary valves (semilunar)
310
Arterial blood pressure is expressed as
systolic over diastolic
311
systolic pressure
pressure generatered during ventricular contraction/ systole
312
Diastolic presure in the
arteries during cardiac relaxation
313
Pulse pressure is the
difference btween systolic and diastolic
314
MAP
average pressure n the arteries during cardiac cycle
315
MAP = eqn
DBP + .33x (SBP-DBP)
316
Korotkoff sounds first phase
a clear tapping sound, onset of the sound for 2 consecutive beats is considered systolic
317
Korotkoff sounds second phase
the tapping sound followed by a murmur
318
Korotkoff sounds 3rd phase
a loud crisp tapping sound
319
Korotkoff sounds 4th phase
abrupt, distinct muffling sound, gradually decreasing intensity (pre diastolic)
320
Korotkoff sounds 5th phase
The disapperance of sound, is considere diastolic BP- 2 points below last sound heard
321
Normal BP
<80
322
Pre HTN
120-139/80-89
323
Stage 1 HTN
140-159/90-99
324
Stage 2 HTN
>/= 160/ >/= 100
325
Stage 3 HTN
180/110 to 215/125
326
hypotension
327
HTN bp = to or above
140/90 mm Hg
328
Primary/essential HTN cuase
etiology unkown
329
primary/essential HTN % of HTN
90% of HTN
330
Secondary HTN result of some other
disease process
331
HTN is risk factor for:
LVH Atherosclerosis and MI Kideny Damage stroke
332
Factors that influence ABP
MAP determinatns, short and long term regulation
333
Determinants of MAP
Q | TVR
334
MAP = formula
Q x TVR
335
Short term regulation is what NS
SNS
336
Short term regulation happens with what
baroreceptors in aorta and carotid arteries
337
Increase BP causes baroreceptors to do what?
decrease SNS activity
338
Decrease BP causes baroreceptors to ?
increase SNS activity
339
Long term regualtion of BP is by what organ
kidney and either direct or indirect mech
340
How down kidney regulate long term bp?
via control of blood volume (renin-angiotensin-aldosterone/ diuretics)
341
Renin-angiotensin-aldoseterone is what mechanims?
longterm indirect mechanism
342
Decreased arterial bp causes release of
renin
343
Renin does what
catalyzes conversion of angiotensinogen from Liver to angiotensin I
344
ACE from lungs and endothelial converts
angiotensin I to angiotensin II
345
angiotensin II increases
blood volume
346
How does angiotensin II increase blood volume?
stimulates aldosterone secretion from renal cortex promotes ADH release triggers hypothalamic thirst center
347
Angiotensin II directly increases BP how , and most potent one of these
vasoconstriction
348
5 factors increasing BP
``` blood volume increases HR increases SV increases (Q increases) Blood viscosity increases Peripheral resistance increase (TVR ) ```
349
Contraction of heart depends on
electrical stimulation of the myocardium
350
Components of conduction system
``` SA node AV node AV bundle bundle branches purkinje fibers ```
351
SA node is located over what and does what?
right atrium | pacemaker, initiates depolarization
352
AV node is located where and does what
floor of atria | pass depolarization to ventricles
353
why brief delay at AV node?
Breif delay at AV node allows for ventricular filling
354
Bundle branches where located
to left and right ventricle
355
purkinje fibers located
throughout ventricles
356
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
357
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
358
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
359
4th step in conduction system of heart
AP are carrried by the Purkinje fibers from the bundle branches to the ventricular walls
360
EKG
records the electrical activity of the heart
361
P wave
artrial depolarization
362
QRS complex time afer the P wave
0.10 second after P
363
QRS complex whats really happening hot stuff
Ventricular depolarixation and atrial repolarization
364
T wave is what
ventricular repolarization
365
ECG abnormalities may indicate
coronary heart disease
366
ST-segment depression can indicate what
myocardial ischemia
367
ECG during GXT used to eval
cardiac function
368
GXT and EKG allows person to
observe EKG during exs and changes in BP
369
Atherosclerosis
fatty plaque that narrows coronary arteries
370
atherosclerosis reduces
blood flow to myocardium resulting in myocardial ischemia
371
S-T segment depression suggests
myocardial ischemia
372
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
373
2) Epinephrine/norepinephrine are ___________- acting hormones and will provide glucose in the liver through ____________________ breakdown, instead of gluconeogenesis.
fast-acting | glycogen breakdown
374
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
375
4) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause glucagon release.
Beta-adrenergic | Alpha pancreatic cell
376
5) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause insulin suppression.
alpha-adrenergic | beta
377
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
378
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
379
8) Because trained individuals are more/less sensitive to hormones levels, glucagon levels will change little/greatly in trained people during exercise.
more | little
380
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
381
10) Fatigue can be defined as the inability to maintain _____________________ or ________________________ during repeated muscular contractions.
power output or force
382
Fitness is what ? 2 parts
General health promotion | stresses moderation of activity
383
Performance is what sports?
competitive sports
384
Does performance or fitness require higher dose needed for success?
Performance
385
Fitness is what to performance
Fitness is a secondary benefit of activity
386
performance has many factors affected by what?
fatigue
387
6 sites of fatigue
``` CNS Function Diet Strength and Skill Environment Energy Production Anaerobic Aerobic Energy Production ```
388
Fatigue
Inability to maintain power output or force during repeated muscle contractions
389
Central fatigue
Central nervous system
390
Peripheral fatigue
Neural factors Mechanical factors Energetics of contraction
391
Reduction in motor units activated is what kind of fatigue?
central fatigue
392
Reduction in motor unit firing frequency is what kind of fatigue?
central fatigue
393
Central nervous system arousal can alter the state of fatigue what kind of fatigue By facilitating motor unit recruitment Increasing motivation Physical or mental diversionis this?
central fatigue
394
Serotonin linked to what 3 things?
relaxation, euphoria, arousal suppression
395
Amino acid tryptophan (Trp) is precursor to
serotonin
396
Free (unbound) Trp (f-Trp) shares carrier across
BBB into brain with BCAA
397
Prolonged exercise:
↑ lipolysis; FFAs compete with Trp in binding to albumin; more f-Trp available for transport to brain
398
Hypothesis for prolonged exercise : more BCAA will compete with
f-Trp for transport across BBB; less serotonin synth; less fatigue
399
Peripheral Fatigue: Neural Factors site
Sarcolemma and transverse tubules
400
Sarcolemma and transverse tubules is the ability of muscle
membrane to conduct an action potential
401
Peripheral Fatigue neural factor inability of what pump to do what
Inability of Na+/K+ pump to maintain action potential amplitude and frequency
402
Neural factor for peripheral fatique can be improved by
Can be improved by training
403
An action potential block in the T-tubules | Reduction in Ca+2 release from sarcoplasmic reticulum
neural factor
404
Peripheral Fatigue: Mechanical Factors (3)
Cross-bridge cycling and tension development High H+ concentration may contribute to fatigue Longer “relaxation time” is a sign of fatigue
405
Cross-bridge cycling and tension development depends on:
Arrangement of actin and myosin Ca+2 binding to troponin ATP availability
406
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
407
Longer “relaxation time” is a sign of fatigue Due to
slower cross-bridge cycling
408
Peripheral Fatigue: Energetics of Contraction
Imbalance in ATP requirements and ATP generating capacity Rate of ATP utilization is slowed faster than rate of ATP generation Muscle fiber recruitment in increasing intensities of exercise
409
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
410
Rate of ATP utilization is slowed faster than rate of ATP generation due to
Maintains ATP conc. – protective effect – minimize change in homeostasis!
411
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
412
The Energy Continuum
Energy systems do not “turn on/turn off” | All 3 are working simultaneously at any given time, just at different percentages
413
Ultra Short-Term Performances duration
Events lasting <10 seconds
414
Ultra Short-Term Performances Dependent on recruitment of Type II muscle fibers why?
Generate great forces that are needed
415
Ultra Short-Term Performances what is important?
Motivation, skill, and arousal are important
416
Ultra Short-Term Performances what is energy source?
Primary energy source is anaerobic ATP-PC system and glycolysis Creatine supplementation may improve performance
417
Short-Term Performances duration
Events lasting 10–180 seconds
418
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
419
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
420
Intermediate-Length Performances duration
Events lasting 21–60 minutes
421
Intermediate-Length Performances energy system
Predominantly aerobic Usually conducted at <90% VO2 max High VO2 max is important
422
Intermediate-Length Performances Other important factors
``` Running economy High percentage of type I muscle fibers Environmental factors Heat Humidity State of hydration ```
423
Long-Term Performances duration
Events lasting 1–4 hours
424
Long-Term Performances energy system
Clearly aerobic
425
Long-Term Performances and VO2max
High VO2max not as important
426
what is is vital for long-term performances?
Environmental factors more important
427
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
428
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
429
long term Performance also determined by:
%VO2 max at which runner can perform Estimated by the lactate threshold Running economy
430
Training program should match the
anaerobic and aerobic demands of the sport
431
Overload
Increased capacity of a system in response to training above the level to which it is accustomed
432
Specificity
Specific muscles involved | Specific energy systems that are utilized
433
Reversibility
When training is stopped, the training effect is quickly lost
434
Men and women respond
similarly to training programs
435
Exercise prescriptions should be
individualized
436
Training improvement is always greater in individuals
with lower initial fitness
437
50% increase in VO2 max in
sedentary adults
438
10–15% improvement in
normal, active subjects
439
3–5% improvement in
trained athletes
440
1-2% improvement in
elite athletes
441
Genetics plays an important role in
how an individual responds to training
442
Åstrand and Rodahl: quote
“If you want to become a world-class athlete, you must choose your parents wisely.”
443
Anaerobic capacity is more genetically determined
than aerobic capacity
444
Training can only improve anaerobic performance to
a small degree
445
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
446
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
447
Workout
Training session
448
Cool-down
Return blood “pooled” in muscles to central circulation | Reduce hypotensive response
449
Aerobic power: measure determined by
VO2max | Determined by max cardiac output, a-v O2 diff
450
Training to Improve Aerobic Power
Long, slow distance High-intensity, continuous exercise High-intensity interval training (HIIT, which includes supramaximal sprint interval training (SIT)
451
Aerobic power should be geared toward improving:
VO2 max Lactate threshold Running economy
452
Long, Slow Distance benefits
economy, VO2max
453
Long, Slow Distance intensity
Low-intensity exercise | 50-60% VO2 max or 70% HRmax
454
Long, Slow Distance duration
Duration greater than would be expected in competition
455
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
456
High-Intensity, Continuous Exercise appears to be what?
Appears to be the best method of increasing VO2 max and lactate threshold
457
High-intensity exercise
At or slightly above lactate threshold 80–90% HRmax ≥90% HRmax or 95% HRR also suggested
458
High-Intensity, Continuous Exercise duration
Duration of 25–50 min | Depending on individual fitness level
459
High-Intensity Interval Training Benefits
Benefit: lactate and H+ clearance
460
High-Intensity Interval Training are
Repeated exercise bouts | Separated by brief recovery periods
461
High-Intensity Interval Training Work effort
(repetition) Distance to be covered Intensity: 85–100% HRmax Duration: >60 seconds to improve VO2 max
462
High-Intensity Interval Training Rest interval
Light activity such as walking | 1:1 ratio of work to rest; can be up to 1:3
463
High-Intensity Interval Training Number of interval sets and repetitions depends on
Depends on purpose of training and fitness level
464
Supramaximal Sprint Repeats are % vo2max
100-150% VO2max
465
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
466
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
467
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
468
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
469
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.
470
The “Live-High, Train-Low” altitude training program provides significant
endurance performance gains compared to training and living at sea level.
471
Most injuries are a result
of overtraining Short-term, high-intensity exercise Prolonged, low-intensity exercise
472
The “ten percent rule” for increasing training load
Increase intensity or duration ≤10% per week
473
Other injury risk factors
``` Strength and flexibility imbalance Footwear problems Malalignment Poor running surface Disease (arthritis) ```
474
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
475
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
476
Strength Training Adaptations
Increased muscle mass Conversion of IIx to IIa fibers Central nervous system changes
477
Hypertrophy
Increased muscle fiber diameter | Responsible for most of the increase in muscle size
478
Hyperplasia
Increased number of muscle fibers
479
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” ```
480
Delayed onset muscle soreness (DOMS) occurs
Appears 24–48 hours after strenuous exercise
481
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
482
What type of exercise/ contraction causes DOMS?
Eccentric exercise causes more damage than concentric exercise
483
How to avoid DOMS?
Slowly begin a specific exercise over 5–10 training sessions to avoid DOMS
484
Why more damage with eccentric exercise?
More force production Due to LESS cross bridge detachment throughout the contraction More attachment = more force production
485
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
486
A bout of unfamiliar exercise results
in DOMS
487
Following recovery, another bout of same exercise results
in minimal injury
488
Theories for the repeated bout effect
Neural theory Connective tissue theory Cellular theory
489
Neural Theory
Recruitment of larger number of muscle fibers
490
Connective tissue theory
Increased connective tissue to protect muscle
491
Cellular theory
Synthesis of protective proteins within muscle fiber
492
Overtraining not overload
Workouts that are too long or too strenuous | Greater problem than undertraining
493
Performing non-specific exercises do not
enhance energy capacities used in competition
494
Failure to schedule a long-term training plan results in
Misuse of training time
495
Failure to taper before a performance results in
Inadequate rest; compromises performance
496
Common Training Mistakes
``` Overtraining Undertraining Performing non-specific exercises Failure to schedule a long-term training plan Failure to taper before a performance ```
497
Overtraining SX
``` Decrease in performance loss of BW Chronic fatigue increased number of infections psychological staleness Elevated HR and blood lactate levels during EXS ```
498
Tapering
Short-term reduction in training load prior to competition
499
Tapering allows what?
Allows muscles to resynthesizes glycogen and heal from training-induced damage
500
Tapering Improves performance in both
strength and endurance events | Athletes can reduce training load by 60% without a reduction in performance