Final Exam Flashcards
L12-28 (198 cards)
1
Q
when do glycolysis and glycogenolysis occur in comparison to each other
A
- at the same time ALWAYS
2
Q
how much ATP is stored in the body
A
- only 80-100g
- lasts for about two seconds
3
Q
how do energy needs change during exercise
A
- increase 100x
- there are minimal changes to concentration of ATP
4
Q
what is the immediate system for ATP resynthesis
A
- 8-15 seconds of exercise
- kicks in as soon as muscles are contracted
- ATP is hydrolyzed to ADP +pi + H+ (these byproducts plus Ca2+ activate CK enzyme)
- CK accelerates breakdown of PCr
- PCr gives a Pi to ADP to make ATP
5
Q
how can carbohydrates generate ATP
A
- both anaerobically and aerobically
- only macronutrient that can do both
6
Q
What is glycolysis
A
- process in which one glucose molecule turns into 2 pyruvate molecules for cellular respiration to continue
-glucose brought into the cell via GLUT1 and GLUT4
-NAD+ goes in NADH comes out
-2 ATP produced
-pyruvate produced
7
Q
where does glycolysis occur
A
- inside of the cell (cytosol)
- not in the mitochondria
8
Q
what is the glycolytic system (anaerobic metabolism)
A
- glycogenolysis
- glycolysis
- lactate production
9
Q
Where is carbohydrate available from during exercise
A
- blood
- muscle
- liver (to muscle via blood)
- ingested (from digestion to muscle via blood)
10
Q
how does glucose enter a muscle cell
A
- glucose transporter 4 (GLUT4)
-transport protein
-specific to muscle cells
-follows concentration gradient (facilitated diffusion)
-insulin sensitive
11
Q
what does Hexokinase (HK) do
A
- converts glucose to glucose-6-phosphate (G6P)
- G6P cannot leave the cell so glucose is now trapped (irreversible reaction)
- ATP is hydrolyzed to ADP, Pi, H+ and the Pi attaches to glucose to produce G6P
12
Q
what two things can happen to G6P after HK converts glucose to G6P
A
- undergoes glycolysis - when doing PA
-phosphoglucomutase converts G6P to G1P - stored at glycogen - at rest
-glycogen synthase converts G1P to glycogen
13
Q
what is phosphofructokinase
A
- rate limiting enzyme
- activated by ADP, AMP, Pi, G6P because that would indicate you are doing PA
- inhibited by ATP and H+
14
Q
what is glycogen phosphorylase (PHOS)
A
- rate limiting enzyme
- increased activity vis Ca2+, AMP, Pi, EP
- decreased activity via H+, ATP, G6P
- catalyses glyocogenolysis
15
Q
what is glycogenolyis
A
- occurs in sarcoplasm
- glycogen breaks down G1P
- Yields 3ATP
-1 required, 4 produced
16
Q
what are the two glycolysis pathways
A
- anaerobic
- aerboic
17
Q
what are the trademarks of aerobic glycolysis
A
- O2 present
- slow
- high ATP production
- product is pyruvate to continue through to the mitochondria
18
Q
what are the trademarks of anaerobic glycolysis
A
- no o2 present
- fast
- low ATP production
- product is lactate
19
Q
how is lactate produced
A
- process called lactate dehydrogenase (LDH)
- when pyruvate and NADH+H+ accumulate lactate is formed
- they accumulate when there is a mismatch between glycolytic rate and capacity of mitochondria to accept pyruvate
20
Q
how is lactate removed
A
- goes into the bloodstream
- goes to brain, liver, heart to be used as fuel
21
Q
what exercise intensity does lactate get produced at
A
- all
- exponentially increases about 80% exertion
22
Q
does lactate cause fatigue?
A
- no - just buffers the acidity
- it is produced when ATP demand > aerobic metabolism ATP supply so fatigue is felt with it
23
Q
what happens to each of the energy systems during a 30 second maximal intensity workout
A
- PCr declines
- glycolysis declines
- oxidative phosphorylation increases
24
Q
how much glycogen is stored in the muscles and liver, and how much glucose is stored in the blood?
A
- Muscle glycogen = 500g
- liver glycogen = 80 g (hard to access)
- blood glucose = 5g
25
what percentage of a muscle cell is mitochondria
4-10%
26
what happens to pyruvate as it enters the mitochondria
- goes into mitochondrial matrix
- pyruvate is converted into acetyl-coA and co2
- once converted its trapped in the mitochondria
- process used PDH
- NAD+ gets converted to NADH and H+
27
what is pyruvate dehydrogenase (PDH)
- PDH reduces the levels of lactate
- PDH controls the rate of carb entry to the mitochondria
- PDH is activated by Ca2+
- PDH is deactivated by acetyl-coA, ATP, NADH
28
what is an enzyme
- a protein that speeds up a chemical reaction
29
what is a coenzyme
- a non protein substance that is required for an enzyme to catalyze a reaction
- coenzymes by themselves cannot catalyze a reaction
30
what are the two coenzymes used for ATP production
- NAD+ or NADH and H+
- FAD or FADH2
- they are electron transporters
31
what is the citric acid cycle (TCA)
- activated by Ca2+, ADP, NAD+
- oxaloacetate is reformed each cycle
- ADP goes in ATP comes out
- NAD+ goes in NADH comes out
- FAD goes in FADH2 comes out
- CO2 exits
32
what happens in the electron transport chain (ETC)
- COMPLICATED COME BACK
33
how much ATP comes from 1 NADH
- 2.5 ATP
34
1 FADH2 = ? ATP
1.5 ATP
35
when is a low carb diet good
- after training
- good for mitochondrial biogenesis
36
what does a low carb diet impair
- high intensity exercise performance
- especially if continued for multiple days
37
what amount of carbs classifies high/low
- ketogenic diet = <50g/day
- low-carb diet = 150-200g/day
- moderate carb diet = 200-400g/day
- high carb diet = >400g/day
38
what are triglycerides
- the only lipid that is a major source of energy (ATP) for muscle
- has glycerol backbone and 3 FFA tails
- connected via three ester bonds
39
what is lipolysis
- break down of triglycerides
- releases the attached FFA from the glycerol backbone
- H2O is added (hydrolysis) to break the C-O bond
40
how are FFA carried in the blood
- albumin (transport protein)
- enter cells via carrier proteins or facilitated diffusion
41
how is FFA carried in the cell
- chaperoned by fatty acid binding protein (FABP)
42
what happens to FFA once in the cell in order to enter the mitochondria
- must be converted into fatty acyl-coA
- requires 2 ATP
- once converted it is considered the active form and cannot leave the cell
43
what is the carnitine shuttle
- essential to transfer long chain fatty acetyl coA across the inner mitochondrial membrane
44
what is beta oxidation
- converts fatty acyl coA into acetyl coA
-1NAD+ in 1NADH, H+ out
- FAD in FADH2 out
- coenzyme A added
45
what determines the number of cycles for beta oxidation
- carbon length/2 -1
* shrinks by 2 C each cycle
46
what is P/O ratio
- ATP per oxygen
47
what is the P/O of carb oxidation
- 2.67
48
what is the P/O of fat oxidation
2.31
49
why are women more aerobically predisposed than men
- more oxidative muscle profile
- 7-23% more type I muscle fibers
- oxidate more fat and less carbs
- slower muscle relaxation
- lower rates of sarcoplasmic reticulum Ca2+ ATPase activity
- higher capillary density
50
What is VO2
- oxygen uptake
- a rate measured in L/min or mL/min
51
what is VCO2
- carbon dioxide production
- a rate measured in L/min or mL/min
52
what is respiratory exchange ratio (RER)
- carbon dioxide produced/oxygen consumed
- RER = Vco2/VO2
53
what does an RER of 1.0 mean
- carbohydrate is the fuel
54
what does an RER of 0.71 mean
- lipid is the fuel source
55
what influences substrate oxidization
- exercise intensity
- exercise duration
- substrate availability
- sex
- training status
56
for what exercise intensity is fat the major fuel source
- resting state to 60/65% of VO2 max
- fat oxidation (specifically plasma FF acid)
57
when is carbohydrate oxidation initiated
- at 60-65% VO2 max
58
where does maximal triglyceride utilization occur
at 65% of vo2 max
59
What is the influence of carb loading on performance
- NO effect on high-intensity exercise lasting less than 5 minutes
- NO effect on moderate intensity lasting 60-90minutes
- postpones fatigue by 20% in endurance events lasting longer than 90 minutes
60
which sex experiences more fat oxidation during exercise
- females
61
when compared to untrained individuals how do athletes use substrates
- reminder: athletes should perform a task at a lower relative exercise intensity (%vo2 max)
- derive a lower percentage of energy from carbs and higher energy from lipid sources
62
what is the advantage of lipid oxidation
- more cals/g
63
what controls hormone secretion
- activation of NS
- chemical stimuli (release of ion, NT, change in substrate)
- another hormone
64
what is the control of hormone secretion during exercise
- increased sympathetic activation/decrease parasympathetic activation
- decreased plasma glucose
- increased growth hormone
- pancreatic islet beta cells are targeted to decrease insulin secretion
65
what is the control of hormones during rest
- Decreased sympathetic activation/increased parasympathetic activation
- high plasma glucose
- increased growth hormone
- pancreatic islet beta cells are targeted to increase insulin secretion
66
what are the important catabolic hormones
- epinephrine/norepinephrine, cortisol, growth hormone, glucagon
- they increase in response to exercise
- they mobilize fat and preserve carb
67
what is the important anabolic hormone
- insulin
- decreases in response to exercise
- stores fuels and lowers blood glucose
68
what is the role of EP and NEP during exercise
- tells the liver to convert glycogen to glucose
- tells adipocyte to convert triglycerides to FFA +glycerol
- tells tissues to increase FFA oxidation
- glucose entry to the muscles is reduced (insulin antagonism)
69
which hormones are counter-regulating
- insulin and glucagon
- do opposite things
- the ratio of glucagon to insulin controls the mobilization of glucose and FFA
70
what are the two mechanisms for skeletal muscle glucose uptake
- both involve GLUT4 translocation to the membrane
- muscle contractions and mechanical stress (increased Ca2+ and AMP) cause GLUT4 to translocate onto cell membrane so that glucose can enter the cell
71
what is the role of insulin
- mediates the entry of glucose into most cells (increases diffusion vis GLUT4)
- increases muscle protein synthesis and decreases muscle protein breakdown
- Increases FFA and triglyceride synthesis in adipose tissue and liver
- increases glycogen synthesis and decreases glycogenolysis in the liver and muscle
72
what are the benefits of decreased plasma insulin during exercise
- maintain the level of plasma glucose and prevent a decline in plasma glucose
- mobilization of glucose and FFA and adipocytes
- decrease chronic insulin resistance
73
what is lipolysis increased by
- increased EP
- increase NEP
- increased cortisol
- increased growth hormone
- decreased insulin
74
how is mitochondrial density increased
training
75
how long does it take to increase mitochondrial density
- adaptations will occur after 1 month of training
- need 2hr/day everyday
76
how do skeletal muscles adapt to training
- mitochondria- increases in number, volume, size and enzyme content
- changed substrate utilization- reduced carb use and increased fat use
- reduced lactate production/ increased lactic threshold
77
what happens to carb oxidation with training
it reduces
78
what happens to fat oxidation with trainin
it increases
79
what happens to lactate threshold with training
- shifts to higher power output
- right shift
- is higher
80
what happens to glucose at rest, early exercise and late exercise
- Rest: extra glucose is converted to glycogen and there are very few GLUT4 proteins at the level of the cell membrane
- with early exercise, translocation of GLUT4 occurs due to muscle contraction and this increases the number of GLUT4 at the cell membrane. Facilitates glucose influx but sise glycogen gets broken down there is low demand on plasma glucose
- with late exercise: translocated GLUT4 proteins remain on the cell membrane and help to reduce the necessity of insulin secretion. Prevents insulin resistance
81
what is the total partial pressure exerted by a gas equal to
- the sum of the partial pressures of each individual gas in the mixture
82
what is atmospheric pressure at sea level
760mmHg
83
what is the concentration and partial pressure of nitrogen
- concentration: 79.03%
- Partial pressure: 600mmHg
84
what is the concentration and partial pressure of Oxygen
- concentration: 20.93%
- Partial pressure: 159.1mmHg
85
what is the concentration and partial pressure of carbon dioxide
- concentration: 0.03%
- Partial pressure:0.3mmHg
86
what is gas exchange
- exchange of gasses (in body this means o2 and co2)
- o2 moved from environment to mitochondria
- co2 moved from mitochondria to environment
87
how does gas exchange occur
- via diffusion
- each gas follows its concentration gradient
88
where does gas exchange occur
- lungs to blood
- blood to tissues
89
diffusion vs perfusion
- diffusion: moving from high to low concentration often through membranes
- perfusion: flowing (like in the blood)
90
how does the partial pressure of oxygen change throughout the body
- Inspired air: 159 mmHg
- alveolus: 100 mmHg
- arterial blood: 100 mmHg
- skeletal muscle: 40 mmHg
- venous blood: 40 mmHg
91
How does the partial pressure of CO2 change throughout the body
- Inspired air: 0.3 mmHg
- alveolus: 40 mmHg
- arterial blood: 40 mmHg
- skeletal muscle: 46 mmHg
- venous blood: 46 mmHg
92
what happens to atmospheric air as it is moved to the trachea
- the air is humidified
- Po2 goes from 159 to 149 mmHg
- when air is humidified it now is the volume of gas and water
- PP of H2O is 47mmHg (constantly)
- this means we subtract 27 mmHg from the total pressure of 760 before multiplying by the O2 constant
93
what happens to air from the trachea to the alvelus
- in the alveoli, the concentrations of each gas is changed
-O2 20.9% - 14.5%
- CO2 0.03% - 5.5%
- N 79.03 - 80%
- this is because CO2 continually enters the alveoli from the blood
- PP from 149 to 103 mmHg
94
what happens to o2 content from the alveoli to the arterial blood
- PP goes from 103 to 100 mmHg
- due to shunting (anatomical structures that makes some blood more difficult to reoxygenate)
- some alveoli are poorly ventilated
95
what happens to PP of O2 between arterial and capilaries
from 100 mmHg to 40 mmHh
- due to shunting
96
What happens to PO2 from capillaries to mitochondria
- from 40 - 2-3mmHg
- because oxygen is actively being consumed here
- steep gradient allows mitochondria to constantly receive more O2
97
what are all of the important PO2
- atmosphere 159 mmHg
- trachea 149 mmHg
- alveolar 103 mmHg
- arterial 100 mmHg
- mean capillary 40 mmHg
- mitochondria 2-3 mmHg
98
what PO2 values remain unchanged with exercise
- atmospheric
- tracheal
- alveolar
- arterial
- increased ventilation (Ve) offsets increased O2 uptake (Vo2)
** Arterial side constant
99
what respiration values do change with exercise
- venous Po2 decreases more (around 15 mmHg with intense exercise) - more o2 taken up by the muscles
- venous Pco2 increases more (around 60 mmHg with intense exercise) - more co2 produced by muscles
** venous side is exercise dependent
100
what is the arteriovenous oxygen difference
- difference between the o2 content of arterial blood and mixed venous blood
- a-vo2 difference
101
what is the oxygen content and saturation of blood leaving the lungs
- 16 to 24 mL/100mL blood
- saturation of 95-98%
102
what is the a-vo2 difference at rest
- 4-5mL/100mL
- 25% of o2 uptake
103
what is the a-vo2 difference during intense exercise
- 15 to 20 mL/100mL blood
- 75-100% of o2 uptake
104
how does blood carry co2
- dissolved in solution: 10% total, 5% plasma and 5% RBCs
- transported as bicarbonate: 65% total
- carbamino compounds: 25% total, 5% plasma and 20% in RBC
105
make fc off of the co2 diagrams l19 s 6,7
106
what are the buffer systems and why are they important
- they resist changes in pH
- chemical buffers: bicarbonate, protein (hemoglobin), phosphate
- physiological buffers: ventilatory
107
what is ventilatory regulation of pH
- increasing ventilation lowers PAco2 allowing more co2 to diffuse into the lung and to be exhales
108
what is hemoglobin
- main carrier of o2
109
is hemoglobin always 100% saturated with o2
- no
110
what determines arterial saturation
- arterial Po2
- this concept directly determines how much hemoglobin is bound to oxygen
111
what is the relationship between Pao2 and Sao2
- s-shaped
- increased o2 availability increases the affinity of hemoglobin to o2
112
what is the haldane effect
- left shift or increased affinity for o2
- more binds even with less avaliable o2
113
what is the bohr effect
- right shift or decreased affinity
114
what causes the haldane effect (left shift)
- increased pH
- decreased temo
- decreased co2
115
what causes the bohr effect (right shift)
- decreased pH
- increased temp
- increased co2
116
what are neural factors of ventilatory control
- predominantly active during exercise
- there are neural inputs related to movement
-motor cortex (voluntary movements)
-stretch receptors in lungs and airways (mechanoreceptors)
-proprioceptors in muscles, joints, tendons
- the intrinsic firng of the respiratory center is also a neural input
-fight or flight/emotional status
117
what are humoral factors of ventilatory control
- predominant at rest
- central chemoreceptors (in medulla responds to decreased pH and increased co2)
- peripheral chemoreceptors (in aortic and carotid bodies decreased PO2, decreased pH and increased co2) - monitors arterial blood
- vagal tone is also important for rest - from a neural factor
118
what are the phases of ventilation in response to constant load exercise
- anticipation is neural
- exponential (increase as u start exercise) is neural and humoral
- steady state is both
- recovery is neural first (vagal tone initiates), humoral second (Paco2 and H+)
119
does ventilation limit performance in untrained individuals?
- NO
- their respiratory system is overbuild for the capacity of their cardiovascular and muscle systems
120
does ventilation limit performance in trained individuals?
- YES
- adaptations from training are primarily in the mitochondria
- lungs become the limiting factor
121
what are the components of the cardiovascular system
- pump = heart
- high pressure circuit = arteries and arterioles
- exchange vessels = capillaries
- low pressure circuit = veins and venules
- fluid = blood
122
what is the velocity of blood flow related to
- inversely related to the total cross sectional area (CSA) of blood vessels
- causes a u-shaped velocity of blood flow where it is the slowest in the capillaries to allow for adequate nutrient exchange
123
why does blood speed up in the veins (even tho they are low pressure)
- skeletal pumps
- respiratory pump
- increased diameter of veins
124
what is myocardium structure
- fibers are shorter than skeletal muscle
- homogenous type I (cant fatigue)
- fibers are connected end to end by and intercalcated disk
- there are to satellite cells in myocardium (dont want fiber type to change)
125
what are the mechanics of myocardium
- cardiac muscle contractions are involuntary
- calcium-induced calcium release
126
how does the myocardium generate electrical signals
- internally (there are no motor endplates around)
- due to anatomical coupling with gap junctions
127
which specialized cells coordinate the hearts excitations
- sinoatrial (SA) node
- atrioventricular (A) node
- AV bundles of his
- purkinje fibers
128
why is there a delay between the AV node to AV bundle
- allows blood from atria to fully drain to ventricles
129
what are the 3 things that contribute to extrinsic control of heart rate
- parasympathetic NS
- sympathetic NS
- endocrine system
130
parasympathetic NS role on HR
- originate from medulla oblongata
- vagus nerve sends signals to SA and AV nodes and releases ACh
- vagal tone sets HR around 60-80bpm
131
Sympathetic NS role on HR control
- increases the rate of depolarization of SA node
- increases HR
132
what is the endocrine system role on HR control
- EP and NEP from adrenal glands and triggered by sympathetic stimulation during stress
133
what is diastole
- relaxation phase
- ventricles fill with blood
- passive flow 70% and contraction of atria 30%
- 2x as long as systole
134
what is systole
- contraction phase
- ventricles contract
- eject blood into aorta and pulmonary artery
135
which cardiac cycle component gets changed from rest to exercise
- diastole is extremely shortened
136
what is the function of arteries
- establish bulk flow and driving pressure
137
what is the fxn of arterioles
- regulators of blood flow
138
what is stroke volume
- the volume of blood pumped during one beat of the heart
- SV = EDV-ESV
139
what is ejection fraction
- fraction of blood pumped out of the left ventricle relative to the total volume of the left ventricle
- EF = SV/EDV
140
does EF change between trained and untrained individuals
- no, just a fraction of two things that are both smaller than trained individuals
141
what is cardiac output
- total volume of blood pumped by the heart in one minute
- Q = HR x SV
142
what is the fick equation
- VO2 = Q x a-vo2 difference
- product of cardiac output and oxygen extraction
143
why does a-vo2 difference increase with intense exercise
- steady Cao2 - increased ventilation ensures nearly complete arterial saturation
- declining Cvo2 - more o2 used by muscles
144
what does the heart maintain its own rhythm at
100 bpm - which can be adjusted up 25-200 bpm by extrinsic regulation
145
which factor of the fick equation plateaus with exercise and why
- stroke volume (initially increased before plateauing at 30-50% of vo2 max)
- EDV doesnt change much as its just venous return and ventricular distensibility
- ESV doesnt change as it is ventricular contractility and aortic pressure
146
what happens to SV during prolonged constant intensity exercise
- gradual decrease due to water loss (sweat), which also causes increase in HR
147
what is the frank starling law of the heart
- stretching ventricle increases the force of contraction
- greated EDV (within limits) yields greater SV
148
what does vo2 max measure physiologically
- an individuals capacity for aerobic ATP resynthesis
149
how can we measure vo2 max
- ramp incremental
- step incremental
- constant intensity
150
what is the effect of sex on vo2 max
- seen due to the differences in lean body mass between the sex
- if they have the same training, and muscle vs fat vo2 will be the same
151
what happens to vo2 max with age
- declines
- around 8% a decade
152
what happens during moderate intensity exercise (before GET)
- linear increase in o2 consumption
- linear increase in co2 production
- linear increase in ventilation
- metabolic stability
- BL/H+ are consistent
153
what happens between GET and RCP ( heavy domain)
- linear increase in o2 consumption
- nonlinear co2 production (GET)
- Ve increases in a faster rate in relation to increased workload or vo2
- metabolic stability
- BL/H+ are consistent but at a higher level (ie clearance is at equilibrium)
154
what occurs at GET
- co2 and H+ are buffered by bicarbonate causing an increase in co2 production
- activation of glycolytic pathway increases rate of H+ production
155
what happens after RCP
- linear increase in o2 consumption
- nonlinear co2 production (GET)
- hyperventilation can compensate the rise in H+
- no metabolic stability
- BL/H+ exeeds the clearnace
156
RCP and beyond
- nonlinear increase in ventilation compared to co2 production
- to compensate for the decrease in pH =, Ve increases out of proportion to vco2
157
why does ventilation exceed co2 in the severe domain
- H+
158
what is mean response time
- the time that it takes for the adaptations that are occurring at the legs to reach the mouth (air being measured)
- power increasing while vo2 doesnt match it
159
how do you correct for MRT
- left shift
- 10-15W should be subtracted from the RAMP power output
- in all exercise domains
160
what happens if you do not correct for MRT
- exercise intensity will be underestimated
161
what are the reasons for dissociation of vo2 during constant load exercise vs RIT
- the muscle consumes most (>80%) of the additional vo2
- results from increased ATP turnover in muscle fibers
- there is an increased metabolic cost with fatiguing fibers - as type I fatigue you get more type II which use more vo2 for the same power
162
which domains is vo2 slow component important in?
heavy and severe domain
163
why are exercise intensity thresholds important
- prescribe exercise accurately
- predicts exercise performance
164
how long can one be in the severe domain
- seconds to 45 mins
165
how long can one be in the heavy domain
45min-2hr
166
how long can one be in the moderate domain
>2hr
167
what is meant by "thresholds are very individual"
- GET can be 40-80% of vo2 max
- RCP can be 65-95% of vo2 max
- even at the same percentage of vo2 max, individuals are not necessarily feeling the same metabolic stresses
168
how does the slope of RIT impact power output
- no matter how steep, it will be similar for GET
- for RCP a steeper slope will have a higher power output - you dont fatigue as much (shorter)
169
what is critical power
- maximal rate of work that a muscle can do without fatigue (without needing to stop)
- greatest metabolic rate that results in wholly oxidative energy provision
170
what value is critical power (CP) equal to
- RCP or MLSS
171
what is W'
- the shape of the hyperbolic curve under the power/speed vs time graph above CP
- the amount of work that can be performed above critical power
- trained athletes will have greater W'
172
how do you test CP
- need multiple time to task failure exercise visits
- if you needed to do it one session you would have athlete go all out in any activity until failure and the speed/power 30s before failure is CP
173
what muscle fiber type is correlated with high CP
- type I (slow twitch)
174
what muscle fiber type is a high W' associated with
- type IIx
175
what are systemic adaptations in response to aerobic training
- blood volume
- o2 carrying capacity of blood
- cardiac output
176
what are skeletal muscle adaptations in response to aerobic training
- capillarization
- mitochondrial content
177
write slides on adaptations time specific l25 s5-6
178
what is responsive to mechanical deformation and intramuscular metabolic disturbance
- pain sensitive receptors (afferent neurons)
179
what is the effect of a second bout of eccentric exercise after the first bout
- less muscle stiffness and soreness
- this is because the muscle rapidly adapts to avoid further damage
180
What are the 5 steps that lead to DOMS
1. overstretched sarcomeres
2. disrupted sarcomeres
3. E-C coupling distribution
4. local contracture
5. swelling and soreness
181
what are overstretched sarcomeres
- sarcomere inhomogeny
- descending phase of the length tension curve
- weaker sarcomeres are stretched beyond myofilament overlap
182
what is sarcomere inhomogenety
- most of the length is taken by weakest half sarcomeres in myofilament
183
what is the popping sarcomere hypothesis
- uncontrolled extension of individual half sarcomeres in each myofibril
- occurs one at a time from weakest to strongest
184
what is damage to the E_C coupling machinery
- damage would be to t-tubule rupture
- torn tubule ends would be leading to inactivation of some sarcomeres
- fall in muscle tension and force output
185
what is local contracture
- after a period of eccentric exercise there is a rise in passive tension in the muscle
- the potential mechanisms are:
1. increases in resting Ca2+ levels in muscle fibers damaged by eccentric contractions
2. shortening of parallel, non contractile elements in the muscle
186
what is the pain experienced during muscle contractions after eccentric exercise related to
- damage and shortening of the non contractile elements
- damage to the muscle fiber membranes (shown by increased CK enzyme)
- activation of group III/IV afferents
187
what is the repeated bout effect (RBE)
- magnitude of muscle damage in a subsequent exercise bout after performing a single bout of exercise is reduced
188
how long does RBE last
- 6-9 months based on the damage of the initial bout
189
what are the benefits of RBE
- further muscle damage is prevented
- the recovery of muscle strength is accelerated
- less soreness
190
contractions performed at a longer muscle length result in ________ symptoms of damage
greater
191
what happens when recovering from eccentric contraction induced muscle damage
- additional sarcomeres in series are created in muscle fibers
- causes a shift in the length tension curve toward longer lengths
- the tension declined with increasing length could be avoided - less sarcomere disruption
192
what are the three main predictors of performance in endurance events
1. vo2 max
2. % of vo2 max associated with LT
3. Efficiency (economy)
193
from order of greatest to least, what is adaptable about the cardiovascular system
PERIPHERY
- skeletal muscles
- o2 carrying capacity
- cardiac output
- pulmonary diffusing capacity
CENTRAL
194
what determines endurance performance in heterogenous groups
- vo2 max
195
what determines endurance performance in homogenous groups
- running economy
- or who utilizes less o2 for a given speed or power
196
what is the effect of having a LT at a higher percentage of vo2 max
you can do the same activity before producing unmanageable blood lactate making exercise more manageable
197
if you induce mental fatigue before the cycling exercise, the RPE will ____________ during the cycling task and the time to task failure will be ________ compared to the control condition
increase, decrease
198
if you induce left leg fatigue followed immediately by the right leg cycling exercise (called pre induced fatigue), right leg time to task failure will __________, and the right leg MVC and resting twitch will ____________ compared to the control session
decrease, decrease less
