HPHY 371 Midterm 2
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What are the common fuel forms? And what are their roles during exercise?
- carbohydrates- readily available and easily metabolized, transported as glucose and stored as glycogen
- fats- triglycerides (glycerol + 3 FAs)
On a graph... How does oxygen uptake change from rest to steady-statesub maximal exercise?
- oxygen deficit- increase in VO2 proportional to energy expenditure required for task
- VO2 does not respond immediately
- energy paid for by other sources (not oxidative)
- O2 deficit is never resolved at supra-maximal work loads
Where does ATP come from during the transition period from rest to steady-state exercise?
anaerobic systems- PCr and glycolysis
On a graph... How does oxygen uptake change during recovery after exercise? What is EPOC?
- EPOC: excess post-exercise O2 consumption
- elevated VO2 for minutes to hours
- fast component (initially after): resynthesis of PCr using oxidative system & replacing muscle and blood O2 stores
- slow component:
- 1. inc HR and breathing - internal mechanical work
- 2. inc BT - inc metabolic rate - internal work
- 3. inc epinephrine- inc metabolic rate - internal work
- 4. conversion of lactate to glucose - chemical work
What is the effect of training on the oxygen deficit?
- - trained athletes reach steady state more quickly
- - increased quantity of mitochondrial enzyme = increased responsiveness
- - as substrate inc, enzyme activity inc
- - no change in individual enzyme capacity
glycerol + 3 fatt acids
breaking down of triglycerides
synthesis of glucose in the liver from amino acids + lactate + glycerol
mobilization of glucose from liver glycogen stores
- 1. lactate produced in muscle via glycolysis
- 2. lactate uptake by liver
- 3. lactate converted into glucose
- 4. glucose used in glycolysis by muscles
What is the role of the catecholamines and intracellular factors in the mobilization of muscle glycogen during exercise?
- SNS: dec insulin and inc glucagon
- increased gluconeogenesis and glycogenolysis
- increased plasma glucose
- Plasma catecholamines reinforce the effects of the glucagon on the cells
- 1. adipose cells: mobilization of FFAs
- 2. liver cells: mobilization of glucose into blood
What's the difference between intracellular factors and plasma catecholamines in the mobilization of muscle glycogen during exercise?
- catecholamines work to break down glucagon in liver
- intracellular factors (calcium and calmodulin) work to break down glucagon in muscle
Four mechanisms involved in maintaining blood glucose concentration
- 1. glycogenolysis (mobilization from liver)
- 2. gluconeogenesis (liver)
- 3. mobilization of FFA from adipose cells
- 4. block of glucose entry into cells so FFAs are used (catecholamines)
On a graph describe how hormones change during graded and prolonged exercise...
- inc catecholamines release (highjack pancreas)
- inc glucagon (maintains plasma glucose)
- dec insulin (dec glucose uptake and prevents suppression of gluconeogenesis and glycogenolysis)
Describe the effect of hormones on glycogenolysis and gluconeogenesis...
- mobilized during 1) inc glucose concentrations 2) exercise - local active muscle
- allow for glucose to be taken into muscle cell at a high rate during exercise even though plasma insulin is reduced
- GLUT-1: insuline dependent (always present on membrane) & passive response
- GLUT-4: most glucose uptake during exercise
Timing of pre-competition meals within the context of the insulin response to feeding...
- right before exercise: insulin mediated GLUT-4 uptake of glucose (dec plasma glucose) BAD
- every 15 mins: inc power output, pancreas already highjacked so no insulin, glucose spared for brain and heart (no benefit with exercise less than an hour)
- high carb diet allows for inc initial muscle glycogen stores (longer time to deplete stores= longer time to exhaustion)
- more readily available in case of extending workout for longer (ex marathon)
- follicle stimulating hormone
- stimulated development of follicles in ovaries
- anterior pituitary
- luteinizing hormone
- maturation of the follicle, stimulation of ovulation and endometrial growth
- anterior pituitary
- maintains endometrium
- if egg is not fertilized, progesterone levels drop and endometrium is shed
- released from ovary
- stimulates LH surge
- released from ovary
3 components of the female athlete triad
- low energy availability
Discuss physiological explanations for the links between three components of the Female Athlete Triad
- 1. low energy availability - disordered eating, expending more energy than taking in
- 2. low energy ---> dec GnRH pulse ---> no stimulation of FSH and LH ---> dec estrogen ---> amenorrhea
- 3. osteoporosis is due to decreased estrogen
other consequences of low energy availability
- vaginal dryness
- elevated LDL cholesterol
- impaired skeletal muscle oxidative metabolism
- impaired endothelium- dependent vasodilation
list the ways low estrogen impacts bone density
- low estrogen= risk for osteoporosis
- dec calcium absorption
- inc calcium loss
- inc osteoclastic activity
On the graph... How does oxygen uptake and blood lactate concentration change during graded exercise to maximal exercise?
- lactate threshold: point where lactate suddenly rises during incremental exercise
- occurs because glycolysis can provide ATP at faster rates than oxidation
Explain, biomechanically, the reasons for lactate production in muscle cells
- 1. glycolysis runs at a faster rate than oxidative metabolism- high lvls of pyruvate and NADH that cannot be accepted by the already saturated mitochondria
- 2. pyruvate builds up in the muscle cells
- 3. lactate dehydrogenase converts pyruvate to lactate
- 4. allows for lactate to recycle NADH to NAD+ (by accepting proton)
- 5. keeps glycolysis running at high rate
Why does blood lactate begin to rise rapidly during graded exercise?
- supply of oxygen stops matching the demand of ETC- inc pyruvate = inc lactate
- rises b/c body is producing lactate faster than it is removing it (lactate going through cori cycle, less active muscle, brain and heart)
Identify the biomechanical adaptations to blood pH and lactate removal.
- 1. buffers acid produced by muscle by consuming hydrogen ions in conversion of pyruvate to lactate - pyruvate + NADH + H <---> lactate + NAD
- 2. symport with hydrogen ions reduces acid load in muscle
Newer biochemical models for
lactate and acid production during exercise
- -Trained individuals lactate threshold = 70-80% VO2 max
- -Untrainted individuals lactate threshold = 50-60% VO2 max
- -Sets a limit of what you can sustain for a longer workout
- -Pacing: run at a speed/VO2 below your lactate threshold
- -Lactate does not accumulate and rate can be maintained
contraction and lengthening muscle
contraction with no change in joint angle
contraction with shortening of a muscle
a response that occurs in muscles due to a brief electrical stimulus applied to a nerve innervating it
the addition of successive twitches
a continual increase in frequency until contraction is sustained
The 3 intrinsic factors that affect the production of force in an isolated muscle.
- 1. muscle twitch/ tetany
- 2. length tension relationship
- 3. number of motor units recruited
Described the size principal with respect to the orderly recruitment of motor units
- small (more fatigue resistant) motor units recruited first
- large (more powerful) motor units recruited last
On a graph... Describe the relationship between movement velocity and the amount of force exerted during muscular contraction.
- inc resistance, dec velocity
- inc velocity, dec force
- amount of force produced at different velocities of contraction
Define the factors that may
influence the strength of a contraction “in situ”.
- "in situ" - within the specific muscle
- 1. coactivation of agonist/antagonist muscles
- 2. biomechanics of joint
- 3. autogenic inhibition
- 4. muscle structure
describe the basis for classifying motor units based on the speed of twitch and resistance to fatigue
- motor unit: motor neuron and muscle cell innervated
- functional assessment
Large vs. Small cross sectional area (in terms of force generated and velocity of shortening)
- at a given length, large cross-sectional areas have a greater force production than smaller cross-sectional areas
- at a given velocity, large cross-sectional areas have greater force production
Longer muscle fibers vs. Shorter muscle fibers (force generated and velocity of shortening)
- longer muscle fibers can produce force over a large range of lengths and can produce greater velocities at a give force
- shorter muscle fibers can produce a greater force but have a dec range of lengths and velocities
How does angle of pennation affect the physiological cross-sectional area and fiber length?
- inc angle of pennation will dec force from a single muscle fiber
- inc angle of pennation also allows for grater number of muscle fibers in the volume of a muscle
- inc in angle of pennation will cause a greater physiological cross sectional area and therefor produce a greater force
How does angle of pennation link muscle structure to muscle function?
- (smallest) fusiform>unipennate>bipennate>multipennate
- smaller angle: inc velocity, range of length but dec force
- larger angle: dec velocity, range of length but inc force
What are the major biochemical and mechanical properties of human skeletal muscle fiber types?
- the myosin isoform type
- quantities of bioenergetic enzymes
What are the basic characteristics of muscle fiber types that can be determined from a muscle biopsy?
- Type I: slow, fatigue resistant and highly oxidative
- Type IIa: fast, hard to fatigue, oxidative/glycolytic
- Type IIx: fastest, easy to fatigue, highly glycolytic
What are the fundamental muscle fiber types that are predominant in endurance vs. power athletes?
- endurance: small fibers, high % of Type I fibers , greater muscular endurance
- strength/power: large fibers, inc number of Type II fibers, dec muscular endurance
Describe the transformations in muscle fiber type that can be demonstrated with exercise training.
- change in fiber type is due to change in gene expression
- training shifts muscle to slower myosin heavy chain isoforms
- starts at type IIx --> IIx/IIa --> IIa --> IIa/I --> Type I
- strength training programs converts Type IIx --> Type IIa
- oxidative stimulus is needed to convert Type IIa --> Type I
Describe the patterns in muscular fiber type that are observed in cases of reduced activity like paralysis
- by being active you naturally drift towards type I fibers
- paralysis no shift to faster fibers like Type IIx
Graph the relationship between HR and work intensity
- linear relationship beginning with resting HR and peaking on average at about 220 depending on the individual
- as work increases, HR increases
Force, power velocity and efficiency of Type I vs. Type II
- Type I (slow): lower force at same velocity, dec velocity, dec ATP consumption, inc efficiency
- Type II (fast): greater force at same velocity, inc velocity, inc ATP consumption, dec efficiency
Estimate maximum heart rate for an individual when their age is provided.
220-age (empirical equation)
Graph the relationship between stroke volume (SV) and work intensity of a sedentary individual and an elite athlete.
- increases with work intensity up to about 40%-60% VO2max. May increase up to VO2max in highly trained athletes
- increased by frank-starling mechanism and intensity-dependent increase in cardiac SNS activity (contractility)
- at a given HR an elite athlete will have a greater SV in comparison to a sedentary individual
Describe the affect of the Frank Starling mechanism on SV during exercise
- SV at rest or during exercise is regulated by:
- increase in venous return...
- - increased preload= increased stretching of ventricles
- -increased contraction (frank starling)
- -increased SV
- -EDV- volume of blood in ventricles at end of diastole (FSM)
- -strength of ventricular contraction (correlates with FSM bc enlargement of EDV causes inc ventricular contraction)
Describe the affect of the ANS on SV during exercise
- increased SNS:
- - increased contractility
- - increased SV
- - circulating epinephrine-norepinephrine and direct SNS stimulation of heart by cardiac accelerator nerves- both increase cardiac contractility by inc calcium availability
State the Fick Equation and define each term
- VO2=Q*(a-v O2 diff)
- VO2: rate at which your heart, lungs and muscles use and take up oxygen during exercise
- Q: cardiac output
- (a-v O2 diff): difference in the content of O2 in arteries versus that in "mixed venous" sample
Define the three primary cardiovascular adjustments that must occur if vigorous large muscle-mass exercise is to be maintained.
- increased cardiac output via ANS adjustments
- redistribution of the augmented cardiac output
- increased venous return to the heart in EXACT proportion to the increase in cardiac output
How does cardiac output increase via ANS adjustments?
- decreased cardiac vagal (PNS) nervous system activity (primary mechanism under 100bpm)
- increased cardiac sympathetic nervous system activity (primary mechanism above 100bpm)
How is augmented cardiac output redistributed?
- parallel distribution allows us to redistribute to different areas of body
- regulated by SNS- there is a tonic level but can dial up or dial down certain areas from NE influence
- circulation is not able to perfuse all muscle during maximal exercise-- redistributes to areas where it is most needed (brain)
How is venous return increased in EXACT proportion to the increase in cardiac output?
- vasoconstriction of compliant vessels (decreased pooling of blood)
- -vasoconstriction of skin and splanchnic vessels (both very compliant)
- vasodilation of skeletal muscle blood vessels (does effect of preload because of shift from compliant to non-complicant vasculature bed)
Given the necessary values, calculate VO2 using Fick equation.
- VO2=(HR*SV)(a-v diff)
- factors limiting our ability to inc VO2 during exercise:
- age by affecting HR max
- changes in SV max via adaptations in training
Define the terms mixed blood and arterial-venous oxygen difference.
- mixed venous blood- representative of all blood coming back form the peripheral system to the right atrium of the heart (blood from both inactive and active muscle)
- arterial venous oxygen difference- the difference in content of O2 in the arteries versus that in mixed venous venous sample
Graph the relationship between cardiac output and work intensity.
- (resting cardiac output= 5L/min)
- increased linearly with increasing exercise intensity
- can increase up to 20-40L/min depending on body size and level of aerobic/endurance training
Explain how exercise influences venous return in terms of Krogh Hydraulic Model.
- vasodilation and vasoconstriction modify the passive properties of circulation
- during exercise splanchnic and skin circulation beds vasoconstrict (inc NE=less venous pooling)
- while skeletal muscle vasodilates its vessels in order to inc blood flow to exercising tissue (functional sympatholysis exercise hyperemia)
Describe the ANS changes that result in the rise in HR during exercise.
- initial are PNS under 100bpm
- rest is due to SNS above 100bpm
Graph the relationship between total peripheral resistance and power output.
TPR decreases linearly with increase in power output due to the functional sympatholysis
Discuss the pattern of redistribution of blood flow during exercise and how it is regulated.
- increase in arterial pressure causes increase in blood flow
- vasoconstriction of splanchnic, skin and non exercising tissues
- vasodilation of exercising tissues
- important to get blood flow to heart, brain and exercising tissues
Define the terms exercise hyperemia and functional sympatholysis.
- Exercise Hyperemia (allowing vessels to vasodilate): increase in blood flood to muscles when contracting rhythmically due to local vasodilators (muscle metabolites: adenosine, ATP, K+, CO2 or decreases in O2)
- also signals from endothelium such as phospholamdin
- Functional sympatholysis (not letting them vasoconstrict): blunted SNS mediated vasoconstriction in active muscle via increase in adenosine and/or ATP only
- leads to localized vasodilation
Identify the factors that regulate local blood flow during exercise.
- from muscle:
- inc in adenosine, ATP, K+, H+, CO2
- dec in O2
- from endothelium:
- inc in NO and prostaglandins
Describe the importance of reducing splanchnic, renal and cutaneous blood flow during exercise.
- these areas are compliant an take up a lot of blood unnecessary for exercise
- vasoconstriction of these areas causes an increase in venous return
Explain how increased SNS activity to skin, splanchnic, and renal arterioles results in passive displacement of the venous blood toward the heart.
- SNS causes vasoconstriction in these areas
- vasoconstriction causes decreased blood flow to these areas= less blood pooling
- constricting vessels in these areas allows for increased venous return to heart
Explain how increased SNS activity to skin and splanchnic veins results in active displacement of blood toward the heart.
- inc SNS to skin and splanchnic veins only causes venoconstriction due to the NE binding to alpha receptors
- helps blood return to heart
Explain how the contraction of skeletal muscle contributes to venous return.
- skeletal muscle pump pushes blood against gravity toward heart (stiffens veins so they appear non compliant)
- inc in respiratory pump and greater rate and depth of breathing= inc venous return because of lung expansion and inc thoracic pressure
Explain the central command theory of cardiovascular regulation during exercise.
- Central command initiated when exercise is expected and contributes to increased HR and SNS response (feed forward mechanism)
- continues throughout exercise
- muscle afferents are feed back
Describe the role of the arterial baroreflex in the cardiovascular response to exercise.
- reflex occurs to inhibit baroreceptor neuron to think BP is lower than actual
- Maintains high SNS activity throughout exercise (diagram)
Describe the role of feedback from actively contracting muscle in the cardiovascular response to exercise.
Explain what happens to HR, SV, and Q during prolonged exercise in hot and or humid enviroment.
- cardiovascular drift:
- -inc HR
- -dec SV
- -thus Q is fairly level
- competition for skin blood flow to keep core temperature down
- inc in blood flow to skin causes dec in venous return thus reducing SV
Describe the ventilatory response to the onset of exercise.
- More CO2 coming from tissues to unload at lungs
- More O2 to bring at working tissues
- need to protect alveolar PO2 and PCO2
Describe the ventilatory response to graded/incremental exercise.
- need proportional change in ventilation to the change in PO2 and PCO2 to maintain gas levels in the alveoli
- VE= VT * FB (frequency of breathing)
- at onset of exercise ventilation increases due to thought of exercise (central command)
- ventilation matches workload until threshold is passed ---> hyperventilation (respiratory compensation due to metabolic acidosis)
Identify some of the possible regulators of ventilatory responses to exercise.
- central command or neural impulses at the onset of exercise
- early: linear increases in ventilation in proportion to graded/incremental exercise (exercise hyperpnea)
- later: steep increase in ventilation out of proportion to metabolism (hyperventilation)
List the major challenges exercise presents to the respiratory system.
- dec O2 and inc CO2 in venous blood returning to lung
- inc pulmonary blood flow=inc vascular pressure
- inc in pulmonary blood flow=dec in perfusion time
- inc in ventilation=increased work of breathing
How does the respiratory system accommodate for dec O2 and inc CO2 in venous blood returning to lung?
Explain how the respiratory system accommodates for inc pulmonary blood flow=inc vascular pressure.
- recruit more alveoli
- inc distention of current alveoli
- opening of larger diameter vessels
Explain how the respiratory system accommodates for inc pulmonary blood flow=dec perfusion time
increased capillary blood volume with increased pulmonary blood flow keeps mean transit time long enough to maintain adequate loading of O2 in alveolus
Explain how the respiratory system accommodates for inc ventilation=inc work of breathing
- respiratory steal phenomenon!
- body overcomes this by minimizing energy expenditure of breathing by working at a more optimal range of lungs volumes and pressures
Explain how changes in metabolic rate and alveolar ventilation alter PAO2 and PACO2 and how this affects arterial blood gases.
- increased in metabolic rate
- -more CO2 produced in tissues
- -more O2 utilized in tissues
- arterial blood gases returning to the heart will have more CO2 and less O2
How does exercise affect O2-hemaglobin interactions? Is this beneficial or detrimental?
- exercise causes an inc in CO2, H+, and temperature
- allows more O2 to be unloaded at muscle
- *see o2 dissociation curve
Describe how ventilation changes during mild, moderate and severe exercise.
- mild to moderate: exercise induced hypernea
- -hypothesis: neural signals initiate increase VE at exercise onset (feed forward) and
- CO2 load to lungs "fine tunes" VA to VCO2 (feed back)
- high intensity: hyperventilation
- -hypothesis: respiratory compensation for metabolic acidosis (occurs because rise in CO2 causes blood to become acidic)
- -no longer in sync with metabolism because responding to other stimulus
Explain current models of what causes the changes in ventilation at each exercise intensity
Compare and contract hyperpnea and hyperventilation
Describe when does hyperventilation begin with respect to exercise
- dec in transit time of RBC during exercise
- respiratory system increases capillary blood volume to decrease mean transit time to maintain adequate loading of O2
- if RBC transit time drops below 0.5 seconds, adequate equilibrium can't occur because equilibrium of O2 molecules takes 0.5 seconds
Perfusion limited at rest is limited by
amount of blood flow to long capillaries
diffusion limited at exercise because
so much blood is flowing through capillaries that mean transit time decreased and limited by the time it takes to diffuse O2
Does the respiratory system typically limit exercise in healthy untrained adult human?
- training induces inc in demand for max O2 transport with no coincident adaptation in the lung
- untrained: respiratory system overbuilt
- trained: respiratory system still overbuilt (limited mostly by cardiovascular system)
- elite: respiratory system is the limiting system (not so much cardiovascular and muscle)
- cardiovascular and muscle system capacity has surpassed the respiratory system because the system cannot adapt
Using the variables identified in the Fick equation, explain how the increase VO2max comes about for the sedentary subject who participates in an endurance training program.
- VO2 max higher in endurance mostly because increased Q
- -increased SV (from larger LV)
- -heart becomes more compliant (inc frank starling mechanism)
Describe the changes in muscle structure that are responsible for the increase in the maximal arterial-venous O2 difference with endurance training.
- capillary angiogenesis: increased capillary density
- -inc physiological cross sectional area
- increased A-V O2 difference b/c more O2 dropped off and more CO2 "washed away"
Describe the changes in the heart, vasculature and blood that occur with exercise training.
- higher Q and more capillaries means
- -inc opening of existing capillaries in trained muscles
- -inc percentage of capillaries that can go to active muscle (more effective blood distribution)
- increased blood volume
- - inc in plasma and a little inc in RBC
- inc the rate at which the O2 gets to the muscles
How do changes in the heart produce greater SV?
- heart is adapting to high flow and high pre-oad in order to inc cardiac output
- 1) ventricular expansion (eccentric cardiac hypertrophy)
- 2) slight ventricular wall thickening- inc contractility
Define angiogenesis and major signal involved
- development or growth of new blood vessels
- increased capillary density reduce the distance for O2 diffusion and more CSA for blood flow through the muscle
- signal: vascular endothelial growth factor and other factors in metabolic demand
Explain how these cardiovascular adaptations to training support work at higher rates or the achievement of higher VO2max levels.
- allow more blood to be distributed to working muscles
- cardiovascular adaptations:
- inc SV at rest, submax and max exercise
- inc EDV
- slight inc in wall thickness
- training bradycardia (slowing of HR at rest- max HR remains unchanged or dec slightly)
- Q unchanged at rest and submax exercise but increased at max
Describe changes that result in a higher lactate threshold following training
- inc in mitochondria enzyme density
- leads to less lactate production
- oxidative system working at a faster rate=less lactate needs to be converted to pyruvate
- greater lactate removal, tissues are better suited to taking up lactate to use in oxidative metabolism
Be able to show how each of the following variables respond to increasing workrates for a sedentary versus an endurance trained person: HR, SV and Q
- SV- inc at rest, submax and max
- HR- dec at rest, slightly dec at max
- Q- unchanged at rest and sub max, inc at max
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