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)
-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 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.
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.
inc in adenosine, ATP, K+, H+, CO2
dec in O2
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.
-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