Discuss how genetics, body size, sex, mode of exercise, and environmental factors influence VO2max. Relate to the data collected during the session. (lab 2)
body size
- VO2 is divided by body weight to accommodate differences in size
- typically increases as body mass increases (to the power of 0.81) (in animals)
- when adjusted to body mass, small animals typically have higher VO2 max
sex
- males typically have greater haemoglobin levels –> greater oxygen delivery = increased VO2 max
- males typically have a larger heart –> higher stroke volume increases O2 delivery = increased VO2max
envoinrmental factors
- altitude (decreased inspired O2 will decrease VO2 max)
- heat (inhibits enzymes causing earlier muscle fatigue, dehydration)
- humidity ( more difficult to cool the body vis sweat evaporation)
genetics
- in an untrained subject, 50% of VO2max is determines b heritability
- on average , with training individuals can improve 15-20% in their but there are high responders and low responders due to heritabiltiy
max SV –> high CO, influenced by genetics and training
mode of exercise
- training specififty
- treadmill generally sees greater results –> greater anaerobic fatigue with cycling
Do the lungs and ventilation influence or limit VO2max? What is the ventilation perfusion mismatch? Could this limit maximal exercise? Relate to the data collected during the session. (lab 2)
a mismatch between airflow to alveoli(ventilation v) and blood flow through pulmonary capillaries (perfusion , Q).. the ideal V/Q ratio is about 1.0
- linear increase with ventilation at first but then a steep incline because it’s also helping to regulate pH and contributes to thermoregulation not only delivery of O2
- with heavy exercise, ventilation goes up but the persuasion at the lung is not effienict so the participant is breathing out more oxygen near the end of the test ( FEO2 goes up to 17.6 later in the test)
- So yes, lungs and ventilation can influence Vo2max and ventilation-perfusion mismatch can limit maximal exercise
How do central cardiovascular factors influence or limit VO2max? How will training alter this response? Relate to the data collected during the session. (lab 2)
- max Cardiac output is primary function in determining VO2max (CO = SV x HR)
- approximately 70-805 of the limitation in VO2max is linked to maximal cardiac output
- trained individuals have a much higher maximal cardiac output than untrained individuals
- leads to changes in VO2 Max
- ranges of VO2 max values are due to variation in SV
- E.G. cardiac hypertrophy, atrophy, contraction time
- to increase VO2 max with training, must have increase in O2 delivery and blood flow
-endurance training increases RBC count and direct blood flow to skeletal muscles for O2 delivery - increases in Vo2 max from bed to rest to sedentary to a trained individual are primary due to increase in cardiac output
How do peripheral (muscle cell) factors influence or limit VO2max? How will training influence these factors? Relate to the data collected during the session. (lab 2)
Vo2 max is limited by blood flow
- skeletal muscles have capacity for increasing blood flow and Vo2
- more muscular concentrations lead to the mitochondria consuming more O2 –> lower intracellular PO2 ( low PO2 relative to blood PO2 is needed to maintain driving force for diffusion)
increase in mitochondrial enzymes and mitochondria
training:
- improves muscle fiber recruitment –> type 1 fibers - improved oxygen utilization (have more mitochondria) –> want these to utilized for longer before recruiting type 2 fibers
- increase mitochondria = smaller disturbances in homeostatis
–> 2 effects: - muscles adapted to endurance exercise will oxidize fat at higher heat, - decrease lactate production during exercise
–> increase mitochondria main effect = improved endurance performance not increase Vo2 max
- endurance training specifically, allows muscles to adapt to exercise and oxidize fat at a higher rate
- decreased lactate production during exercise as well
training athlete therefore RER would have likely strayed low for a longer time (using fats over carbs) = no build up of lactate and less burning
Define oxygen deficit, explain what causes it, show & compare the O2 deficit on both graphs of VO2 from the activity today. (lab 3)
oxygen deficit : lag in O2 uptake at the bringing of exercise. It refers to the difference between the amount of oxygen required to perform an activity at a given intensity and the actual oxygen consumed in the early stages of exercise
causes:
- bringing exercise, your body’s demand for ATP (energy) increases immediately, but your aerobic energy systems take time to catch up
- slow activation of aerobic pathways: heart rate, breathing and blood flow need time to deliver O2 to working muscles
- there is an inadequate supply of oxygen to the working muscles at the onset of exercise
- key stimulators of oxidative phosphorylation do not instantaneously rise (ADP and Pi_
- mitochondria need time to increase aerobic ATP production using oxygen ) oxidative phosphorylation)
the body relies on aneraboic energy systems (ATP-Pc and anaerobic glycolysis) at the begining, until the demand is caught up with.
oxygen deficit light exercise:
- O2 deficit is smaller
oxygen Deficit Moderate exercise:
- O2 deficit is larger
Define EPOC, explain what causes it, explain how & why EPOC differs for each of the two exercise bouts. What is fast and slow EPOC and is it apparent in the data collected today? (lab3)
EPOC stands for excess post-exercise oxygen consumption
caused by:
- lactate being converted into glucose
- replenishing ATP and Pc stores
- re-oxygenating myoglobin and hemoglobin ( from O2 deficit)
- elevated body temp and hormones like E and NE
how they differ per bout
- higher intensity drives a greater O2 deficit per unit of time
- results in greater EPOC, particularly from the slow component
why they differ per exercise bout
- lower bouts require lower oxygen and put the body in a smaller deficit to meet metabolic demands
- higher bouts deplete more stores as it places a higher demand on the body so which will take longer to replenish
what is fast and slow + data today
- rapid portion = the steep decline following exercise: restoration of PC and oxygen stores in muscles ( first 2-3 minutes)
- slow portion = slow decline in O2 following exercise: involves elevated HR, body temp, + hormonal changes+ lactacte –> glucose
Using the RER, fuel utilization can be estimated, compare fuel utilization before, during, and after exercise for both exercise conditions. Are the results expected? Why/why not? What are the limitations to using RER to estimate fuel utilization?(lab3)
light exercise
- before 0.7 (100 fats)
- during 0.71( 100 fats)
- after 0.9 ( 33% fats and 67% carbs
moderate exercise
- before 0.8 ( 33% carbs and 67% fat
- during 0.8( 33% carbs and 67% fat
- after 1 ( 100% carbs)
results
- these results were expected, as he increased intensity there was an increase in carbohydrate utilization. As we increase intensity, glycolysis increases. It is expected that fats were primary fuels source as the crossover point in fuel utilization occurs at higher intensity activity
- ratio of CO2 and O2 consumption increased during moderate intensity exercise meaning more CO2 was expired compared to the amount of O2 inspired
limtiations:
- has to be at a steady state for an accurate reflection of gas exchange at tissue
- does not take into account protein metabolism ( neglitabel amount doh)
- RER stays elevated post exercise b/c the VCO2 doesn’t go down right away ( takes time to drop as bicarbonate is still in system and takes time to be released) but the Vo2 does decrease ( consuming less)
How many kcal of energy were used from each of the three energy macronutrients; carbohydrates, fats, and protein? Given the energy demands of the light and moderate exercise intensities observed today, what exercise limitations might be due to energy substrate availability? (lab3)
rest 0.7 RER = 100 fats = 4.69 kcal/LO2
light exercise = 0/71 RER = 100% fats = 4.69 kcal/LO2
moderate exercise = 0.8 RER = 67%fats 33% carbs = 4.7 kcal
protein : around 2-5% used during exercise of less than an hour
at rest: has 2158kcal/24hr - body has this much storage
- if exercising at moderate, VO2 2.00 RER 0.8, they would exercise for 3.7 hours without refuels.
- 576 kcal/HR*3.7 HR = 2158
- fat storage is a lot higher and wouldn’t be the limitation during light to moderate exercise ( approx 100,000 kcal)
What happened to heart rate (HR) and VO2 as power output (PO) increased? Describe the physiology explaining the changes in these two measures seen during incremental exercise.(lab 4)
VO2
- increase in VO2 to facilitate oxygen delivery to muscles
- VO2 primarily increases via increases cardiac output ( CO = HR x SV), an increase in HR facilitates this
- O2 deficit: lag of O2 uptake at the bringing of exercise
–> slight O2 deficit at onset of exercise
–> reflects anaerobic energy system use
heart rate
- heart rate increase at beingnging of exercise to deliver more blood to working skeletal muscles to allow for continued energy production
- cardiorespiratory system will increase its output by increasing heart rate and ventilation to match energy demand ( aka power output) during exercise
- as workload increase each stage, oxygen demand increases as more muscle fibers are recruited. This is reflected in the increasing values of HR and VO2 as wattage increases.
change in sympathetic input reedition in parasympathetic activity
first leg pause - contraction of muscle –> immediate change in ATP
- first contraction stimulates alpha motor neurone which stimulate
- increase Venus return –> spikes venous return to the heart –> increase heart filling which results in frank stealing effect –> increase ventricle filling increase contractility of heart
- combines with parasympathetic and sympathetic change result in increase in heart rate
- first leg push increase heart rate and increases cardiac output
Using the oxyhemoglobin dissociation curve as the basis of the discussion, how would changes in body temperature and blood acidity alter oxygen delivery in the current experiment?(lab4)
blood acidity –> decrease in pH –> increase in H+
bohr effect
- increased acidity decrease O2 and hemoglobin affinity ( right shift)
- leads to O2 unloading at the tissues during heavy exercise
why? –> H+ binds to hemoglobin –> reduces O2 transport capacity
Temperature
- increased temperature causes shift to the right and weakens the bond of the O2-Hb, leading to more O2 being offloaded into the tissues to be used for energy metabolism
- these changes occur so that more oxygen is offloaded at the tissues to favour aerobic metabolism as anaerobic systems are creating more lactate which could lead to metabolic acids
changes to current experiment
- increased temperature and blood acidity would lead to an increase in O2 unloading to working tissues
- helps prolong a more optimal state before we cross ventilatory and lactate threshold( maintain aerobic system longer, increased buffering)
Identify ventilatory threshold (Tvent)? What trend was seen in ventilation before Tvent? After? Describe the physiology behind the change in ventilation before and after Tvent.(lab4)
Event = ventilation threshold = the “breakpoint” at which pulmonary ventilation and CO2 output begin to increase exponentially during an incremental exercise test
- event is 58l.min and occurs around 19min
trend before : constant linear increase:
trend after: exponential increase in VE
physiology behind the change in ventilation before Tvent:
- H+ ions being produced, increase ventilation to expire CO2 alongside our buffering system ( no lactate accumulation yet)
- linearly increases as intensity increases until Tvent
physiology behind the changes in ventilation after Tvent:
- primary H+ ion buildup from glycolysis
- secondary : increase in potassium, increase in catecholamines, increase in temperature, changes in neural drive
- must increase ventilation exponentially to expel CO2 after we’ve saturated our buffering system in attempt to deal with lactate accumulation
Identify lactate threshold (Tlactate)? What trend was seen in blood lactate before Tlactate? After? Describe the physiology behind the change in blood lactate before and after Tlactate.(lab4)
lactate threshold occurs at around 160 watts
before lactate threshold: lactate levels remain relatively stable and low, begin to rise and as it gets close to lactate threshold
After lactate threshold: blood lactate levels rise rapidly ( lactate production is exceeding clearance through buffering and the blowing off of CO2)
physiology explained:
- before the threshold, exercise is mainly supported by aerobic engird metabolism, slow twitch fibers produce little lactate, mitochondria and blood clear lactate well ( lactic acid is blown off as CO2)
- at this point the buffering systems are also able to keep up with the amount of lactate produced to keep it within the low range as well as through blowing off more CO2
- as intensity increase, fast twitch fibers are recruited, they produce more lactate, rate of glycolysis increases, leading to increase pyruvate production and increased lactate production ( under low oxygen conditions) , clearance mechanisms cannot keep up ( liver, heart, and muscles)
Produce a graph of oxygen consumption (mL.kg-1.min-1) by time. Use the course text book to discuss the concept of VO2 drift and use the graph to illustrate the concept.(lab 5)
VO2 drift - 2 conditions
1) exercise in a hot/humid environment results in an upward “drift” in oxygen consumption over time
2) exercise at a high relative work rate ( >75% VO2 max) results in a slow rise in oxygen uptake across time
In both cases, VO2 drift due to the effects of increasing body temperature and to rising blood levels of the hormones E and NE –> increase metabolic rate, resulting in increased oxygen uptake across time
given that core temperature is proportional to work rate, metabolic heat production plays an important role in the overall heat load the body experiences during exercise
mechanisms to increase ventilation 9Ve) during work in heat
- increase in core temp –> stimulates respiratory control centre
- increase in Ve due to increase in breathing frequency and dead-space ventilation
- but, little increase in PCO2
oxygen cost in hot/humid evoirnment increases the VO2 –> elevated increase not drift for this lab because not gradual increase
- need to ventilate more as the rising E and NE
- work of breathing can be increased as you restrict breathing ie adding constructive backpack
- sending more blood to skin leading to an increase in ventilation
Produce a graph of heart rate (b.min-1) by time. Use the course text book to discuss the concept of cardiovascular drift and use the graph to illustrate the concept.(lab5)
Cardiovascular drift is the increase in heart rate and decrease in stroke volume during prolonged exercise
- due to to rising body temperature during a decrease in hydration and plasma volume
- decrease plasma volume leads to a reduction in venous return to the heart and therefore reduces stroke volume
- increase in heart rate to make up for the decrease in stroke volume
prolonged exercise in hot/humid environment increase in heart rate and decrease in stroke volume is exaggerated
- minute 15 was rest and min 20 and 25 was exercise in firefighter suit where we see an 20bpm increase compared to exercise in normal clothing
sweating reduces plasma volume, functional decrease in plasma volume as the blood goes to skin to cool( less blood going to the working muscles) decrease stroke volume to maintain cardiac output we increase heart rate) steady state is around change in 5bpm
Produce a graph for ear & mean skin temperatures, by time. Use the graph to discuss blood flow changes during thermal challenge.(lab 5)
muscle blood flow increase to 100x due to
- decrease vascular resistance( vasodilation)
- increase capillary recruitment (capillaries open = more o2 delivery)
- this is caused by
- Nitric oxide, prostaglandins, ATP, adenosine, EDHF
- local vasodilators inhibit vasoconstriction in active muscles (selective inhibition - sympatholysis)
- as core temperature rises, more cardiac output is redirected toward the skin
- this increase skin temp, promoting heat loss through convection, conduction, and exaporation
- with the gear on, the skin termpature is already at a higher level and during exercise it procesds to get closer to the eat temperate which represents core temp
–> as this gradient gets smaller (closing gap between) the skin temp approaching the core temp, we are losing the ability to diffuse heat form the body as the skin is in the same temp and no longer cooler to release heat
–> once the skin temp = the core temp, there is no longer thermal gradient and core temp ) and skin temp) is going to rise rapidly after that
–> skin and air is normally cooler than the core
Define heat acclimation and how this would alter the results of this experiment.(lab 5)
heat acclimation is the process of physiologically adapting to heat
heating rate: decrease resting and exercising heart rate due to plasma volume expansion and improved stroke volume
ventilation: decrease ventilation response at a given workload, reducing respiratory strain
HIF-1 ( hypoxia-induced factor 1) : increase activation promotes cellular protection, angiogensisi, and improved oxygen utilization
metabolism: decrease muscle glycogen use, increase fat oxidation, and improved mitochondrial efficiency
sweat: easier onset of sweat ,increase sweat rate but decrease salt loss
overall: enhances heat tolerance, endurance, and cardiovascular stability
those acclimatized to heat would exerpience these adaptations in response to heat after 7-14 days and likely have a lower perceived exertion
Describe the relationship between HRV and caffeine consumption. What does our data reveal? What does the literature suggest? What are the mechanisms of the effects?(lab 6)
relationship between HRV and caffine
- no effect on HRV within 90 minutes after consuming 100-200 mg habitually
- no difference in LF/HF ratio 60 minutes after acute ingestion of 300mg caffine
Our data:
- moderate relationship between caffine and noise disturbance
literature:
- BP and MSA(muscle sympathetic nervous activity) increased for Non-habitual drivers of caffine/coffee
- habitual drinkers lack of BP increase despite MSA activation to coffee
mechanisms of effect
- short-term administration of caffine in non-coffee drinkers increases BP, plasma renin acidity and catecholamines
- sympathetic nerve activity showed a sustained increase after coffee drinking
Question #2
Describe the relationship between mood, illness, and HRV. What does our data reveal? What does the literature suggest? What are the mechanisms of the effects?
(lab6)
MOod:
positive emotions - more stable HRV frequencies (showing high ability of coherence, maximizing the efficiency of the sagas nerve)
negative emotions - more dispersed frequency disruptions( showing that the SNA and PNS are “fighting” or firing asynchronously)
Illness:
- lower HRV indicated body is stresses
- HRV taps directly into the nervous system making it a sensitive and fast-acting indicator for illness
- low HRV is a sign of poor health indicating that your body is less resilient to changing situistions
OUr data:
- moderate negative reslaship between VLF and Mood ( R = -0.56)
moderate negative relationship between illness and %difference ration 7-12(R = -0.38)
mechanisms : illness or depression/anxiety - increased sympathetic activity, increase HR and BP - less HRV between mood and not sick - better balance between sympathetic and parasympathetic activity - increase HRV
Question #3
Describe the relationship between acute exercise and HRV. What does our data reveal? What does the literature suggest? What is the effect of chronic exercise? What are the mechanisms of the effects?
(lab6)
exercise training and HRV
Acute: HRV decreases in response to acute exercise
- rise in sympathetic activity needed to increase the cardiac output and systemic vascular tone needed to meet physiological demands of exercise
- regular exercise training can modify atomic balance
chronic: increase HRV and promotes greater vagal tone and cardiac electrical stability, whereas acute exercise typically causes a temporary decrease in HRV due to elevated sympathetic activation
chronic exercise increases HRV through:
- enhanced parasympathetic activity at rest( vagal tone)
- improved baroreflex sensiisty
- increased SV and EDV at rest( reduced need for sympathetic drive)
Question #4
Select two or three individuals from the group data set and explore them as case studies. What could explain some of the changes/differences/similarities?
(lab6)
women tends to have a lower LF to HF ration compared to men. This difference reflects variation in auomtomic cardiac control, suggesting that women tend to have higher parasympathetic ( vagal acitivyt) and Lowe rsympathetic activity than men
there are substantial sex differences in autonomic regulation of the heart. HRV in women is characterized by a relative dominance of vagal acidity despite a hgierh resting heart rate, which can result in lower LF/HF ratio as observed in the case study
Question #1
At the onset of occlusion, end of occlusion, and post-occlusion (reperfusion), how does the HRV response relate to the hemodynamic response?
(lab7)
blood flow = change in pressure/resistance
onset of occlusion
- sympathetic acuity increases and parasympathetic activity decreases causing a decrease in HRV
- the increase in sympathetic activity increase heart rate, blood pressure, and mean partial pressure which can be seen in the lab data
- this would also cause an increase in cardiac output
- there are the same responses seen due to decrease HRV at the onset of exercise
- middle HRV response: increase in resistance causes a decrease in blood flow so HR needs to increase to make for this
end of occulsion
- sustained ischemica at the end of occlusion maintains chi sympathetic tone and accumulated metabolites to preserve blood pressure
- HRV start low due to reduced baroreceptors input and dominance of sympathetic tone this is reflected in the hemodynamic response seen is elevated vascular resistance and reduce venous return
least HRV response: blood oxygen saturation is at its lowest in occluded limb, and blood pressure is low so syptahtic tone is still growing
post occulsion
- rapid vasodilation, less TPR and a decrease in blood pressure. This is detected by baroreceptors
- sympathetic activity decrease and parasymptahtis activity increases causing increase HRV
- helping heart rate slow down, resulting in increase HRV
- most HRV response: increased vagal tone allows for more HR changes decreae resistance causes an increase in blood flow
Question #2
At the onset of occlusion, end of occlusion, and post-occlusion (reperfusion), how and why is oxygenation affected centrally and peripherally?
(lab7)
onset of occlusion
centrally: steady( reliant on arterial oxygen content and cardiac output, not affected by peripheral occlusion)
peripherally: sharp linear decline caused by continuous consumption of O2, but no further delivery of O2
TSI drops due to deoxygenation increases and oxyhemoglobin decrease
end of occulsion
centrally: steady or a small decrease ( increase sympathetic>increase HR and bp>increase O2 demand)
peripherally: O2 occurred tissue is depleted further, metabolism shifts toward anaerobic glycolysis, this can cause a lactate build-up, lower pH and very low O2 saturation ( like we see during an exercise response as well)
- central homeostasis treis to compensate for local hypoxia vic cv response
post-occlusion (repercussion)
centrally :
- steady, brain maintains constant persuusion
- can elevate slightly due to the systemic hyperaemic response, but not caused by an central ischemic debt
peripherally:
- oxygen rebounds and overshoots above baseline
- due to accumulation of metabolies( H+, CO2, etc)
- causes vasodilatory response, reperfusing tissues and hemoglobin and flushes out metabolic byproducts
Question #3
At the onset of occlusion, end of occlusion, and post-occlusion (reperfusion), how and why is blood pressure affected? (lab 7)
onset occlusion
- blood pressure rises
- bue to more peripheral vascular resistance ( increase in sympathetic nervous system activity ==> vasoconstriction)
end of occlusion
- further increase in sympathetic activity causes sustained increase in BP due to continuous vasoconstriction
post occlusion
- vasodilation = decrease blood pressure
- result of decrease sympathetic acidity post-occlusion which caused vasoconstriction, relaxation
- increase parasympathetic system causes vasodilation lowering resistance in the blood vessels and therefore aiding in lowering blood pressure = hyperaemic response –> more blood flow to occluded limb
- the systemic BP will increase again once sympathetic tone stabilizes it back to normal –> reaches homeostasis
Question #4
Explain the physiological mechanisms involved in the hyperaemic response seen post-occlusion.
(lab 7)
reactive hyperaemic (RH) - a temporal, exaggerated increase in tissue blood flow following short-term vascular occulasion
during the period of occlusion:
- tissue hypoxia and a buildup of vasodilator metabolites(sympatholysis: eg, Nitric oxide, H+, adenosine, etc) dilate arterioles and decrease vascular resistance
occlusion released:
- flow becomes elevated because of the reduced vascular resistance
- accumulated metabolites cause smooth muscle relaxation
- shear stress also causes endothelium release of NO and PGS
- transient vasodilation of the microcirudlation facilities an increased red blood cell (RBC) flux and O2-delivery to the capillary bed of the previously O20deprived tissue
during hyperaemia:
- tissue deoxygenation and metabolite washout restore vascular tone: longer occlusions amplify the magnitude and duration of RH
- myogenic mechanisms: decreased arteriolar pressure during occlusion can induce myogenic-mediated vasodilation
