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CV Exercise Physiology > Cardiorespiratory Physiology > Flashcards

Cardiorespiratory Physiology Flashcards

1
Q

fuel use during exercise and intensity
1. intensity and percent fuel selection
2. intensity and rate of fuel selection
3. keto diet

A
  1. measured using RER, during low intensity increase lipid oxidization; at higher intensity use more carbs since they req less O2 for oxidization, supply greater portion with muscle glycogen
  2. measure using indirect calorimetry (kcals); at low intensity greater fat use, at moderate hit lipid threshold; at higher intensities greatly increase carbs oxidation to supply E
  3. increase lipid burning assoc with increased VO2 since lipid req more O2 to oxidize; harder to maintain high VO2 so have to decrease intensity to maintain steady state
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2
Q
  1. duration on fuel selection
  2. how to determine specific fuel use?
A
  1. increase duration, decrease glycogen use as it runs out, fill in with glucose from liver and gluconeogenesis, increased reliance on blood fuels
  2. more specific is more invasive; VO2 measures rate of E use, RER determine % CHO and fat; biopsy measure muscly glycogen use; A-V catheters measure muscle uptake FFA
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3
Q

neuroendocrinology
1. def
2. hormone def and sources
3. hormone classification
4. major functions of hormones

A
  1. activity of tissue regulating hormone release to control physiological processes
  2. chemical substance released into bloodstream that specifically acts on local or distant tissues; endocrine glands, SNS nerves (neurotransmitters), other tissues
  3. peptide hormones derived from PRO secreted straight into blood, soluble, fast-acting; steroid hormones derived from cholesterol are insoluable, req carrier molecule, slow acting
  4. peptide hormones alter enzyme activity and membrane transport; steroid alter rate of PRO synth
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4
Q

key hormones in exercise metabolism
1. function
2. location
3. conc with intensity

A
  1. insulin released from beta cells of pancreas increase fuel uptake, storage, and synthesis and decrease lipolysis, decrease with exercise intensity
  2. glucagon from the alpha cells of the pancreas increase liver glycogenolysis and gluconeogenesis; increase with exercise intensity
  3. epinephrine from adrenal medulla increase muscle glycogenolyis and lipolysis in muscle and adipose tissue; increase with exercise intensity
  4. norepinephrine from SNS fibres and adrenal medulla increase lipolysis of adipose tissue and cardioresp func; increase with exercise intensity
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5
Q
  1. cyclic AMP sys
  2. muscle glucose uptake during exercise
A
  1. hormone binds to receptor on membrane, G PRO converted to adenylate cyclase which facilitates rxn converting ATP to cAMP, cAMP activates protein kinase which produces a cellular response depending hormone that bound to receptor; Epi increase muscle glycogenolysis, Epi/NE increase lipolysis in muscle and adipose tissue, glucagon increase liver glycogenolysis
  2. muscle contraction stimulate GLUT1 transporters to uptake glucose into cell via Ca2+; insulin stim release of GLUT 4 receptors from vesicles (some sensitive to insulin some to contractions) into membrane, GLUT 4 uptake glucose
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6
Q
  1. insulin circulation to muscle
  2. glucose and insulin during feeding and exercise
  3. how blood glucose is maintained during exercise
A
  1. controlled by concentration in blood and BF to muscle; 15 units/min at rest; 100 units/min during exercise; decrease to other tissues during exercise
  2. during feeding blood glucose increases, insulin increases to take in more glucose into skeletal muscle (glucose sink, why ppl with greater lean body
    mass have better control of Bglu) and body tissues; during exercise blood insulin decease as increased release of contraction sensitive GLUT4 transporters, Bglu stay constant because rate of glucose use by muscle is the same as release from liver, prolonged exercise sees decrease in Bglu, increase glucose to active muscles and decrease to inactive muscles and other body tissues
  3. decrease insulin and BF to less active tissues to minimize their glucose use, increased NE stim lipolysis in adipose tissue to mobilize alt fuels, Epi increase phosphorylase activity to stim muscle glycogen use, increase glucagon to increase glucose release from liver sources (glycogenolysis and gluconeogenesis)
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7
Q

key metabolic adaptations to training (aerobic)

A
  1. increased mitochondria number, size, and oxidative enzymes (measured using citrate synthase as mitochondrial marker)
  2. increase fuel (glycogen) storage capacity
  3. increased efficiency of fuel use; decreased CHO use (decreased RER) and decreased lactate production (increase LT)
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8
Q

aerobic training on:
1. RER
2. LT
3. peak sustainable workload

A
  1. with training decreased RER at given workload and increased workload at given RER; decreased workload per mitochondria, increased lipid delivery to mitochondria, increased enzymes for lipid oxi, decrease Epi, decreased CHO use
  2. increased LT indicates efficiency CHO utilization; post-training decrease lactate at given workload or increase workload at given lactate; increase mitochondria, increased lactate clearance, increases pyruvate oxidation (increase PDH), decreased pyruvate production (decrease PFK)
  3. percentage of VO2max that can be maintained (steady state) increases along with higher VO2max
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9
Q
  1. key components of CV sys
  2. 3 major CV adjustments to acute exercise
  3. anatomy of the heart
A
  1. Heart (pump), vessels (tubing), blood ( fluid medium)
  2. CO (Q) increase from resting 5 L/min to 75 L/min during exercise, Q redistribution from 20% to 80% skeletal muscle, adjusted rate of O2 removal from blood
  3. AV valve reg BF in heart, SL valves reg flow out of heart; electrical system with SA node pacemaker 100 bpm (slows down through PNS inhibition of HR at rest, during exercise PNS withdrawal for higher HR), signal slows through AV node to L&R bundle branches and purkinje fibres
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10
Q

ECG

A
  1. P wave is atrial depolarization, QRS complex show dip then great increase in electrical activity rep ventricular depolarization (ventricles have more electric signal than atria since they are bigger) masking atrial repolarization, ST segment show ventricular repolarization
  2. PR interval from P to Q shows atrial depolarization, QT interval from Q to end of T shows ventricular activity
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11
Q

Cardiac cycle
1. At rest vs. Exercise
2. Phases, pressure, and volume changes

A
  1. Events at occur b/w successive heart beats; systolic contraction phase and diastolic relaxation phase; at rest cycle 0.8 sec with HR 75 bpm, 40% systole, 60% diastolic to allow for proper filling of heart, during exercise at cycle shortens with intensity, systolic increase, diastolic decrease, ventricular filling decrease
  2. ventricular filling, volume in ventricles increases as blood flows from atria to ventricle through AV valves, increase in atrial pressure as it contracts; isovolumetric contraction, AV valves close as pressure in ventricles exceeds atria as it contracts, no change in volume since increasing pressure in ventricles is not great enough to open the SL valves; ventricular ejection, pressure high enough to open SL valves, decrease in blood vol as it is ejected; isovolumetric relaxation, ventricles relax, pressure decreases closing SL valves, atrial fills passively
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12
Q

ventricular volumes
1. end diastolic volume at rest
2. stroke volume at rest and ejection fraction
3. exercise
4. muscle pump
5. Frank-Starling Law

A
  1. volume of blood in ventricle at end of diastole, around 100-160 mL, is the preload determining the stretch on the ventricles
  2. volume of blood ejected per beat, SV = EDV-ESV, approx 70 mL, ejection fraction is SV/EDV (approx 60%) indicating how well the heart function, if EF decrease, increase HR to sustain CO via exercise training to increase heart func or acutely with NE to increase HR
  3. increase EDV (greater preload contraction) while decreasing ESV (better EF) to increase SV; SV is greatest factor for req VO2 max
  4. pressure by muscles approx 20-30 to squeeze veins to return blood to heart but not compromise arterial pressure sending blood to muscle; why EDV increase during exercise despite decrease in diastole
  5. greater stretch (increased EDV) within physiological limit, increase elastic recoil, increase contraction strength (and SV); if stretched beyond limit, unoptimal CB can’t contract properly, pathophysiological, use diuretic to decrease BV to relieve stretch
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13
Q

CO (Q) at rest
1. untrained male
2. trained male
3. untrained female
4. trained female

A
  1. unchanged after training, unless great change in body comp
  2. UTM: HR 70, SV 80, Q 6.0
  3. TRM: HR 55, SV 110, Q 6.0
  4. UTF: HR 70, SV 60, Q 4.5
  5. TRF: HR 55, SV80, Q 4.5
  6. females with smaller SV bc smaller bodies; TR increase SV to maintain Q due to increased EDV and EF
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14
Q

CO (Q) at max
1. untrained male
2. trained male
3. untrained female
4. trained female
5. components of Qmax and effect of training

A
  1. HR 200, SV 100, Q 20
  2. HR 200, SV 140, Q 28
  3. HR 200, SV 80, Q 16
  4. HR 200, SV 120, Q 24
  5. HR is fixed at 220-age, SV is semi-adjustable with genetic and training; HR displays linear change with VO2 in UT and TR until max; SV plateaus at 50% in UT while TR increases slowly resulting in slowed increase in Q at 50% in UT while TR increases
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15
Q

using HR to predict fitness and training intensity
1. variability in max HR
2. assumptions and procedures in using HR to predict VO2max
3. Karvonen Formula

A
  1. high SD, can use max HR to assume max workload and thus VO2max, cheap and highly reproducable by those who can’t reach max effort but v. inaccurate for individual
  2. assume linear relation b/w HR and workload and HR; measure HR at >= 2 submax workloads, extrapolate line to predicted HRmax, determine predicted VO2max
  3. heart rate reserve (HRR) = HRmax - HRrest; training HR (THR) = HRrest + %VO2max*HRR; %HRmax tends to underestimate workload at a %VO2max but error decreases as VO2 approach max
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16
Q

Regulating CO:
1. influences
2. nervous control of CO

A
  1. chronotropic mod rate of contraction using neural and hormonal; inotropic mod strength of contraction using neural, hormonal, and mech factors
  2. cardiovascular control centres in sp cd have PNS and SNS pathways; PNS using vagus nerve to release Ach to chronotropically slow HR at the SA and AV nodes, withdrawal of vagal tone is initial increase HR; SNS release NE through cardiac accelerator nerves to chronotropically increase in HR at the SA and AV node and inotropically increase contractility in ventricles to increase SV
17
Q

vasculature
1. structure and function of different vessels
2. hemodynamics
3. radius and resistance

A
  1. thickest diameter of great vessels 2.5 cm high-velocity BF, low SA, big arteries near heart est bulk flow velocity and driving pressure, small arterioles vasodilate or constrict to regulate BF, thinnest capillaries 6 um for highest SA and slowest BF for sufficient gas exchange; veins 3.0 cm allow pooling of blood to regulate venous return via muscle pump
  2. dynamics of blood circulation dependent on flow, pressure, and resistance; flow proportional to pressure difference on both ends of tube, flow inversely proportional to resistance
  3. resistance = viscosity*length/radius^4; changes in radius leads to great change in flow since viscosity and length of vessel don’t change much; training can increase length and dehydration can increase viscosity but not by much
18
Q

Q rest v. max
1. skeletal muscle
2. splanchnic + renal
3. heart

A

CO rest 5 L/min; CO max 25 L/min
1. 20% Q, 1 L; 80% Q, 20 L
2. 40% Q, 2 L; 5% Q, 1 L
3. 4% Q, 0.2 L; 4% Q, 1 L

19
Q

muscle BF and transit time

A
  1. vasodilation of local arterioles controlled by smooth muscle around it to increase BF to muscle capillaries
  2. transit time is the amount of time it takes for the RBC to pass through capillary, time available for gas exchange, 0.8 s at rest, 0.4 s during exercise despite 20 fold increase in BF, TT maintained by precapillary sphincters opening more capillary beds for greater area of exchange
20
Q

vascular control during exercise

A
  1. neurohumoral control work through the SNS to release NE to vasoconstrict in most tissues especially splanchnic tissues
  2. local control uses changes concentration of blood gases such as decreased O2, increased CO2, and increase in H+, reflecting metabolism in muscle as signal to smooth muscles of arterioles and to dilate to increase BF to replenish fuel and remove waste
  3. contraction of muscle stretches arterioles to release nitric oxide signalling precapillary sphincters to open more capillary beds for gas exchange, nitric oxide then gets degraded, viagra blocks break down of NO, continued signal for vasodilation to increase BF
21
Q

muscle oxygen extraction
1. overview
2. Fick equation

A
  1. arterial blood O2 maintained at 200 mL during normal respiratory function, at rest A-V difference is 50 mL O2/L, during exercise 150 mL/L, more O2 extracted supply metabolism, lower venous O2 as result, higher intensity greater A-V O2 difference
  2. VO2 = Q(a-V O2 diff), why VO2 greatly influenced by SV

CV Exercise Physiology (4 decks)

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