Exam 2- Lectures 9-11 Flashcards
functions of cardiovascular system during exercise
- provide tissues with oxygen and nutrients
- remove carbon dioxide and metabolic waste products
- maintain body temperature
- transport hormones
Oxygen delivery =
cardiac output x arterial oxygen content
when does cardiac output increase?
in proportion to dynamic exercise intensity
what stays relatively constant during exercise?
arterial oxygen content (CaO2)
what do increases in oxygen delivery depend on?
increases in cardiac output
stroke volume =
end diastolic volume - end systolic volume
how do autonomic nerves affect HR?
- vagus (parasympathetic) activation lowers HR
- sympathetic nerves raise HR and cardiac contractility
how does oxygen consumption change with exercise?
- VO2 can increase from 1 MET to 12-20 in untrained to highly trained
- CO increases from 5-20 l/min in untrained (4x increase)
- O2 extraction can increase from 4 ml to 15-20 ml in untrained (3-4x increase)
arteriovenous oxygen difference
- represents the amount of oxygen transferred from the blood to the interstitial space and/or tissue
- a-v O2 difference = arterial O2 content - venous O2 content
BP =
CO x TPR
CO response during exercise
- depends on increases in SV and HR
- both increase at onset of exercise
- SV plateaus during moderate exercise, while HR increases linearly until maximal HR is reached
in most individuals, what is the further increase in CO during moderate to heavy exercise due to?
increases in HR
- often use HR as a surrogate marker for exercise intensity
change in heart rate –>
change in cardiac output –> change in oxygen delivery –> change in VO2 with increasing workload
what dominates heart rate at rest?
vagal activity with minor influence from SNS
Heart rate initial response to exercise
- rapid withdrawal of vagal (PNS) activity
- activation of SNS is slower
what happens as HR continues to rise above 100 b/m
- balance of vagal to SNS tone shifts more and more towards SNS dominant
- during maximal exercise, the HR response is very strongly dependent on SNS
why is there a decrease in HR max due to age?
the reduction in intrinsic HR and decrease in beta-adrenergic responsiveness
what are the consequences of increased heart rate during exercise
- decreased left ventricular filling time
- but filling is well maintained until close to max HR
what helps maintain filling time?
increased rate of relaxation with SNS stimulation
second consequence of an increase in HR during exercise
- can increased cardiac contractility and thus SV –> “treppe” or the force-frequency relationship
- at higher HR there is more calcium available to contractile proteins
- SV will increase as a result of increased contractility
major determinants of stroke volume
preload, after load, and contractility
what occurs to stroke volume during dynamic exercise
increases
can increase from 70 to 100 ml in the untrained
what is preload
ventricular wall tension at the end of diastole
what is used as a major index of preload?
end diastolic volume
what occurs to EDV during exercise?
- increases at the onset of upright exercise (40-60%)
- plateaus at higher levels of exercise
- increased EDV results in larger SV due to Frank-starling mechanism
determinants of EDV
- blood volume
- position
- venous return
SV =
EDV- ESV
Determinants of EDV: Blood volume
- a greater blood volume increases EDV
- exercise in the heat and/or of long duration may lead to dehydration and reduced EDV
determinants of EDV: position
- supine: at rest, EDV is already elevated, so that exercise in the supine position results in small, if any, further increase in EDV
- during exercise in upright position EDV will increase with intensity
determinants of EDV: venous return
increases immediately with muscular contraction:
- muscle pump: skeletal muscle contraction forces venous blood centrally
- respiratory pump: reduced intrathoracic pressure (with large inspiration) favors blood flow into the thoracic cavity from peripheral veins
- venoconstriction: reduced venous compliance mobilizes blood from periphery to central veins (especially from splanchnic organs)
what is after load?
- myocardial wall stress or tension during systolic ejection
- the force that must be overcome in order to eject any blood
what is a major index of after load?
MAP
What occurs to after load with exercise?
- stays the same or increases slightly during exercise
- vasodilation of skeletal muscle resistance vessels attenuates rise in MAP that should have occurred due to the larger increases in CO (MAP = CO x TPR)
what is contractility?
an increase in strength of contraction independent of fiber length
contractility increases during exercise as a result of:
- increase HR (treppe)
- increase beta-adrenergic signaling due to enhanced sympathetic nerve activity and increased plasma levels of epinephrine and norepinephrine
what does increased contractility cause?
- a decrease in ESV, leading to an increase in ejection fraction and therefore a greater SV
- increased contractility maintains early preload (EDV) - augmented rise in SV
increased EDV is due to:
- increase venous return
muscle pump, reparatory pump, increased circulating blood volume due to venoconstriction
decrease ESV
- increased contractility
increased sympathetic nerve activity, increased plasma catecholamines, increased HR
a-v O2 difference determinants
- O2 extraction increases from 4-5 to about 15-16 from rest to maximal exercise
- determinants:
1. tissue PO2 (diffusion gradient), change in pH, PCO2, temperature
2. increased blood flow and increased recruitment of capillaries
increased a-vO2 difference is due to:
increased blood flow
increased capillary recruitment
low PO2 in tissue
decrease Hb affinity for O2
what causes increased LVEDV?
increase venous return:
muscle pump
respiratory pump
splanchnic venoconstriction and visceral vasoconstriction
what occurs to MAP during maximum exercise?
- increases approximately 25-30% while CO may increase 4 fold
- systolic blood pressure may increase by 60% whereas diastolic pressured increases by 10% and therefore pulse pressure increases
why are the relative increases in MAP small compared to CO?
because TPR decreases considerably during dynamic exercise
redistribution of blood flow during exercise
- compliant regions may hold large blood volumes (splanchnic veins and liver)
- during exercise, arterial flow reduced to these visceral organs (via sympathetic vasoconstriction)
- “stored” venous blood mobilized by sympathetic vasoconstriction
what is the receptor type that mediates the veno- and vasoconstriction?
decreases in blood flow during exercise
visceral organs
gut, liver, renal, reproductive organs
increases in blood flow during exercise
heart (but same % of CO), active skeletal muscle, and skin when core temperature increases
At rest, how much blood flow does skeletal muscle receive?
5-10 ml/kg/100g
how much blood flow can skeletal muscle get with maximal exercise?
> 250 ml/min/100g (25-50x resting)
what is blood flow to active skeletal muscle proportional to?
amount of work (oxygen consumption) the muscle is doing
Exercise hyperemia at onset of exercise –> what drives initial hyperemic response?
- flow begins to increase at muscular contraction
- muscle pump: venous pressure reduction
- active vasodilation: mechanical arteriole compression, potassium induced hyperpolarization, NO/PG mediated
skeletal muscle pump
- decreases venous pressure
- pushes venous blood towards the heart
- since a-v pressure difference is higher, blood flow into the vein will be higher when the muscle relaxes
what does mechanical compression of the arterioles promote?
active vasodilation
primary mechanism underlying the rapid active vasodilation associated with a single muscle contraction
interstitial potassium-mediated vascular cell hyper polarization and simultaneous endothelial NO and PG release
what follows vascular compression during skeletal muscle work?
vascular relaxation
exercise hyperemia as exercise continues
- flow mediated vasodilation: as flow begins to increase, so does endothelial cell shear stress
- increased shear stress activates endothelial prostaglandins or NO –> vasodilation and increased flow
metabolic vasodilation at the arterioles-mechanisms include:
- increased interstitial K (hyper polarize vascular smooth muscle and closes calcium channel)
- lower tissue PO2, plus increased interstitial ATP, PGs, acidosis, lactate ion, phosphate ion
functional sympatholysis
- inhibition of alpha-adrenergic mediated signaling at the level of the vascular smooth muscle cell
- even though adrenergic SNS activity is still present to the active skeletal muscle arteries, the vasoconstrictor effect is less than what would occur at rest
flow induced arterial vasodilation
increase in blood flow in artery –> increase in sheer stress on the endothelium –> increase release of NO, PGI and decrease release of endothelin –> vasodilation
is there any neural control of skeletal muscle during activity?
- yes, sympathetic neural activity is still present but effects are blunted at higher levels of exercise
- purpose: avoid fall in arterial BP during exercise due to excessive metabolic dilation because if during heavy activity the skeletal muscle was allowed to maximally dilate, TPR would fall too far and BP would decrease
One factor that contributes to the high level of skeletal muscle blood flow observed during heavy exercise is:
an increase in the skeletal muscle arteriovenous pressure gradient due to the action of the muscle pump
Static resistance exercise
generation of large muscle forces but with little to no change in whole muscle length (ex: pushing against a wall, handgrip exercise)
dynamic resistance exercise
high muscle forces through a distance
Aerobic (endurance or dynamic) exercise is classified as:
- “volume-load” exercise
- is characterized by muscle contractions at a low % of maximal capacity and no mechanical occlusion of blood flow
- volume- load refers to the large increases in preload, SV, and CO during the endurance exercise
resistance exercise is classified as:
- “pressure-load” exercise
- is characterized by muscle contractions at a high % of maximal capacity which results in significant partial or full occlusion of muscle blood flow
- pressure-load refers to the unchanged or higher TPR and definitely high MAP during resistance exercise
CV responses in resistance exercise
- the amount of muscle mass activated, and the intensity of the exercise greatly influences the CV responses to resistance exercise
- the higher the intensity or muscle mass, the greater the increases in MAP and TPR
key differences in CV responses in dynamic vs resistance exercise –> dynamic exercise
- TPR is greatly decreased
- SBP increases modestly, DBP no change, MAP modest increase
- tight linear relationship between HR and VO2
- SV greatly increases
- tight relationship between CO and VO2
- VO2 can increase to maximal values due to CO
key differences in CV responses in dynamic vs resistance exercise –> resistance exercise
- TPR is variable and may increase
- large increases in SBP, DBP, and MAP
- HR does increase but not a good relationship between HR and VO2
- SV same or lower
- CO increases due to HR only; doesn’t reach max values
- VO2 moderately increases; doesnt reach max values
what causes decrease in SV during resistance exercise?
reduced central venous pressure and increased after load
does resistance or dynamic exercise induce a greater MAP?
resistance
what is valsalva maneuver
- a forcible expiration against a closed glottis or against a high resistance
- stabilizes chest wall when lifting
- immediately raises intrathoracic pressure
high intrathoracic pressure leads to
impeded venous return by decreasing CO and BP
results in reflex tachycardia and increased SNA to periphery via arterial baroreflex
what occurs upon release of valsalva maneuver
- there is a large increase in venous return that greatly enhances CO
- CO is pumped into a very constricted vasculature and there is a large increase in blood pressure
- may precipitate angina, acute stroke, retinal hemorrhage in susceptible individuals
MVO2
myocardial oxygen consumption
reflects workload of the heart
determinants of MVO2
- heart rate
- preload
- afterload
- contractility
what is an index of MVO2
rate-pressure product
“double product”
RPP=
HR x SBP
external work
useful work
stroke volume x ventricular pulse pressure
internal work
- elongating vicious or elastic muscle elements and rearranging cardiac muscle architecture in order to contract
- contraction against the closed aortic valve
- proportional to wall stress and degraded as heat
what does increased volume work result from?
an increased preload, which increases both external and internal work
what does increased pressure work result from?
an increased after load, which greatly increases wall stress (internal work) with little change or decrease in SV
which type of work is less economical?
pressure work
greater MVO2 for same external work
a greater proportion of total work is
internal work with pressure work when compared to volume work
a heart that has limitations in coronary flow due to coronary artery disease may have:
- maximally dilated resistance vessels at rest
- if met with greater pressure work, coronary flow will not meet the oxygen requirement resulting in cardiac muscle ischemia and Angelina, which could lead to arrhythmias and sudden cardiac death
patients with hypertension or coronary artery disease:
- may be counseled to avoid heavy resistance training especially static exercise with valsalva maneuver to avoid large acute increase in after load and thus MVO2
what type of exercise is encouraged in cardiac patients?
- moderate dynamic resistance training
- improves or maintains muscular strength and endurance
A patient with CAD experiences angina when he tries resistance training, but is asymptomatic when performing a comparable workload while walking on a treadmill. The mechanism that best explains this difference in response is that during lifting:
MAP increases more compared to walking
does arm or leg exercise induce a greater increase in HR and SBP?
arm exercise
- involves smaller muscle mass to generate same power output
- less economical than leg work (higher VO2 at a given external work)
- lower VO2 max and maximal HR
