10.2 Flashcards by Kiera Joy

The cardiovascular adjustments in exercise consist of a

combination and integration of neural and local chemical factors

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the neural factors apart of CV adjustments in exercise consist of

central command
reflexes originating in the contracting muscle
the baroreceptor reflex

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examples of reflexes originating in contracting muscle

mechanoreceptors and metaboreflexes

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central command is the

cerebrocortical activation of the sympathetic NS that produces cardiac acceleration, increased myocardial contractile force, and peripheral vasoconstriction

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reflexes can be activated intramuscularly by

stimulation of mechanoreceptors (by stretch, tension) and of chemoreceptors (by-products of metabolism) in response to muscle contraction (metaboreflex)

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impulses from the reflex receptors travel

centrally via small myelinated (group III) and unmyelinated (group IV) afferent nerve fibers

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what does the group IV unmyelinated fibers represent

the muscle chemoreceptors (chemically sensitive)

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what has not been identified

no morphological chemoreceptor

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what is unknown about chemoreceptors reflexes

the central connections

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what is the efferent limb of the muscle chemoreceptors composed of

the sympathetic nerve fibers to the heart and peripheral blood vessels

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how do muscle fibers change with disease

aerobic to glycolytic
fast twitch
exercise intolerant
blood flow decreases to muscle, fatigues quicker, blood vessels constrict

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in humans and in trained animals, anticipation of PA

inhibits vagus nerve impulses to heart

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what does the withdrawal of vagal nerve activity underly

the initial increase in heart rate

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eventually after the inhibition of vagal nerve activity

sympathetic nerve discharge also increases

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the concerted inhibition of parasympathetic areas and activation of sympathetic areas of the medulla

increase the heart rate and myocardial contractility

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what does the tachycardia and the enhance contractility due to inhibition of para and increased symp cause

increase in cardiac output, in turn raising the arterial pressure

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as increase in CO what is there a change in

central venous pressure
higher CVP indicative of CV disease

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peripheral resistance declines during

exercise

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at the same time that the heart is stimulated, the sympathetic NS elicits

vascular resistance changes in the periphery

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sympathetically mediated vasoconstriction

increases vascular resistance

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where does vasoconstriction increase vascular resistance and divert blood away from these areas

skin, kidneys, splanchnic regions, and inactive muscle

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what persists throughout exercise

the greater resistance in vascular beds of inactive tissues

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in muscle beds that are not metabolically active what happens

sympathetic constriction

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why does pressure still rise during exercise even when vasodilation occurs

flow is greater than dilation

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what can the increase in blood flow to active muscles at onset of exercise not be attributed to

neural mechanism because a chemical block of the autonomic nervous system does not alter this blood flow response

the increase in muscle blood flow may be caused by

modest elevation of blood pressure or by some unknown mechanism

what do cardiac output and blood flow to active muscles increase with

progressive increments in the intensity of exercise

what decreases as intensity of exercise increases

visceral blood flow (splanchnic and renal vasculatures)

what happens to myocardium blood flow as exercise intensity increases

increases

what happens to brain blood flow as exercise intensity increases

unchanged

what happens to skin blood flow as exercise intensity increases

initially decreases during exercise it then increases, as body temp rises with increments in duration and intensity (serves to help control)

when does skin blood flow finally decrease with exercise

when the skin vessels constrict, as the total body VO2 nears max values

what does the graph of the organ blood flow show

approximate distribution of CO at rest and at different levels of exercise up to peak VO2

what gets most blood

muscle

what happens to blood flow to viscera during exercise

decreases as muscle blood flow increases

what does the major circulatory adjustment to prolonged exercise involve

the vasculature of the active muscles

what progresses as the intensity level of exercise increases

local formation of vasoactive metabolites induces marked dilation of the resistance vessels (of active muscles)

what is one of substance released by contracting muscle

potassium

what is pottasium released from active muscle be in part responsible for

the initial decrease in vascular resistance in the active muscles

what can elevated interstitial K+ cause

vasodilation

how does elevated interstitial K+ cause vasodilation

stimulation of Na-K pump and by activation of the conductance of other K+ channels

the more metabolites released

the further dilation of arterioles

why does BP increase

increase in CO increase in CO must be greater than decrease in TPR

K+

important vasodilator

either action caused by K+ causes

hyperpolarization of vascular smooth muscle membrane, thereby reducing Ca++ entry

what are other contributing factors to vasodilation of arterioles

release of adenosine and nitric oxide (NO), activation of KATP channels, and decrease in pH during sustained exercise

what does reducing Ca++ entry do

allows smooth muscle to relax

all of the factors can

act locally to dilate arterioles in contracting muscle

adenosine release and KATP channel activation are

thought to act at more distal arterioles to increase blood flow

the mechanism for the transmission of the dilating effect to distal arterioles

is not understood

local accumulation of matabolites

relaxes the terminal arterioles

blood flow through the muscle may rise

15-20 times above the resting level

what occurs very soon after the onset of exercise

this metabolic vasodilation of the precapillary vessels in active muscles

the decrease in TPR enables the heart to

pump more blood at a lesser load and more efficiently (less pressure work) than if TPR were unchanged

what is perfused at rest

only a small % of the capillaries

whereas in actively contracting muscle how much is perfused

nearly all of the capillaries contain flowing blood (capillary recruitment)

what is secondary to arteriolar vasodilation

decrease in TPR

in heart failure what happens to TPR

less dilation unchanged TPR higher afterload not only pump function impaired but also squeezing against harder resistance

the contracting muscle avidly extracts

O2 from the perfusing blood (increased A-VO2 diff) and release of O2 from blood is facilitated

what is the release of O2 from the blood facilitated by

nature of oxyhemoglobin dissociation

what shifts oxyhemoglobin dissociation curve to the right

reduction in pH caused by high concentration of CO2, the formation of lactic acid and increase in temp in contracting muscle

what is the oxyhemoglobin dissociation curve shifting right an example of

the Bohr effect (facilitating offloading of O2)

fick equation

VO2 = CO x AVO2 diff

SV equation

EDV - ESV

Leftward shift

not facilitating O2 offloading

what does the oxyhemoglobin dissociation curve show

the saturation of hemoglobin as a function of the partial pressure of O2 (Po2) in blood

at any given partial pressure of O2

less O2 is bound by the hemoglobin in the RBCs consequently O2 removal from the blood is facilitated

Oxygen Vo2 consumption may increase

as much as 60 fold

muscle blood flow only increases

15 fold

muscle myoglobin serves as a

limited O2 store in exercise it can release attached O2 at very low partial pressures

muscle myoglobin facilitates

O 2 transport from capillaries to mitochondria by serving as an O2 carrier

blood flow not a 1:1 relationship with

VO2

O2 consumption increases much higher than

blood flow (lungs designed to exceed what heart can do)

in anticipation of exercise, the

vagus nerve impulses to the heart are inhibited and the sympathetic nervous system is activated by central command

results of sympathetic NS being activated

increase in HR, myocardial contractile force, cardiac output, and arterial pressure

with exercise, vascular resistance

increases in skin, kidneys, splanchnic regions, and inactive muscles and decreases in active muscles