13.1 Flashcards by Kiera Joy

panel 3 similar to

4 and 7

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panel 3 looking at

HR and CO2 production

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panel 3:

HR versus VO2 and VCO2 versus VO2 (anaerobic threshold)

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x axis is

VO2 not work or time

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the anaerobic threshold is defined as

the level of exercise VO2 above which aerobic energy production is supplemented by anaerobic mechanisms

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anaerobic threshold is reflected by an increase in

lactate and lactate-to-pyruvate (L/P) ratio in muscle and arterial blood

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the underlying mechanism for the AT measurement depends on

the onset of anaerobic glycolysis leading to a net increase in lactic acid production

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at work rates below the AT

The muscle and blood L/P ratio is the same as at rest, and no metabolic acidosis develops

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above the AT

lactic acidosis develops

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lactic acidosis occurs when

rate of rise of VCO2 is greater then VO2
greater lactic acid buffering

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the ventilatory threshold can be defined physiologically as

VO2 above which the critical capillary PO2 has been reached and production of ATP through anaerobic glycolysis supplements the aerobic ATP production

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ventilatory threshold can also be defined in terms of changing redox state within the cell as

vo2 at which lactate and L/P ratio increase (LT)

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ventilatory threshold can also be defined it terms of acid base balance change as

the vo2 at which lactic acidosis develops (lactic acidosis threshold LAT)

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like the VO2max the threshold measurement is influenced by

the size of the muscle groups involved in the activity

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what increases occur during incremental exercise in trained and sedentary normal subjects and in patients with cardiac disease

lactate increase and bicarbonate decrease

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as lactate rises

bicarbonate decreases
develops very early

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H+ production is increased when

lactate concentration is elevated in the cell

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at the pH of cell water, virtually all of the increase in H+

production must be buffered

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the H+ produced with the first 0.5 mmol/L increase in lactate appears

to be buffered by newly generated HCO3-

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in the buffering of H+ what is the new HCO3- resulting from

the reaction accompanying hydrolysis of PCr in muscle during early exercise

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above this initial increase in lactate, HCO3- buffers

newly produced H+

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at work rates above the threshold, an obligatory

increase in CO2 production is produced above that from aerobic metabolism

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why is there an obligatory increase in CO2 production above that from aerobic metabolism

because HCO3- buffers newly produced H+

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what is H+ buffered by

HCO3
CO2 released as we ventilate because of buffering

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what do we use as indicator of buffering

co2 exiting

what is equivalent to the co2 generated from the dissociation of HCO3 buffering of lactic acid

new lactate accumulating during exercise

what is easy to detect

the developnent of cellular lactic acidosis

how do you measure cellular lactic acidosis

measure the rate of increase in VCO2 relative to that of VO2 during a progressively increasing exercise test

if Vco2 vs VO2 relationship below threshold has

a slope consistently at or slightly less than 1.0

IF vco2 and vo2 relationship above the AT

The slope changed to a value greater than 1.0

what can a short, progressive work-rate test rapidly determine

the VO2 at which lactic acidosis develops when gas exchange is measured breath by breath or as avg of several breaths

what is the reason gas exchange is so effective at detecting the development of cellular metabolic acidosis

the time delay between HCO3 buffering lactic acid in cell and its appearance in the lung gas is only a few seconds

mechanism 1

describes gas exchange that results solely from buffering of newly formed lactic acid

increase lactate -> increase HCO3 ->

- voc2 increase non-linear with WR - VO2 increase linear with WR - decrease pH

v-slope is for

determining AT

v-slope

plot of VCO2 vs vo2

AT on graph is where

VCO2 starts to increase faster than VO2, so slope of plot becomes steeper than 1

when the net increase in lactate accumulation produces acidosis

VCO2 accelerates relative to VO2

When vo2 and vco2 plotted against each other the relationship is composed

of two apparently linear components, the lower had slope of slightly less than 1.0, whereas upper had slope steeper than 1.0

intercept of these two slopes is

the AT as measured by gas exchange

what drives the change in slope

buffering of lactic acid causes obligatory increase in VO2 relative to VO2 from the co2 produced when HCO3 buffers lactic acid

technique is referred to as v-slope method because

it relates the increase in volume of vco2 output to volume of vo2 uptake

with increasing work rate exercise hr normally increses

linearly with vo2

in heart diseases unrelated to conduction defects the HR often

increases relatively steeply for the increase in vo2 because the SV is reduced

in heart diseases unrelated to conduction defects VO2 commonly shows its

rate of increase with work rate when the myocardium becomes ischemic, as in patients with coronary artery disease

because HR typically continues to increase in patients not on B-adrenergic blockade,

the rate of increase in hr relative to vo2 becomes steeper, deviating from linearity established at lower work rates

with HD, HR

has steeper rise for given VO2

The increasing HR at later parts implies

sv is decreasing to offset hr and CO may not be increasing in pace with vo2 requirement

although curvilinear increase in HR VO2 relationship not always seen in patients with HD, it is usually useful diagnostic observation and suggests

significant worsening in LV fuction with increasing WR

What is pulmonary vascular disease also associated with

steep HR

why is pulmonary disease associated with steep HR

because venous return to left side of heart and therefore LV output is low

Heart rate reserve

measure of the difference between predicted maximal HR based on age, and measured HR at peak vo2

normally HRR is

relatively small (less than 15bpm)

HRR is usually normal in patients with

silent myocardial ischemia and valvular HD and in patients iwth disorder of pulmonary circulation (No pain, exercise lipmitation due to CV function)

patients with peripheral arterial disease and COPD become

symptom limited before pred. max HR reached no intrinsic limitation, but symptoms stop before max HR

patients with disorders of the conducting system of the heart, or SA node

may also have low max HR

Patients who take B-adrenergic blocking drugs or who are limited in exercise because of heart block or sinus syndome have

large HRR

Patients who make a poor effort have an

increased HRR becuase they fail to maximally stress their CV system at time they stop exercising

In normal subjects HR

increases linearly with VO2 to predicted maximums

in patients with heart failure and without chronotropic incompetence

the HR increase is steep

HR and VO2 relationship may lose

its linearity with HR increasing progressively more rapidly than vo2 in patients with myocardial ischemia

VCO2 increases linearly with

vo2 with a slope of 1 or slighlty less than 1, up to the AT

The vco2 increases more rapidly above

AT causign steepening of slope

the degree of steepening of s2 depends on the

rate of HCO3 buffering of lactic acid

AT is low in patients with

poor CV function (early onset lactic acidosis)