D. look at pics of heart to see how much blood in it at rest vs exervise using nts.

Measure end diastolic volume and end systolic volume. As go from rest to mild
exercise, get a big increase in filling and a small dec in end systolic volume. At
peak/max exercise, have greatly increased SV. Done that largely by increase
preload (end diastolic volume) and by virtue of Beta 1, the heart is contracted more
vigorously and dec end systolic volume. Net effect is that SV has gone up. So if
were to look at a PV loop:

So during exercise: increased preload, dec end systolic volume thanks to more
vigorous contraction. So get a bigger SV.

Might think that since have so much more filling of LV, would end up with an inc
diastolic P in the LV and in the LA. But in fact during vigorous exercise of a healthy
heart, it actually drops. So left ventric pressures during diastole are actually lower.
Good bc don’t want LA Pressures to rise. So how can LA P drop? The heart muscle is
sort of like a rubber ball. Semirigid. The harder you push it the better it relaxes
(recoil). The ventricular muscle recoils and P drops during diastole from what it
would be at rest. So LV p does not rise despite the fact that you increased end
diastolic volume. So pre load went up yet end diastolic P did not go up. If LAP goes
up that would dec delta P of flow thru lung. And also would cause edema in lung due
to the starling forces.

Exercise 2

The csrotid baroreceptors, during ecxercise, are they acting to increase sympathetic
output or would they be acting to decrease sympth output? They fire in response to
pressure/stretch. So if systolic P goes up, baroreceptors firing more. Also respond to
change in pressure. When exercising change in P with each beat is greater bc
systolic goes up and diastolic stays the same. The point is that the baroreceptors
actually are checking sympathetic output, preventing it from going enormously high
during exercise. They are actually acting as a break during strenuous exercise.

Now gonna look at metabolic changes during exercise. (E)

When vigorously exercising, E and NE have gone up bc the exercise produces a big
increase in NE and E. that promotes glycogen breakdown both in the active muscle
(accomplished in part bc u get more intracellular Ca which directlryu activates
phosphorylase which activates glycogen breakdown idepenetedly of E and NE)..,
end product of which is anaerobic conditions in lactate. Same thing happens in
inactive muscle, don’t have Ca doing it bc the muscle is not contracting but
neverthe less the E and NE is causing glycogen breakdown, lactate coming out as
the product during anaerobic conditions and during vigorous exercise at least part
of the muscle metabolism is anerobic.
Lactate goes to liver gets converted into glucose. Glucose can be sec by the liver, E
promotes this. So the glycogen from the muscle actually creates glucose which is
aavailabe then for the RBCs and the CNS. Some of the glucose gose back to the
muscle and gets utlizied, to CO2 and H20 and generates ATP.

Because insulin sec is decreased, not an excessive amt of the glucose gets into the
muscle. IMPORTANT. Dec insulin tends to dec glucose uptake into the muscle. But
because are using glucose in the muscle theres still a reasonable gradient so
glucose does go in. glucose metabolism during exercise by the muscle
INCREASES> not because of this hormonal change but inspite of it. Why bc of
increased blood flow at least 20 fold to the working muscle. So if increase delivery
of glucose 20 fold, even if you’ve made it more difficult for glucose to get in you still
end up using more glucose by the exercising muscle. Were it not for the dec sec of
insulin and the other change (inc glycolysis that occurs means that more FFAs are
entering the muscle and that activates the FA part of the glucose-FA cycle. So the
mere fact that FAs get into the muscle tends to decrease the glycolysis and glucose
uptake into the muscle) prevents an enormous increase in glucose metabolism by
the muscle during exercise. Were it not for this all of the glucose would be utilized
by the muscle.

**now gonna look at a couple of figures that we saw earlier.

Looking at work rate Kg/m/min so what we’re really looking at is power (work/time).
Measuring these parameters at various work rates/power levels.

HR- the greater the power output, the greater the HR. so HR approximately tripled
from 60>>170.

CO went from ~6 to ~17/18. SO CO ~ tripled.

SV went up and then came down, but not quite to original level. So SV increased
and was still larger than it was at rest during exercised. In a person with a well-
conditioned heart, SV going down bc at rapid heart rates don’t have adequate time
for filling-you jmust don’t get that. Even at a HR of 200 SV is still larger at intense
ex

HR- the greater the power output, the greater the HR. so HR approximately tripled
from 60>>170.

CO went from ~6 to ~17/18. SO CO ~ tripled.

SV went up and then came down, but not quite to original level. So SV increased
and was still larger than it was at rest during exercised. In a person with a well-
conditioned heart, SV going down bc at rapid heart rates don’t have adequate time
for filling-you jmust don’t get that. Even at a HR of 200 SV is still larger at intense
exercise than original.
Systolic P increases. Mean P goes up a little. Diastolic P stays essentially constant,
maybe increase a bit. Net effect is PP increases., PP= SV/C. So SV went up a little
bit. And compliance-=w/shypmathetic input, the aorta and large arteries may have
become a little more stiff so C decreased a bit. SO these are why PP goes up.

**TPR decreases, at least 3 fold.

**O2 consumption went up from about 300 to 2200. SO ~7 fold inc in oxygen
consumption.

How can you have CO going pu only 3 fold but oxygen consumption going up 7 fold.
The answer is in AV diff.

VO2 (amt of oxygen you use that you deliver to tissues and that will be used) = CO
x (a-v) AV diff in O2 content. Arterial content of O2 doesn’t change. Mixed
venous content goes down. So AV diff gets larger. CO gets larger too and that’s
how get a 7 fold increase in oxygen u tilization (Vo2). This is the FICK equation.
KNOW IT.

F. Figure from Dr. Ebihara.

Looking at work rate (power) expressed as watts. Measuring several parameters.

pCO2 of alverolar (and therefore arteriolar) did not increase with exercise. May
have decreased a bit towards the end.

Alverolar O2 and therefore arteriolar O2 does not dec, may inc a little with intense
exercise. That comes back to the point that we ventilate more during exercise for
several reasons but not bc of chemical signals from O2 or Co2 bc O2 does not drop
and CO2 does not increase.

Measure of oxygen utilization as a function or work-directly related to amt of work.

CO2 otuput also directly related to amt of work

Ve= amt of air moved/minute=Vt. Not Va, which will be a little less (bc have to
ventilate DAS too). But essentially they are similar bc DAS comprises such a small
amount.
As increase power, O2 and CO2 go up at the same rate. The O2 slope never
changes, but at a certain point the CO2 slope changes as increase work rate. CO2
slope becomes steeper as does Ve slope. The moment when those two curves
differ is supposed to be a measure of anaerobic threshold. What it represents is the
point at which lactic acid starts to build up in the blood so H ion starts to bulid up in
blood which stimulates ventilation. So ventilation goes up so CO2 output goes up bc
the amt of CO2 you get rid of is proportional to alverolar ventilation (which is inc).
so the point at which those two curves change their slope is the anaerobic threshold
which is stimulated by accumulation of H stimulating the carotid body
chemoreceptors (NOT THE BRAIN). In fact, the brain gets its H ion from CO2, which
is decreasing. The brian doesn’t measure H ion directly. So this is increased
ventilation in response to the H ion, a byproduct of lactic acid production.
Presumably when you train well you can increase your anaerobic threshold. So you
can exercise more before u have to become anaerobic.

Anaerobic threshold-point at which lactic acid starts to stimulate ventilation so

much that the two curves now differ

Also at the anaerobic threshold, bicarb starts to dec in blood. Tahts bc when you
blow of CO2 bicarb decreases (davenport diagram!). at this point you are
hyperventilating (hypernia too). Ph of blood drops as bicarb drops.

***Clinical

Splanchnic and renal blood flow. Percent of resting value. At rest, the athlete, NA
adult, and MS patients, not much difference. All start out at 100%. As you exercise
and CO flow goes way up, athlete can go to ** 65? oxygen consumption. The % of
CO going to viscera decreases considerably. This dec happens in all three groups
but it happens at a lower oxygen consumption for ppl w/MS bc they can’t achieve a
higher Oxygen consumption. Still when they exercise they still see the same kind of
dec in blood flowing thru the viscera due to inc NE, E, etc.

As we exc our HR goes up and the percentage of blood that is going to the viscera
decreases (renal aplanchnic both dec). NE goes up and that is presumably the
reason why the splanchnic goes down = a-1 mediated constriction during exercise.