KINS 4500 chapter 13 what changes when you keep doing it

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Last updated 5:10 PM on 10/10/26
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25 Terms

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Heart rate falls from 72 to 58 over six months of running

adaptation

heart rate changes in Fick equation

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Heart rate rises from 72 to 140 in the first two minutes of a jog

response

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Stroke volume falls over 45 minutes at a fixed pace

response

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The capillary to fibre ratio in the quadriceps goes up.

adaptation

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the athlete’s heart is a bigger heart

left and right ventricular mass in endurance athletes and untrained controls, measured by cardiac MRI

both chambers grew, and by the same share

21 male endurance athletes against 21 untrained men, matched for age, height, and weight. Cardiac MRI

left ventricle 35% heavier. Right ventricle 38% heavier. The right side is not long for the ride, it adapts too

mass ratio, left to right: 2.6 in the athletes and 2.6 in the controls. Ejection fraction was the same in both groups, near 59% left and 63% right

scharhag’s phrase for it: a balanced enlarged heart, bigger everywhere, not remodeled out of proportion

<p>left and right ventricular mass in endurance athletes and untrained controls, measured by cardiac MRI</p><p>both chambers grew, and by the same share </p><p>21 male endurance athletes against 21 untrained men, matched for age, height, and weight. Cardiac MRI</p><p>left ventricle 35% heavier. Right ventricle 38% heavier. The right side is not long for the ride, it adapts too</p><p>mass ratio, left to right: 2.6 in the athletes and 2.6 in the controls. Ejection fraction was the same in both groups, near 59% left and 63% right</p><p>scharhag’s phrase for it: a balanced enlarged heart, bigger everywhere, not remodeled out of proportion </p>
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a big heart that is fine, and a big heart that is not

wall and cavity moving TOGETHER is the physiological pattern. Wall without city is the one that needs a cardiologist

athlete’s heart

Pathological remodeling

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athlete’s heart

wall thickening and cavity enlargement together. Chamber fills and empties normally. Function normal or better than normal. Regresses when training stops.

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pathological remodeling

wall thickens without the cavity enlarging. Filling is impaired. Function is reduced. Does not regress

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same test, trained, and untrained

cardiac output, stroke volume, and heart rate through a graded test to exhaustion trained against untrained

three adaptations, and they are all one adaptation

the same graded test, run to exhaustion

higher maximal cardiac output. Higher stroke volume at every point. Lower heart rate at every sub maximal point. And the trained subject lasts longer

maximal heart rate is the SAME in both. Training does not raise. Ask the room why before you tell them

every one of those is a bigger stroke volume. A bigger stroke volume times an unchanged maximal heart rate is a bigger material cardiac output, and the same delivery at rest needs fewer beats to achieve

more blood per squeeze for trained

<p>cardiac output, stroke volume, and heart rate through a graded test to exhaustion trained against untrained</p><p><strong>three adaptations, and they are all one adaptation</strong></p><p>the same graded test, run to exhaustion</p><p>higher maximal cardiac output. Higher stroke volume at every point. Lower heart rate at every sub maximal point. And the trained subject lasts longer </p><p>maximal heart rate is the SAME in both. Training does not raise. Ask the room why before you tell them </p><p>every one of those is a bigger stroke volume. A bigger stroke volume times an unchanged maximal heart rate is a bigger material cardiac output, and the same delivery at rest needs fewer beats to achieve </p><p>more blood per squeeze for trained </p>
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back to the question we left open

  • On September 29, we said the stroke volume response is trained athletes is unsettled, and the chapter itself calls it debated. Chapter 13 then prints out a figure showing trained stroke volume rising continuously to maximum, from a paper titled "endurance athletes" stroke volume does not plateau"

  • Your textbook takes both positions, one chapter apart

  • This is not a mistake you need to resolve. It is what a live question looks from the outside

  • What you should be able to do is say what evidence would settle it


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what the figure actually shows

stroke volume against heart rate in trained and untrained men matched at the same heart rates

the plateau is not a law

seven trained and seven untrained men, matched at the same heart rates on a cycle ergometer

untrained store volume flattens by 120 b/min and then moves 3 mL for the rest of the test. That is the plateau the last slide drew

trained stroke volume never flattens. It climbs another 40 mL past that same point, all the way to maximum heart rate.

the Lowe panel is not new data. It is this panel times the x axis, behave cardiac output is heart rate times stroke volume. Same fasct, and now the size of it is visible

<p>stroke volume against heart rate in trained and untrained men matched at the same heart rates</p><p><strong>the plateau is not a law</strong></p><p>seven trained and seven untrained men, matched at the same heart rates on a cycle ergometer</p><p>untrained store volume flattens by 120 b/min and then moves 3 mL for the rest of the test. That is the plateau the last slide drew</p><p>trained stroke volume never flattens. It climbs another 40 mL past that same point, all the way to maximum heart rate.</p><p>the Lowe panel is not new data. It is this panel times the x axis, behave cardiac output is heart rate times stroke volume. Same fasct, and now the size of it is visible </p>
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three more adaptations, and where each one acts

everything on this slide widens one of the two terms in the Fick’s equation

vascular structure

vascular function

blood volume

do not do cardio > lose

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vascular structure

the athlete's artery. Larger vessel diameter, thinner wall, greater capillary density. More surface for exchange and less resistance to flow

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vascular function

better endothelial function, so greater ability to vasodilate. Directly tied to endothelial nitric oxide production

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blood volume

 a 20-25% larger blood volume in highly trained endurance athletes, mostly plasma. More filling, so more stroke volume

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blood volume moves in eight days, both ways

eight days of training. All of its plasma

blood volume rose about 550 mL over eight days

plasma volume rose about 550 mL. Red cell volume did not rise at all

so the early gain in water, not cells. Cells take weeks; plasma takes days. The top line here is not measured, it is the other two added together

stop training and it drains away again within a week, most of the way back to where it started

drawn from zero, these are changes of a few percent in a large number. The original broke its axes and make them look like cliffs

  • Plasma volume and red cell volume across eight days of training and the days after stopping

  • Someone who loses faster more adaptive to the environment

  • Muscle tissue expensive


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every adaptation in one table

the stroke volume is the only one that reads the same way in all three columns

<p>the stroke volume is the only one that reads the same way in all three columns </p>
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how much training buys how much gain

spread of the change in VO2max attributable to intensity, duration, and starting fitness

frequency, not duration

frequency and starting fitness move it most. Duration moves it least, by a factor of six, and duration is the one people add first

pooled across many studies, so the four are not independent: a 90 to 100% program was rarely also a 45 min one

<p>spread of the change in VO2max attributable to intensity, duration, and starting fitness</p><p><strong>frequency, not duration </strong></p><p>frequency and starting fitness move it most. Duration moves it least, by a factor of six, and duration is the one people add first</p><p>pooled across many studies, so the four are not independent: a 90 to 100% program was rarely also a 45 min one</p>
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what resistance training does, and does not, do

resistance training produces real cardiovascular adaptations, but they are not the aerobic ones, and the evidence on muscle oxidative capacity genuinely conflicts

resting heart rate: little or no change. Resting blood pressure: decrease or no change

on mitochondrial content: some studies show a decrease or no change and others a small increase

on capillary number; some show a small increase and others a small decrease

ask what would make studies disagree: training status, program design, and how long the study ran

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sex differences at maximal exercise

maximal heart rate is 195 in all four groups. Everything else moves with sex, with training or with both

<p>maximal heart rate is 195 in all four groups. Everything else moves with sex, with training or with both </p>
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how much of this is genetics?

  • In the HERITAGE family study, the heritability estimate was 47%. That is the heritability of the RESPONSE TO TRAINING, not of your starting VO2max

  • 481 sedentary adults from 98 two-generation families, trained for 20 weeks.

  •  There was about 2.5 times more variance between families than within them.

  • So how much you gain from the same programme runs in families. What you start with is a different question.


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the same comparison, forty years later

comparison of cardiovascular responses to maximal exercise in sedentary and trained elderly individuals. 60 to 70 years

<p>comparison of cardiovascular responses to maximal exercise in sedentary and trained elderly individuals. 60 to 70 years</p>
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decline with age, and what this figure gets wrong

  • Decline in peak oxygen uptake per decade, the cross sectional assumption against longitudinal data

  • The rate of decline is not constant

  • Usually around age 30

  • cross sectional studies said 5 to 10% per decade, the same every decade. Follow the same people for years instead and the rate ACCELERATES: about 3 to 6% in the 20s and 30s, about 20% past 70

  • now the dashed line. Maximal heart rate falls at a flat 4 to 5% per decade the whole way across

  • so ask the room: if oxygen uptake is cardiac output times extraction, and cardiac output is heart ate times stroke volume, and the heart rate term is NOT accelerating, what is? > stroke volume or a-vO2 diff

  • hollow markers are interpolated, not Fleg’s value


<ul><li><p><span>Decline in peak oxygen uptake per decade, the cross sectional assumption against longitudinal data</span></p></li><li><p><span><strong>The rate of decline is not constant</strong></span></p></li><li><p><span>Usually around age 30</span></p></li><li><p><span>cross sectional studies said 5 to 10% per decade, the same every decade. Follow the same people for years instead and the rate ACCELERATES: about 3 to 6% in the 20s and 30s, about 20% past 70</span></p></li><li><p><span>now the dashed line. Maximal heart rate falls at a flat 4 to 5% per decade the whole way across</span></p></li><li><p><span>so ask the room: if oxygen uptake is cardiac output times extraction, and cardiac output is heart ate times stroke volume, and the heart rate term is NOT accelerating, what is? &gt; stroke volume or a-vO2 diff</span></p></li><li><p><span>hollow markers are interpolated, not Fleg’s value </span></p></li></ul><p></p>
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detraining: what goes first

  • The adaptations are not permanent, and they do not all leave at the same rate. Plasma volume is among the fastest, measurably down within about eight days

  • Blood volume comes back off in roughly the time it took to come on

  • Stroke volume and maximal cardiac output that follow

  • The structural changes take longer than the volume changes

  • Reduced training is not the same as no training: frequency and duration can drop a long way before VO2max does


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close: one adaptation, many consequences

  • Trained people have a lower heart rate at rest, a lower heart rate at any submaximal workload, the same maximal heart rate, and a higher maximal cardiac output

  • Explain all four with ONE adaptation

  • Then: why does maximal heart rate not increase with training > we can have harder squeezes but we can not change, can not change filling time, TIME