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Heart rate falls from 72 to 58 over six months of running
adaptation
heart rate changes in Fick equation
Heart rate rises from 72 to 140 in the first two minutes of a jog
response
Stroke volume falls over 45 minutes at a fixed pace
response
The capillary to fibre ratio in the quadriceps goes up.
adaptation
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

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
athlete’s heart
wall thickening and cavity enlargement together. Chamber fills and empties normally. Function normal or better than normal. Regresses when training stops.
pathological remodeling
wall thickens without the cavity enlarging. Filling is impaired. Function is reduced. Does not regress
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

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
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

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
vascular structure
the athlete's artery. Larger vessel diameter, thinner wall, greater capillary density. More surface for exchange and less resistance to flow
vascular function
better endothelial function, so greater ability to vasodilate. Directly tied to endothelial nitric oxide production
blood volume
 a 20-25% larger blood volume in highly trained endurance athletes, mostly plasma. More filling, so more stroke volume
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
every adaptation in one table
the stroke volume is the only one that reads the same way in all three columns

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

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

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.
the same comparison, forty years later
comparison of cardiovascular responses to maximal exercise in sedentary and trained elderly individuals. 60 to 70 years

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

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
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