Two one’s individual ability to reach their maximum

Two factors that limit cardiac
output (Q) are heart rate (HR) and stroke volume (SV). The HR is limited by age
and one’s individual ability to reach their maximum heart rate, but this factor
does not change with training5. Stroke volume is limited by the amount the
ventricles can fill (end-diastolic filling) which is both determined by a
reduction in pericardial resistance, and an increase in blood volume5,6 found
in elite trained athletes. SV is also limited by the ejection volume possible
by the ventricles which can be explained by the Frank-Starling mechanism in
which a reduction in pericardial resistance would provide more filling, and
greater contractility to increase the ejection volume6. Increased heart size
would also explain the increase in SV with elite trained athletes due to chronic
and prolonged training leading to increased ventricular wall size6. Thus, with
proper training, stroke volume appears to be the main limiting central factor
that if improved, can greatly increase cardiac output and consequently, VO2max.


In conclusion, the research
supports the fact that cardiac output, a central limitation in trained
athletes, is the primary limiting factor to maximal oxygen uptake. This is
despite the fact that at VO2max, athletes may demonstrate a decrease in the
a-vO2 difference, perhaps due to very high blood flow limiting the full
oxyhemoglobin saturation . Consistent across many research findings 1,3–6,
oxygen delivery is the primary limiting factor for VO2.

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trained athletes had larger
hearts and the size was attributable to adaptive processes within the heart
that caused ventricular hypertrophy. This hypertrophy of the main pump allows
for more powerful contractions of the left ventricle which, in turn, causes
more blood to be pumped per beat of the heart. It goes without saying that the
more blood that can be pumped out into the arteries per beat, the more oxygen
that is available to working muscles. If the average, untrained individual has a
maximum cardiac output of 20 l/min. and the elite, aerobic athlete has a
maximum cardiac output of 40 l/min., it can be assumed that if oxygen
saturations are the same, twice as much oxygen is being transported within the
arteries per minute in the elite athlete and this increased amount of oxygen
results in greater muscle contraction and increased performance.


increases in cardiac output (and
VO2 max) seems to be reflective of increases in stroke volume

the heart muscle react to
increased levels of aerobic exercise by growing larger (hypertrophy) and being
able to handle increased levels of aerobic work. This hypertrophy is most
evident in the left ventricle as this is the primary “pumper” of
blood out into the system. The cavity increases in size to accommodate larger
volumes of blood and the muscle increases in cross-sectional area which allows
for greater contractility and more forceful contractions. This combination of
adaptive mechanisms leads to increased stroke volumes which can vary from
minimal in recreationally trained individuals to extreme in the most elite
endurance athletes.

It is a fact that aerobically
trained athletes have higher VO2 max values than their untrained counterparts
(with the exception of extreme cases of genetic predisposition which can never
be ruled out). It is also a fact that endurance-type athletes have higher
cardiac outputs than sedentary individuals. It can then be postulated that the
higher VO2 max values are the result of greater oxygen delivery which is a
result of increased cardiac output