Hi, I originally responded to this question directly to Hansel and my
reply to him where I zip through the VO2 calculations using his example
results is at the end of the email. However, I feel some of the postings
on sportscience deserve some clarification, so I am compelled to chime in.

Beginning with this quote:

“Based on your friend's intake (6000 ml of O2/min)his mass specific
VO2max consumption would be 6000/80 or 75 ml of O2/(kg-min). That value
is pretty high. Ed Coyle measured Lance Armstrong's VO2max in the same
area, but he is
exceptional.”

1. For average folks this value is very high, but for international class
cyclists, 75 ml/kg/min VO2 max is not exceptional at all, more like the
average I would say, based on published data from various sources.
However, most international class road cyclists weigh 10-15kg less than
the 80kg fellow in question, so his absolute VO2 og 6.0 liters/min IS
quite high and is more typical of what we see in elite XC skiers and
rowers. A 65kg athlete with a VO2 max of 75 ml/kg/min is nothing to write
home about in a high performance setting. An 80 kg athlete with the same
is very impressive. A 100kg athlete (like a 2m rower) with 75 ml/kg/min
is (7.5 Liters/min) is well, higher than I have ever heard of. Allometric
scaling is an interesting topic.....

2. There seems to be some confusion about ejection fraction (EF) versus
stroke volume (SV). They are related but not the same. Ejection fraction
= (End diastolic volume-End systolic volume)/ end diastolic volume)*100.
EF tells us something about the contractile function of the heart. It
increases some during exercise due to sympathetic stimulation, but as Carl
Foster pointed out, not much. On the other hand, EF is dramatically lower
in failing hearts as Ian Shriar points out.

What normally DOES increase during exercise is End diastolic volume (EDV).
The heart fills with more blood during diastole due to increased venous
return. So, even with no change in ejection fraction, SV goes up, since
the same fraction of a larger EDV gives a higher SV. But, with a
combination of both increased EF and increased cardiac filling, SV can and
does increase relatively more than EF during intense exercise. I have to
admit the table Ian Shrier presented does not support this contention, but
those data are not consistent with a lot of other data I have seen (see
refs below for example) and they are from untrained men at 65% max as I
recall.


3. “At very high heart rates experienced at VO2max, there is less time
for the heart to fill, end- systolic volume therefore decreases, and this
leads to decreases in stroke volume (not sure if ejection fraction
declines but I think so).”

I also learned 20+ years ago as an exercise physiology student that stroke
volume invariably plateaus at about 40% of VO2 max and even declines at
very high heart rates due to inadequate filling time between the beats.
This “fact” is still commonly stated in textbooks. However, there have
been several studies in the last 15 years demonstrating that SV does NOT
plateau in well-trained endurance athletes (see references at end of
post). Exceptional diastolic filling performance seems to explain the
finding that stroke volume can continue to increase at even 90% or more of
VO2 max. However, the old dogma does persist despite new evidence and
better understanding of the underlying mechanisms, kind of like the term
“anaerobic threshold”. And when you think about it, if stroke volume (and
end diastolic volume) plateaus at 40% of VO2 max, why would doing interval
training at 90% of VO2 max have beneficial effects on cardiac performance?




My original response to the question:

The equation for VO2 is HR x SV X a-vO2diff. HR x Stroke volume gives
the cardiac output, and thereby the oxygen delivery. Arterio-venous O2
difference represents the amount of oxygen extracted from the blood by the
tissues( primarily exercising muscle here) or the difference in the
arterial and venous blood oxygen content, expressed in ml O2 per
100mlblood. Oxygen extraction increases significantly during exercise.

So 200 x 175ml/beat (a good guess for stroke volume for this person)
=about 35 L/ min cardiac output. Remember that A-V O2 diff is measured in
ml O2 per 100ml/blood. Oxygenated blood leaves the heart with about
20ml/O2 per 100ml. At rest the AVO2 diff is 3-5ml/100ml (meaning 75-80%
of
the oxygen is left in the blood and returns to thelungs). During exercise
a-v O2 diff may increase to 16-18 ml/100ml. So 35 L (350 dL) x
17 ml/dl = = 5,950 ml O2 or about 6L min.




Stroke volume (non)plateau references:

Gledhill N, Cox D, Jamnik R. Endurance athletes' stroke volume does not
plateau: major advantage is diastolic function. Med Sci Sports Exerc.
1994 Sep;26(9):1116-21.

Zhou B, Conlee RK, Jensen R, Fellingham GW, George JD, Fisher AG. Stroke
volume does not plateau during graded exercise in elite male distance
runners. Med Sci Sports Exerc. 2001 Nov;33(11):1849-54.

Ferguson S, Gledhill N, Jamnik VK, Wiebe C, Payne N.
Med Sci Sports Exerc. 2001 Jul;33(7):1114-9.
Cardiac performance in endurance-trained and moderately active young women.


Wiebe CG, Gledhill N, Jamnik VK, Ferguson S. Exercise cardiac function in
young through elderly endurance trained women. Med Sci Sports Exerc. 1999
May;31(5):684-91.

Wiebe CG, Gledhill N, Warburton DE, Jamnik VK, Ferguson S. Exercise
cardiac function in endurance-trained males versus females. Clin J Sport
Med. 1998 Oct;8(4):272-9.



Stephen Seiler Ph.D FACSM
Institute of Public Health, Sport, and Nutrition
Service box 422
University of Agder
4604 Kristiansand, Norway