EXERCISE AND FATIGUE
The limiting factor in exercise, by healthy individuals, is cardiac
output, not ventilation. In severe
exercise, cardiac output may rise from 4 times to 6 times above resting level, but
ventilation can increase up to 25-fold beyond resting level. Healthy people run “out of blood” not air;
the heart can’t pump enough blood fast enough.
It’s the build up of PCO2 that increases respiratory drive, not
oxygen deficit; the PO2 receptor sites in the aorta and carotid
arteries detect normal oxygen as a result of proper ventilation in the lungs. Dissolved oxygen and oxygen bound to
hemoglobin in arteries are normal.
Arterial
carbon dioxide (PaCO2) regulation during exercise is the same as it
is at rest, 35 - 45 mmHg. The PCO2,
as per the Henderson-Hasselbach equation, required for maintaining pH and acid-base-balance
has not changed. To maintain normal
levels of PCO2, however, the actual quantity of CO2
exhaled increases dramatically. Lactic
acid generated during exercise is buffered by bicarbonates and then utilized by
the body to resynthesize glucose, or is oxidized (broken down into CO2
and H2O). The bicarbonates
are returned to the system for buffering new production of acids. Under normal circumstances, the rate of
lactic acid generation and its utilization by the body are equivalent; bicarbonate
buffer supplies remain relatively constant.
During severe exercise, cardiac output limitation leads to an oxygen content
deficit, which results in anaerobic metabolism in cells. Cellular respiration is compromised, which
means that there is an exponential increase the production of lactic acid. Acid generation is greater than its
utilization, and bicarbonate buffers are thus not restored fast enough to the
system. The result is lactic acidosis. The solution is compensatory
overbreathing, reduction of PCO2, which can be
accomplished immediately and effectively, simply by ventilating air from the
lungs faster than the heart pumps blood into the lungs (perfusion).
Click here to learn more about
compensatory breathing.
Chronic hypocapnia, the result of
overbreathing, compromises bicarbonate reserves. What does this mean to an athlete? Reduced physical endurance! What does this mean to a “burned out”
corporate executive? Generalized fatigue
symptoms! And, how are these symptoms normally
accounted for? “Stress,” is the quick
and easy explanation for everything.
Click here to learn
more about
kidney physiology.
Exercise testing and ETCO2
measurement, while working out on an exercise bike or a treadmill, tells us
about buffering capacity, and ultimately about physical endurance and fatigue,
valuable information to athlete and corporate manager alike:
(1) Take a baseline of ETCO2,
while sitting on the bike, without exercise.
(2) Introduce light pedaling, almost work free, for three minutes.
(3) Increase workload to a higher level for three minutes.
(4) increase the workload, three minutes at a time, until ETCO2
drops.
(5) Stop the exercise, and record ETCO2 for a final three minutes.
● If overbreathing occurs with
relatively little exercise, buffers have been depleted quickly.
● If overbreathing occurs only after major
physical output, we know that buffer pool is substantial.
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Behavioral Physiology Institute,