◄     EXERCISE AND FATIGUE     
Main Menu

 

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 haemoglobin in arteries are normal.

 

Arterial partial pressure carbon dioxide (PaCO2) regulation during exercise is the same as it is at rest, 35 - 45 mmHg.  The PCO2, as per the Henderson-Hasselbalch 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 utilised by the body to resynthesise glucose, or is oxidised (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 utilisation 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 utilisation, and bicarbonate buffers are thus not restoured 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?  Generalised 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 pedalling, 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.

 

Copyrighted by Behavioral Physiology Institute, Boulder, Colorado USA