It has been suggested that hyperventilation and the disproportionate increase in V̇CO2versus V̇O2above the ventilatory threshold (VTH) in ramp exercise are due to the production of nonmetabolic CO2in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a ∼1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2production in muscle (no nonmetabolic CO2is produced in tissues); (4) the CO2flow to the lungs, which should not be confused with V̇CO2at the mouth, does not increase at a faster rate above than below VTH. The disproportionate increase in V̇CO2at the mouth above VTHis due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body. © 2005 Elsevier B.V. All rights reserved.
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