For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (V̇O2), CO2 production (V̇CO2), arterial blood gases, arterial lactate concentration ([LA-](a)), and rectal temperature (T(re)) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in V̇CO2), PaCO2 fell 5.5 ± 0.6 Torr, and despite a small but significant increase in [LA-](a), respiratory alkalosis prevailed [change in arterial pH (ΔpH(a)) = 0.034 ± 0.006]. Arterial PO2 (PaO2) increased 4.1 ± 1.5 Torr and T(re) increased 0.6 ± 0.1 °C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, V̇O2 increased 3.4-fold (72 ± 1.50 ml · kg-1 · min-1) and V̇CO2 increased 4.5-fold (74 ± 1.90 ml · kg-1 · min-1), resulting in a 9-fold increase in [LA-](a) and a severe metabolic acidosis (pH(a) 7.31 ± 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 ± 1.4 Torr] resulted in partial compensation of pH(a), but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e. at <65% maximum V̇O2 (V̇O2max)], and the increased [H+](a) with further elevations in V̇O2 produced no further hypocapnia. The rat, like many other nonhuman species, responds to short-term treadmill exercise with a progressive hyperventilation and hypocapnia. Although this hyperventilatory response is important to arterial [H+] regulation. It is not dependent on an attendant metabolic acidosis during moderate or maximum exercise.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - Jan 1 1984|
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