Arterial blood acid-base regulation during exercise in rats

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.