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Cardiorespiratory Effects of Forced Activity and Digestion in Toads

Digestion and physical activity are associated with large and sometimes opposite changes in several physiological parameters. Gastric acid secretion during digestion causes increased levels of plasma bicarbonate ([ \( \mathrm{HCO}\,^{-}_{3} \) ]pl), whereas activity leads to a metabolic acidosis with increased lactate and decrease in plasma bicarbonate. Here we describe the combined effects of feeding and activity in the toad Bufo marinus to investigate whether the increased bicarbonate buffering capacity during digestion (the so‐called alkaline tide) protects the acid‐base disturbance during activity and enhances the subsequent recovery. In addition, we describe the changes in arterial oxygen levels and plasma ion composition, as well as rates of gas exchange, heart rates, and blood pressures. Toads were equipped with catheters in the femoral artery and divided into four experimental regimes: control, digestion, forced activity, and forced activity during the postprandial period (N = 6 in each). Digestion induced a significant metabolic alkalosis with increased [ \( \mathrm{HCO}\,^{-}_{3} \) ]pl that was completely balanced by a respiratory acidosis; that is, increased arterial Pco2 (Paco2), so that arterial pH (pHa) did not change. Forced activity led to a substantial reduction in pHa by 0.43 units, an increase in plasma lactate concentration by 12.5 mmol L−1, and a reduction in [ \( \mathrm{HCO}\,^{-}_{3} \) ]pl of similar magnitude. While digesting animals had higher Paco2 and [ \( \mathrm{HCO}\,^{-}_{3} \) ]pl at rest, the magnitude and duration of the changes in arterial acid‐base parameters were similar to those of fasting animals, although the reduction in pHa was somewhat lower (0.32 units). In conclusion, while recovery from the acidosis following exercise did not seem to be affected by digestion, the alkaline tide did slightly dampen the reduction in pHa during activity.