The response to hypercapnia was studied in western painted turtles, Chrysemys picta bellii at 20°C. Ventilation, metabolic rate, arterial blood gases, blood pH and blood plasma ions were monitored periodically on individual turtles exposed to 5.7% CO2 for 72 h and then allowed to recover in air.

In response to hypercapnia, there is an immediate 10- to 15-fold increase in ventilation from control levels, which was maintained throughout the entire 5.7% CO2 breathing period. The first hour of CO2 breathing caused an increase in PaCOCO2 from 24–39 mmHg with a concomitant decrease in pH and rise in [HCO3]. [HCO3] rose from 42 to 50mmol1−1 in the next 24 h of CO2 breathing and remained at this level for the rest of the hypercapnic period. Small, significant increases in total [Ca2+] and total [Mg2+] were found; however, no changes were observed in the plasma Na+, K+ or Cl concentrations and the overall change in measured ions could not account for the increased [HCO3]. The maximum change in [HCO3] attained in Chrysemys exposed to a more severe acidosis (14.3% CO2) for up to 18 h was the same as that seen in the animals breathing 5.7% CO2 (10mmol1−1) implying that there is an upper limit for the accumulation of [HCO3] in Chrysemys at 20°C.

The blood pH of turtles recovering in air returned to the control value (7.56–7.74) within the first hour although PaCOCO2 did not return to the control value. The HCO3 ion concentration also remained elevated throughout the 48-h recovery period, which suggests that ionic compensation is a slower process.

The freshwater turtle employs two mechanisms to reduce the severity of an imposed respiratory acidosis: increased ventilation and changes in the strong ion difference. In spite of these responses, blood pH is not restored to the control value.

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