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.