Following spinal cord injury, it is not known whether the respiratory rhythm generator undergoes plasticity to compensate for respiratory insufficiency. To test this hypothesis, respiratory variables were measured in adult semi-aquatic turtles using a pneumotachograph attached to a breathing chamber on a water-filled tank. Turtles breathed breathing room air (2 hr) before being challenged with two consecutive 2-hr bouts of hypercapnia (2% and 6% CO₂ or 4% and 8% CO₂). Turtles were spinalized at dorsal segments D₈-D₁₀ so that only pectoral girdle movement was used for breathing. Measurements were repeated at 4- and 8-weeks post-injury. While breathing room air, breathing frequency, tidal volume (Vt) and ventilation (Ve) were not altered by spinalization; single breath (singlet) frequency increased 7-fold. While breathing 6-8% CO₂, spinalized turtles had lower Ve due to decreased frequency and Vt, episodic breathing (breaths/episode) was reduced, and singlet breathing was increased 7-fold. Respiratory variables in sham-operated turtles were unaltered by surgery. Isolated brainstems from control turtles, spinalized and sham turtles produced similar respiratory motor output and responded the same to increased bath pH. Thus, spinalized turtles compensated for pelvic girdle loss while breathing room air, but were unable to compensate during hypercapnic challenges. Since isolated brainstems from control and spinalized turtles had similar respiratory motor output and chemosensitivity, breathing changes in spinalized turtles in vivo were probably not due to plasticity within the respiratory rhythm generator. Instead, caudal spinal cord damage probably disrupts spinobulbar pathways that are necessary for a normal breathing.