SUMMARY1. The ventilatory response to electrically induced exercise was studied in thirteen patients with traumatic spinal cord transaction at or about the level of T6. The steady-state and on-transient responses to this exercise were compared with those obtained in eighteen normal subjects (Adams, Garlick, Guz, Murphy & Semple, 1984).2. Exercise was produced by surface electrode stimulation of the quadriceps and hamstring muscles so as to produce a pushing movement at 1 Hz against a spring load.3. At rest there was no significant difference between normals and patients, except that the patients had a lower CO2 elimination (Pco2) and end-tidal Pco, (PET,Co2) and a higher heart rate. 5. In the steady state there was a mean rise in PETCO, of 0-9 mmHg (S.D. 1-4) in the normals, and 3-2 mmHg (S.D. 2 7) in the patients, but there was overlap between the two groups. In many experimental runs in both groups, PET,Co2 did not rise, and sometimes fell. Where PCO2 did rise, the ventilatory response to exercise could not be accounted for on the basis of the ventilatory sensitivity to CO2 inhalation. From arterial sampling in three of the patients it was found that when PETC02 rose, the corresponding change in Paco2 was less.6

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Cerebral blood flow (CBF) was measured using a technique of continuous infusion of 4-radio-iodoantipyrine with external scintillation counting. Rectal temperature (T,), mean arterial pressure (MAP), heart rate (HR), respiration rate (RR), pa029 p&20,, and pH, were measured at T,s of 38,40, 42, and 43 C. Cerebrovascular resistance (CVR) and the ratio of CBF/Paooz (apparent CO2 sensitivity of cerebral circulation) were calculated. Pao, was elevated and Pacoz was depressed at all hyperthermic T,s. CBF was not significantly altered from control values during hyperthermia. CVR was reduced and apparent CO2 sensitivity increased at T,s of 42 and 43 C. These data indicate that during hyperthermia and its accompanying hypocapnia CBF stability resulted, in part, from apparent

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