An increase in rate of respiration was recorded for intact roots of seven native Australian species 16 h after inoculation with Phytophthora cinnamomi. By 24 h the magnitude of the increase ranged from 2—159% above that of the uninoculated controls and was evidently not related to host susceptibility. A time sequence study of lesion extension and the associated increased respiration rates for both susceptible and tolerant eucalypts demonstrated a difference in response. The rate of respiration in the tolerant species increased 2 % and only at the site of inoculation, whereas in the susceptible species the respiration rate increased in a wave which began at the inoculation site and continued along the root with the advancing fungal invasion. Respiration rate only increased in regions of the root actually inhabited by the pathogen. The fungal contribution to the total respiration of infected roots was less than 1 % and was determined by measuring respiration of inoculated killed roots. Respiration rates were measured in the presence of potassium cyanide (KCN) and salicylhydroxamic acid (SHAM). Both KCN‐sensitive and SHAM‐sensitive respiration occurred in normal uninfected E. marginate seedlings. A large proportion of the increase in total respiration rate of infected seedlings compared with uninoculated controls was due to the alternate, SHAM‐sensitive pathway. The physiological implications of these results are discussed.