When exposed to temperatures below their critical thermal minimum (CT(min)), insects enter chill-coma and accumulate chilling injuries. While the critical thermal limits of water-breathing marine animals may be caused by oxygen- and capacity-limitation of thermal tolerance (OCLT), the mechanisms are poorly understood in air-breathing terrestrial insects. We used thermolimit respirometry to characterize entry into chill-coma in a laboratory population of fall field crickets (Gryllus pennsylvanicus). To detect potential oxygen limitation, we quantified muscle ATP, lactate and alanine concentrations in crickets following prolonged exposure to 0°C (a temperature that causes chill-coma, chilling injury and eventual death). Although there was a sharp (44%) drop in the rate of CO(2) emission at the CT(min) and spiracular control was lost, there was a low, continuous rate of CO(2) release throughout chill-coma, indicating that the spiracles were open and gas exchange could occur through the tracheal system. Prolonged exposure to 0°C caused muscle ATP levels to increase marginally (rather than decrease as OCLT would predict), and there was no change in muscle lactate or alanine concentration. Thus, it appears that insects are not susceptible to OCLT at low temperatures but that the CT(min) may instead be set by temperature effects on whole-animal ion homeostasis.