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Interval exercise typically involves repeated bouts of relatively intense exercise interspersed by short periods of recovery. A common classification scheme subdivides this method into high-intensity interval training (HIIT; 'near maximal' efforts) and sprint interval training (SIT; 'supramaximal' efforts). Both forms of interval training induce the classic physiological adaptations characteristic of moderate-intensity continuous training (MICT) such as increased aerobic capacity (V̇O2 max ) and mitochondrial content. This brief review considers the role of exercise intensity in mediating physiological adaptations to training, with a focus on the capacity for aerobic energy metabolism. With respect to skeletal muscle adaptations, cellular stress and the resultant metabolic signals for mitochondrial biogenesis depend largely on exercise intensity, with limited work suggesting that increases in mitochondrial content are superior after HIIT compared to MICT, at least when matched-work comparisons are made within the same individual. It is well established that SIT increases mitochondrial content to a similar extent to MICT despite a reduced exercise volume. At the whole-body level, V̇O2 max is generally increased more by HIIT than MICT for a given training volume, whereas SIT and MICT similarly improve V̇O2 max despite differences in training volume. There is less evidence available regarding the role of exercise intensity in mediating changes in skeletal muscle capillary density, maximum stroke volume and cardiac output, and blood volume. Furthermore, the interactions between intensity and duration and frequency have not been thoroughly explored. While interval training is clearly a potent stimulus for physiological remodelling in humans, the integrative response to this type of exercise warrants further attention, especially in comparison to traditional endurance training.