A hallmark of skeletal muscle remodeling elicited by exercise training in an increased oxidative capacity as measured using various biomarkers of mitochondrial content. This response is influenced by many factors that fundamentally include the type, intensity, duration, and volume of exercise performed. It was shown almost 50 years ago that a two-month program of intermittent (INT) or continuous (CONT) cycling exercise, matched for total work, elicited similar increases in succinate dehydrogenase activity in mixed human skeletal muscle (1). The response to each type of training differed between type I and type II fibres, however, an effect that was attributed to the pattern of fibre recruitment during exercise. Studies on rodents at the time that characterized the influence of intensity and duration on skeletal muscle responses showed that brief INT exercise increased mitochondrial content like CONT exercise despite a lower training volume, and these effects were influenced by fibre type (2). It was concluded, “the typical endurance training response of a biochemical change in mitochondrial content can be achieved at relatively intense exercise (i.e. exceeding VO2max) maintained for relatively short durations… (and) there seems to be a point where exercise duration becomes unimportant and the magnitude of the adaptive change is established by the intensity of exercise” (2). Despite many studies over the ensuing decades on human skeletal muscle responses to INT and CONT exercise, a vigorous debate endures regarding the most important factors to promote training-induced increases in mitochondrial content and the regulatory mechanisms involved (3,4). Recent work includes the finding based on single-leg cycling exercise (which facilitates a within-subject comparison of responses) that mixed skeletal muscle mitochondrial content increased to greater extent after short-term INT compared to CONT training matched for total work (5). This suggests that exercise intensity per se, and/or the pattern of contraction, is an important determinant of exercise-induced skeletal muscle remodelling in humans. Acute INT compared to CONT exercise has been shown to elicit greater activation of molecular signaling cascades linked to mitochondrial biogenesis, including in type II fibres, which could be important for exercise-type specific responses (6). Other work has revealed that while “sprint”-type INT training increases mixed skeletal muscle mitochondrial content like CONT training despite a lower training volume, there are differential responses in some fibre types (7). It has also been shown in trained individuals with an already well-developed oxidative capacity that adding sprint INT to CONT exercise training augments the increase in mitochondrial proteins in mixed skeletal muscle and type II fibers despite matched total work (8). A considerate recent review by Bishop and colleagues (9) examines current controversies in the field including the role of INT and CONT exercise for promoting mitochondrial biogenesis and discusses methodological issues that need to be addressed to resolve existing conflicts. From an integrative perspective, there are of course many cellular processes that ultimately determine the skeletal muscle response to different training modalities including peripheral vascular remodeling (10).