Mechanistic and methodological perspectives on the impact of intense interval training on post‐exercise metabolism

Abstract

The post‐exercise recovery period is associated with an elevated metabolism known as excess post‐exercise oxygen consumption (EPOC). The relationship between exercise duration and EPOC magnitude is thought to be linear whereas the relationship between EPOC magnitude and exercise intensity is thought to be exponential. Accordingly, near‐maximal and supramaximal protocols such as high‐intensity interval training (HIIT) and sprint interval training (SIT) protocols have been hypothesized to produce greater EPOC magnitudes than submaximal moderate‐intensity continuous training (MICT). This review updates previous reviews by focusing on the impact of HIIT and SIT on EPOC. Research to date suggests small differences in EPOC post‐HIIT compared to MICT in the immediate (<1 hour) recovery period, but greater EPOC values post‐HIIT when examined over 24 hours. Conversely, differences in EPOC post‐SIT are more pronounced, as SIT tends to produce a larger EPOC vs MICT at all time points. We discuss potential mechanisms that may drive the EPOC response to interval training (eg, glycogen resynthesis, mitochondrial uncoupling, and protein turnover among others) and also consider the role of EPOC as one of the potential contributors to fat loss following HIIT/SIT interventions. Lastly, we highlight a number of methodological shortcomings related to the measurement of EPOC following HIIT and SIT.

Exercise training‐induced visceral fat loss in obese women: The role of training intensity and modality

“…24 Indeed, the greater elevation of post-exercise EE was deemed as one of potential contributors to the promising effects of HIIT and SIT interventions on fat loss. 25 It has been shown that a single session of SIT could induce an elevation of daily EE of >225 kcal, 26 markedly greater than that mediated by the MICT counterparts. 25 The elevated post-exercise EE following vigorous exercise, which is likely a consequence of the restoration of physiological equilibrium from the exercise-mediated metabolic perturbations, appears to be relied on fat oxidation.…”

Huddling relieves myocardial glycogen synthesis of Brandt’s voles in mild cold environment

“…In general, huddling behavior completely or partially alleviated the increase in glycogen content caused by the increase in glycogen synthesis in the myocardium of voles following cold environment exposure. Normal glycogen metabolism is the basis of exercise in mammals [39,40]. Earlier studies on Brandt's voles showed that activity is higher in huddling groups than separated groups under cool environments [19].…”

Acute metabolic responses after continuous or interval exercise in post‐menopausal women with overweight or obesity

“…9 Fat oxidation could be facilitated by a higher oxygen consumption observed after exercises performed at an intensity above 75% of VO 2max . 14,15 Therefore, using a randomized crossover design, we compared the 2 hours post-exercise VO 2 and fat utilization after three isoenergetic exercise sessions (MICE, and two HIIE with different active phase duration but at the same intensity). The first one [60 × (8-s cycling − 12-s recovery) at 80%-90% HR max ] has been extensively tested by our group and by others in pre-and post-menopausal women.…”

“…9 These adaptations are probably facilitated by the higher excess post-exercise oxygen consumption (EPOC) generally observed after exercise performed above 75% of the maximal oxygen uptake (VO 2max ). 14,15 Moreover, a decrease of post-exercise appetite could also contribute to the larger fat mass loss. 9 Indeed, acute high-intensity intermittent exercise (HIIE) may stimulate anorexigenic signals that could limit energy intake for few hours.…”