Two Minutes of Sprint-Interval Exercise Elicits 24-hr Oxygen Consumption Similar to That of 30 min of Continuous Endurance Exercise

Abstract

Six weeks (3 times/wk) of sprint-interval training (SIT) or continuous endurance training (CET) promote body-fat losses despite a substantially lower training volume with SIT. In an attempt to explain these findings, the authors quantified VO₂ during and after (24 h) sprint-interval exercise (SIE; 2 min exercise) vs. continuous endurance exercise (CEE; 30 min exercise). VO₂ was measured in male students (n = 8) 8 times over 24 hr under 3 treatments (SIE, CEE, and control [CTRL, no exercise]). Diet was controlled. VO₂ was 150% greater (p < .01) during CEE vs. SIE (87.6 ± 13.1 vs. 35.1 ± 4.4 L O₂; M ± SD). The observed small difference between average exercise heart rates with CEE (157 ± 10 beats/min) and SIE (149 ± 6 beats/min) approached significance (p = .06), as did the difference in peak heart rates during CEE (166 ± 10 beats/min) and SIE (173 ± 6 beats/min; p = .14). Total O₂ consumed over 8 hr with CEE (263.3 ± 30.2 L) was greater (p < .01) than both SIE (224.2 ± 15.3 L; p < .001) and CTRL (163.5 ± 16.1 L; p < .001). Total O₂ with SIE was also increased over CTRL (p < .001). At 24 hr, both exercise treatments were increased (p < .001) vs. CTRL (CEE = 500.2 ± 49.2; SIE = 498.0 ± 29.4; CTRL = 400.2 ± 44.6), but there was no difference between CEE and SIE (p = .99). Despite large differences in exercise VO₂, the protracted effects of SIE result in a similar total VO₂ over 24 hr vs. CEE, indicating that the significant body-fat losses observed previously with SIT are partially due to increases in metabolism postexercise.

Physiological and molecular responses to an acute bout of reduced-exertion high-intensity interval training (REHIT)

“…The strong reliance on glycolysis for ATP resynthesis will also result in a reduction in both intramyocellular and blood pH levels (Robergs et al 2004). Consistent with previous observations following more strenuous and time-consuming HIT protocols (Chan and Burns 2013;Hazell et al 2012) we observed a sharp increase in RER immediately after REHIT, demonstrating the immediate bicarbonate-mediated buffering of the metabolic acidosis associated with the all-out sprints. The subsequent drop in RER below 0.70 reflects the retention of CO2 to replenish the depleted blood bicarbonate stores during recovery (Laforgia et al 1997).…”

“…Since direct exercise energy expenditure is much lower with HIT compared with aerobic exercise, the (potentially superior) reductions in fat mass following HIT have been hypothesised to be a result of either an increase in energy expenditure through a more prolonged EPOC and/or a reduction in energy intake through suppression of appetite (Boutcher 2011). There are now several studies reporting that HIT results in an increase in total daily energy expenditure (Hazell et al 2012;Skelly et al 2014;Beaulieu et al 2015;Sevits et al 2013), and this increase is similar to that elicited by 30-50 minutes of moderate-vigorous aerobic exercise (Hazell et al 2012;Skelly et al 2014). However, the magnitude of the increase is typically modest and is only evident for 1-2 hours into the recovery period (Hazell et al 2012;Skelly et al 2014;Beaulieu et al 2015;Sevits et al 2013;Kelly et al 2013;Williams et al 2013;Chan and Burns 2013).…”

“…The subsequent drop in RER below 0.70 reflects the retention of CO2 to replenish the depleted blood bicarbonate stores during recovery (Laforgia et al 1997). Given that the majority of glycogenolysis, and hence metabolic acidosis, occurs during the first sprint of a repeated sprint protocol (Parolin et al 1999) it is not surprising that a protocol involving a smaller number of shorter sprints poses a similar challenge to buffering mechanisms compared with more strenuous HIT protocols, and hence still has this effect on RER (Hazell et al 2012;Chan and Burns 2013). It can be speculated that this regular overloading (and recovery) of muscle and blood buffering mechanisms provides an explanation for the adaptations in buffering capacity observed following six weeks of HIT (Gibala et al 2006).…”

“…Previous studies investigating more time-consuming and more strenuous HIT protocols have demonstrated a molecular response which includes a 20-30% drop in muscle glycogen concentrations, substantial lactate accumulation, an altered ATP:ADP ratio, and increases in AMPK activity (1.4-fold), p38 MAPK activity (1.5-fold), and a 6-fold increase in mRNA expression of PGC1α (Esbjornsson-Liljedahl et al 1999;Gibala et al 2009;Parolin et al 1999). Furthermore, the acute disturbance in muscle metabolism is associated with a substantial disruption of wholebody/systemic homeostasis, including a prolonged increase in post-exercise oxygen consumption (EPOC), and alterations in the appetite regulating hormones acylated ghrelin and peptide YY in a direction which would be expected to suppress appetite (Hazell et al 2012;Williams et al 2013;Deighton et al 2013). Such changes may explain why studies have observed beneficial alterations in body composition following several weeks of HIT (Whyte et al 2010;Gillen et al 2013;Heydari et al 2012;Trapp et al 2008).…”

“…In study 2, we examined differences between REHIT and a bout of moderate-intensity aerobic exercise in a range of post-exercise physiological responses including oxygen consumption and appetite regulating hormones. As intensity has been highlighted as the key determinant of exercise-induced changes in these variables (Hazell et al 2012;Deighton et al 2013), we hypothesised that REHIT would be associated with a more pronounced disturbance of physiological homeostasis and a greater suppression of appetite compared to aerobic exercise.…”