Low-volume High-intensity Interval Exercise Research Articles

Acute Low-Volume High-Intensity Interval Exercise and Continuous Moderate-Intensity Exercise Elicit a Similar Improvement in 24-h Glycemic Control in Overweight and Obese Adults.

Background: Acute exercise reduces postprandial oxidative stress and glycemia; however, the effects of exercise intensity are unclear. We investigated the effect of acute low-volume high-intensity interval-exercise (LV-HIIE) and continuous moderate-intensity exercise (CMIE) on glycemic control and oxidative stress in overweight and obese, inactive adults.Methods: Twenty-seven adults were randomly allocated to perform a single session of LV-HIIE (9 females, 5 males; age: 30 ± 1 years; BMI: 29 ± 1 kg·m−2; mean ± SEM) or CMIE (8 females, 5 males; age: 30 ± 2.0; BMI: 30 ± 2.0) 1 h after consumption of a standard breakfast. Plasma redox status, glucose and insulin were measured. Continuous glucose monitoring (CGM) was conducted during the 24-h period before (rest day) and after exercise (exercise day).Results: Plasma thiobarbituric acid reactive substances (TBARS; 29 ±13%, p < 0.01; mean percent change ±90% confidence limit), hydrogen peroxide (44 ± 16%, p < 0.01), catalase activity (50 ± 16%, p < 0.01), and superoxide dismutase activity (21 ± 6%, p < 0.01) significantly increased 1 h after breakfast (prior to exercise) compared to baseline. Exercise significantly decreased postprandial glycaemia in whole blood (−6 ± 5%, p < 0.01), irrespective of the exercise protocol. Only CMIE significantly decreased postprandial TBARS (CMIE: −33 ± 8%, p < 0.01; LV-HIIE: 11 ± 22%, p = 0.34) and hydrogen peroxide (CMIE: −25 ± 15%, p = 0.04; LV-HIIE: 7 ± 26%; p = 0.37). Acute exercise provided a similar significant improvement in 24-h average glucose levels (−5 ± 2%, p < 0.01), hyperglycemic excursions (−37 ± 60%, p < 0.01), peak glucose concentrations (−8 ± 4%, p < 0.01), and the 2-h postprandial glucose response to dinner (−9 ± 4%, p < 0.01), irrespective of the exercise protocol.Conclusion: Despite elevated postprandial oxidative stress compared to CMIE, LV-HIIE is an equally effective exercise mode for improving 24-h glycemic control in overweight and obese adults.

Low volume–high intensity interval exercise elicits antioxidant and anti-inflammatory effects in humans

The purpose of the present study was to compare acute changes in oxidative stress and inflammation in response to steady state and low volume, high intensity interval exercise (LV-HIIE). Untrained healthy males (n = 10, mean ± s: age 22 ± 3 years; VO2MAX 42.7 ± 5.0 ml · kg−1 · min−1) undertook three exercise bouts: a bout of LV-HIIE (10 × 1 min 90% VO2MAX intervals) and two energy-matched steady-state cycling bouts at a moderate (60% VO2MAX; 27 min, MOD) and high (80% VO2MAX; 20 min, HIGH) intensity on separate days. Markers of oxidative stress, inflammation and physiological stress were assessed before, at the end of exercise and 30 min post-exercise (post+30). At the end of all exercise bouts, significant changes in lipid hydroperoxides (LOOH) and protein carbonyls (PCs) (LOOH (nM): MOD +0.36; HIGH +3.09; LV-HIIE +5.51 and PC (nmol · mg−1 protein): MOD −0.24; HIGH −0.11; LV-HIIE −0.37) were observed. Total antioxidant capacity (TAC) increased post+30, relative to the end of all exercise bouts (TAC (µM): MOD +189; HIGH +135; LV-HIIE +102). Interleukin (IL)-6 and IL-10 increased post+30 in HIGH and LV-HIIE only (P < 0.05). HIGH caused the greatest lymphocytosis, adrenaline and cardiovascular response (P < 0.05). At a reduced energy cost and physiological stress, LV-HIIE elicited similar cytokine and oxidative stress responses to HIGH.

High-Intensity Interval Exercise and Postprandial Triacylglycerol.

This review examined if high-intensity interval exercise (HIIE) reduces postprandial triacylglycerol (TAG) levels. Fifteen studies were identified, in which the effect of interval exercise conducted at an intensity of >65% of maximal oxygen uptake was evaluated on postprandial TAG levels. Analysis was divided between studies that included supramaximal exercise and those that included submaximal interval exercise. Ten studies examined the effect of a single session of low-volume HIIE including supramaximal sprints on postprandial TAG. Seven of these studies noted reductions in the postprandial total TAG area under the curve the morning after exercise of between ~10 and 21% compared with rest, but three investigations found no significant difference in TAG levels. Variations in the HIIE protocol used, inter-individual variation or insufficient time post-exercise for an increase in lipoprotein lipase activity are proposed reasons for the divergent results among studies. Five studies examined the effect of high-volume submaximal interval exercise on postprandial TAG. Four of these studies were characterised by high exercise energy expenditure and effectively attenuated total postprandial TAG levels by ~15-30%, but one study with a lower energy expenditure found no effect on TAG. The evidence suggests that supramaximal HIIE can induce large reductions in postprandial TAG levels but findings are inconsistent. Submaximal interval exercise offers no TAG metabolic or time advantage over continuous aerobic exercise but could be appealing in nature to some individuals. Future research should examine if submaximal interval exercise can reduce TAG levels in line with more realistic and achievable exercise durations of 30 min per day.

Effects of resistance training combined with moderate-intensity endurance or low-volume high-intensity interval exercise on cardiovascular risk factors in patients with coronary artery disease

To determine the effects of resistance training combined with either moderate-intensity endurance or low-volume high-intensity interval training on cardiovascular risk profiles in patients with coronary artery disease. Factorial repeated-measures study design. Nineteen patients were randomized into moderate-intensity endurance (n = 10) or high-intensity interval (n = 9) groups, and attended 2 supervised exercise sessions a week for 6-months. The first 3-months involved exclusive moderate-intensity endurance or high-intensity interval exercise, after which progressive resistance training was added to both groups for the remaining 3-months. Fitness (VO(2)peak), blood pressure and heart rate, lipid profiles and health related quality of life assessments were performed at pretraining, 3 and 6-months training. VO(2)peak increased from pretraining to 3-months in both groups (moderate-intensity endurance: 19.8 ± 7.3 vs. 23.2 ± 7.4 ml kg(-1)min(-1); high-intensity interval: 21.1 ± 3.3 vs. 26.4 ± 5.2 ml kg(-1)min(-1), p<0.001) with no further increase at 6-months. Self-evaluated health and high-density lipoprotein were increased following 6-months of moderate-intensity endurance exercise, while all remaining indices were unchanged. Low-volume high-intensity interval exercise did not elicit improvements in lipids or health related quality of life. Blood pressures and heart rates were unchanged with training in both groups. Findings from our pilot study suggest improvements in fitness occur within the first few months of training in patients with coronary artery disease, after which the addition of resistance training to moderate-intensity endurance and high-intensity interval exercise elicited no further improvements. Given the importance of resistance training in cardiac rehabilitation, additional research is required to determine its effectiveness when combined with high-intensity interval exercise.

Low-Volume, High-Intensity Interval Training in Patients with CAD

Isocaloric interval exercise training programs have been shown to elicit improvements in numerous physiological indices in patients with CAD. Low-volume high-intensity interval exercise training (HIT) is effective in healthy populations; however, its effectiveness in cardiac rehabilitation has not been established. This study compared the effects of 12-wk of HIT and higher-volume moderate-intensity endurance exercise (END) on brachial artery flow-mediated dilation (FMD) and cardiorespiratory fitness (VO2 peak) in patients with CAD. Twenty-two patients with documented CAD were randomized into HIT (n = 11) or END (n = 11) based on pretraining FMD. Both groups attended two supervised sessions per week for 12 wk. END performed 30-50 min of continuous cycling at 58% peak power output (PPO), whereas HIT performed ten 1-min intervals at 89% PPO separated by 1-min intervals at 10% PPO per session. Relative FMD was increased posttraining (END, 4.4% ± 2.6% vs 5.9% ± 3.6%; HIT, 4.6% ± 3.6% vs 6.1% ± 3.4%, P ≤ 0.001 pre- vs posttraining) with no differences between groups. A training effect was also observed for relative VO2 peak (END, 18.7 ± 5.7 vs 22.3 ± 6.1 mL · kg(-1) · min(-1); HIT, 19.8 ± 3.7 vs 24.5 ± 4.5 mL · kg(-1) · min(-1), P < 0.001 for pre- vs posttraining), with no group differences. Low-volume HIT provides an alternative to the current, more time-intensive prescription for cardiac rehabilitation. HIT elicited similar improvements in fitness and FMD as END, despite differences in exercise duration and intensity.

Effects of acute and chronic low-volume high-intensity interval exercise on cardiovascular health in patients with coronary artery disease

The merits of low-volume high-intensity interval exercise (HIT) have been established in healthy populations; however, no studies have examined this exercise prescription in patients with coronary artery disease (CAD). The present thesis examined the acute and chronic effects of HIT in patients with CAD. The first study demonstrated transient improvements in brachial artery endothelial-dependent function, which was assessed using flow-mediated dilation (FMD) 60 min following a single bout of either HIT or moderate-intensity endurance exercise (END) in habitually active patients. The second study demonstrated no effects of training status on the acute endothelial responses to exercise; following 12-weeks of either HIT or END training. However, there was a significant reduction in endothelial-independent function immediately postexercise, at both pre- and post-training, which requires further examination. The third study demonstrated comparable increases in fitness and resting FMD following 12-weeks of END and HIT, lending support to the notion that favourable adaptations are obtainable with a smaller volume of exercise. Finally, the fourth study demonstrated no change in heart rate recovery following 12-weeks of END and HIT. However, pre-training heart rate recovery values reported by our sample were in a low risk range, which suggests training induced improvements may only be achievable in populations with attenuated pre-training values. The results of this thesis provide preliminary evidence that supports the use of HIT in patients with CAD. The findings of favourable transient and chronic improvements following HIT are notable, especially given that the HIT protocol involves less time and work than END, which was modelled after the current exercise prescription in cardiac rehabilitation. Further investigations are necessary, including the assessment of additional physiological indices; the feasibility and adherence to HIT; the inclusion of CAD populations with comorbidities, including heart failure and diabetes; as well as other forms of HIT training, including HIT combined with resistance training.

Heart rate recovery and heart rate variability are unchanged in patients with coronary artery disease following 12 weeks of high-intensity interval and moderate-intensity endurance exercise training

Decreased heart rate variability and attenuated heart rate recovery following exercise are associated with an increased risk of mortality in cardiac patients. This study investigated the effects of 12 weeks of moderate-intensity endurance exercise (END) and a novel low-volume high-intensity interval exercise protocol (HIT) on measures of heart rate recovery and heart rate variability in patients with coronary artery disease (CAD). Fourteen males with CAD participated in 12 weeks of END or HIT training, each consisting of 2 supervised exercise sessions per week. END consisted of 30-50 min of continuous cycling at 60% peak power output (PPO). HIT involved ten 1-min intervals at 88% PPO separated by 1-min intervals at 10% PPO. Heart rate recovery at 1 min and 2 min was measured before and after training (pre- and post-training, respectively) using a submaximal exercise bout. Resting time and spectral and nonlinear domain measures of heart rate variability were calculated. Following 12 weeks of END and HIT, there was no change in heart rate recovery at 1 min (END, 40 ± 12 beats·min(-1) vs. 37 ± 19 beats·min(-1); HIT, 31 ± 8 beats·min(-1) vs. 35 ± 8 beats·min(-1); p ≥ 0.05 for pre- vs. post-training) or 2 min (END, 44 ± 18 beats·min(-1) vs. 43 ± 19 beats·min(-1); HIT, 42 ± 10 beats·min(-1) vs. 50 ± 6 beats·min(-1); p ≥ 0.05 for pre- vs. post-training). All heart rate variability indices were unchanged following END and HIT training. In conclusion, neither END nor HIT exercise programs elicited training-induced improvements in cardiac autonomic function in patients with CAD. The absence of improvements with training may be attributed to the optimal medical management and normative pretraining state of our sample.

Flow-Mediated Dilation Is Acutely Improved after High-Intensity Interval Exercise

Cardiovascular disease is characterized by decreased endothelial function. Chronic exercise training improves endothelial function in individuals with cardiovascular diseases; however, the acute endothelial responses to a single bout of exercise are not consistent in the literature. This study investigated whether a single bout of moderate-intensity endurance exercise (END) and low-volume high-intensity interval exercise (HIT) on a cycle ergometer resulted in similar acute changes in endothelial function. Ten individuals (66 ± 11 yr) with coronary artery disease (CAD) participated in two exercise sessions (END and HIT). Endothelial-dependent function was assessed using brachial artery flow-mediated dilation (FMD) preexercise and 60 min postexercise. Brachial artery diameters and velocities were determined using Doppler ultrasound before and after a 5 min ischemic period at all time points. Endothelial-independent function was assessed using a 0.4-mg sublingual dose of nitroglycerin. The total work performed was higher in END (166 ± 52 kJ) compared with HIT (93 ± 28 kJ) exercise (P < 0.001). Endothelial-dependent function improved (P = 0.01) after END (absolute FMD preexercise, 0.24 ± 0.18 mm; postexercise, 0.31 ± 0.24 mm) and HIT (absolute FMD preexercise, 0.25 ± 0.13 mm; postexercise, 0.29 ± 0.13 mm), with no differences between exercise conditions. A time effect for FMD normalized to the shear rate area under the curve was also observed (P = 0.02) after END (preexercise, 0.005 ± 0.004; postexercise, 0.010 ± 0.011) and HIT (preexercise, 0.005 ± 0.004; postexercise, 0.009 ± 0.011). Endothelial-independent function responses were unchanged after END and HIT (P > 0.05). HIT and END resulted in similar acute increases in brachial artery endothelial-dependent function in a population with dysfunction at rest, despite the difference in exercise intensities.

Reply from M. J. Gibala, J. P. Little, M. J. MadDonald and J. A. Hawley

Thank you for the opportunity to respond to the letter submitted by Gayda and colleagues in response to our recent review published in The Journal of Physiology (Gibala et al. 2012). With regards to their first comment regarding our new ‘practical’ high-intensity interval exercise (HIIE) protocol, we disagree with the assertion that ‘exercise intensity at 60% of peak power cannot be considered high intensity.’ In our efforts to develop a low-volume HIIE protocol that can be applied across different cohorts including clinical populations, we devised a model comprising 10 × 60 s work bouts at an intensity eliciting ∼85–90% of maximal heart rate (HRmax; averaged over the 10 intervals), interspersed by 60 s of recovery. We have found that the percentage of peak power output (PPO; determined using a standard ramp test to volitional fatigue which does not always elicit peak O2 uptake) that approximates the desired target heart rate (i.e. the % of HRmax) varies considerably between subjects and is exercise-mode specific. For example, in the study by Hood et al. (2011) which was conducted on sedentary healthy adults, a workload equivalent to 60% of PPO during upright cycling was sufficient to elicit a training intensity of ∼90% HRmax. However, in our recent study conducted on patients with type 2 diabetes, the intensity required to elicit ∼90% HRmax was ∼95% of PPO determined during recumbent cycling (Little et al. 2011). We agree with the assertion by Gayda and colleagues that ‘acute physiological responses during different HIIE protocols as well as patient's safety, tolerance and comfort should be tested before their implementation into training programs’. Ongoing protocol optimization work in our laboratory reveal that when interval exercise was prescribed as 80% of PPO in coronary artery disease (CAD) patients – most of whom were taking beta-blocker medication – the 10 × 60 s protocol resulted in peak heart rates during the exercise that averaged ∼85% of age-predicted HRmax. Further, the 10 × 60 s protocol was best tolerated and rated as most preferred by CAD patients in comparison with a modified Wingate protocol (repeated 30 s efforts at 100% PPO with 4 min unloaded cycling for recovery), the standard aerobic interval training protocol used by Wisloff and colleagues (2007), or a moderate-intensity continuous exercise (MICE) protocol. It is likely that high-intensity interval training (HIT) does not conform to a ‘one size fits all’ approach and the interval training stimulus needs to be tailored to individuals depending on their initial level of fitness, exercise tolerance, use of prescription medications and other factors. We also concur with the other main comment by Gayda and colleagues that ‘the superiority of this HIIE protocol [our 10 × 60 s ‘hard’/60 s ‘easy’ model]… needs to be demonstrated.’ Indeed, our review concluded ‘One aspect that is unclear from the present literature is the precise intensity and minimal volume of training that is needed to potentiate the effect of the stimulus-adaptation on outcomes such as mitochondrial biogenesis and relevant health markers. To answer such questions, a complex series of studies needs to be undertaken that systematically ‘titrate’ levels of the ‘training impulse’ and determine subsequent cellular, performance and clinical responses after divergent training interventions.’ Specifically with respect to the use of HIIE in patients with cardiovascular risk or cardiovascular disease, the letter by Gayda and colleagues highlights four references from their laboratory that were not cited in our review. Given the relatively broad scope of our review and the fact that Journal guidelines restricted the number of references to 50, it was obviously not possible to cite all relevant work. Moreover, two of the citations listed by Gayda et al. were acute exercise studies (whereas the focus of our review was training adaptations) and the other two citations were a journal abstract and a recent paper published in February 2012 (neither of which we had access to at the time of submission of our original manuscript). We are also aware of the pioneering research conducted by Meyer and colleagues (e.g. Meyer et al. 1998) and have acknowledged this work in a previous commentary (MacDonald & Currie, 2009). We apologize to all authors whose work on interval training we could not cite due to the broad focus of our review and referencing limitations imposed by The Journal.