The precise magnitude of the effect of acute exercise on subsequent energy intake is not well understood. Identifying how large a deficit exercise can produce in energy intake and whether this is compensated for, is important in design of long-term exercise programs for weight loss and weight maintenance. Thus, this paper sought to review and perform a meta-analysis on data from the existing literature. Twenty-nine studies, consisting of 51 trials, were identified for inclusion. Exercise duration ranged from 30 to 120min at intensities of 36-81% VO(2)max, with trials ranging from 2 to 14h, and ad libitum test meals offered 0-2h post-exercise. The outcome variables included absolute energy intake and relative energy intake. A random effects model was employed for analysis due to expected heterogeneity. Results indicated that exercise has a trivial effect on absolute energy intake (n=51; ES=0.14, 95% CI: -0.005 to 0.29) and a large effect on relative energy intake (creating an energy deficit, n=25; ES=-1.35, 95% CI: -1.64 to -1.05). Despite variability among studies, results suggest that exercise is effective for producing a short-term energy deficit and that individuals tend not to compensate for the energy expended during exercise in the immediate hours after exercise by altering food intake.

An acute bout of exercise may influence appetite by suppressing levels of acylated ghrelin while simultaneously increasing levels of PYY, GLP-1 and PP, which may contribute to alterations in food and drink intake after acute exercise. Further longitudinal studies and exploration into mechanisms of action are required in order to determine the precise role these hormones play in long-term appetite responses to an exercise intervention.

These results suggest that exercise intensity, mode, duration and the nature of meal/fluid ingested all influence GE during and after acute exercise. The relationship of GE parameters with appetite regulation after exercise remains largely unexplored. Further integrative studies combining GE and alterations in gut hormones, as well as in populations such as overweight and obese individuals are needed.

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Alterations in maximal oxygen uptake (VO2max), heart rate (HR), and fat oxidation occur in response to chronic endurance training. However, many studies report frequent incidence of “non-responders” who do not adapt to continuous moderate exercise. Whether this is the case in response to high intensity interval training (HIT), which elicits similar adaptations as endurance training, is unknown. The aim of this retrospective study was to examine individual responses to two paradigms of interval training. In the first study (study 1), twenty active men and women (age and baseline VO2max = 24.0±4.6 yr and 42.8±4.8 mL/kg/min) performed 6 d of sprint interval training (SIT) consisting of 4–6 Wingate tests per day, while in a separate study (study 2), 20 sedentary women (age and baseline VO2max = 23.7±6.2 yr and 30.0±4.9 mL/kg/min) performed 12 wk of high-volume HIT at workloads ranging from 60–90% maximal workload. Individual changes in VO2max, HR, and fat oxidation were examined in each study, and multiple regression analysis was used to identify predictors of training adaptations to SIT and HIT. Data showed high frequency of increased VO2max (95%) and attenuated exercise HR (85%) in response to HIT, and low frequency of response for VO2max (65%) and exercise HR (55%) via SIT. Frequency of improved fat oxidation was similar (60–65%) across regimens. Only one participant across both interventions showed non-response for all variables. Baseline values of VO2max, exercise HR, respiratory exchange ratio, and body fat were significant predictors of adaptations to interval training. Frequency of positive responses to interval training seems to be greater in response to prolonged, higher volume interval training compared to similar durations of endurance training.

The present meta-analysis suggests that consumption of flaxseed may lower blood pressure slightly. The beneficial potential of flaxseed to reduce blood pressure (especially diastolic blood pressure) may be greater when it is consumed as a whole seed and for a duration of >12 wk.

These data suggest that 12 wk of either moderate or more strenuous interval training similarly enhance fat oxidation in sedentary women but do not alter body weight or body composition.

Increased whole-body fat oxidation (FOx) has been consistently demonstrated in response to moderate intensity continuous exercise training. Completion of high intensity interval training (HIIT) and its more intense form, sprint interval training (SIT), has also been reported to increase FOx in different populations. An explanation for this increase in FOx is primarily peripheral adaptations via improvements in mitochondrial content and function. However, studies examining changes in FOx are less common in response to HIIT or SIT than those determining increases in maximal oxygen uptake which is concerning, considering that FOx has been identified as a predictor of weight gain and glycemic control. In this review, we explored physiological and methodological issues underpinning existing literature concerning changes in FOx in response to HIIT and SIT. Our results show that completion of interval training increases FOx in approximately 50% of studies, with the frequency of increased FOx higher in response to studies using HIIT compared to SIT. Significant increases in β-HAD, citrate synthase, fatty acid binding protein, or FAT/CD36 are likely responsible for the greater FOx seen in these studies. We encourage scientists to adopt strict methodological procedures to attenuate day-to-day variability in FOx, which is dramatic, and develop standardized procedures for assessing FOx, which may improve detection of changes in FOx in response to HIIT.