Summary: The aim of this meta‐analysis was to quantify the effects of high‐intensity interval training (HIIT) on markers of glucose regulation and insulin resistance compared with control conditions (CON) or continuous training (CT). Databases were searched for HIIT interventions based upon the inclusion criteria: training ≥2 weeks, adult participants and outcome measurements that included insulin resistance, fasting glucose, HbA1c or fasting insulin. Dual interventions and participants with type 1 diabetes were excluded. Fifty studies were included. There was a reduction in insulin resistance following HIIT compared with both CON and CT (HIIT vs. CON: standardized mean difference [SMD] = −0.49, confidence intervals [CIs] −0.87 to −0.12, P = 0.009; CT: SMD = −0.35, −0.68 to −0.02, P = 0.036). Compared with CON, HbA1c decreased by 0.19% (−0.36 to −0.03, P = 0.021) and body weight decreased by 1.3 kg (−1.9 to −0.7, P < 0.001). There were no statistically significant differences between groups in other outcomes overall. However, participants at risk of or with type 2 diabetes experienced reductions in fasting glucose (−0.92 mmol L⁻¹, −1.22 to −0.62, P < 0.001) compared with CON. HIIT appears effective at improving metabolic health, particularly in those at risk of or with type 2 diabetes. Larger randomized controlled trials of longer duration than those included in this meta‐analysis are required to confirm these results.

Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 ± 0.3 yr, body mass index 23.1 ± 0.4 kg/m², maximum oxygen uptake 62.1 ± 1.8 ml·kg⁻¹·min⁻¹ (means ± SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant ( P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 ± 110, resistance 1,381 ± 97, aerobic 1,750 ± 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.

Weight loss is an important goal in the management of several chronic conditions, including type 2 diabetes mellitus, and pharmacological therapies that aid weight loss are appealing. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter 2 inhibitors (SGLT2is) are novel glucose-lowering therapies that have been shown to induce clinically significant reductions in body weight. However, this weight loss may not be attributed solely to fat mass (FM). Given the importance of skeletal muscle and lean body mass (LBM) on cardio-metabolic health and physical function, we reviewed the available literature reporting the effects of GLP-1RAs and SGLT2is on body composition. Results demonstrate that, in most circumstances, the weight loss associated with both therapies predominantly comprises a reduction in FM, although significant heterogeneity exists between studies. In over half of the studies identified, the proportion of LBM reduction ranged between 20% and 50% of total weight lost, which is consistent with diet-induced weight loss and bariatric surgery. No clear differences existed between GLP-1RAs and SGLT2is. Consequently, the loss of LBM and skeletal muscle associated with weight loss induced by GLP-1RAs and SGLT2is warrants attention. Strategies to preserve skeletal muscle and improve physical function, for example through structured exercise, are of great importance.

Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.

The effects of prolonged treadmill running on appetite, energy intake and acylated ghrelin (an appetite stimulating hormone) were examined in 9 healthy males over the course of 24h. Participants completed 2 experimental trials (exercise and control) in a randomised-crossover fashion. In the exercise trial participants ran for 90 min at 68.8 + or - 0.8% of maximum oxygen uptake followed by 8.5 h of rest. Participants returned to the laboratory on the following morning to provide a fasting blood sample and ratings of appetite (24 h measurement). No exercise was performed on the control trial. Appetite was measured within the laboratory using visual analogue scales and energy intake was assessed from ad libitum buffet meals. Acylated ghrelin was determined from plasma using an ELISA assay. Exercise transiently suppressed appetite and acylated ghrelin but each remained no different from control values in the hours afterwards. Furthermore, despite participants expending 5324 kJ during exercise there was no compensatory increase in energy intake (24 h energy intake; control 17,191 kJ, exercise 17,606 kJ). These findings suggest that large energy deficits induced by exercise do not lead to acute compensatory responses in appetite, energy intake or acylated ghrelin.