We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.

Sprint interval training (SIT) has demonstrated reductions in fat mass through potential alterations in postexercise metabolism. This study examined whether exercising in the fasted or fed state affects postexercise metabolism following acute SIT. Ten active males performed a bout of modified SIT (8 × 15-s sprints; 120 s recovery) in both a fasted (FAST) and fed (FED) state. Gas exchange was collected through 3 h postexercise, appetite perceptions were measured using a visual analog scale, and energy intake was recorded using dietary food logs. There was no difference in energy expenditure between conditions at any time point (p > 0.329) or in total session energy expenditure (FED: 514.8 ± 54.9 kcal, FAST: 504.0 ± 74.3 kcal; p = 0.982). Fat oxidation at 3 h after exercise was higher in FED (0.110 ± 0.04 g·min−1) versus FAST (0.069 ± 0.02 g·min−1; p = 0.013) though not different between conditions across time (p > 0.340) or in total postexercise fat oxidation (FED: 0.125 ± 0.04 g·min−1, FAST: 0.105 ± 0.02 g·min−1; p = 0.154). Appetite perceptions were lower in FED (–4815.0 ± 4098.7 mm) versus FAST (–707.5 ± 2010.4 mm, p = 0.022); however, energy intake did not differ between conditions (p = 0.429). These results demonstrate the fasted or fed state does not augment postexercise metabolism following acute SIT in a way that would favour fat loss following training. Novelty Energy expenditure was similar between conditions, while fat oxidation was significantly greater in FED at 3 h after exercise. Appetite perceptions were significantly lower in FED; however, energy intake was not different between conditions. Current findings suggest that performing SIT in the fed or fasted state would not affect fat loss following training.

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ObjectiveIn obesogenic states and after exercise, interleukin (IL)‐6 elevations are established, and IL‐6 is speculated to be an appetite‐regulating mechanism. This study examined the role of IL‐6 on exercise‐induced appetite regulation in sedentary normal weight (NW) males and those with obesity (OB).MethodsNine NW participants and eight participants with OB completed one non‐exercise control (CTRL) and one moderate‐intensity continuous training (MICT; 60 minutes, 65% V̇O2max) session. IL‐6, acylated ghrelin, active peptide tyrosine‐tyrosine3‐36, active glucagon‐like peptide‐1, and overall appetite perceptions were measured fasted, pre exercise, and 30, 90, and 150 minutes post exercise.ResultsFasted IL‐6 concentrations were elevated in OB (p = 0.005,  = 0.419); however, increases following exercise were similar between groups (p = 0.934,  = 0.000). Acylated ghrelin was lower in OB versus NW (p < 0.017, d > 0.84), and OB did not respond to MICT (p > 0.512, d < 0.44) although NW had a decrease versus CTRL (p < 0.034, d > 0.61). IL‐6 did not moderate/mediate acylated ghrelin release after exercise (p > 0.251). There were no observable effects of MICT on tyrosine‐tyrosine3‐36, glucagon‐like peptide‐1, or overall appetite (p > 0.334,  < 0.062).ConclusionsThese results suggest that IL‐6 is not involved in exercise‐induced appetite suppression. Despite blunted appetite‐regulatory peptide responses to MICT in participants with OB, NW participants exhibited decreased acylated ghrelin; however, no differences in appetite perceptions existed between CTRL and MICT or NW and OB.