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Unlabelled: Changes in glucose and insulin are potentially involved in the appetite-regulatory effects of exercise considering their role post-prandially.

Purpose: To examine if glucose and insulin play a role in post-exercise appetite regulation.

Methods: 12 participants (M=8; 26±5 y) completed 3 experimental sessions in a systematically rotated randomized crossover design: 1) no-exercise control (CTRL); 2) moderate-intensity continuous training (MICT; 30-min, 70% maximal oxygen consumption (V̇O2max)); and 3) sprint interval training (SIT; 4 x 30-s "all-out" sprints, interspersed with 4-min rest).

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Background: Growth differentiation factor 15 (GDF-15) is a potential therapeutic target for obesity due to its role in appetite suppression. Although acute exercise stimulates GDF-15 secretion, its relationship with appetite regulation remains unclear. It is also unknown whether preexercise carbohydrate intake would affect GDF-15 responses.

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Rare defects in the promoter region of SLC16A1, the gene encoding monocarboxylate transporter 1 (MCT-1), result in exercise-induced hyperinsulinism. In this disorder, inappropriate insulin secretion is triggered by anaerobic exercise with consequent hypoglycaemia. We describe the case of a 41-year-old man presenting with a generalised tonic-clonic seizure and severe hypoglycaemia following strenuous exercise.

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The potential mechanisms involved in lactate's role in exercise-induced appetite suppression require further examination. We used sodium bicarbonate (NaHCO) supplementation in a double-blind, placebo-controlled, randomized crossover design to explore lactate's role on neuropeptide Y (NPY), agouti-related peptide (AgRP), and alpha-melanocyte-stimulating hormone (α-MSH) concentrations. Twelve adults (7 males; 24.

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