The hormone leptin acts as an appetite suppressor. Some people see Obesity as being a result of leptin resistance - the body no longer reacts to leptin.....appetite is no longer suppressed. So this study suggests that sprinting kicks off the same cascade of signals as does leptin. It signals you to stop eating....
The conclusion is really provocative - restoration of leptin sensitivity via sprinting:
In conclusion, this study shows that most of the signaling pathways activated by leptin in rodent skeletal muscle are also activated by sprint exercise in human skeletal muscle, despite a small reduction of leptin serum concentration after the sprint exercise. These findings imply that sprint exercise behave as a leptin mimetic and could be used to stimulate the leptin signaling pathways in human skeletal muscle. This opens the possibility of using sprint exercise to circumvent leptin resistance in obese humans and may lead to increased leptin sensitivity. We provide some evidence to support that the effects of sprint exercise on ERK, STAT3, STAT5, and SOCS3 are not mediated by changes in either serum leptin or IL-6 concentrations, while the expression of SOCS3 and the phosphorylation of STAT5 may have been induced by GH. Importantly, we showed that glucose ingestion 1 h prior to the sprint exercise abolishes or delays some of the exercise-elicited signaling responses, implying that the adaptative responses to sprint exercise training may be modulated by the postabsorp- tive state.
Is sprint exercise a leptin signaling mimetic in human skeletal muscle?
This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.