Abstract
The possible direct role of exercise intensity and duration on leptin concentrations is conflicting. The aim of this study was to evaluate the acute effects of high intensity interval (HIIE) and moderate intensity continuous (MICE) exercise on plasma leptin response. Seven young volunteers underwent three tests: 1) a treadmill graded exercise test to identify running peak velocity (PV); 2) HIIE: 5 × 2 min work bouts at 90% of PV, interspersed by 2 min of passive recovery and; 3) MICE: 30 min at 70 % of PV. Blood samples were drawn for the assays of leptin before and 30 minutes after HIIE and MICE. A 2-way repeated measures ANOVA showed a significant main effect of time [F(1,6) =17,52; p=0,006], no significant effect of condition (type of exercise) (F(1,6) = 0,16; p = 0,68) and no significant interaction (condition × time) (F(1,6)= 0,48, p=0,51). Leptin decreased 30 min after HIIE (t= 2,95, p=0,025) and MICE (t=4,18; p=0,005). There was no difference between the HIIE and MICE conditions immediately after exercise (t=0,90; p=0,40). After HIIE and MICE, leptin decreased in the same magnitude. It appears that both exercise modalities result in physical stress which is sufficient to improve short-term leptin sensibility.
Highlights
Several hormonal responses may contribute to control of energy balance, weight management, body fat distribution and inflammatory status Fisher et al (2001)
The acute effects of the two exercise regimens on serum leptin levels are presented in table 2
This study investigated the effect of HIIE compared with traditional MICE on acute leptin response after exercise
Summary
Several hormonal responses may contribute to control of energy balance, weight management, body fat distribution and inflammatory status Fisher et al (2001). A 167-amino-acid polypeptide hormone that is produced by adipocytes in proportion to their triglyceride content, influences food intake and control of body weight by binding to and activating the long form of its receptor in the brain Park; Ahima (2015). Leptin action is required for energy stores to be sensed in the central nervous system (CNS), is essential for normal energy homeostasis and its major physiological role is to respond to and defend against reductions of body fat, that might impair survival and reproductive fitness Myers et al (2010). The coexistence of elevated leptin levels with obesity is considered a strong evidence of “leptin resistance” Myers et al (2010 e Park; Ahima (2015)
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