Abstract

It remains unknown whether the high insulin (INS) levels in the brain affect fat oxidation during exercise. We examined the effects of the intranasal administration of INS, which increases the INS concentration in the cerebrospinal fluid when peripheral effects are lacking, on the maximum fat oxidation rate (maxFOR) and its intensity (FATmax) during exercise in 15 young normal-weight (N group) and eight young overweight (O group) individuals. On two separate days, either INS or placebo (PL) was randomly administered intranasally before a graded exercise test. Indirect calorimetry was used to assess maxFOR and FATmax during exercise. Blood INS and glucose levels did not change after INS administration. In the N group, maxFOR and FATmax were significantly smaller in the INS trial than in the PL trial. MaxFOR was significantly smaller in the O group than in the N group and was not influenced by INS administration. Exercise-induced elevation in blood epinephrine levels tended to be reduced by INS administration only in the N group. Intranasal INS administration reduces fat oxidation during exercise without any peripheral effects, possibly by suppressing sympathetic nerve activity. This inhibitory effect is diminished in overweight subjects, suggesting that cerebral insulin effects are attenuated in this population.

Highlights

  • IntroductionThe skeletal muscle must use both fat and carbohydrates as energy sources

  • During endurance exercise, the skeletal muscle must use both fat and carbohydrates as energy sources

  • The intranasal administration of INS acutely reduces the appetite and food intake [16] and chronically reduces the body fat in healthy subjects [17]. These results suggest that INS in central nervous system (CNS) contributes to the regulation of eating behavior and energy metabolism, especially to facilitating catabolic action, as opposed to the effects of peripheral INS; it is unclear whether INS delivery to CNS influences fat oxidation during exercise

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Summary

Introduction

The skeletal muscle must use both fat and carbohydrates as energy sources. MaxFOR and the exercise intensity at which maxFOR occurs are lower in obese individuals in relation to their insulin (INS) resistance compared with those in subjects of normal weight [4,5]. This “low metabolic fitness” might explain, at least in part, an impaired exercise capacity or the reduced effect of aerobic exercise on reducing body fat in obese subjects. Animal studies have shown that INS infusion into the cerebral ventricle reduces blood glucose levels and food intake [10,11]

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