Annals of nutrition & metabolism
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Prior to 1969, athletes were advised to avoid drinking during exercise. At least 4 subsequent events led to the adoption of a radically different approach. By 1996, all exercisers were advised to drink 'as much as tolerable' in order to insure that they did not lose any weight during exercise - the 'zero percent dehydration' doctrine. This advice requires that athletes drink enough to 'stay ahead of thirst'. The act of drinking is a basic survival instinct that has been regulated by complex, unconscious controls ever since the first fish-like creatures moved onto land and should not require conscious adjustment. ⋯ Drinking ad libitum appears to optimize performance and safety during exercise in many situations. The presence of thirst, not of water loss, may be the biological signal that impairs exercise performance in those who drink less than their thirst dictates during exercise.
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Knowledge about the relationship between exercise and appetite is important both for athletes wishing to optimise performance and for those interested in maintaining a healthy body weight. A variety of hormones are involved in appetite regulation including both episodic hormones, which are responsive to episodes of feeding, and tonic hormones, which are important regulators of energy storage over the longer term (e.g. insulin and leptin). Notable among the episodic appetite-regulating hormones is ghrelin, which plays a unique role in stimulating appetite and energy intake. ⋯ The lack of a full compensatory response of appetite to exercise may facilitate the development of a negative energy balance and weight loss although there is individual variability in the response to exercise. From a practical standpoint athletes should not feel concerned that exercise will cause overeating as there is limited evidence to support this. For those desiring weight loss there may be some merit in performing exercise in the postprandial period as a means of enhancing the satiating effect of a meal but additional evidence is required to confirm the effectiveness of this strategy.
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The aim of our study was to investigate the interaction between the tumor necrosis factor-α (TNF-α) gene -308G/A promoter and the leptin receptor (LEPR) gene Lys656Asn polymorphisms and their effects on serum leptin levels in obese subjects. ⋯ There is an interaction between TNF-α gene G308A promoter and LEPR gene Lys656Asn polymorphisms, with higher concentrations of leptin in the G308A and A308A genotypes combined with the mutant LEPR genotype.