Energy balance of 10 male and 8 female triathletes participating in an Ironman event (3.8-km swim, 180-km cycle, 42.2-km run) was investigated. Energy intake (EI) was monitored at 7 designated points by dietary recall of food and fluid consumption. Energy expenditure (EE) during cycling and running was calculated using heart rate-VO, regression equations and during swimming by the multiple regression equation: Y = 3.65v+ 0.02W- 2.545 where Yis VO,in L x min(-1), v is the velocity in m s(-1), Wis the body weight in kilograms. Total EE (10,036 +/- 931 and 8,570 +/- 1,014 kcal) was significantly greater than total EI (3,940 +/- 868 and 3,115 +/- 914 kcal, p <.001) for males and females, respectively, although energy balance was not different between genders. Finishing time was inversely related to carbohydrate (CHO) intake (g x kg(-1) x h(-1)) during the marathon run for males (r = -.75,p <.05), and not females, suggesting that increasing CHO ingestion during the run may have been a useful strategy for improving Ironman performance in male triathletes.

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Obesity is considered a major public health concern throughout the world among children, adolescents, as well as adults and several therapeutic, preventive and dietary interventions are available. In addition to life style changes and medical interventions, significant milestones have been achieved in the past decades in the development of several functional foods and dietary regimens to reduce this menace. Being a multifactorial phenomenon and related to increased fat mass that adversely affects health, obesity has been associated with the development of several other co-morbidities. A great body of research and strong scientific evidence identifies obesity as an important risk factor for onset and progression of several neurological disorders. Obesity induced dyslipidaemia, metabolic dysfunction, and inflammation are attributable to the development of a variety of effects on central nervous system (CNS). Evidence suggests that neurological diseases such as Parkinson's disease and Alzheimer's disease could be initiated by various metabolic changes, related to CNS damage, caused by obesity. These metabolic changes could alter the synaptic plasticity of the neurons and lead to neural death, affecting the normal physiology of CNS. Dietary intervention in combination with exercise can affect the molecular events involved in energy metabolism and synaptic plasticity and are considered effective non-invasive strategy to counteract cognitive and neurological disorders. The present review gives an overview of the obesity and related neurological disorders and the possible dietary interventions.

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