Question

Horowitz and Coyle (1993) tested six meals, each with carbohydrate at a dose of 0.7 g/kg...

Horowitz and Coyle (1993) tested six meals, each with carbohydrate at a dose of 0.7 g/kg body weight, fed 30 min prior to 60 min of exercise at 50-70% VO2max. The carbohydrate sources were either potato, rice, or sucrose. Each carbohydrate source was consumed alone in one trial and in another trial with added fat. The addition of fat reduced the glycemic responses of the carbohydrate sources. Of the six treatments, the three with the highest glycemic effects were potato, sucrose, and sucrose plus fat. The other three feedings caused less of an increase in blood glucose and insulin at rest. The lower insulin concentration coincided with a nonsignificant trend toward a higher free fatty-acid concentration during exercise for the lower GI foods. Maximal performance was not evaluated; all individuals did identical cycling bouts. The fact that RPE did not differ by treatment suggests that onset of fatigue was not different. However, the average RPEs ranged from 10.2-12.9, indicating that the exercise bout was not very demanding for these physically fit males. The authors concluded that although there were differences in metabolic responses prior to exercise, these metabolic factors converged among groups by about 20 min of exercise and were unlikely to affect ability to do endurance exercise. However, it should be noted that these individuals were clearly not metabolically or physiologically highly stressed by this exercise bout. Differences may not appear unless individuals are pushed to fatigue.

20 Why did the addition of fat reduce the glycemic responses of the carbohydrate sources?

Homework Answers

Answer #1

Addition of fat to carbohydrate source reduces glycemic responses by delaying gastric emptying and stimulating insulin secretion.

Adding fat to carbohydrate is thought to reduce glycemic responses by mechanisms, namely, delayed gastric emptying, mediated by gut hormones such as gastric inhibitory polypeptide and glucagon-like peptide-1 (GLP-1), and increased insulin secretion mediated by direct effects of fatty and amino acids and/or by the hormones of the entero-insulin axis.

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