|Image 1: With just bacon and eggs for breakfast you would not run the "risk" of reducing fatty acid oxidation.|
Orange juice with breakfast? Better not...
The question, whether GI and carbohydrate type of a meal would have a significant impact on the postprandial glucose, lactate and free fatty acids levels, as well as the insulin response and the subsequent carbohydrate and fatty acid oxidation in the course of a low intensity 1h walk, has been bothering Feng-Hua Sun and his (or her?) colleagues from the Department of Sports Science and Physical Education at the Chinese University of Hong Kong, too. In a counter-balanced crossover design (>=7 days between trials; identical, recorded diet in the 3 days before each trial), all 10 healthy male subjects reported fasted (10-12h) at the laboratory, where they consumed one out of three meals with identical macronutrient composition, yet varying carbohydrate sources and glycemic indexes (cf. figure 1).
|Figure 1: Macronutrient (in g) and ingredient composition of |
the three test meals (according to Sun. 2011)
After all participants had finished eating their "delicious" breakfast, they remained seated for another 120min, in the course of which they had to drink 2ml of water per kg of body weight every 30 minutes "to ensure adequate hydration and balance the water content of the meals".
After these sedentary 2 hours, the subjects performed a standardized 5 min warm-up at 40% of their individual VO2 and then completed 60 min of brisk walking at 50% of their VO2max.
|Figure 2: Differential postprandial (2 hours) glucose (left) and insulin (right) response to the three test meals |
(data adapted from Sun. 2011)
|Figure 3: Postprandial (2 hours) lactate concentration in the 10 subjects after ingestion of the three test meals |
(data adapted from Sun. 2011)
|Figure 4: Postprandial, during exercise and total substrate utilization (in g) subsequent to the ingestion of the three different test meals (data adapted from Sun. 2011)|
With respect to the underlying reasons of this disadvantageous shifts in substrate utilization, Sun et al. speculate, that the mechanism
[...] behind this may be the reduced hyperglycemia and hyperinsulinaemia during the postprandial period following LGI meal consumption. [...] In addition, it is well known that insulin can suppress the lipolysis. This suppression appears to be long lasting, even when insulin concentration has returned to basal levels.The last part, here, is of particular interest, because, obviously, after a few minutes of walking and with the increased need for carbohydrates the insulin levels of all subjects (regardless of the composition of their prior meals) dropped to levels ~2-3mU/L. Now the insulin response in the LGF group was still smaller than the one of the high GI (HG) group, so that the scientists assume that the ability of the fructose to bypass first rate-limiting enzymes of glycolosis in the liver, which renders it readily available for oxidation, must explain why the ratio of carbohydrate to fat oxidation was still similarly skewed in both, the low GI, plus fructose, and the high GI groups.
|Image 2: I wonder if nutritionists will ever understand that there is difference between fructose powder (left) and an apple (right)|