Fructose Impairs Fatty Acid Oxidation: Replacing 26g of Starch and Lactose in low GI Meal by Fructose Decreases Postprandial and Exercise Fatty Acid Oxidation by -21%

Image 1: With just bacon and eggs for breakfast you would not run the "risk" of reducing fatty acid oxidation.

A carby meal, i.e. a meal with a high amount of carbohydrates, right before workout triggers a shift in substrate utilization, i.e. the type of energy resource, your body will use to fuel the subsequent workout, from fats to carbohydrates, right!? But does it make difference whether you eat a Snickers bar or drink a can of Coca Cola, if both contained the same amount of carbs? Or, in other words, does the source and/or the glycemic index of your pre-workout meal have an impact on the respiratory quotient (RQ), which is the quotient of the amount of exhaled CO2 and inhaled oxygen, with higher RQs (towards 1.0) indicating that you are predominantly running on carbs, and low RQs (towards 0.7) indicating that you derive a greater part (not all!) of your energy from fatty acids.

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)

As you can see, the meals have identical caloric values and macronutrient compositions. Unfortunately, the differences between the ingredients go beyond their plain sugar vs. starch vs. fructose content. After all, spaghettis are not rice and milk is not ham ... this is a design flaw, of which I think that it impairs the significance of the results, but hey! At least the Chines have grasped the idea that calorie is not a calorie...

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)

As you can see in figure 2, there were significant difference in the postprandial (120 min before exercise) glucose and insulin response to the different meals. Yet, while the difference between the low and high GI meals was something you should have expected, judged by the GI, the fructose enriched LGF meal should not have produced greater glucose (+63% area under the curve, cf. figure 2, left, small graph) and insulin (+62% area under the curve, cf. figure 2 right, small graph) responses than the low GI, no fructose meal, which, in fact, had a slightly lower glycemic index.

Figure 3: Postprandial (2 hours) lactate concentration in the 10 subjects after ingestion of the three test meals
(data adapted from Sun. 2011)

What is yet even more striking is the profound increase in lactate concentration during the prostprandial (not the exercise phase) in the subjects who consumed the fructose-containing meal (cf. figure 3). With +211% (lactate AUC) the postprandial lactate concentration in the LGF group is more than 3x higher than in the LG group! A clearcut sign for an increase in hepatic glycolysis and probably part of the reason that we are seeing increased carbohydrate and decreased fatty acid oxidation rates in the course of the subsequent walking exercise (cf. figure 4).

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)

Postprandially, the increase in carbohydrate oxidation is even more pronounced in the LGF group than in the HG (sugar) group. That being said, the total reductions in fatty acid oxidation are -21% for the low GI fructose (LGI) and -23% for the high GI sugar (HG) group and thusly, within their respective statistical margins, identical!

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)

Although these results stand in line with the detrimental effects of fructose sweetened foods, I would still like to see two methodologically flawless studies with a) meal 1 not using different foods (I mentioned that in the 4th paragraph of this post already) and b) fructose from whole fruit and not in the form of the powdered poison Sun et al. just dissolved in water and added to their meals... and you know, in case these studies will be done - sometime in the distant future, when mainstream nutritionists will finally understand that not only is a calorie not a calorie, but that powdered fructose is also not an apple, you will read about that on the SuppVersity, first!