"The effect on the blood ketone body concentration of a 100 g oral dose of either alanine, glucose or starch was studied in forty-four healthy men. Twenty of the subjects were highly trained long-distance runners who underwent 'glycogen stripping' as previously described by us (Koeslag et al. 1980). Twelve non-athletic subjects fasted for 65 h before the test, and twelve were studied on a normal day after a normal breakfast."Trained athletes were tested after running 2 hours. They ate a low carbohydrate diet for 48h prior to the experiment. The starvation group was composed of 12 non trained subjects, fasted for 65 hours.
|The arrow shows the point in which the different solutions were ingested.|
"The ingestion of glucose or alanine after exercise caused the mean blood ketone body concentration to fall to less than 0 5 mmol/l in 2 h. The fall was more prompt, less variable and longer lasting after 100 g alanine was ingested than after 100 g glucose. At 15.00 the mean blood ketone body concentration was rising again in the subjects who had taken glucose, but not in those who had taken alanine. The difference between the mean blood ketone body concentrations of the two groups at 15.00 is statistically significant (P < 0-01).
(...) Starch ingestion caused the blood ketone body concentrations to fall, but to a lesser extent than after alanine or glucose ingestion. After starch ingestion, as after glucose, the mean blood ketone body concentration was rising again at 16.00 (Fig. 1), thus reaffirming the evanescence ofthe antiketogenic effects of carbohydrate administration."So the antiketogenic effect was alanine > glucose > starch. We are talking about 100g of each, after either 65h of fasting (almost 3 days) and running 22km plus a low carbohydrate diet. This is by no means a "typical" scenario. But it shows us that starch is less antiketogenic than glucose. Evolutionary reasons perhaps?
Extrapolating the findings to real life situations, there shouldnt be much of a problem about getting back to ketosis consuming carbohydrates only post workout, specially if you follow a very low carbohydrate diet, fast daily and train in a fasted state. This is the winning combo for minimizing glucose oxidation and maximizing non-oxidative glucose disposal after a glucose load.
Studies have shown that adaptation to a high fat-low carbohydrate diet produces a shift in glucose metabolism, reducing glucose oxidation and increasing glycogen synthesis and glucose storage. A similar metabolic response is triggered by short term fasting and resistance training.
Further reading on high fat diets and glucose metabolism:
High-fat/low-carbohydrate diet reduces insulin-stimulated carbohydrate oxidation but stimulates nonoxidative glucose disposal in humans: An important role for skeletal muscle pyruvate dehydrogenase kinase 4.
Low-carbohydrate diet alters intracellular glucose metabolism but not overall glucose disposal in exercise-trained subjects.
Carbohydrate refeeding after a high-fat diet rapidly reverses the adaptive increase in human skeletal muscle PDH kinase activity.
Koeslag JH, Noakes TD, & Sloan AW (1982). The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation. The Journal of physiology, 325, 363-76 PMID: 7050344