Here is why I suggest no carbs post-workout, particularly on an established keto diet
The finding that endurance-trained individuals have elevated fat utilization in the resting state (1, 2) has raised the possibility that exercise can produce an overall increase in fat oxidation, particularly in the postexercise state. This effect is particularly relevant for obesity-prone individuals who are known to have reduced fat oxidation after weight reduction (3).
Bielinski et al (4) studied energy expenditure and substrate oxidation in the postexercise recovery period using whole-body indirect calorimetry. They showed that 17 h after a 3-h exercise session at 50% of maximal oxygen consumption ( O2max) there was a 4.7% increase in resting energy expenditure and a significant decrease in respiratory quotient (RQ). Other studies also showed a persisting increase in metabolic rate after exercise bouts of different durations and intensities (5, 6) as well as reduced RQs (5, 7, 8). Conversely, Weststrate et al (7) did not find any effect of exercise on resting metabolic rate (RMR) 12 h after a 90-min exercise bout at 25?35% of O2max. These results may be related to an exercise intensity that was too low, as shown previously (6).
The enhancement in fat oxidation after exercise reflected by the decrease in RQ may be secondary to the glycogen depletion and to the acute negative energy balance induced by the exercise stimulus. It is possible then that the reduced carbohydrate availability promotes a shift from glucose to fat oxidation. To verify this hypothesis, Calles-Escandon et al (9) submitted 21 subjects to one of four 10-d treatments: 1) control, 2) overfeeding, 3) exercise, and 4) overfeeding and exercise. They found that after an exercise session at 50% of maximal oxygen consumption representing 50% of daily RMR, fat oxidation increased at rest independently of a postexercise dietary compensation matching the cost of exercise.
According to the classic concept developed by Randle et al (10), fat metabolism can substantially alter carbohydrate metabolism. However, little evidence has supported this concept in exercise studies. In a recent study, it was shown that fatty acid oxidation is regulated by carbohydrate metabolism via changes in blood insulin concentrations during exercise (11), probably by controlling the rate of fatty acid entry into the mitochondria (12). Thus, during recovery, the exercise-induced glycogen depletion and the decrease in circulating insulin could provoke an increase in fat oxidation by enhancing fatty acid metabolism, perhaps until carbohydrate stores are replenished. Specifically, this may mean that the substrate mix oxidized is altered in the postexercise state as long as carbohydrate balance is not restored, which seems concordant with the theory proposed by Flatt (13).
In the present study, we attempted to document this phenomenon by measuring postexercise macronutrient oxidation under conditions in which liquid supplementation compensating for the carbohydrate and lipid oxidized (over the resting rate) was provided immediately after exercise. We submitted 8 volunteers to an exercise session followed by 61 h in a respiratory chamber to measure postexercise energy expenditure and substrate oxidation.