Introduction: An increased ability to oxidize fat during exercise is associated with training status and with a series of health parameters (Robinson et al., 2015; Rosenkilde et al., 2010). Fat oxidation is influenced by substrate availability of both fat and carbohydrate shown by a positive correlation between the availability of free fatty acids and peak fat oxidation (PFO) (Romijn et al., 1995) and by a reduced PFO after consuming a carbohydrate-rich meal prior to exercise (Achten & Jeukendrup, 2003). Glycogen stores in muscle and liver serve as key energy substrates during exercise and the content can be manipulated by diet and physical activity (Bergström & Hultman, 1967). Depending on the filling-degree, the muscle glycogen content can cause a shift in substrate metabolism, yet no study has investigated how changes in glycogen availability will influence the PFO.

 

Aim: The aim of the study was to investigate the influence of muscle glycogen content on PFO and the intensity that elicits PFO (FAT_max). We hypothesized that both PFO and FAT_max would increase when endogenous carbohydrate delivery was limited by depletion of the muscle glycogen stores.

 

Methods: Nine healthy, trained men was included (age (years): 26.8±2.1, BMI (kg/m²): 23.5±1.6, VO_2peak (ml O₂/min): 4736±369) in a crossover study consisting of two consecutive trial days separated by 7-14 days. Test day 1 consisted of a DXA scan, a blood sample, a muscle biopsy and a graded exercise test on a bike ergometer to measure PFO, FAT_max and VO_2peak. Lastly, a 2,5-3-hour glycogen depletion protocol was performed on a bike ergometer to deplete muscle and liver glycogen. Test day 2 consisted of a venous blood sample, a muscle biopsy and a graded exercise test. Between test day 1 and 2, the participants, in random order, consumed an isocaloric diet high or low in carbohydrate to induce high and low muscle glycogen content, respectively. A high fat content compensated for the low carbohydrate content in the low-carbohydrate diet. Test day 1 and 2 was performed again in the second week, but with the opposite diet.

 

Results: PFO increased significantly with both high (Δ0.097±0.02 g/min, p=0.0343) and low (Δ0.366±0.01 g/min, p=<0.0001) carbohydrate feeding, and the increase in PFO with low carbohydrate feeding was significantly higher (p=<0.0001). FAT_max increased significantly with low (from 41±4.8 to 57±7.4 % of VO_2peak, p=<0.001), but not with high (from 42±4.8 to 45±4.4 % of VO_2peak, p=0.533) carbohydrate feeding.

 

Conclusion: In conclusion, and in line with our hypothesis, the low carbohydrate feeding and expected low content of glycogen increased both PFO and FAT_max. However, the expected high glycogen content also increased PFO. This may be explained by inadequate refilling of the glycogen content after the high carbohydrate feeding. The results have implications towards a health perspective relative to understanding and optimizing fat oxidation during exercise as a read out of metabolic flexibility.