Author(s): LANGE, K., BECKER, L., RØMER, T., HASSING, M., HØYBYE, S.T., SMAILES, N., PARDO, P., DANISMAN, B., ANDERSEN, P.F., LARSEN, S., HELGE, J.W., Institution: UNIVERSITY OF COPENHAGEN, Country: DENMARK, Abstract-ID: 1229

INTRODUCTION:
Whole-body fat oxidation correlates with mitochondrial oxidative capacity, emphasising the role of mitochondrial function in systemic and skeletal muscle substrate utilisation during exercise – a relationship that may be modulated by the prevailing fuel availability (Demine et al., 2014). Muscle glycogen is an important fuel during exercise due to its pronounced effects on substrate metabolism. To date, no study has explored whether a change in muscle glycogen content and thus substrate availability influences peak fat oxidation (PFO) and mitochondrial coupling control and efficiency (MCCE). The aim was therefore to investigate the influence of muscle glycogen content on PFO, the intensity that elicits PFO (Fatmax) and MCCE. It was hypothesised that PFO and Fatmax would increase in a state of low muscle glycogen availability, whereas MCCE was expected to be higher in a state of medium to high muscle glycogen.
METHODS:
Ten trained men (age: 26.1±3.0 years, BMI: 23.3±1.6 kg/m2, 𝑉̇O2peak: 4.72±0.35 L O2/min) participated in a crossover study involving two interventions each consisting of two test days. Day 1 consisted of anthropometrics, blood sampling, a muscle biopsy, and a graded exercise test to measure PFO, Fatmax and 𝑉̇O2peak using an automated online system (Quark CPET, COSMED, Rome, Italy), followed by a 2.5-3-hour glycogen depletion protocol. On the following day, a blood sample and a muscle biopsy were collected, and the graded exercise test was repeated. An isocaloric diet high or low in carbohydrate was consumed between the days to manipulate glycogen levels and constituted a high-carbohydrate (H-CHO) and low-carbohydrate (L-CHO) intervention. The alternative diet was repeated 7-14 days later. Muscle samples were analysed for muscle glycogen content, and MCCE was assessed in isolated mitochondria using high-resolution respirometry (Oxygraph-2k; Oroboros Instruments GmbH, Innsbruck, Austria) . A two-way mixed-model ANOVA was used to assess both within-intervention changes in PFO and Fatmax and between-intervention differences. Changes in muscle glycogen and MCCE were analysed by a one-way ANOVA.
RESULTS:
Compared to baseline, muscle glycogen content was reduced by 30.5 % and 69.3 % in the H-CHO and L-CHO intervention, respectively. PFO increased under conditions of low muscle glycogen availability and was lower in H-CHO when compared to baseline values. Fatmax was elevated only under low muscle glycogen availability. Muscle glycogen content did not influence MCCE.
CONCLUSION:
The study design successfully manipulated muscle glycogen content through dietary and exercise interventions. As hypothesised, muscle glycogen content influenced both PFO and Fatmax. However, contrary to the hypothesis, diet and exercise induced short-term changes in muscle glycogen content did not significantly influence MCCE.