Abstract
Muscle glycogen and intramuscular triglycerides (IMTG, stored in lipid droplets) are important energy substrates during prolonged exercise. Exercise-induced changes in lipid droplet (LD) morphology (i.e. LD size and number) have not yet been studied under nutritional conditions typically adopted by elite endurance athletes, that is, after carbohydrate (CHO) loading and CHO feeding during exercise. We report for the first time that exercise reduces IMTG content in both central and peripheral regions of type I and IIa fibres, reflective of decreased LD number in both fibre types whereas reductions in LD size were exclusive to type I fibres. Additionally, CHO feeding does not alter subcellular IMTG utilisation, LD morphology or muscle glycogen utilisation in type I or IIa/II fibres. In the absence of alterations to muscle fuel selection, CHO feeding does not attenuate cell signalling pathways with regulatory roles in mitochondrial biogenesis. We examined the effects of carbohydrate (CHO) feeding on lipid droplet (LD) morphology, muscle glycogen utilisation and exercise-induced skeletal muscle cell signalling. After a 36h CHO loading protocol and pre-exercise meal (12 and 2gkg-1 , respectively), eight trained males ingested 0, 45 or 90gCHOh-1 during 180min cycling at lactate threshold followed by an exercise capacity test (150% lactate threshold). Muscle biopsies were obtained pre- and post-completion of submaximal exercise. Exercise decreased (P<0.01) glycogen concentration to comparable levels (∼700 to 250mmolkg-1 DW), though utilisation was greater in type I (∼40%) versus type II fibres (∼10%) (P<0.01). LD content decreased in type I (∼50%) and type IIa fibres (∼30%) (P<0.01), with greater utilisation in type I fibres (P<0.01). CHO feeding did not affect glycogen or IMTG utilisation in type I or II fibres (all P>0.05). Exercise decreased LD number within central and peripheral regions of both type I and IIa fibres, though reduced LD size was exclusive to type I fibres. Exercise induced (all P<0.05) comparable AMPKThr172 (∼4-fold), p53Ser15 (∼2-fold) and CaMKIIThr268 phosphorylation (∼2-fold) with no effects of CHO feeding (all P>0.05). CHO increased exercise capacity where 90gh-1 (233±133s)>45gh-1 (156±66s; P=0.06)>0gh-1 (108±54s; P=0.03). In conditions of high pre-exercise CHO availability, we conclude CHO feeding does not influence exercise-induced changes in LD morphology, glycogen utilisation or cell signalling pathways with regulatory roles in mitochondrial biogenesis.
Highlights
Muscle glycogen and intramuscular triglycerides (IMTG) provide important energy substrates during prolonged endurance exercise (Van Loon, 2004)
The aim of the present study was to test the following hypotheses: (1) CHO feeding during prolonged endurance exercise does not affect IMTG and muscle glycogen utilisation in both type I and type II muscle fibres, (2) CHO feeding does not impair the activation of skeletal muscle cell signalling pathways with regulatory roles in training adaptation and, (3) CHO feeding improves exercise capacity in a dose dependent manner
Confirming our hypothesis, our data demonstrate that CHO feeding during prolonged endurance exercise does not alter IMTG and glycogen utilisation in either type I or type II/IIa muscle fibres
Summary
Muscle glycogen and intramuscular triglycerides (IMTG) provide important energy substrates during prolonged endurance exercise (Van Loon, 2004). We observed that prolonged endurance exercise reduces IMTG content in the central region (indicative of the intermyofibrillar region) of type I fibres but not the peripheral (i.e. subsarcolemmal) region (Jevons et al 2020) It is noteworthy, that different methodological protocols may affect our interpretation of the subcellular utilisation patterns of IMTG, given that the choice of lipid dye (Oil Red O versus BODIPY) and chosen size of peripheral region (i.e. 2 versus 5 μm) may contribute additional artefacts upon the quantification of changes in substrate pools during exercise (Jevons et al 2020; Strauss et al 2020). Such data demonstrate that further research is required to further characterise the exercise-induced subcellular changes in LD morphology within specific fibre types
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