Leucine-enriched protein feeding does not impair exercise-induced free fatty acid availability and lipid oxidation: beneficial implications for training in carbohydrate-restricted states

Given that the enhanced oxidative adaptations observed when training in carbohydrate (CHO) restricted states are potentially regulated through free fatty acid (FFA) mediated signalling and that leucine rich protein elevates muscle protein synthesis, the present study aimed to test the hypothesis that leucine enriched protein feeding enhances circulating leucine concentration but does not impair FFA availability nor whole body lipid oxidation 56 during exercise. Nine males cycled for 2 h at 70% VO2peak when fasted (PLACEBO) or having consumed a whey protein solution (WHEY) or a leucine enriched whey protein gel (GEL), administered as 22 g 1 hour pre-exercise, 11 g/h during and 22 g thirty minutes post-exercise. Total leucine administration was 14.4 g and 6.3 in GEL and WHEY, respectively. Mean plasma leucine concentrations were elevated in GEL (P= 0.001) compared 60 with WHEY and PLACEBO (375 ± 100, 272 ± 51, 146 ± 14 μmol.L-1 respectively). No differences (P= 0.153) in plasma FFA (WHEY 0.53 ± 0.30, GEL 0.45 ± 0.25, PLACEBO 0.65 ± 0.30, mmol.L-1) or whole body lipid oxidation during exercise (WHEY 0.37 ± 0.26, GEL 0.36 ± 0.24, PLACEBO 0.34 ± 0.24 g/min) were apparent between trials, despite elevated (P= 0.001) insulin in WHEY and GEL compared with PLACEBO (38 ± 16, 35 ± 16, 22 ± 11 pmol.L-1 respectively). We conclude that leucine enriched protein feeding does not impair FFA availability nor whole body lipid oxidation during exercise, thus having practical applications for athletes who deliberately train in CHO restricted states to promote skeletal muscle adaptations

The effect of different exercise regimens on mitochondrial biogenesis and performance [Elektronisk resurs]

Endurance training is a powerful tool to improve both health and performance. Physical activity is now recognized as an effective treatment and prevention therapy for a wide range of diseases. One of the most profound adaptations to endurance training is increased mitochondrial function and content within the exercising muscles. Mitochondrial quality and quantity are closely related to several of the positive health effects reported after training. High mitochondrial content strongly correlates with muscle oxidative capacity and endurance performance. Even though it is well known that endurance training increases mitochondrial content, it is unclear which type of training is the most efficient to promote mitochondrial biogenesis. Therefore, the basis for current exercise recommendations relative to mitochondrial biogenesis is poor or absent. Thus, the main objective of this thesis was to evaluate the effect of different training strategies on mitochondrial biogenesis. Recent developments in molecular methods have made it possible to study the initial adaptations to training through measurement of mRNA gene expression of exercise induced genes. One such gene is transcriptional coactivator peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α). PGC-1α is a key regulator of mitochondrial biogenesis and the expression of PGC-1α can therefore be used as a marker of this process. The first four studies presented in this thesis are acute exercise studies where two different exercise models were compared using a cross-over design. Muscle biopsies were obtained pre and post exercise and analysed for gene expression and glycogen, apart from study II. The final study was a long-term training study where muscle biopsies were obtained before and after the training period and analysed for mitochondrial enzyme activities and protein content. Study I: The expression of PGC-1α and related genes were examined after 90 min of continuous and interval exercise in untrained subjects. The exercise protocols influenced the expression of genes involved in mitochondrial biogenesis and oxidative metabolism in a similar manner. Both interval and continuous exercise were potent training strategies for relatively sedentary individuals. Study II: The expression of PGC-1α and related genes were examined after low-volume sprint interval (SIT) and high-volume interval (IE) exercise in highly trained cyclists. SIT induced a similar increase in PGC-1α expression as IE despite a much lower time commitment and work completed. Sprint interval exercise might, therefore, be a time efficient training strategy for highly trained individuals. Study III: The expression of PGC-1α and related genes, as well as the activity of upstream proteins, were examined after concurrent (ER: cycling + leg press) and single-mode (E: cycling only) exercise in untrained subjects. PGC-1α expression doubled after ER compared with E. It was concluded that concurrent training might be beneficial for mitochondrial biogenesis in untrained individuals. Study IV: The expression of PGC-1α and related genes were examined after exercise performed with low (LG) and normal (NG) muscle glycogen in well-trained cyclists. PGC-1α expression increased approximately three times more after LG compared with NG. This finding suggested that low glycogen exercise is a potent inducer of mitochondrial biogenesis in well-trained individuals. Study V: Mitochondrial enzyme activity, protein content and endurance performance were examined after eight weeks of concurrent (ES: cycling + leg press) or single-mode (E: cycling only) training in cyclists. ES did not affect enzyme activity, protein content or endurance performance differently than E. The beneficial effect previously observed in untrained subjects did not translate to higher numbers of mitochondria in trained individuals. In three of the studies, I, III, and IV, both glycogen and PGC-1α expression were measured after exercise. These data were then pooled and examined. The highest PGC-1α mRNA expression levels were identified when glycogen levels were low, and vice versa. This suggests that low glycogen might play an important role in the regulation of mitochondrial biogenesis also during interval and concurrent strength and endurance exercise. In conclusion, key markers of mitochondrial biogenesis can be effectively up-regulated by interval, concurrent and low glycogen exercise. A possible explanation for this might be that though the exercise protocols are quite divergent in nature, they all have a pronounced effect on muscle glycogen and/or perturbation in energetic stress

Dataset related to the article "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle"

This dataset is related to the figures presented in the paper "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle" published in JAPPL 2019. The dataset is provided so that interested parties can do additional analysis and interpretations. Each individual row in the Excel spreadsheet corresponds to the same subject across the tabs. Training, biopsies, 1RM and muscle thickness measurements where performed at GIH by Niklas Psilander and colleagues. Please contact Niklas regarding questions related to that dataset. Histochemical analysis were performed at NIH by Kristoffer Toldnes Cumming and colleagues. Please contact Kristoffer regarding questions related to that dataset (nuclei per fiber cross section and fiber CSA) Single fiber analysis were performed at UiO by Einar Eftestøl and colleagues. Please contact Einar regarding questions related to that dataset (nuclei per sarcomere from single fibers, volume per fiber segment and myonuclear domain size

Dataset related to the article "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle"

This dataset is related to the figures presented in the paper "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle" published in JAPPL 2019. The dataset is provided so that interested parties can do additional analysis and interpretations. Each individual row in the Excel spreadsheet corresponds to the same subject across the tabs. Training, biopsies, 1RM and muscle thickness measurements where performed at GIH by Niklas Psilander and colleagues. Please contact Niklas regarding questions related to that dataset. Histochemical analysis were performed at NIH by Kristoffer Toldnes Cumming and colleagues. Please contact Kristoffer regarding questions related to that dataset (nuclei per fiber cross section and fiber CSA) Single fiber analysis were performed at UiO by Einar Eftestøl and colleagues. Please contact Einar regarding questions related to that dataset (nuclei per sarcomere from single fibers, volume per fiber segment and myonuclear domain size

Dataset related to the article "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle"

This dataset is related to the figures presented in the paper "Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle" published in JAPPL 2019. The dataset is provided so that interested parties can do additional analysis and interpretations. Training, biopsies, 1RM and muscle thickness measurements where performed at GIH by Niklas Psilander and colleagues. Please contact Niklas regarding questions related to that dataset. Histochemical analysis were performed at NIH by Kristoffer Toldnes Cumming and colleagues. Please contact Kristoffer regarding questions related to that dataset (nuclei per fiber cross section and fiber CSA) Single fiber analysis were performed at UiO by Einar Eftestøl and colleagues. Please contact Einar regarding questions related to that dataset (nuclei per sarcomere from single fibers, volume per fiber segment and myonuclear domain size

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