Nutritional Manipulation of Exercise Induced Skeletal Muscle Cell Signalling: Implications for Acute Training Adaptations

Traditional nutritional approaches for endurance training typically advise high carbohydrate (CHO) availability before, during and after each training session to suppor high training volume, intensity and recovery. However, during the last decade, accumulating data demonstrate that carefully scheduled periods of reduced CHO availability actually augment training-induced oxidative adaptations of skeletal muscle, the so-called train-low paradigm. In accordance with this movement there is also growing rationale ot consume protein before, during and/or after train-low sessions in an attempt to simultaneously promote mitochondrial biogenesis, muscle protein synthesis (MPS) and improve net muscle protein balance. The aim of this thesis was to assess the effects of reduced CHO but high protein availability on the regulation of molecular pathways associated with modulation of the aforementioned components of training adaptation. On the basis of characterising such molecular responses, a secondary aim was to formulate a nevel framework for which to practically apply train-low paradigms. Given the enhanced oxidative adaptatios observed when training in CHO restricted state is potentially regulated through free fatty acid (FFA)-mediated signalling, the aim of study 1 (chapter 4) was to test the hypothesis that leucine-enriched protein feeding before and during exercise does not impair FFA availability or whole body lipid oxidation during exercise. Here I utulised a novel leucine enriched protein gel and compaired this agains a whey drink or placebo gel in a repeated masures design. This study showed that despite the insulemic effects of protein provision, there was no imparment in FFA availability or whole body lipid oxidation during exercise. Therefore, suggesting that protein feeding does not hinder a key objective of train-low sessions. Building on the results from study 1, I next saught to characterise the effects of reduced CHO but high leucine availability on exercise capacity and cell-signalling responses associated with exercise-induced regulation of mitochondrial biogenesis and MPS. While low CHO availability inhibited exercise capacity, comparible mitochondrial signalling responces were seen at the point of fatigue despite participants performing significantly more work in high CHO condition. This demonstrated that training with low CHO is work-efficient in eliciting beneficial signals regulating mitochondrial biogenesis. Despite providing leucine rich protein before, during and after exercise, MPS related signalling could not be rescued during the CHO restriced post-exercise period in the low CHO condition. The data from this study suggest that although there are potential metabolic benefits associated with reduced pre-exercise CHO availability, the post-exercise meal should contain sufficient CHO to restore muscle glycogen to sufficient levels and/or provide the nexessary energy to support post-exercise remodelling process. Having identified the potential detrimental effects of low CHO recovery, the aim of study 3 (Chapter 6) was to examine the role of leucine availability in regulating post-exercise skeletal muscle remodelling processes in recovery from a train-low training session. Here I fed one of two protein types, a collagen (naturally low in leucine) or a whey (naturally high in leucine) protein during a low CHO training session, in a repeated measures design. When considered with study 2, the data from this study suggested that leucine is essential for reactivation of signalling mechanisms involved in protein translation, interestingly while low CHO training appeared to activate components of the system that selectively degrades malfunctional parts of the cell, leucine content had no effect on these processes. When taken together, the novel data presented in this thesis allude to a potential muscle glycogen threshold hypothesis surmising that reduced pre-exercise muscle glycogen may enhance the activation of those pathways regulating mitochondrial biogenesis but also suggest that keeping glycogen (and energy) at critically low levels may impair the regulation if post-exercise remodelling processes. From a practical perspective, data lend support for a potential “fuel for the work required” train-low paradigm in that athletes could strategically reduce CHO availability prior to completing pre-determined training workloads that can be redily performed with reduced CHO availability, thereby inducing a work efficient approach to training. Alternativly, when the goals of the training session are to complete the highest workload possible over more prolonged duration, then adequate CHO should be provided prior to and during the specific training session