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      Carbohydrate availability and exercise training adaptation: Too much of a good thing?

      , ,
      European Journal of Sport Science
      Informa UK Limited

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          Abstract

          Traditional nutritional approaches to endurance training have typically promoted high carbohydrate (CHO) availability before, during and after training sessions to ensure adequate muscle substrate to meet the demands of high daily training intensities and volumes. However, during the past decade, data from our laboratories and others have demonstrated that deliberately training in conditions of reduced CHO availability can promote training-induced adaptations of human skeletal muscle (i.e. increased maximal mitochondrial enzyme activities and/or mitochondrial content, increased rates of lipid oxidation and, in some instances, improved exercise capacity). Such data have led to the concept of 'training low, but competing high' whereby selected training sessions are completed in conditions of reduced CHO availability (so as to promote training adaptation), but CHO reserves are restored immediately prior to an important competition. The augmented training response observed with training-low strategies is likely regulated by enhanced activation of key cell signalling kinases (e.g. AMPK, p38MAPK), transcription factors (e.g. p53, PPARδ) and transcriptional co-activators (e.g. PGC-1α), such that a co-ordinated up-regulation of both the nuclear and mitochondrial genomes occurs. Although the optimal practical strategies to train low are not currently known, consuming additional caffeine, protein, and practising CHO mouth-rinsing before and/or during training may help to rescue the reduced training intensities that typically occur when 'training low', in addition to preventing protein breakdown and maintaining optimal immune function. Finally, athletes should practise 'train-low' workouts in conjunction with sessions undertaken with normal or high CHO availability so that their capacity to oxidise CHO is not blunted on race day.

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          Most cited references36

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          Carbohydrates for training and competition.

          An athlete's carbohydrate intake can be judged by whether total daily intake and the timing of consumption in relation to exercise maintain adequate carbohydrate substrate for the muscle and central nervous system ("high carbohydrate availability") or whether carbohydrate fuel sources are limiting for the daily exercise programme ("low carbohydrate availability"). Carbohydrate availability is increased by consuming carbohydrate in the hours or days prior to the session, intake during exercise, and refuelling during recovery between sessions. This is important for the competition setting or for high-intensity training where optimal performance is desired. Carbohydrate intake during exercise should be scaled according to the characteristics of the event. During sustained high-intensity sports lasting ~1 h, small amounts of carbohydrate, including even mouth-rinsing, enhance performance via central nervous system effects. While 30-60 g · h(-1) is an appropriate target for sports of longer duration, events >2.5 h may benefit from higher intakes of up to 90 g · h(-1). Products containing special blends of different carbohydrates may maximize absorption of carbohydrate at such high rates. In real life, athletes undertake training sessions with varying carbohydrate availability. Whether implementing additional "train-low" strategies to increase the training adaptation leads to enhanced performance in well-trained individuals is unclear.
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            Repeated transient mRNA bursts precede increases in transcriptional and mitochondrial proteins during training in human skeletal muscle.

            Exercise training induces mitochondrial biogenesis, but the time course of molecular sequelae that accompany repetitive training stimuli remains to be determined in human skeletal muscle. Therefore, throughout a seven-session, high-intensity interval training period that increased (12%), we examined the time course of responses of (a) mitochondrial biogenesis and fusion and fission proteins, and (b) selected transcriptional and mitochondrial mRNAs and proteins in human muscle. Muscle biopsies were obtained 4 and 24 h after the 1st, 3rd, 5th and 7th training session. PGC-1α mRNA was increased >10-fold 4 h after the 1st session and returned to control within 24 h. This 'saw-tooth' pattern continued until the 7th bout, with smaller increases after each bout. In contrast, PGC-1α protein was increased 24 h after the 1st bout (23%) and plateaued at +30-40% between the 3rd and 7th bout. Increases in PGC-1β mRNA and protein were more delayed and smaller, and did not persist. Distinct patterns of increases were observed in peroxisome proliferator-activated receptor (PPAR) α and γ protein (1 session), PPAR β/δ mRNA and protein (5 sessions) and nuclear respiratory factor-2 protein (3 sessions) while no changes occurred in mitochondrial transcription factor A protein. Citrate synthase (CS) and β-HAD mRNA were rapidly increased (1 session), followed 2 sessions later (session 3) by increases in CS and β-HAD activities, and mitochondrial DNA. Changes in COX-IV mRNA (session 3) and protein (session 5) were more delayed. Training also increased mitochondrial fission proteins (fission protein-1, >2-fold; dynamin-related protein-1, 47%) and the fusion protein mitofusin-1 (35%) but not mitofusin-2. This study has provided the following novel information: (a) the training-induced increases in transcriptional and mitochondrial proteins appear to result from the cumulative effects of transient bursts in their mRNAs, (b) training-induced mitochondrial biogenesis appears to involve re-modelling in addition to increased mitochondrial content, and (c) the 'transcriptional capacity' of human muscle is extremely sensitive, being activated by one training bout.
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              The Glycogen-Binding Domain on the AMPK β Subunit Allows the Kinase to Act as a Glycogen Sensor

              Summary AMPK β subunits contain a conserved domain that causes association with glycogen. Although glycogen availability is known to affect AMPK regulation in vivo, the molecular mechanism for this has not been clear. We now show that AMPK is inhibited by glycogen, particularly preparations with high branching content. We synthesized a series of branched oligosaccharides and show that those with a single α1→6 branch are allosteric inhibitors that also inhibit phosphorylation by upstream kinases. Removal of the outer chains of glycogen using phosphorylase, thus exposing the outer branches, renders inhibition of AMPK more potent. Inhibition by all carbohydrates tested was dependent on the glycogen-binding domain being abolished by mutation of residues required for carbohydrate binding. Our results suggest the hypothesis that AMPK, as well as monitoring immediate energy availability by sensing AMP/ATP, may also be able to sense the status of cellular energy reserves in the form of glycogen.
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                Author and article information

                Journal
                European Journal of Sport Science
                European Journal of Sport Science
                Informa UK Limited
                1746-1391
                1536-7290
                October 23 2014
                January 02 2015
                June 19 2014
                January 02 2015
                : 15
                : 1
                : 3-12
                Article
                10.1080/17461391.2014.920926
                24942068
                c6dcac87-3e7f-4fe5-9b99-4ec45f12eb3b
                © 2015
                History

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