Version classiqueVersion mobile

Nutrition and Performance in Sport

Christophe Hausswirth

Chapter 1. Nutrition: from training to competition

Topic 2. Training adaptations by timed nutrition: recent knowledge and practical applications for Rio 2016 perspectives

John A Hawley


Acute alterations in substrate availability modify the immediate exercise response and when repeated over days and weeks, modulate many adaptive processes in skeletal muscle that ultimately underpin the phenotype-specific characteristics observed in highly trained athletes. Macronutrient intake rapidly alters the concentration of blood-borne substrates and hormones, causing marked perturbations in the storage profile of skeletal muscle and other insulin-sensitive tissues. In turn, muscle energy status exerts profound effects on resting fuel metabolism and patterns of fuel utilization during training, as well as acute regulatory processes underlying gene expression and cell signalling. As such, these nutrient-exercise interactions have the potential to activate or inhibit many biochemical pathways with putative roles in training adaptation. This paper focuses on how nutrient availability can optimize adaptations to endurance, strength and repeated sprint activities that are common to the majority of Olympic sports.

Texte intégral

1. Historical background

1The interaction between training capacity and nutrient availability has long been recognized and it has generally been assumed that the optimal adaptation to the demands of repeated training sessions requires a diet that preserves muscle energy stores. Indeed, The International Olympic Committee’s Consensus Statement on Sports Nutrition published in 2003 reflected this viewpoint and recommended that “athletes should aim to achieve carbohydrate intakes to meet the fuel requirements of their training programme and to optimize restoration of muscle glycogen stores between workouts” (Burke, 2003). In real life, however, competitive athletes preparing for the majority of Olympic sports follow an intricate periodization of both diet and training load in their competitive build-up (Burke, 2010). As such, the latest guidelines for the daily training environment acknowledge the complexity of these practices by encouraging “strategies to promote carbohydrate availability for the majority of workouts as is practical and within the athletes total energy budget” (Burke, 2010; Burke et al. 2011).

2In recent years there has been a growing interest in the systematic manipulation of carbohydrate availability before and after selected training sessions and the subsequent effects on cell metabolism, training adaptation and performance. Such an approach is intended to form part of a periodized training programme during which athletes intentionally commence specific workouts with either low muscle glycogen reserves and/or low exogenous carbohydrate availability (for reviews see Burke, 2010; Hawley and Burke, 2010; Hawley et al. 2011). Support for such a practice is slowly emerging: several investigations have reported that when endurance-based training sessions are commenced with low carbohydrate availability, training adaptation is augmented to a greater extent than when similar workouts are undertaken with normal glycogen stores (Hawley and Burke, 2010; Hawley et al. 2011; Philp et al. 2012; Bartlett et al. 2014, Hawley, 2014). What is apparent is that nutrient availability alters many training-induced skeletal muscle adaptations and could potentially be a valuable coaching strategy to modulate training efficiency.

3In this brief review, the cellular events that occur in skeletal muscle during endurance-based exercise are discussed and evidence is provided demonstrating that nutrient availability plays important roles in promoting many of the adaptive responses to training. Emphasis is on human studies that have determined the regulatory role of muscle glycogen availability on cell metabolism, endurance training capacity and performance. This review concludes with the description of a new training strategy which has recently emerged, and describes its practical applications for athletes. The reader is referred to several recent reviews for detailed discussion of other nutritional strategies that impact on training-induced skeletal muscle adaptations (Hawley and Burke, 2010; Hawley et al. 2011).

2. Training adaptation

4The key components of any endurance training programme are the volume, intensity and frequency of exercise sessions, with the sum of these inputs being the “training stimulus” that either promote (fitness) or decrease (fatigue) performance capacity (for a review, see Hawley, 2002). Modifications in skeletal muscle cells that persist as a consequence of training are termed chronic adaptations, whereas cellular alterations that occur in response to a single training session are said to be acute responses. Chronic adaptations in skeletal muscle are likely to be the result of the cumulative effect of repeated (acute) bouts of exercise, with the initial signalling responses leading to these adaptations occurring during recovery after each training session (Pilegaard et al. 2000). From a molecular perspective, training adaptation can be simplistically viewed as the accumulation of specific proteins (i.e. enzymes) with increased gene expression promoting changes in protein concentrations which are pivotal to the adaptation process (Hansen et al. 2005).

5In recent years, advances in molecular biology have allowed scientists to determine how endurance exercise training stimulates mitochondrial biogenesis (for review, see Coffey and Hawley, 2007). An emerging field of interest arising from our understanding of the molecular bases of training adaptation is how nutrient availability alters the regulation of many of the contraction-induced events in muscle in response to endurance-based exercise. Nutrient-gene and nutrient-protein interactions can promote or inhibit the activities of a number of cell signalling pathways and thereby modulate training adaptation and subsequent performance capacity.

3. Effects of altering endogenous carbohydrate availability on cell metabolism, training adaptation and physical performance

6Acute alterations in muscle glycogen availability alter the immediate exercise-induced response of a number of signalling pathways involved in the training response and when repeated over weeks and months have the potential to modulate many adaptive processes in skeletal muscle and ultimately drive the phenotype-specific characteristics observed in highly trained athletes. In the first investigation to test this hypothesis, Hansen et al. (2005) employed a study design in which the left and right legs of the same (untrained) individual undertook the same total work during a 10 wk training intervention, albeit with different pre-exercise muscle glycogen availability for half the training sessions. These authors reported that resting muscle glycogen levels, the maximal activities of citrate synthase and exercise time to exhaustion were all enhanced to a greater extent in the leg that commenced half the workouts with low compared to normal, glycogen availability.

7To investigate whether competitive athletes with a prolonged history of endurance training might attain the same benefit as less fit individuals who undertake a training regimen with reduced glycogen availability, Yeo et al. (2008) recruited 12 competitive male cyclists/triathletes and divided them into two groups matched for age, VO2peak and training history. One group (HIGH) trained 6 days/wk with one rest day (day 7) for 3 wk, alternating between 100-min steady-state aerobic riding (AT; ˜70% VO2peak) on the first day and high-intensity interval training (HIT; 8 x 5-min work bouts at maximal effort with 1-min recovery in between work bouts at ˜100 W) the next day. The AT and HIT session were deliberately chosen as both these workouts deplete ˜50% of resting muscle glycogen stores in the fed state in well-nourished, trained athletes. The other group (LOW) trained twice a day, every second day for three weeks, performing the AT in the morning to decrease muscle glycogen content, followed by ˜2 h of rest without nutrient intake and then HIT. Thus, the HIGH group completed all HIT sessions at a time when muscle glycogen levels were restored, whereas the LOW group undertook this interval set at a time when muscle glycogen stores were 50% lower than normal. During week 1 (HIT sessions 1 to 3), the LOW group trained at a significantly lower average power output compared to the HIGH group (P < 0.05). During the second week (HIT sessions 4 to 6) there was a trend for the average training intensity to be lower for the LOW group (P = 0.06), but by the third week (HIT sessions 7 to 9), the training intensities for the LOW and HIGH groups were no different. Resting muscle glycogen content, the maximal activities of citrate synthase and β-hydroxyacyl-CoA dehydrogenase (β-HAD) and the content of the electron transport chain component COX subunit IV were all enhanced to a greater extent in LOW compared with HIGH after the three-week intervention. However, while markers of training adaptation were augmented when athletes trained LOW, the performance during a 1-h time trial undertaken after a 60-min steady-state ride was similar after both training programmes. These findings were subsequently confirmed by Hulston et al. (2010). More recently, Bartlett et al. (2013) reported greater levels of PDK4, Tfam, Cox IV and PGC-1α transcripts after exercise commenced with reduced versus normal carbohydrate (i.e. muscle glycogen) availability. Taken collectively, these findings suggest that the training-induced signalling pathways to mitochondrial biogenesis may be amplified in the face of low glycogen status (for recent reviews see Bartlett et al. 2015; Hawley and Morton, 2014).

Figure 1: Overview of the putative cell signalling pathways involved in regulating the enhanced mitochondrial adaptations observed when endurance-based training is undertaken under conditions of reduced carbohydrate availability (from Hawley and Morton, 2014).

Figure 1: Overview of the putative cell signalling pathways involved in regulating the enhanced mitochondrial adaptations observed when endurance-based training is undertaken under conditions of reduced carbohydrate availability (from Hawley and Morton, 2014).

8Training with reduced glycogen availability induces shifts in substrate utilization, increasing lipid oxidation while concomitantly reducing glycogenolysis and blood glucose oxidation (Hansen et al. 2005; Yeo et al. 2008; Hulston et al. 2010; Marquet et al. 2014). The enhanced lipid oxidation appears to be due to increased use of intramuscular triglycerides rather than blood-borne fatty acids, although the elevated FFA acids serve as substrates for ß-oxidation in the mitochondria and as signalling intermediates for the regulation of proteins involved in lipid metabolism.

4. Effects of altering exogenous carbohydrate availability on cell metabolism, training adaptation and physical performance

9In addition to altering endogenous carbohydrate stores, other exercise/diet protocols have been utilized to manipulate exogenous glucose availability, including training after an overnight fast, prolonged training with or without an overnight fast, and withholding carbohydrate intake during the session and/or withholding carbohydrate during the first hours of recovery. In contrast to the robust effects of commencing endurance training sessions with low muscle glycogen stores, studies that have manipulated glucose availability before, during, and/or after endurance exercise have provided less convincing results on selected muscle adaptations. Several investigations report that, after six to ten-week intervention periods, a range of training-responsive metabolic markers (including succinate dehydrogenase activity, GLUT4, and hexokinase II content) are increased by a similar extent with or without carbohydrate supplementation. Cox et al. (2010) determined the effects of varying daily carbohydrate intake by providing or withholding carbohydrate during daily training on endurance performance, whole body rates of substrate oxidation, and selected mitochondrial enzymes. Sixteen endurance-trained cyclists or triathletes were pair matched and randomly allocated to either a high-carbohydrate group (High group; n = 8) or an energy-matched low carbohydrate group (Low group; n = 8) for 28 days. The novel finding of that study (Cox et al. 2010) was that, in contrast to a matched group who exercised with lower carbohydrate availability, well-trained athletes who trained under conditions of high-carbohydrate availability (a high daily carbohydrate intake scheduled during daily training) achieved 1) a greater increase in maximal muscle citrate synthase activity and 2) an increase in the oxidation of glucose consumed during submaximal exercise. From a practical perspective, athletes who trained with high-carbohydrate availability increased exogenous glucose oxidation when subjects consumed glucose throughout a performance exercise trial. While no clear advantage was apparent to performance during a ˜2-h cycling protocol preceded by a carbohydrate-rich meal compared with training with lower carbohydrate availability, these findings suggest that athletes should practise “train-low” workouts in conjunction with sessions undertaken with normal or high-carbohydrate availability so that their capacity to oxidize carbohydrate is not blunted on race day.

10To date, only one study has examined the interactive effects of endogenous muscle glycogen and exogenous glucose availability on training adaptation. Morton et al. (2009) employed a variety of training protocols (twice/day, 2 days/wk, or once/day, 4 days/wk) and dietary manipulations (with or without carbohydrate support before and during exercise) in recreational subjects for six weeks. All protocols were associated with an increase in the levels of cytochrome c oxidase IV and the peroxisome proliferator-activated receptor-coactivator-1 (PGC-1) at the protein level, with no differences in the versus magnitude of change between groups who trained with low vs. high-carbohydrate availability. Only the maximal activity of succinate dehydrogenase was greater in subjects who commenced training with lowered muscle glycogen stores and who did not receive carbohydrate support during/after training.

5. A novel training strategy: “train high, sleep low”

11Recently a novel strategy termed “train high, sleep low” has emerged which may provide a more practical means to prolong the exposure to low carbohydrate availability. Hansen et al. (2005) and Yeo et al. (2008) observed that, under conditions of low carbohydrate availability, the average self-selected power output of high-intensity workouts was reduced by 8% under conditions of low muscle glycogen availability. Under the modified protocol, athletes would perform their high-intensity training session in the evening (with normal or high-carbohydrate availability), then sleep “low” (i.e. without post-exercise carbohydrate). A second prolonged training session is undertaken the following morning. In this scenario, training intensity is not compromised, and the athlete has a longer period of low carbohydrate availability (i.e. 10 to 12 hr) but can still perform low to moderate continuous exercise the next day.

12A recent study (Psilander et al. 2013) applied this strategy and investigated the impact of exercising with low glycogen availability on mitochondrial biogenesis in ten highly trained cyclists. Subjects undertook a glycogen depletion exercise in the evening. For the low glycogen group, dinner and breakfast were both low CHO meals (with CHO corresponding to less than 1% of total energy intake). The results revealed increased transcription of the regulator of mitochondrial biogenesis (PGC-1α) and of oxidative metabolism enzymes (PDK4 and COX I), once again confirming that training with restricted carbohydrate availability promotes the oxidative potential of muscles.

13Recently, Lanet et al. (2015) determined the effects of “training high” and “sleeping low” on acute responses of genes and proteins with roles in endurance training adaptation. Seven cyclists completed two trials and received isoenergetic diets differing only in the timing of ingestion. In one trial subjects consumed 8 g·kg-1 BM of carbohydrate (CHO) throughout the day before an evening high-intensity training session (HIT) and sleeping fasted (FAST). In the other they consumed 4 30 g·kg-1 BM of CHO before HIT then 4 g·kg-1 BM of CHO before sleeping (FED). The next morning subjects completed 2 h cycling (120SS) fasted. Muscle biopsies were taken before and 2 h after HIT (D1) and pre-, post-, and 4 h after 120SS (D2). Muscle [glycogen] was higher in FED at all times post-HIT (P<0.001). HIT increased PGC1α mRNA in both conditions (P <0.01) while PDK4 mRNA was elevated to a greater extent in FASTED (P<0.05). Phosphorylation of AMPKThr172, p38MAPKThr180/Tyr182 and p-ACCSer79 at rest (D2) was greater in FASTED (P<0.05). Fat oxidation during 120SS was higher in FASTED (P=0.01), coinciding with increases in ACCSer79 and CPT1, as well as mRNA expression of CD36 and FABP (P<0.05). Methylation on the gene promoter for COX4IA and FABP3 increased 4 h after 120SS in both trials, while methylation of the PPARδ promoter increased in FASTED. Trainhigh, sleeplow upregulated markers of lipid metabolism but failed to augment cellular markers of mitochondrial biogenesis.

14Marquet et al. (2014) were also interested in the chronic effects of the “train high, sleep low” strategy and its impact on endurance performance. These workers recruited 21 endurance-trained triathletes, randomly divided between two groups. All athletes completed the same three-week training programme, but with different nutritional guidelines. The total daily carbohydrate intake for both groups was set at 6 g. kg-1.d-1, but one group (LOW) consumed all their carbohydrate between the end of the morning training session and the beginning of the evening training session, and were not allowed to consume carbohydrates during the training sessions. The other group (HIGH) spread their carbohydrate intake throughout the day (carbohydrate was eaten at each meal and during all training sessions). In this study, unusually, performance was measured in the field (10 km running performance on a track after 40 min cycling, mimicking the end of a triathlon). This is the first study to observe a clear improvement in performance with a “train high, sleep low” strategy (-2.9% on the time to complete the 10-km running trial for the LOW group; -0.04% for the HIGH group). The results also showed an improvement in body composition (-1.05% fat mass for the LOW group,-0.27% for the HIGH group). These improvements were associated with other indicators of training adaptations (decreased heart rate, decreased RER, increased cycling efficiency during a submaximal cycling trial at fixed intensity). No impairment of the immune response was noted (based on analysis of white blood cells), nor was there any effect on the prevalence of URTI (WURSS-21 questionnaire) or sleep pattern disturbances.

15Taken collectively, the results of these studies suggest that carbohydrate should no longer be considered as a simple energy substrate, but rather as a regulator of training adaptation. Indeed, independent of prior training status, short-term (three to ten-week) training programmes during which some workouts are commenced with either low muscle glycogen and/or low exogenous glucose availability augment training adaptation (i.e. they increase the maximal activities of selected enzymes involved in carbohydrate and/or lipid metabolism and promote mitochondrial biogenesis) to a greater extent than when all workouts are undertaken with normal or elevated glycogen stores (Hawley et al. 2011). Commencing exercise with low glycogen stores induces a metabolic stress (elevated circulating catecholamine levels (Marquet et al. 2014) and initiates responses designed to maintain energy supply. This strategy will therefore improve the capacity for fatty acid oxidation to a greater degree than training with normal glycogen availability. Significant improvements in performance have been achieved with a strategy known as “train high, sleep low” which extends the time-course of the exposure to low glycogen availability. This new strategy is also more compatible with what athletes naturally do in terms of eating patterns.

16From a coaching perspective, however, it is important to note that carbohydrate availability is not the only variable manipulated in all of these investigations. The studies employed different modes of training and a range in the number of training sessions (both in total number and those undertaken under conditions of low carbohydrate availability), along with variable intervention periods. Some of the results may not even be directly attributable to differences in carbohydrate availability, but rather to the effects of the exercise training protocol itself (i.e. differences in recovery time between workouts, training once/day versus twice every second day). Notwithstanding this possibility, there is no evidence of impaired adaptation (or poorer performance outcomes) after short-term training with low carbohydrate availability. The only study to show a clear performance improvement was that applying the “train high, sleep low” strategy. We therefore recommend that nutritional scheduling be adjusted as part of training blocks, but further studies will be needed to determine how long these blocks should last, and how long before a competition they should be programmed. Other studies mimicking “real-life” practices will also be needed to confirm the gain in endurance performance. Finally, none of the studies reviewed involved elite athletes and, as usual, we are left to ponder whether or not the results for well-trained recreational individuals are relevant in any way to Olympic-calibre athletes.

6. Practical adaptations

171. Practical approaches to training-low include training in the fasted state (i.e. 6 to 10 h after the last meal); training twice per day (where the second session is thus performed with reduced glycogen stores); and/or restricting CHO intake in the recovery period post-exercise (see Table 1). Although it is presently not known which of these approaches provides the most potent training stimulus, it is recommended that where training intensity and duration lend themselves to the training-low approach (i.e. training loads are not overly compromised), then athletes would benefit from incorporating elements of train-low into their training programme.

182. In order to minimise any exercise-induced immunosuppression, training-low should be undertaken during sessions that are not dedicated to uncustomary training loads (i.e. supramaximal efforts, prolonged, intense workouts).

193. In an attempt to maintain training intensity during train-low sessions, athletes would benefit from pre-training caffeine ingestion (Lane, Areta et al. 2013) and/or CHO mouth rinse during exercise (Lane, Bird, Burke, & Hawley, 2013) as both approaches can partially offset the reduced training intensity that accompanies training with low endogenous and/or exogenous CHO availability.

204. Protein ingestion (e.g. 20 to 25 g) should be ingested before, during and/or immediately after exercise in order to attenuate muscle protein breakdown, and to promote protein synthesis. Increased protein availability before/during/after exercise does not attenuate the activation of the key signalling cascades associated with train-low (e.g. AMPK-PGC-1), suggesting that amino acid provision will not downregulate the beneficial adaptations induced by training low.

215. The practice of training low should also be undertaken alongside deliberate sessions of training high where the intended competition fuelling schedule (glycogen loaded, pre-exercise meal and exogenous CHO provision during exercise) is simulated (Stellingwerff, 2012). These sessions are likely to be best undertaken when the intensity and duration of training simulate the physiological demands of competition.

Table 1: Exercise-diet strategies for the Olympic endurance athlete.

Exercise diet strategy

Main outcomes


Training twice a day (low muscle glycogen availability for the second session)

↓ Muscle glycogen availability
↑ Enzyme activities
↑ Rates of fat oxidation
↓ Training intensity
↔ Performance
↔ Effects on immune system unknown

Should be included as part of any endurance athletes periodized diet-training regimen during selected training sessions

Chronically low carbohydrate diet (carbohydrate intake less than fuel requirements of training)

↓ Endogenous and exogenous carbohydrate availability
↓ Training capacity and performance
↓ Immune function

Not recommended

Training after overnight fast

↓ Exogenous carbohydrate availability
↑ Rates of fat oxidation
↔ Performance
↔ Effects on immune system unknown

Should be included as part of any endurance athletes periodized diet-training regimen for specific sessions

Training after overnight fast combined with withholding carbohydrate during training session

↓ Endogenous and exogenous carbohydrate availability
↔ Effects on immune system unknown

Should be included as part of any endurance athletes periodized diet-training regimen for specific sessions

Withholding carbohydrate during recovery

↓ Glycogen resynthesis
↑ Training adaptation?

Could be on benefit to “drive” the training response-adaptation process, but has not been investigated

Repeatedly training after an overnight fast while also withholding carbohydrate during training sessions

↓ Endogenous and exogenous carbohydrate availability
↑ Endurance performance
↑ Training adaptation?
↔ Effects on immune system

During training camp with increased training volume. In the weeks preceding the tapering period

7. Unanswered questions and directions for future research

22“Train low” has now become a catchphrase in athletic circles as well as in the scientific literature. This terminology is frequently used to describe a range of practices differing from the original protocol (i.e. commencing training sessions with low muscle glycogen availability) and as a generic or “one-size-fits-all” theme promoted as a replacement to the era of the high-carbohydrate diet in sport. However, there are many ways of achieving low carbohydrate availability before, during and after training sessions which differ in the site targeted for low carbohydrate availability (i.e. intra-versus extra-muscular), in the duration of exposure, the number of tissues affected as well as the frequency and timing of their incorporation into an athlete’s periodized training programme.

23A common finding from many of the studies discussed (Hansen et al. 2005; Hulston et al. 2010; Yeo et al. 2008) is the mismatch between changes in many of the cellular “mechanistic” variables (e.g. increases in the phosphorylation status of signalling molecules and/or increases in the expression of genes and proteins involved in mitochondrial biogenesis) and whole body functional outcomes (changes in training capacity or measures of laboratory-based endurance performance). There are several potential reasons that might help explain the “disconnect” and each warrants further investigation. First, there may be no direct relationship between the performance of highly trained athletes and some of the training-induced changes in selected cellular events that have been measured; the functions achieved by up-regulating various muscle proteins may be important in promoting the capacity for exercise when moving from an untrained to moderately-trained status, but are not quantitatively correlated, or indeed rate-limiting for high-level Olympic performance outcomes. Indeed, skeletal muscle function is only one factor in determining performance, and the role of the central nervous system in determining pacing strategies and perceptions of fatigue or effort have not been measured in the vast majority of studies of “train-low”. Second, there is a growing feeling from some sport scientists that we currently lack the appropriate tools to accurately measure exercise/sports performance, in particular the ability to detect small changes that are worthwhile to a competitive athlete in order to change the outcomes of real-world events (see Hopkins et al. 1999). For example, in some cases the technical variability of various enzymatic assays and/or gene measurements (typically 5 to 10%) exceed by several orders of magnitude the small (1 to 2%) biological changes that manifest as improvements in performance.

24The third possibility is that when undertaken for prolonged periods (i.e. weeks to months), some “train low” strategies may have a negative impact on parameters related to an athlete’s health or performance. Such impairments might directly result because of the complex interactions between pathways of substrate utilization; as systems to upregulate one pathway occur there may be a downregulation of others. An indirect outcome of dietary periodization may be changes in the training stimulus; a common finding when training sessions are undertaken with low carbohydrate availability is that subjects frequently chose a lower workload or intensity because they perceive the effort to be higher, at least in their initial exposure to “training low” (Yeo et al. 2008). This outcome would seem counter-intuitive for the preparation of competitive athletes, where high-intensity workouts and the generation of high power outputs are a critical component of a periodized training programme. Interference with such sessions is likely to impair other adaptations to training such as muscle fibre recruitment. Training with low carbohydrate availability is also likely to be associated with reduced immune function, and expose the athlete to an increased risk of illness, and an increased risk of injury has also been associated with exercise in a glycogen-depleted state.

25Finally, it may simply be the case that few published studies have been sophisticated enough to integrate various combinations and permutations of “train-low” strategies into the periodized training programmes of highly trained athletes. The preparation of elite athletes involves a range of training activities with various goals. It may be that “training low” needs to be carefully integrated into parts of this complex system to allow a performance benefit to be achieved in concert with the measurable cellular changes. It should also be considered whether highly trained athletes have a different response or require a different stimulus to untrained or even moderately trained individuals.

26One aspect that is currently unclear from the sparse scientific literature is the degree of glycogen depletion or restricted carbohydrate availability that is needed to potentiate the effect of the training stimulus on outcomes such as mitochondrial biogenesis, or the length of time periodic low-glycogen/low-carbohydrate training needs to be undertaken to demonstrate functional changes to training and/or performance outcomes (e.g. weeks or months?). To answer such questions, a complex series of studies would need to be undertaken that systematically “titrate” levels of carbohydrate availability and determine subsequent cellular and performance response after a standardized training regimen. Unfortunately, few of the present studies have measured actual muscle glycogen content pre-and post-training in the train-low or control conditions; some have simply assumed that restricted intake of carbohydrate and/or an abbreviated recovery period between training sessions will deliver depleted muscle glycogen stores for subsequent sessions. Investigations to date (Hansen et al. 2005; Yeo et al. 2008) have utilized a limited number of total training sessions during the study duration (18 to 45 sessions) when determining both muscle adaptation and functional performance outcomes. However, many elite endurance athletes undertake ˜500 total training sessions per year, of which ˜25-30% would be classified as difficult or hard. It is clearly impractical to extrapolate the effect of short-term laboratory supervised training studies to an entire year of periodized training and competition.

27Perhaps more importantly, we know surprisingly little about glycogen utilization during the training sessions typically undertaken by competitive athletes in Olympic sports, or how their current real-world training and dietary practices interact to determine carbohydrate availability for various workouts. Although current sports nutrition guidelines recommend practices to promote carbohydrate availability for training, particularly key sessions involving high-intensity workouts, it is likely that elite athletes who undertake several sessions per day already undertake some of these workouts with reduced carbohydrate availability, either deliberately or unintentionally. Some athletes have already adopted specific train-low practices due to the present and previous interests in this strategy and some athletes in weight-category sports may also restrict carbohydrate intake below training requirements as part of the reduced energy or carbohydrate-modified diets designed to achieve lower body mass or fat levels. Prior to embarking on further lab-based investigations of “train low”, it may be beneficial to clarify whether successful athletes have already refined optimal nutrient-training protocols that enhance endurance performance and can better inform future scientific enquiry. Such an approach may ultimately result in scientists being in a better position to advise coaches about the optimal nutrient-exercise strategies that best modulate training efficiency!


8. Bibliographic references

Bartlett JD, Louhelainen J, Iqbal Z, Cochran AJ, Gibala MJ, Gregson W, Close GL, Drust B, Morton JP. 2013. “Reduced carbohydrate availability enhances exercise-induced p-53 signaling in human skeletal muscle: implications for mitochondrial biogenesis.” In Am J Physiol Regul Interg Comp Physiol. 304: R450-R458.

Bartlett JD, Hawley JA, Morton JP. 2015. “Carbohydrate availability and exercise training adaptation: Too much of a good thing?” In Eur J Sport Sci. 19:1-10.

Burke LM. 2003. “The IOC consensus on sports nutrition 2003: new guidelines for nutrition for athletes.” In Int J Sport Nutr Exerc Metab. 13:549-52.

Burke LM. 2010. “Fueling strategies to optimize performance: training high or training low?” In Scand J Med Sci Sports. 20 (Suppl 2): 48-58.

Burke LM, Hawley JA, Wong SH, Jeukendrup AE. 2011. “Carbohydrates for training and competition.” In J Sports Sci. 29 (Suppl 1): S17-27.

Coffey VG, Hawley JA. 2007. “The molecular bases of training adaptation.” In Sports Med. 37:737-63.

Cox GR, Clark SA, Cox AJ, Halson SL, Hargreaves M, Hawley JA, Jeacocke N, Snow RJ, Yeo WK, Burke LM. 2010. “Daily training with high-carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling.” In J Appl Physiol. 109: 126-134.

Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK. 2005. “Skeletal muscle adaptation: training twice every second day vs. training once daily.” In J Appl Physiol. 98:93-9.

Hawley JA. 2002. “Adaptations of skeletal muscle to prolonged, intense endurance training.” In Clin Exp Pharmacol Physiol. 29:218-22.

Hawley JA, Burke LM. 2010. “Carbohydrate availability and training adaptation: effects on cell metabolism.” In Exerc Sport Sci Rev. 38:152-60.

Hawley JA. 2014. “Manipulating carbohydrate availability to promote training adaptation.” In Sports Science Exchange. 134: 1-7.

Hawley JA, Burke LM, Phillips SM, Spriet LL. 2011. “Nutritional modulation of training-induced skeletal muscle adaptations.” In J Appl Physiol. 110:834-845.

Hawley JA and Morton JP. 2014. “Ramping up the signal: promoting endurance training adaptation in skeletal muscle by nutritional manipulation.” In Clin Exp Pharmacol Physiol. Aug 41(8): 608-13.

Hopkins WG, Hawley JA, Burke LM. 1999. “Design and analysis of research on sport performance enhancement.” In Med Sci Sports Exerc. 31:472-85

Hulston CJ, Venables MC, Mann CH, Martin C, Philp A, Baar K, Jeukendrup AE. 2010. “Training with low muscle glycogen enhances fat metabolism in well-trained cyclists.” In Med Sci Sports Exerc. 42:2046-55.

Lane SC, Camera DM, Lassiter DG, Areta JL Bird SR, Yeo WK, Jeacocke NA, Krook A, Zierath JR, Burke LM, Hawley JA. 2014. “Train-high, sleep-low: investigation of a new training protocol for promoting endurance training adaptation.” Submitted to JAP.

Marquet L, Louis J, Brisswalter J, Tiollier E, Burke LM, Hawley JA, Hausswirth C. 2014. “Enhancing endurance performance by nutritional manipulation: a sleep low strategy.” ECSS conference. Amsterdam, 3-6 July.

Morton JP, Croft L, Bartlett JD, Maclaren DP, Reilly T, Evans L, McArdle A, Drust B. 2009. “Reduced carbohydrate availability does not modulate training-induced heat shock protein adaptations but does upregulate oxidative enzyme activity in human skeletal muscle.” In J Appl Physiol. 106:1513-21.

Philp A. Hargreaves M, Baar K. 2012. “More than a store: regulatory roles for glycogen in skeletal muscle adaptation to exercise.” In Am J Physiol Endocrinol Metab. 302: E1343-E1351.

Pilegaard H, Ordway GA, Saltin B, Neufer PD. 2000. “Transcriptional regulation of gene expression in human skeletal muscle during recovery from exercise.” In Am J Physiol Endocrinol Metab. 279: E806-14.

Psilander N, Frank P, Flockhart M, Shalin K. 2013. “Exercise with low glycogen increase PGC-1α gene expression in human skeletal muscle.” In Eur J Appl Physiol. 113:951-963

Yeo WK, Paton CD, Garnham AP, Burke LM, Carey AL, Hawley JA. 2008. “Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens.” In J Appl Physiol. 105:1462-70.

Table des illustrations

Titre Figure 1: Overview of the putative cell signalling pathways involved in regulating the enhanced mitochondrial adaptations observed when endurance-based training is undertaken under conditions of reduced carbohydrate availability (from Hawley and Morton, 2014).
Fichier image/jpeg, 124k


PhD. Exercise & Nutrition Research Group School of Exercise Sciences 8-18 Brunswick St Australian Catholic University (ACU) Locked Bag 4115 – Fitzroy – Victoria 3065 AUSTRALIA
Address for correspondence:

© INSEP-Éditions, 2015

Licence OpenEdition Books


Rechercher dans OpenEdition Search

Vous allez être redirigé vers OpenEdition Search