596 research outputs found

    Nutrition Strategies for Triathlon

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    Contemporary sports nutrition guidelines recommend that each athlete develop a personalised, periodised and practical approach to eating that allows him or her to train hard, recover and adapt optimally, stay free of illness and injury and compete at their best at peak races. Competitive triathletes undertake a heavy training programme to prepare for three different sports while undertaking races varying in duration from 20 min to 10 h. The everyday diet should be adequate in energy availability, provide CHO in varying amounts and timing around workouts according to the benefits of training with low or high CHO availability and spread high-quality protein over the day to maximise the adaptive response to each session. Race nutrition requires a targeted and well-practised plan that maintains fuel and hydration goals over the duration of the specific event, according to the opportunities provided by the race and other challenges, such as a hot environment. Supplements and sports foods can make a small contribution to a sports nutrition plan, when medical supplements are used under supervision to prevent/treat nutrient deficiencies (e.g. iron or vitamin D) or when sports foods provide a convenient source of nutrients when it is impractical to eat whole foods. Finally, a few evidence-based performance supplements may contribute to optimal race performance when used according to best practice protocols to suit the triathlete’s goals and individual responsiveness

    Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers

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    We investigated the effects of adaptation to a ketogenic low carbohydrate (CHO), high fat diet (LCHF) during 3 weeks of intensified training on metabolism and performance of world-class endurance athletes. We controlled three isoenergetic diets in elite race walkers: high CHO availability (g kg−1 day−1: 8.6 CHO, 2.1 protein, 1.2 fat) consumed before, during and after training (HCHO, n = 9); identical macronutrient intake, periodised within or between days to alternate between low and high CHO availability (PCHO, n = 10); LCHF (< 50 g day−1 CHO; 78% energy as fat; 2.1 g kg−1 day−1 protein; LCHF, n = 10). Post-intervention, ˙V O2peak during race walking increased in all groups (P < 0.001, 90% CI: 2.55, 5.20%). LCHF was associated with markedly increased rates of whole-body fat oxidation, attaining peak rates of 1.57±0.32 gmin−1 during 2 h of walking at 80% ˙V O2peak.However, LCHFalso increased the oxygen (O2) cost of race walking at velocities relevant to real-life race performance: O2 uptake (expressed as a percentage of new ˙V O2peak) at a speed approximating 20 km race pace was reduced in HCHO and PCHO (90% CI:−7.047,−2.55 and−5.18,−0.86, respectively), but was maintained at pre-intervention levels in LCHF. HCHO and PCHO groups improved times for 10 km race walk: 6.6% (90% CI: 4.1, 9.1%) and 5.3% (3.4, 7.2%), with no improvement (−1.6% (−8.5, 5.3%)) for the LCHF group. In contrast to training with diets providing chronic or periodised high-CHO availability, and despite a significant improvement in ˙V O2peak, adaptation to the topical LCHF diet negated performance benefits in elite endurance athletes, in part due to reduced exercise economy

    Dose-response of sodium bicarbonate ingestion highlights individuality in time course of blood analyte responses

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    To defend against hydrogen cation accumulation and muscle fatigue during exercise, sodium 20 bicarbonate (NaHCO3) ingestion is commonplace. The individualised dose-response relationship 21 between NaHCO3 ingestion and blood biochemistry is unclear. The present study investigated the 22 bicarbonate, pH, base excess and sodium responses to NaHCO3 ingestion. Sixteen healthy males (23±2 23 years; 78.6±15.1 kg) attended three randomised order-balanced, non-blinded sessions, ingesting a single 24 dose of either 0.1, 0.2 or 0.3 g.kg-1BM of NaHCO3 (Intralabs, UK). Fingertip capillary blood was 25 obtained at baseline and every 10 min for 1 h, then every 15 min for a further 2 h. There was a significant 26 main effect of both time and condition for all assessed blood analytes (P≤0.001). Blood analyte 27 responses were significantly lower following 0.1 g.kg-1BM compared with 0.2 g.kg-1BM; bicarbonate 28 concentrations and base excess were highest following ingestion of 0.3 g.kg-1BM (P≤0.01). Bicarbonate 29 concentrations and pH significantly increased from baseline following all doses; the higher the dose the 30 greater the increase. Large inter-individual variability was shown in the magnitude of the increase in 31 bicarbonate concentrations following each dose (+2.0-5; +5.1-8.1; and +6.0-12.3 mmol·L-1 for 0.1, 0.2 32 and 0.3 g.kg-1BM) and in the range of time to peak concentrations (30-150; 40-165; and 75-180 min for 33 0.1, 0.2 and 0.3 g.kg-1BM). The variability in bicarbonate responses was not affected by normalisation 34 to body mass. These results challenge current practices relating to NaHCO3 supplementation and clearly 35 show the need for athletes to individualise their ingestion protocol and trial varying dosages prior to 36 competition

    Contribution of Conventional and Quantitative MRI in Leukodystrophies

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    We explored the contribution of magnetic resonance imaging (MRI) in leukodystrophies. Leukodystrophies are genetic diseases mainly affecting the white matter of the central nervous system. A multitude of variants in many different genes can cause leukodystrophies; variants in each gene are related to a specific leukodystrophy, associated with specific underlying pathological changes. These disorders may cause devastating signs and symptoms. Since recently disease-specific therapies are emerging for several leukodystrophies. In part I of the dissertation, we focus on conventional MRI techniques, based on comparing signal intensity between normal and abnormal tissue. Chapter 1.1 and chapter 1.2 describe the natural MRI history of chronic decline and the imaging correlates of acute episodes of decline in the leukodystrophy “vanishing white matter” (VWM). In chapter 1.1, we conclude that the cerebral white matter abnormalities do not improve and reflect the chronic disease course of VWM. Patients with VWM may also suffer from acute episodes of neurological decline. The results in chapter 1.2 indicate that signal abnormalities in deep gray matter structures and the brain stem may appear with acute episodes of neurological decline, and may disappear after recovery of such episodes. These findings aid correct MRI interpretation in VWM patients. In chapter 1.3 the clinical and MRI spectrum of the leukodystrophy “leukoencephalopathy with brainstem and spinal cord involvement and lactate elevation” is broadened, a disease caused by variants in the DARS2 gene. We describe two atypical MRI patterns in 15 severely affected patients. One MRI pattern featured striking cerebral atrophy, and one had a lack of the typical brainstem abnormalities. We discuss that different specific DARS2 variants likely cause detrimental effects to different cell types in the white matter, leading to different disease characteristics. Chapter 1.4 reports on three patients with clinical signs and the MRI pattern pointing to a vascular pathophysiology, in which a specific diagnosis lacked for many years. Genetic testing revealed biallelic NOTCH3 variants. These variants were first ignored, as NOTCH3 variants also cause CADASIL, in which they are mono-allelic. The patients described presented at a much earlier age, and lacked certain hallmarks of CADASIL, indicating that they have a different disease, albeit various similarities suggest a comparable pathophysiological pathway. In part II of the dissertation, we focus on quantitative MRI techniques, aiming to probe microstructural properties. Chapter 2.1 reviews numerous quantitative MRI techniques in the context of leukodystrophies. White matter consists of various cells and components. All can be affected in leukodystrophies. Certain quantitative MRI techniques aim to specifically extract microstructural information. This information may uncover neuropathological changes and aid in monitoring disease progression for different microstructural components separately. Most techniques are novel, and focus on a subset of tissue components. In chapter 2.2 we implemented several promising quantitative MRI methods. Two techniques (MCR-DIMWI and METRICS) that quantify water bound to myelin were used and the results correlated strongly. The techniques are clinically feasible and show large differences between leukodystrophy patients and controls. In chapter 2.3 we analyzed quantitative MRI in two distinct leukodystrophies with a fundamentally different pathology. The quantitative MRI measures distinguished between the leukodystrophies. Also, the degree of changes in quantitative MRI measures correlated to clinical measures, making the MRI measures relevant for monitoring. In this dissertation we show the pivotal role of MRI in leukodystrophy research and clinical care. MRI is central in diagnosing patients, can identify new, as yet unknown diseases or variations of known diseases, and helps to generate hypotheses on disease processes and mechanisms. In the near future, quantitative MRI measures may act as biomarker in monitoring patients and may be used as secondary outcome measure in therapy trials

    Fuel for the work required: a practical approach to amalgamating train-low paradigms for endurance athletes.

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    Using an amalgamation of previously studied "train-low" paradigms, we tested the effects of reduced carbohydrate (CHO) but high leucine availability on cell-signaling responses associated with exercise-induced regulation of mitochondrial biogenesis and muscle protein synthesis (MPS). In a repeated-measures crossover design, 11 males completed an exhaustive cycling protocol with high CHO availability before, during, and after exercise (HIGH) or alternatively, low CHO but high protein (leucine enriched) availability (LOW + LEU). Muscle glycogen was different (P < 0.05) pre-exercise (HIGH: 583 ± 158, LOW + LEU: 271 ± 85 mmol kg(-1) dw) but decreased (P < 0.05) to comparable levels at exhaustion (≈100 mmol kg(-1) dw). Despite differences (P < 0.05) in exercise capacity (HIGH: 158 ± 29, LOW + LEU: 100 ± 17 min), exercise induced (P < 0.05) comparable AMPKα2 (3-4-fold) activity, PGC-1α (13-fold), p53 (2-fold), Tfam (1.5-fold), SIRT1 (1.5-fold), Atrogin 1 (2-fold), and MuRF1 (5-fold) gene expression at 3 h post-exercise. Exhaustive exercise suppressed p70S6K activity to comparable levels immediately post-exercise (≈20 fmol min(-1) mg(-1)). Despite elevated leucine availability post-exercise, p70S6K activity remained suppressed (P < 0.05) 3 h post-exercise in LOW + LEU (28 ± 14 fmol min(-1) mg(-1)), whereas muscle glycogen resynthesis (40 mmol kg(-1) dw h(-1)) was associated with elevated (P < 0.05) p70S6K activity in HIGH (53 ± 30 fmol min(-1) mg(-1)). We conclude: (1) CHO restriction before and during exercise induces "work-efficient" mitochondrial-related cell signaling but; (2) post-exercise CHO and energy restriction maintains p70S6K activity at basal levels despite feeding leucine-enriched protein. Our data support the practical concept of "fuelling for the work required" as a potential strategy for which to amalgamate train-low paradigms into periodized training programs

    Effects of beta-alanine supplementation on brain homocarnosine/carnosine signal and cognitive function: an exploratory study

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    Objectives: Two independent studies were conducted to examine the effects of 28 d of beta-alanine supplementation at 6.4 g d-1 on brain homocarnosine/carnosine signal in omnivores and vegetarians (Study 1) and on cognitive function before and after exercise in trained cyclists (Study 2). Methods: In Study 1, seven healthy vegetarians (3 women and 4 men) and seven age- and sex-matched omnivores undertook a brain 1H-MRS exam at baseline and after beta-alanine supplementation. In study 2, nineteen trained male cyclists completed four 20-Km cycling time trials (two pre supplementation and two post supplementation), with a battery of cognitive function tests (Stroop test, Sternberg paradigm, Rapid Visual Information Processing task) being performed before and after exercise on each occasion. Results: In Study 1, there were no within-group effects of beta-alanine supplementation on brain homocarnosine/carnosine signal in either vegetarians (p = 0.99) or omnivores (p = 0.27); nor was there any effect when data from both groups were pooled (p = 0.19). Similarly, there was no group by time interaction for brain homocarnosine/carnosine signal (p = 0.27). In study 2, exercise improved cognitive function across all tests (P0.05) of beta-alanine supplementation on response times or accuracy for the Stroop test, Sternberg paradigm or RVIP task at rest or after exercise. Conclusion: 28 d of beta-alanine supplementation at 6.4g d-1 appeared not to influence brain homocarnosine/ carnosine signal in either omnivores or vegetarians; nor did it influence cognitive function before or after exercise in trained cyclists

    New Strategies in Sport Nutrition to Increase Exercise Performance.

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    Despite over 50 years of research, the field of sports nutrition continues to grow at a rapid rate. Whilst the traditional research focus was one that centred on strategies to maximize competition performance, emerging data in the last decade has demonstrated how both macronutrient and micronutrient availability can play a prominent role in regulating those cell signalling pathways that modulate skeletal muscle adaptations to endurance and resistance training. Nonetheless, in the context of exercise performance, it is clear that carbohydrate (but not fat) still remains king and that carefully chosen ergogenic aids (e.g. caffeine, creatine, sodium bicarbonate, beta-alanine, nitrates) can all promote performance in the correct exercise setting. In relation to exercise training, however, it is now thought that strategic periods of reduced carbohydrate and elevated dietary protein intake may enhance training adaptations whereas high carbohydrate availability and antioxidant supplementation may actually attenuate training adaptation. Emerging evidence also suggests that vitamin D may play a regulatory role in muscle regeneration and subsequent hypertrophy following damaging forms of exercise. Finally, novel compounds (albeit largely examined in rodent models) such as epicatechins, nicotinamide riboside, resveratrol, β-hydroxy β-methylbutyrate, phosphatidic acid and ursolic acid may also promote or attenuate skeletal muscle adaptations to endurance and strength training. When taken together, it is clear that sports nutrition is very much at the heart of the Olympic motto, Citius, Altius, Fortius (faster, higher, stronger)

    Mouth Rinsing With Carbohydrate Solutions at the Postprandial State Fail to Improve Performance During Simulated Cycling Time Trials.

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    Mouth-rinsing with carbohydrate solutions during cycling time trials results in performance enhancements, however the majority of studies have utilised ∼6% carbohydrate solutions. Therefore, the purpose of this study was to compare the effectiveness of mouth-rinsing with 4%, 6%, and 8% carbohydrate (CHO) solutions on 1-h simulated cycling time trial performance. On four occasions, seven trained male cyclists completed at the postprandial period, a set amount of work as fast as possible in a randomised, counterbalanced order. The subjects mouth rinsed for 5-s, upon completion of each 12.5% of the trial, with 25 mL of a non-CHO placebo, 4%, 6%, and 8% CHO solutions. No additional fluids were consumed during the time trial. Heart rate (HR), ratings of perceived exertion (RPE), thirst (TH) and subjective feelings (SF) were recorded after each rinse. Further, blood samples were drawn every 25% of the trial to measure blood glucose (BG) and blood lactate (BG) concentrations, whilst whole body carbohydrate oxidation was monitored continuously. Time to completion was not significant between conditions with the placebo, 4%, 6%, and 8% conditions completing the trials in 62.0 ± 3.0, 62.8 ± 4.0, 63.4 ± 3.4, and 63 ±4.0 minutes respectively. There were no significant differences between conditions in any of the variables mentioned above however significant time effects were observed for HR, RPE, TH, and SF. Post-hoc analysis showed that TH and SF of subjects in the CHO conditions but not in the placebo were significantly increased by completion of the time trial. In conclusion, mouth-rinsing with CHO solutions did not impact 1-h cycling performance in the postprandial period and in the absence of fluid intake. Our findings suggest that there is scope for further research to explore the activation regions of the brain and whether they are receptive to CHO dose, before specific recommendations for athletic populations are established. Consequently mouth-rinsing as a practical strategy for coaches and athletes is questionable under specific conditions and should be carefully considered before its inclusion. The emphasis should be focused on appropriate dietary and fluid strategies during training and competition

    Functional polymorphisms in the P2X7 receptor gene are associated with stress fracture injury

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    Context: Military recruits and elite athletes are susceptible to stress fracture injuries. Genetic predisposition has been postulated to have a role in their development. The P2X7 receptor (P2X7R) gene, a key regulator of bone remodelling, is a genetic candidate that may contribute to stress fracture predisposition. Objective: To evaluate the putative contribution of P2X7R to stress fracture injury in two separate cohorts, military personnel and elite athletes. Methods: In 210 Israeli Defence Forces (IDF) military conscripts, stress fracture injury was diagnosed (n=43) based on symptoms and a positive bone scan. In a separate cohort of 518 elite athletes, self-reported medical imaging scan-certified stress fracture injuries were recorded (n=125). Non-stress fracture controls were identified from these cohorts who had a normal bone scan or no history or symptoms of stress fracture injury. Study participants were genotyped for functional SNPs within the P2X7R gene using proprietary fluorescence-based competitive allele-specific PCR assay. Pearson Chi-square (χ2) tests, corrected for multiple comparisons, were used to assess associations in genotype frequencies. Results: The variant allele of P2X7R SNP rs3751143 (Glu496Ala- loss of function) was associated with stress fracture injury, while the variant allele of rs1718119 (Ala348Thr- gain of function) was associated with a reduced occurrence of stress fracture injury in military conscripts (P<0.05). The association of the variant allele of rs3751143 with stress fractures was replicated in elite athletes (P<0.05), whereas the variant allele of rs1718119 was also associated with reduced multiple stress fracture cases in elite athletes (P<0.05). Conclusions: The association between independent P2X7R polymorphisms with stress fracture prevalence supports the role of a genetic predisposition in the development of stress fracture injury

    No effect of glutamine supplementation and hyperoxia on oxidative metabolism and performance during high-intensity exercise.

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    addresses: Health and Biology, Liverpool Hope University, Liverpool, UK. [email protected]: Comparative Study; Journal ArticleThis is an Author's Accepted Manuscript of an article published in Journal of Sports Sciences, 2008, Vol. 26, Issue 10, pp. 1081 – 1090 © 2008 copyright Taylor & Francis, available online at: http://www.tandfonline.com/doi/abs/10.1080/02640410801930200Glutamine enhances the exercise-induced expansion of the tricarboxylic acid intermediate pool. The aim of the present study was to determine whether oral glutamine, alone or in combination with hyperoxia, influenced oxidative metabolism and cycle time-trial performance. Eight participants consumed either placebo or 0.125 g kg body mass(-1) of glutamine in 5 ml kg body mass(-1) placebo 1 h before exercise in normoxic (control and glutamine respectively) or hyperoxic (FiO(2) = 50%; hyperoxia and hyperoxia + glutamine respectively) conditions. Participants then cycled for 6 min at 70% maximal oxygen uptake (VO(2max)) immediately before completing a brief high-intensity time-trial (approximately 4 min) during which a pre-determined volume of work was completed as fast as possible. The increment in pulmonary oxygen uptake during the performance test (DeltaVO(2max), P = 0.02) and exercise performance (control: 243 s, s(x) = 7; glutamine: 242 s, s(x) = 3; hyperoxia: 231 s, s(x) = 3; hyperoxia + glutamine: 228 s, s(x) = 5; P < 0.01) were significantly improved in hyperoxic conditions. There was some evidence that glutamine ingestion increased DeltaVO(2max) in normoxia, but not hyperoxia (interaction drink/FiO(2), P = 0.04), but there was no main effect or impact on performance. Overall, the data show no effect of glutamine ingestion either alone or in combination with hyperoxia, and thus no limiting effect of the tricarboxylic acid intermediate pool size, on oxidative metabolism and performance during maximal exercise
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