Abstract

Key points Three weeks of intensified training and mild energy deficit in elite race walkers increases peak aerobic capacity independent of dietary support.Adaptation to a ketogenic low carbohydrate, high fat (LCHF) diet markedly increases rates of whole‐body fat oxidation during exercise in race walkers over a range of exercise intensities.The increased rates of fat oxidation result in reduced economy (increased oxygen demand for a given speed) at velocities that translate to real‐life race performance in elite race walkers.In contrast to training with diets providing chronic or periodised high carbohydrate availability, adaptation to an LCHF diet impairs performance in elite endurance athletes despite a significant improvement in peak aerobic capacity. 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˙O2 peak 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 g min−1 during 2 h of walking at ∼80% V˙O2 peak . However, LCHF also 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˙O2 peak ) 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˙O2 peak , adaptation to the topical LCHF diet negated performance benefits in elite endurance athletes, in part due to reduced exercise economy.

Highlights

  • During continuous exercise lasting more than a few minutes duration, skeletal muscle is fuelled by both intraand extramuscular carbohydrate (CHO) and lipid substrates, with only a minor contribution from amino acids

  • Mean daily intake of CHO was similar between the HCHO and periodised CHO availability (PCHO) diets, the breakdown associated with specific training days partially illustrates the difference in its spread, due to the timing of intake around training sessions designated as high and low CHO availability

  • While this would have contributed towards an improvement in aerobic capacity and walking economy across all groups, we feel that energy availability was preserved and standardised such that it did not interfere with training adaptations or favour one group over another

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Summary

Introduction

During continuous exercise lasting more than a few minutes duration, skeletal muscle is fuelled by both intraand extramuscular carbohydrate (CHO) and lipid substrates, with only a minor contribution from amino acids (for review see Hawley et al 2015) These observations were made over a century ago by Zuntz & Schumburg (1901) who manipulated the proportions of fat and CHO in the diet for several days and showed changes in the non-protein respiratory exchange ratio (RER) during subsequent submaximal exercise. These experiments identified a potential benefit for CHO as a substrate for muscle metabolism by virtue of an ß8% higher energy yield per litre of oxygen (O2) consumed when CHO was the primary fuel oxidised. There is recognition that a periodised programme that includes some training sessions deliberately undertaken with low endogenous and/or exogenous CHO availability (‘train low’; Hawley & Burke, 2010; Bartlett et al 2015) or a delay in replacing muscle glycogen after a session (‘sleep low’) may promote greater cellular adaptations to training (Lane et al 2015) and enhance performance (Marquet et al 2016) to a greater magnitude than undertaking all sessions with high CHO availability

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