4.6 Article

Acute Ketogenic Diet and Ketone Ester Supplementation Impairs Race Walk Performance

期刊

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 53, 期 4, 页码 776-784

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0000000000002517

关键词

B-HYDROXYBUTYRATE; KETOSIS; ATHLETIC PERFORMANCE; LOW-CARBOHYDRATE HIGH-FAT

资金

  1. Australian Catholic University Research Fund (ACURF) [2017000034]
  2. Natural Sciences and Engineering Research Council of Canada (NSERC) Postdoctoral Fellowship

向作者/读者索取更多资源

This study found that the combination of LCHF diet and KE supplementation has limited impact on exercise metabolism and performance, with a negative effect on race performance.
The consumption of a ketogenic low-carbohydrate (CHO), high-fat (LCHF) diet increases skeletal muscle fat utilization but impairs exercise economy. Whether the concomitant increase in circulating endogenous ketone bodies (KB) alters the capacity to metabolize exogenous ketone supplements such as the popular ketone monoester is unknown. Purpose: This study aimed to determine if LCHF and ketone ester (KE) supplementation can synergistically alter exercise metabolism and improve performance. Methods: Elite race walkers (n = 18, 15 males and 3 females; <(V)over dot>O-2(peak), 62 +/- 6 mUmin(-1).kg(-1)) undertook a four-stage exercise economy test and real-life 10,000-m race before and after a 5-d isoenergetic high-CHO (HCHO, similar to 60%-65% fat; CHO, 20% fat; n= 9) or LCHF (75%-80% fat, <50 g.d(-1) CHO, n= 9) diet. The LCHF group performed additional economy tests before and after diet after supplementation with 573 mg.kg(-1) body mass KE (HVMN; HYMN Inc., San Francisco, CA), which was also consumed for race 2. Results: The oxygen cost of exercise (relative <(V)over dot>O-2, mL.min(-1).kg(-1)) increased across all four stages after LCHF (P < 0.005). This occurred in association with increased fat oxidation rates, with a reciprocal decrease in CHO oxidation (P < 0.001). Substrate utilization in the HCHO group remained unaltered. The consumption of KE before the LCHF diet increased circulating KB (P < 0.05), peaking at 3.2 +/- 0.6 mM, but did not alter <(V)over dot>O-2 or RER. LCHF diet elevated resting circulating KB (0.3 +/- 0.1 vs 0.1 +/- 0.1 mM), but concentrations after supplementation did not differ from the earlier ketone trial. Critically, race performance was impaired by similar to 6% (P < 0.0001) relative to baseline in the LCHF group but was unaltered in HCHO. Conclusion: Despite elevating endogenous KB production, an LCHF diet does not augment the metabolic responses to KE supplementation and negatively affects race performance.

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