Changes in metabolism but not myocellular signaling by training with CHO-restriction in endurance athletes.

Kasper D Gejl, Kristian Vissing, Mette Hansen, Line Thams, Torben Rokkedal-Lausch, Peter Plomgaard, Anne-Kristine Meinild Lundby, Lars Nybo, Kurt Jensen, Hans-Christer Holmberg, Niels Ørtenblad

Journal: Physiological reports 2019;6(17):e13847

PMID: 30175557

Abstract

Carbohydrate (CHO) restricted training has been shown to increase the acute training response, whereas less is known about the acute effects after repeated CHO restricted training. On two occasions, the acute responses to CHO restriction were examined in endurance athletes. Study 1 examined cellular signaling and metabolic responses after seven training-days including CHO manipulation (n = 16). The protocol consisted of 1 h high-intensity cycling, followed by 7 h recovery, and 2 h of moderate-intensity exercise (120SS). Athletes were randomly assigned to low (LCHO: 80 g) or high (HCHO: 415 g) CHO during recovery and the 120SS. Study 2 examined unaccustomed exposure to the same training protocol (n = 12). In Study 1, muscle biopsies were obtained at rest and 1 h after 120SS, and blood samples drawn during the 120SS. In Study 2, substrate oxidation and plasma glucagon were determined. In Study 1, plasma insulin and proinsulin C-peptide were higher during the 120SS in HCHO compared to LCHO (insulin: 0 min: +37%; 60 min: +135%; 120 min: +357%, P = 0.05; proinsulin C-peptide: 0 min: +32%; 60 min: +52%; 120 min: +79%, P = 0.02), whereas plasma cholesterol was higher in LCHO (+15-17%, P = 0.03). Myocellular signaling did not differ between groups. p-AMPK and p-ACC were increased after 120SS (+35%, P = 0.03; +59%, P = 0.0004, respectively), with no alterations in p-p38, p-53, or p-CREB. In Study 2, glucagon and fat oxidation were higher in LCHO compared to HCHO during the 120SS (+26-40%, P = 0.03; +44-76%, P = 0.01 respectively). In conclusion, the clear respiratory and hematological effects of CHO restricted training were not translated into superior myocellular signaling after accustomization to CHO restriction.

© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

Address: Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.; Department of Public Health, Section for Sport Science, Aarhus University, Aarhus, Denmark.; SMI, Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark.; Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.; The Centre of Inflammation and Metabolism, Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.; The Centre of Inflammation and Metabolism, Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.; Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.; Swedish Winter Sports Research Centre, Department of Health Sciences, Mid Sweden University, Östersund, Sweden.; Swedish Olympic Committee, Stockholm, Sweden.; Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.; Swedish Winter Sports Research Centre, Department of Health Sciences, Mid Sweden University, Östersund, Sweden.
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