Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes.

Line Jensen,Ulrik Frandsen,Jakob L Nielsen,Kent Sahlin,Niels Ørtenblad,Rune D Bech,Kasper D Gejl,Tobias Nygaard

doi:10.14814/phy2.12184

Abstract

The aim was to determine if the metabolic adaptations, particularly PGC-1α and downstream metabolic genes were affected by restricting CHO following an endurance exercise bout in trained endurance athletes. A second aim was to compare baseline expression level of these genes to untrained. Elite endurance athletes (VO2max 66 ± 2 mL·kg−1·min−1, n = 15) completed 4 h cycling at ∼56% VO2max. During the first 4 h recovery subjects were provided with either CHO or only H2O and thereafter both groups received CHO. Muscle biopsies were collected before, after, and 4 and 24 h after exercise. Also, resting biopsies were collected from untrained subjects (n = 8). Exercise decreased glycogen by 67.7 ± 4.0% (from 699 ± 26.1 to 239 ± 29.5 mmol·kg−1·dw−1) with no difference between groups. Whereas 4 h of recovery with CHO partly replenished glycogen, the H2O group remained at post exercise level; nevertheless, the gene expression was not different between groups. Glycogen and most gene expression levels returned to baseline by 24 h in both CHO and H2O. Baseline mRNA expression of NRF-1, COX-IV, GLUT4 and PPAR-α gene targets were higher in trained compared to untrained. Additionally, the proportion of type I muscle fibers positively correlated with baseline mRNA for PGC-1α, TFAM, NRF-1, COX-IV, PPAR-α, and GLUT4 for both trained and untrained. CHO restriction during recovery from glycogen depleting exercise does not improve the mRNA response of markers of mitochondrial biogenesis. Further, baseline gene expression of key metabolic pathways is higher in trained than untrained.

Highlights

Carbohydrate (CHO) is an important fuel for skeletal muscle both during (Bergstrom et al 1967) and following exercise (Bergstrom and Hultman 1967), and depletion of muscle glycogen during prolonged exercise is linked to fatigue and impairment of performance in training and competition (Jacobs et al 1981).Within the last decade, a new concept of exercising with reduced muscle glycogen levels (“train low”) has been introduced in order to optimize the adaption to training (Pilegaard et al 2002)
The highly trained (HT) athletes displayed an increased number of type I fibers compared to the UT (65.0 Æ 3.1% vs. 48.3 Æ 5.3%, P = 0.010) with a consequent lower proportion of type II fibers (35.0 Æ 3.3% vs. 51.7 Æ 5.3%, Table 1)
Comparing baseline mRNA expressions showed a higher level of expression in HT subjects of nuclear respiratory factor 1 (NRF-1) and cytochrome c oxidase-IV (COX-IV) involved in mitochondrial biogenesis (29 and 94%, respectively) (Fig. 2A)

Summary

Introduction

Carbohydrate (CHO) is an important fuel for skeletal muscle both during (Bergstrom et al 1967) and following exercise (Bergstrom and Hultman 1967), and depletion of muscle glycogen during prolonged exercise is linked to fatigue and impairment of performance in training and competition (Jacobs et al 1981).Within the last decade, a new concept of exercising with reduced muscle glycogen levels (“train low”) has been introduced in order to optimize the adaption to training (Pilegaard et al 2002). Carbohydrate (CHO) is an important fuel for skeletal muscle both during (Bergstrom et al 1967) and following exercise (Bergstrom and Hultman 1967), and depletion of muscle glycogen during prolonged exercise is linked to fatigue and impairment of performance in training and competition (Jacobs et al 1981). Exercising with low muscle glycogen levels or restriction of CHO intake during or after exercise may be a way of increasing training induced transcriptional improvements in muscle oxidative capacity, which can potentially enhance athletic performance. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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Discussion

Conclusion