Training in the fasted state facilitates re-activation of eEF2 activity during recovery from endurance exercise
Department of Biomedical Kinesiology, Research Centre for Exercise and Health, FaBeR-K.U. Leuven, Tervuursevest 101, 3001 Leuven, Heverlee, Belgium. Arbeitsphysiologie
(Impact Factor: 2.19).
12/2010; 111(7):1297-305. DOI: 10.1007/s00421-010-1753-7
Nutrition is an important co-factor in exercise-induced training adaptations in muscle. We compared the effect of 6 weeks endurance training (3 days/week, 1-2 h at 75% VO(2peak)) in either the fasted state (F; n = 10) or in the high carbohydrate state (CHO, n = 10), on Ca(2+)-dependent intramyocellular signalling in young male volunteers. Subjects in CHO received a carbohydrate-rich breakfast before each training session, as well as ingested carbohydrates during exercise. Before (pretest) and after (posttest) the training period, subjects performed a 2 h constant-load exercise bout (~70% of pretest VO(2peak)) while ingesting carbohydrates (1 g/kg h(-1)). A muscle biopsy was taken from m. vastus lateralis immediately before and after the test, and after 4 h of recovery. Compared with pretest, in the posttest basal eukaryotic elongation factor 2 (eEF2) phosphorylation was elevated in CHO (P < 0.05), but not in F. In the pretest, exercise increased the degree of eEF2 phosphorylation about twofold (P < 0.05), and values returned to baseline within the 4 h recovery period in each group. However, in the posttest dephosphorylation of eEF2 was negated after recovery in CHO, but not in F. Independent of the dietary condition training enhanced the basal phosphorylation status of Phospholamban at Thr(17), 5'-AMP-activated protein kinase α (AMPKα), and Acetyl CoA carboxylase β (ACCβ), and abolished the exercise-induced increase of AMPKα and ACCβ (P < 0.05). In conclusion, training in the fasted state, compared with identical training with ample carbohydrate intake, facilitates post-exercise dephosphorylation of eEF2. This may contribute to rapid re-activation of muscle protein translation following endurance exercise.
Available from: Henri Nielens
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ABSTRACT: In this study, we compared the effects of endurance training in the fasted state (F) vs. the fed state [ample carbohydrate intake (CHO)] on exercise-induced intramyocellular lipid (IMCL) and glycogen utilization during a 6-wk period of a hypercaloric (∼+30% kcal/day) fat-rich diet (HFD; 50% of kcal). Healthy male volunteers (18-25 yrs) received a HFD in conjunction with endurance training (four times, 60-90 min/wk) either in F (n = 10) or with CHO before and during exercise sessions (n = 10). The control group (n = 7) received a HFD without training and increased body weight by ∼3 kg (P < 0.001). Before and after a HFD, the subjects performed a 2-h constant-load bicycle exercise test in F at ∼70% maximal oxygen uptake rate. A HFD, both in the absence (F) or presence (CHO) of training, elevated basal IMCL content by ∼50% in type I and by ∼75% in type IIa fibers (P < 0.05). Independent of training in F or CHO, a HFD, as such, stimulated exercise-induced net IMCL breakdown by approximately twofold in type I and by approximately fourfold in type IIa fibers. Furthermore, exercise-induced net muscle glycogen breakdown was not significantly affected by a HFD. It is concluded that a HFD stimulates net IMCL degradation by increasing basal IMCL content during exercise in type I and especially IIa fibers. Furthermore, a hypercaloric HFD provides adequate amounts of carbohydrates to maintain high muscle glycogen content during training and does not impair exercise-induced muscle glycogen breakdown.
Journal of Applied Physiology 05/2011; 111(1):108-16. DOI:10.1152/japplphysiol.01459.2010 · 3.06 Impact Factor
Available from: journals.cambridge.org
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ABSTRACT: Diet can significantly influence athletic performance, but recent research developments have substantially changed our understanding of sport and exercise nutrition. Athletes adopt various nutritional strategies in training and competition in the pursuit of success. The aim of training is to promote changes in the structure and function of muscle and other tissues by selective modulation of protein synthesis and breakdown in response to the training stimulus. This process is affected by the availability of essential amino acids in the post-exercise period. Athletes have been encouraged to eat diets high in carbohydrate, but low-carbohydrate diets up-regulate the capacity of muscle for fat oxidation, potentially sparing the limited carbohydrate stores. Such diets, however, do not enhance endurance performance. It is not yet known whether the increased capacity for fat oxidation that results from training in a carbohydrate-deficient state can promote loss of body fat. Preventing excessive fluid deficits will maintain exercise capacity, and ensuring adequate hydration status can also reduce subjective perception of effort. This latter effect may be important in encouraging exercise participation and promoting adherence to exercise programmes. Dietary supplement use is popular in sport, and a few supplements may improve performance in specific exercise tasks. Athletes must be cautious, however, not to contravene the doping regulations. There is an increasing recognition of the role of the brain in determining exercise performance: various nutritional strategies have been proposed, but with limited success. Nutrition strategies developed for use by athletes can also be used to achieve functional benefits in other populations.
Proceedings of The Nutrition Society 02/2012; 71(1):112-9. DOI:10.1017/S0029665111003211 · 5.27 Impact Factor
Available from: Joke Puype
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In this study, we compared the effect of sprint interval training (SIT) in normoxia versus hypoxia on muscle glycolytic and oxidative capacity, monocarboxylate transporter content, and endurance exercise performance.
Healthy male volunteers (18-30 yr) performed 6 wk of SIT on a cycling ergometer (30-s sprints vs 4.5-min rest intervals; 3 d · wk(-1)) in either normobaric hypoxia (HYP, FiO2 = 14.4%, n = 10) or normoxia (NOR, FiO2 = 20.9%, n = 9). The control group did not train (CON, n = 10). Training load was increased from four sprints per session in week 1 to nine sprints in week 6. Before and after SIT, subjects performed a maximal incremental exercise test plus a 10-min simulated time trial on a cycle ergometer in both normoxia (MAX nor and TT nor) and hypoxia (MAX hyp and TT hyp). A needle biopsy was taken from musculus vastus lateralis at rest 5-6 d after the last exercise session.
SIT increased muscle phosphofructokinase activity more in HYP (+59%, P < 0.05) than that in NOR (+17%), whereas citrate synthase activity was similar between groups. Compared with the pretest, power outputs corresponding to 4 mmol blood lactate in HYP during MAX nor (+7%) and MAX hyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V·O 2max in MAX nor and TT performance in TT nor and TT hyp were increased by ≈ 6%-8% (P < 0.05) in either group. The training elevated monocarboxylate transporter 1 protein content by ≈ 70% (P < 0.05). In CON, all measurements were constant throughout the study.
SIT in hypoxia up-regulated muscle phosphofructokinase activity and the anaerobic threshold more than SIT in normoxia but did not enhance endurance exercise performance.
Medicine and science in sports and exercise 04/2013; 45(11). DOI:10.1249/MSS.0b013e31829734ae · 3.98 Impact Factor
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