1) insulin sensitivity is not improved after ESA treatment despite improved exercise capacity, 2) the calorigenic effects of ESA may be related to increased UCP2 gene expression in skeletal muscle, and 3) training and ESA exert opposite effects on lipolysis under basal conditions, increased FFA levels and liver fat fraction was observed after ESA treatment.

New Findings r What is the central question of this study?Is an erythropoiesis-stimulating agent (ESA), alone or in combination with endurance training, able to induce changes in human skeletal muscle fibre and vascular morphology? r What is the main finding and its importance?Human skeletal muscle morphology and angiogenetic effects did not exhibit sensitivity to ESA treatment alone. Endurance training stimulates angiogenesis and fibre type transition in the direction of a more oxidative fibre phenotype; however, addition of ESA had no further effect.The aim was to investigate the ability of an erythropoiesis-stimulating agent (ESA), alone or in combination with endurance training, to induce changes in human skeletal muscle fibre and vascular morphology. In a comparative study, 36 healthy untrained men were randomly dispersed into the following four groups: sedentary-placebo (SP, n = 9); sedentary-ESA (SE, n = 9); training-placebo (TP, n = 10); or training-ESA (TE, n = 8). The ESA or placebo was injected once weekly. Training consisted of progressive bicycling three times per week for 10 weeks. Before and after the intervention period, muscle biopsies and magnetic resonance images were collected from the thigh muscles, blood was collected, body composition measured and endurance exercise performance evaluated. The ESA treatment (SE and TE) led to elevated haematocrit, and both ESA treatment and training (SE, TP and TE) increased maximal O 2 uptake. With regard to skeletal muscle morphology, TP alone exhibited increases in whole-muscle cross-sectional area and fibre diameter of all fibre types. Also exclusively for TP was an increase in type IIa fibres and a corresponding decrease in type IIx fibres. Furthermore, an overall training effect (TP and TE) was statistically demonstrated in whole-muscle cross-sectional area, muscle fibre diameter and type IIa and type IIx fibre distribution. With regard to muscle vascular morphology, TP and TE both promoted a rise in capillary to muscle fibre ratio, with no differences between the two groups. There were no effects of ESA treatment on any of the muscle morphological parameters. Despite the haematopoietic effects of ESA, we provide novel evidence that endurance training rather than ESA treatment induces adaptational changes in angiogenesis and muscle morphology.

Background: Deliberately training with reduced carbohydrate availability, a paradigm coined training low, has shown to promote adaptations associated with improved aerobic capacity. In this context researchers have proposed that protein may be ingested prior to training as a means to enhance the protein balance during exercise without spoiling the effect of the low carbohydrate availability. Accordingly, this is being practiced by world class athletes. However, the effect of protein intake on muscle protein metabolism during training low has not been studied. This study aimed to examine if protein intake prior to exercise with reduced carbohydrate stores benefits muscle protein metabolism in exercising and non-exercising muscles. Methods: Nine well-trained subjects completed two trials in random order both of which included a high-intensity interval ergometer bike ride (day 1), a morning (day 2) steady state ride (90 min at 65% VO 2 peak, 90ss), and a 4-h recovery period. An experimental beverage was consumed before 90ss and contained either 0.5 g whey protein hydrolysate [WPH]/ kg lean body mass or flavored water [PLA]. A stable isotope infusion (L-[ring-13 C 6 ]phenylalanine) combined with arterial-venous blood sampling, and plasma flow rate measurements were used to determine forearm protein turnover. Myofibrillar protein synthesis was determined from stable isotope incorporation into the vastus lateralis. Results: Forearm protein net balance was not different from zero during 90ss exercise (nmol/100 ml/min, PLA: 0.5 ± 2.6; WPH: 1.8, ± 3.3) but negative during the 4 h recovery (nmol/100 ml/min, PLA: − 9.7 ± 4.6; WPH: − 8.7 ± 6.5); no interaction (P = 0.5) or main effect of beverage (P = 0.11) was observed. Vastus lateralis myofibrillar protein synthesis rates were increased during 90ss exercise (+ 0.02 ± 0.02%/h) and recovery (+ 0.02 ± 0.02%/h); no interaction (P = 0.3) or main effect of beverage (P = 0.3) was observed. Conclusion: We conclude that protein ingestion prior to endurance exercise in the energy-and carbohydraterestricted state does not increase myofibrillar protein synthesis or improve net protein balance in the exercising and non-exercising muscles, respectively, during and in the hours after exercise compared to ingestion of a non-caloric control.

Recent studies demonstrate that protein ingestion immediately before sleep improves muscle recovery during the night following resistance exercise. Whether this feeding strategy benefits recovery from endurance training has yet to be established. The aim of this study was to investigate the effects of whey protein isolate ingested every night before sleep on subsequent performance and circulatory markers of muscular recovery during a week of intensified endurance training mimicking a training camp. In a parallel design, 32 trained runners underwent a 1-week intervention with a rigorously controlled diet (carbohydrate = 7.2 g·kg−1·day−1, protein = 1.8 g·kg−1·day−1, and fat = 1.0 g·kg−1·day−1) and exercise program (11 sessions) while receiving either a protein (0.5 g·kg−1·day−1) or carbohydrate (0.5 g·kg−1·day−1) beverage every night before sleep. Blood samples were obtained on the morning of Days 1, 4, 7, and 8 and analyzed for markers of muscle damage (creatine kinase, lactate dehydrogenase, and myoglobin). The postintervention 5-km time-trial performance was significantly impaired in both groups (11 ± 24 s, p < .01). Plasma creatine kinase (227% ± 221%, p < .01), lactate dehydrogenase (18% ± 22%, p < .01), and myoglobin (72% ± 62%, p < .01) increased gradually throughout the week with no difference between the groups (p > .05). In conclusion, the presleep protein ingestion did not reduce the decline in performance or ameliorate the rise of circulatory markers of muscle damage during a week of intensified training when compared with the isocaloric carbohydrate ingestion.