Carbohydrate consumption and variable-intensity exercise responses in boys and men.

PURPOSE: The effect of carbohydrate (CHO) supplementation on physiological and perceptual responses to steady-state exercise has been studied in children. However, little is known about these responses to variable-intensity exercise (VIE) and how these responses might differ from adults. This study examined the physiological and perceptual effects of CHO on VIE in boys and men. METHODS: Eight boys (11.1 ± 0.9 years) and 11 men (23.8 ± 2.1 years) consumed CHO or a placebo (PL) beverage before and throughout VIE (three 12-min cycling bouts with intensity varying every 20-30 s between 25, 50, 75, and 125% peak work rate). Pulmonary gas exchange was assessed during the second 12-min bout. RPE was assessed twice per bout. RESULTS: In CHO, blood glucose increased and then decreased more from pre-exercise to 12 min and was higher in this trial at the end of exercise in men versus boys. In boys, blood glucose in CHO was higher at 24 and 36 min of exercise than in PL. RER during the CHO trial was higher in both groups; the other physiological responses were unaffected by CHO. All RPE measures (whole body, legs and chest) increased over time, but were not different between groups or trials. CONCLUSION: Blood glucose patterns during VIE were differentially affected by CHO in boys and men, but most physiological and perceptual responses to VIE were unaffected by CHO in either group. Knowledge of the underlying mechanisms of glucose regulation and effects on physical performance during this type of exercise in children is warranted.

SCD1 activity in muscle increases triglyceride PUFA content, exercise capacity, and PPARδ expression in mice.

Stearoyl-CoA desaturase (SCD)1 converts saturated fatty acids into monounsaturated fatty acids. Using muscle overexpression, we sought to determine the role of SCD1 expression in glucose and lipid metabolism and its effects on exercise capacity in mice. Wild-type C57Bl/6 (WT) and SCD1 muscle transgenic (SCD1-Tg) mice were generated, and expression of the SCD1 transgene was restricted to skeletal muscle. SCD1 overexpression was associated with increased triglyceride (TG) content. The fatty acid composition of the muscle revealed a significant increase in polyunsaturated fatty acid (PUFA) content of TG, including linoleate (18:2n6). Untrained SCD1-Tg mice also displayed significantly increased treadmill exercise capacity (WT = 6.6 ± 3 min, Tg = 71.9 ± 9.5 min; P = 0.0009). SCD1-Tg mice had decreased fasting plasma glucose, glucose transporter (GLUT)1 mRNA, fatty acid oxidation, mitochondrial content, and increased peroxisome proliferator-activated receptor (PPAR)δ and Pgc-1 protein expression in skeletal muscle. In vitro studies in C2C12 myocytes revealed that linoleate (18:2n6) and not oleate (18:1n9) caused a 3-fold increase in PPARδ and a 9-fold increase in CPT-1b with a subsequent increase in fat oxidation. The present model suggests that increasing delta-9 desaturase activity of muscle increases metabolic function, exercise capacity, and lipid oxidation likely through increased PUFA content, which increases PPARδ expression and activity. However, the mechanism of action that results in increased PUFA content of SCD1-Tg mice remains to be elucidated.

The influence of maturation on the oxygen uptake efficiency slope.

This study examined the influence of maturation on the oxygen uptake efficiency slope (OUES) in healthy male subjects. Seventy-six healthy male subjects (8-27 yr) were divided into groups based on maturation status: prepubertal (PP), midpubertal (MP), late-pubertal (LP), and young-adult (YA) males. Puberty status was determined by physical examination. Subjects performed a graded exercise test on a cycle ergometer to determine OUES. Group differences were assessed using a one-way ANOVA. OUES values (VO(2)L·min(-1)/log(10)V(E)L·min(-1)) were lower in PP and MP compared with LP and YA (p < .05). When OUES was expressed relative to body mass (VO(2)mL·kg-1·min(-1)/log(10)V(E)mL·kg(-1)·min(-1)) differences between groups reversed whereby PP and MP had higher mass relative OUES values compared with LP and YA (p < .05). Adjusting OUES by measures of body mass failed to eliminate differences across maturational groups. This suggests that qualitative factors, perhaps related to oxidative metabolism, account for the responses observed in this study.

Lipocalin-2 increases fat oxidation in vitro and is correlated with energy expenditure in normal weight but not obese women.

OBJECTIVE: The role of lipocalin-2 (Lcn2) was determined in regulating metabolism in cell, animal, and human models. DESIGN AND METHODS: Adipocytes were treated with recombinant lipocalin-2 (rLcn2) to determine the effect on lipid metabolism. rLcn2 was injected into mice to determine the effect on metabolism in vivo. To assess the relationship between Lcn2 and fat oxidation (FatOx) in humans, normal weight (NW) and obese (OB) women were given three separate high fat (HF) meals followed by indirect calorimetry. The relationship between postprandial Lcn2 with macronutrient metabolism and total energy expenditure (TEE) using Pearson correlations was determined. RESULTS: Lcn2 increased expression of genes involved in ß-oxidation including peroxisome proliferator-activated receptor-δ in adipocytes, as well as (3) H labeled oleate ß-oxidation. Lcn2 injected into chow-fed mice directly increased TEE by 18% after the first dark cycle (232 ± 1.4 cal vs. 341 ± 1.4 cal; PBS vs. Lcn2) and remained significantly elevated by 10% after the second dark cycle (296 ± 1.4 cal vs. 326 ± 1.4 cal; PBS vs. Lcn2). Lcn2 was correlated with TEE in all three HF meal challenges in NW but not OB females. CONCLUSIONS: Lipocalin-2 is a novel adipokine that promotes FatOx and TEE and its function may be impaired in obesity.