Improved walking energy efficiency might persist in presence of simulated full weight regain after multidisciplinary weight loss in adolescents with obesity: the POWELL study.

AIM: Weight loss leads to a reduction of the energy cost of walking but the respective implications of the metabolic and mechanic changes remain unknown. The present study compares the post-weight loss energy cost of walking (Cw) with and without a total reload of the induced weight reduction in adolescents with obesity. METHODS: Energy cost of walking and substrate use were evaluated during a graded walking exercise (4×6-min at 0.75, 1, 1.25, 1.5 m.s-1) before (V1) and after a 12-week intervention in 21 adolescents with obesity (11 girls; 13.8 ± 1.4 y). After weight loss, the walking exercise was randomly repeated once without weight reload (V2) and once with a loading corresponding to the total induced weight loss during the program (V2L). Body composition was assessed before and after the intervention. RESULTS: Body weight and fat mass decreased in response to the 12-week intervention (p < 0.001), while FFM did not change. The absolute gross Cw (ml.m-1) was higher on V1 compared with V2 at every speed. The absolute net Cw (ml.m-1) was higher on V1 compared to V2L at 0.75 m.s-1 (p = 0.04) and 1 m.s-1 (p = 0.02) and higher on V2L compared with V2 at 1.5 m.s-1 (p = 0.03). Net Cw (ml.m-1.kg-1) on V1 being higher than V2 (p < 0.001), and V2L higher than V2 (p = 0.006). The absolute CHO oxidation (mg.min-1) did not show any condition effect (p = 0.12) while fat utilization was higher on V1 compared to V2 and V2L (p < 0.001). Relative to body weight CHO oxidation was lower on V1 compared to V2 (p = 0.04) and V2L (p = 0.004) while relative to body weight fat oxidation was higher on V1 than V2 (p = 0.002). CONCLUSION: Adolescents with obesity might not show an entire rise back to pre-weight loss values of their metabolic cost of walking when weight gain is simulated. These new findings suggest metabolic and physiological adaptations to weight loss of the energy metabolism that remain to be clarified.

Diet- but not exercise-induced iso-energetic deficit induces compensatory appetitive responses.

Although physical exercise and dietary restriction can be both used to induce energy deficits, they have been suggested to favor different compensatory appetitive responses. While dietary restriction might favor increased subsequent energy intake and appetite sensations, such compensatory responses have not been observed after a similar deficit by exercise. The present work provides a first overview of the actual evidences discussing the effects of iso-energetic deficits induced by exercise versus dietary restriction on subsequent energy intake, appetite sensations, and on the potentially involved hedonic and physiological mechanisms.

The effects of a calf pump device on second half performance of a simulated soccer match in competitive youth players.

During soccer matches, performance decrements have been reported that relate to both physical abilities and technical skills. To investigate the effects of low-frequency electrical stimulation LFES (VeinoplusSport®, Ad Rem Technology, France) administered during half-time recovery on performance alterations during the second half. Twenty-two highly trained young players undertook a soccer-match simulation (SAFT90). During half-time, they were randomly assigned to LFES group or Placebo group. Each half was split into 3 bouts of 12 minutes. Following each bout, maximal strike speed (MSS), sprint test (ST), maximal sprint accelerations (MA) and metabolic power (MP) were determined in both groups. Arterial (AF) and venous flows (VF) were measured at rest and at the end of half-time. LEFS group exhibited beneficial effects on performance compared to the Placebo group with a likely effect for MSS, ST, MA, and a possible effect for MP. AF and VF increased statistically more in LEFS group compared to Placebo group. The use of specific calf-pump LFES during half-time of a youth simulated soccer match attenuated the decrease in performance during the second half compared to Placebo group. This effect is most marked at the beginning of the second half with regards to explosive parameters.

Neuregulin 1 improves glucose tolerance in adult and old rats.

AIM: Studies both in vitro and ex vivo of rodent skeletal muscle have highlighted the potential involvement of neuregulin 1 (NRG1) in glucose metabolism regulation, yet nothing is known of the role of NRG1 in systemic glucose homoeostasis. For this reason, it was hypothesized that systemic delivery of NRG1 might improve glucose tolerance and that the effect might be age-dependent. METHODS: Glucose tolerance tests were performed in 6-month-old (adult) and 22-month-old (old) male Wistar rats 15min after a single injection of either NRG1 (50µg/kg) or saline (controls). Skeletal muscle and liver samples were also collected 30min after the acute NRG1 or saline treatment, while the phosphorylation status of ErbB receptors and AKT was assessed by Western blotting. RESULTS: Acute NRG1 treatment decreased the glycaemic response to an oral glucose load in both adult and old rats. NRG1 injection did not activate ErbB receptors in skeletal muscle, whereas phosphorylation of ErbB3 and AKT was markedly increased in the liver of NRG1-treated adult and old rats compared with controls. CONCLUSION: This study shows that NRG1 has a possible glucose-lowering effect in the liver and via an ErbB3/AKT signaling pathway. This NRG1 effect is also maintained in old rats, suggesting that the NRG1/ErbB signaling pathway might represent a promising therapeutic target in insulin resistance states.

Neuregulin 1 affects leptin levels, food intake and weight gain in normal-weight, but not obese, db/db mice.

AIM: Studies in vitro have highlighted the potential involvement of neuregulin 1 (NRG1) in the regulation of energy metabolism. This effect has also been suggested in vivo, as intracerebroventricular injection of NRG1 reduces food intakes and weight gain in rodents. Thus, it was hypothesised that NRG1 might affect serum leptin levels in mice. METHODS: Weight, food intakes, energy expenditure, spontaneous physical activity and serum leptin levels were evaluated in normal-weight C57BL/6JRJ mice following intraperitoneal administration of NRG1 (50 µg/kg, three times/week) or saline for 8 weeks. Based on the results of this first experiment, leptin-resistant obese db/db mice were then given NRG1 for 8 weeks. RESULTS: Leptin serum concentrations were six times higher in C57BL/6JRJ mice treated with NRG1 than in the animals given saline. NRG1 treatment also reduced weight gain by 10% and food intakes by 15% compared with saline treatment, while energy expenditure remained unchanged. In db/db mice, serum leptin concentrations, weight gain, food intakes, energy expenditure and spontaneous physical activity were not altered by NRG1 treatment. CONCLUSION: The decrease in food intakes and weight gain associated with NRG1 treatment in C57BL/6JRJ mice may be partly explained by increased leptin levels, whereas db/db mice were not affected by the treatment, suggesting resistance to NRG1 in this pathological state.