A reproducible, self-reported, field-based tool for monitoring ovarian hormone status and body weight variations in female athletes: the Answ'Her questionnaire.

Background: Intra-individual factors like ovarian hormone profiles and body weight variations may influence sports practice and performance in female athletes and need to be characterized. The "Answ'Her" questionnaire was designed to develop a relevant and reproducible field-based tool to assess self-reported ovarian hormone status (natural menstrual cycle and hormonal contraceptive use) and body weight variations practices among female athletes.

Methods: French females with a regular sports practice responded (once: N.

Overfeeding increases postprandial endotoxemia in men: Inflammatory outcome may depend on LPS transporters LBP and sCD14.

Scope: Low-grade inflammation is a recognized hallmark of obesity. Endotoxins absorbed after high-fat meals have recently been implicated. Plasma lipopolysaccharides binding protein (LBP) and soluble cluster of differentiation 14 (sCD14) have also been suggested as clinical markers of endotoxemia.

Visceral fat accumulation during lipid overfeeding is related to subcutaneous adipose tissue characteristics in healthy men.

Context: The hypothesis of a limited expansion of sc adipose tissue during weight gain provides an attractive explanation for the reorientation of excess lipids toward ectopic sites, contributing to visceral adipose depots and metabolic syndrome.

Objective: Our objective was to define whether the characteristics of sc adipose tissue influence the partition of lipids toward abdominal fat depots during weight gain in healthy men.

Research Design And Methods: Forty-one healthy nonobese volunteers performed a 56-day overfeeding protocol (+760 kcal/d).

Muscle mitochondrial oxidative phosphorylation activity, but not content, is altered with abdominal obesity in sedentary men: synergism with changes in insulin sensitivity.

Context: Abdominal obesity is a major risk factor for muscle insulin resistance. Mitochondria may play a key role in this etiology.

Objective: Changes in muscle mitochondrial content and function were examined according to abdominal obesity and insulin sensitivity in men.

Potential mechanisms of muscle mitochondrial dysfunction in aging and obesity and cellular consequences.

Mitochondria play a key role in the energy metabolism in skeletal muscle. A new concept has emerged suggesting that impaired mitochondrial oxidative capacity in skeletal muscle may be the underlying defect that causes insulin resistance. According to current knowledge, the causes and the underlying molecular mechanisms at the origin of decreased mitochondrial oxidative capacity in skeletal muscle still remain to be elucidated.

Impaired resting muscle energetics studied by (31)P-NMR in diet-induced obese rats.

Objective: Mitochondrial activity is altered in skeletal muscle of obese, insulin-resistant or type 2 diabetic patients. We hypothesized that this situation was associated with profound adaptations in resting muscle energetics. For that purpose, we used in vivo (31)P-nuclear magnetic resonance ((31)P-NMR) in male sedentary Wistar rats fed with obesogenic diets known to induce alterations in muscle mitochondrial activity.

Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice.

Mitochondrial dysfunction in skeletal muscle has been implicated in the development of type 2 diabetes. However, whether these changes are a cause or a consequence of insulin resistance is not clear. We investigated the structure and function of muscle mitochondria during the development of insulin resistance and progression to diabetes in mice fed a high-fat, high-sucrose diet.

Enhanced muscle mixed and mitochondrial protein synthesis rates after a high-fat or high-sucrose diet.

Objective: Obesity and insulin resistance are associated with muscle mitochondrial dysfunction, which might be related to impairment of mitochondrial protein synthesis. This study aimed at investigating mixed and mitochondrial protein synthesis in skeletal muscle in response to dietary manipulations.

Research Methods And Procedures: High-sucrose (SU) and high-fat, high-sucrose (F) diets were provided for 6 weeks to Wistar rats at standard (N) and high (H) energy intakes and compared with controls.

Study of iron metabolism disturbances in an animal model of insulin resistance.

The relationship between iron and insulin-resistance (IR) is documented by the positive correlation between iron stores and IR. Moreover, some patients exhibited a hepatic iron overload associated with IR (HIO-IR) but the mechanism involved in this overload is not known. Thus, we studied the iron metabolism disturbances in an animal model of IR and the influence of provoked hyperglycemia/hyperinsulinemia on plasma iron parameters.

Chronological approach of diet-induced alterations in muscle mitochondrial functions in rats.

Objective: Mitochondrial dysfunction might predispose individuals to develop insulin resistance. Our objective was to determine whether mitochondrial dysfunction or insulin resistance was the primary event during high-fat (HF) diet.

Research Methods And Procedures: Rats were fed an HF diet for 0, 3, 6, 9, 14, 20, or 40 days and compared with control.

Synergistic effects of caloric restriction with maintained protein intake on skeletal muscle performance in 21-month-old rats: a mitochondria-mediated pathway.

Caloric restriction (CR) delays the onset of age-related mitochondrial abnormalities but does not prevent the decline in ATP production needed to sustain muscle protein fractional synthesis rate (FSR) and contractile activity. We hypothesized that improving mitochondrial activity and FSR using a CR diet with maintained protein intakes could enhance myofibrillar protein FSR and consequently improve muscle strength in aging rats. Wistar rats (21 months old) were fed either an ad libitum (AL), 40% protein-energy restricted (PER) or 40% AL-isonitrogenous energy restricted (ER) diet for 5 months.

Diets high in sugar, fat, and energy induce muscle type-specific adaptations in mitochondrial functions in rats.

Obesity is often associated with insulin resistance and mitochondrial dysfunction within skeletal muscles, but the causative factors are not clearly identified. The present study examined the role of nutrition, both qualitatively and quantitatively, in the induction of muscle mitochondrial defects. Two experimental diets [high sucrose (SU) and high fat (F)] were provided for 6 wk to male Wistar rats at 2 levels of energy [standard (N) and high (H)] and compared with a standard energy cornstarch-based diet (C).