Search Results

This study explores the prevalence of disordered eating attitudes in a sample of male first-year university students engaged in a physical education program and examines the relationships between emotional intelligence, coping, and emotional eating in relation to disordered-eating (DE) attitudes. A total of 140 students completed the following questionnaires: the Eating Attitudes Test, the Bar-On Emotional Intelligence Questionnaire, the Coping Inventory Stress Scale, and the Dutch Eating Behavior Questionnaire. The number of participants represented 80% of the male students registered in this discipline at the authors’ university. Twenty percent of students presented DE attitudes even though they were of normal weight. The Bar-On EQ-I results indicated that students with DE attitudes had lower levels of emotional intelligence (EI) scores than students without DE attitudes (control group). Moreover, they scored higher than the control group on coping styles such as avoidance-oriented coping, emotion-oriented coping, and emotional eating. The DE group presented a positive correlation between DE attitudes symptoms and both avoidance- and emotion-oriented coping but a negative correlation between DE attitudes and task-oriented coping. There was also a significant negative correlation between DE attitudes and EI score. Another result from this group indicated an association between EI score and emotional-eating score (p < .05, r = –.44) and also a positive correlation between emotion-oriented coping and emotional eating (p < .01, r = .47). The findings highlight future research potential on the role of emotions and EI in DE symptoms, which may be beneficial in the context of collaborative care management intervention.

This cross-sectional study explored the prevalence of iron deficiency (ID) and associations between dietary factors and incidence of ID in female rhythmic gymnasts during preseason periods. Participants were 60 elite collegiate rhythmic gymnasts (18.1 ± 0.3 years [M ± SD]) who were recruited every August over the course of 8 years. Participants were divided into 2 groups according to the presence or absence of ID. Presence of ID was defined either by ferritin less than 12 µg/L or percentage of transferrin saturation less than 16%. Anthropometric and hematologic data, as well as dietary intake, which was estimated via a semiquantitative food frequency questionnaire, were compared. ID was noted in 48.3% of participants. No significant group-dependent differences were observed in physical characteristics, red blood cell counts, hemoglobin, hematocrit, haptoglobin, or erythropoietin concentrations. The ID group had a significantly lower total iron-binding capacity; serum-free iron; percentage of transferrin saturation; ferritin; and intake of protein, fat, zinc, vitamin B₂, vitamin B₆, beans, and eggs but not iron or vitamin C. The recommended dietary allowance for intake of protein, iron, zinc, and various vitamins was not met by 30%, 90%, 70%, and 22%–87% of all participants, respectively. Multiple logistic analysis showed that protein intake was significantly associated with the incidence of ID (odds ratio = 0.814, 95% confidence interval [0.669, 0.990], p = .039). Participants in the preseason’s weight-loss periods showed a tendency toward insufficient nutrient intake and were at a high risk for ID, particularly because of lower protein intake.

Endurance training in fasted conditions (FAST) induces favorable skeletal muscle metabolic adaptations compared with carbohydrate feeding (CHO), manifesting in improved exercise performance over time. Sprint interval training (SIT) is a potent metabolic stimulus, however nutritional strategies to optimize adaptations to SIT are poorly characterized. Here we investigated the efficacy of FAST versus CHO SIT (4–6 × 30-s Wingate sprints interspersed with 4-min rest) on muscle metabolic, serum metabolome and exercise performance adaptations in a double-blind parallel group design in recreationally active males. Following acute SIT, we observed exercise-induced increases in pan-acetylation and several genes associated with mitochondrial biogenesis, fatty acid oxidation, and NAD⁺-biosynthesis, along with favorable regulation of PDK4 (p = .004), NAMPT (p = .0013), and NNMT (p = .001) in FAST. Following 3 weeks of SIT, NRF2 (p = .029) was favorably regulated in FAST, with augmented pan-acetylation in CHO but not FAST (p = .033). SIT induced increases in maximal citrate synthase activity were evident with no effect of nutrition, while 3-hydroxyacyl-CoA dehydrogenase activity did not change. Despite no difference in the overall serum metabolome, training-induced changes in C3:1 (p = .013) and C4:1 (p = .010) which increased in FAST, and C16:1 (p = .046) and glutamine (p = .021) which increased in CHO, were different between groups. Training-induced increases in anaerobic (p = .898) and aerobic power (p = .249) were not influenced by nutrition. These findings suggest some beneficial muscle metabolic adaptations are evident in FAST versus CHO SIT following acute exercise and 3 weeks of SIT. However, this stimulus did not manifest in differential exercise performance adaptations.

The purpose was to investigate the effects of CYP1A2 −163C > A polymorphism on the effects of acute caffeine (CAF) supplementation on anaerobic power in trained males. Sixteen trained males (age: 21.6 ± 7.1 years; height: 179.7 ± 5.6 cm; body mass: 72.15 ± 6.8 kg) participated in a randomized, double-blind, placebo (PLA) controlled crossover design. Participants supplemented with CAF (6 mg/kg of body mass) and an isovolumetric PLA (maltodextrin) in random order and separated by 7 days, before an all-out 30-s anaerobic cycling test to determine peak, average, and minimum power output, and fatigue index. Genomic deoxyribonucleic acid was extracted to identify each participants CYP1A2 genotype. Six participants expressed AA homozygote and 10 expressed C alleles. There was a treatment by genotype interaction for peak power output (p = .041, η² = .265, observed power = 0.552) with only those expressing AA genotype showing improvement following CAF supplementation compared with PLA (CAF: 693 ± 108 watts vs. PLA: 655 ± 97 watts; p = .039), while no difference between treatments was noted in those expressing C alleles (CAF: 614 ± 92 watts vs. PLA: 659 ± 144 watts; p = .135). There were no other interaction or main effects for average or minimum power output, or fatigue index (p > .05). In conclusion, the ingestion of 6 mg/kg of CAF improved peak power output only in participants with the AA genotype compared with PLA; however, expression of the CYP1A2 did not influence average or minimum power output or fatigue index.

We aimed to investigate the combined effects of aerobic exercise (EXE) and cocoa flavanol (COCOA) supplementation on performance, metabolic parameters, and inflammatory and lipid profiles in obese insulin-resistant rats. Therefore, 32 male Wistar rats (230–250 g) were fed a high-fat diet and a fructose-rich beverage for 30 days to induce insulin resistance. Next, the rats were randomized into four groups, orally administered placebo solution or COCOA supplementation (45 mg·kg⁻¹), and either remained sedentary or were subjected to EXE on a treadmill at 60% peak velocity for 30 min, for 8 weeks. Blood samples and peripheral tissues were collected and processed to analyze metabolic and inflammatory parameters, lipid profiles, and morphological parameters. Supplementation with COCOA and EXE improved physical performance and attenuated body mass gain, adipose index, and adipocyte area. When analyzed as individual interventions, supplementation with COCOA and EXE improved glucose intolerance and the lipid profile reduced the concentrations of leptin, glucose, and insulin, and reduced homeostasis assessment index (all effects were p < .001 for both interventions), while ameliorated some inflammatory mediators in examined tissues. In skeletal muscles, both COCOA supplementation and EXE increased the expression of glucose transporter (p < .001 and p < .001), and combined intervention showed additive effects (p < .001 vs. COCOA alone or EXE alone). Thus, combining COCOA with EXE represents an effective nonpharmacological strategy to treat insulin resistance; it could prevent Type 2 diabetes mellitus by improving physical performance, glucose metabolism, neuroendocrine control, and lipid and inflammatory mediators in the liver, pancreas, adipose tissue, and skeletal muscle in obese male insulin-resistant rats.

The purpose of this study was to investigate the effects of supplementation of whey protein (WP) versus leucine-matched collagen peptides (CP) on muscle thickness MT and performance after a resistance training (RT) program in young adults. Twenty-two healthy untrained participants were randomly assigned to either a WP (n = 11) or leucine-matched CP (n = 11) group and then submitted to a supervised 10-week RT program (3 days/week). The groups were supplemented with an equivalent amount of WP (35 g, containing 3.0 g of leucine) and CP (35 g, containing 1.0 g of leucine and 2.0 g of free leucine) during the intervention period (after each workout and in the evening on nontraining days). MT of the vastus lateralis and biceps brachii, isokinetic peak torque and mean power output of the elbow flexors, and peak power output of the lower body were assessed before and after the RT program. The WP group experienced a greater (interaction, p < .05) increase in the vastus lateralis (effect size, WP = 0.68 vs. CP = 0.38; % Δ, WP = 8.4 ± 2.5 vs. CP = 5.6 ± 2.6%) and biceps brachii muscle thickness (effect size, WP = 0.61 vs. CP = 0.35; % , WP = 10.1 ± 3.8 vs. CP = 6.0 ± 3.2%), with a similar increase in muscle performance (peak torque, mean power output, and peak power output) between groups (time p < .05). Supplementation with WP was superior to leucine content-matched CP supplementation in increasing muscle size, but not strength and power, after a 10-week RT program in young adults.

Assessing bone’s response to physical activity interventions is challenging. This randomized controlled trial investigates if changes in bone turnover markers can offer an early evaluation of a physical activity intervention’s effectiveness in improving bone mineral density (BMD) in premenopausal women. Participants in the intervention group (n = 27, with 24 completing the trial) were instructed to walk at least 10,000 steps every day on a brisk walk and to execute 60 jumps daily, each surpassing 4g of acceleration, using an accelerometer-based wearable device. Meanwhile, the control group (n = 26, with 18 completing the trial) continued with their usual lifestyle. Bone turnover markers, comprising of C-terminal telopeptide of Type I collagen, procollagen Type 1 N-terminal propeptide, and total osteocalcin (carboxylated and undercarboxylated) were measured at baseline and midway through the intervention (3 months). Dual-energy X-ray absorptiometry scans of the hip and lumbar spine were conducted at baseline and the end of the intervention (6 months) to estimate BMD. Analysis of covariance exhibited significant differences between groups in procollagen Type 1 N-terminal propeptide (−6.74 μg/L, p = .023) and C-terminal telopeptide of Type I collagen (−83 ng/L, p = .043) after 3 months, and in femoral neck BMD (+0.024 g/cm², p = .016), total hip BMD (+0.036 g/cm², p = .004), and lumbar spine BMD (+0.026 g/cm², p = .020) after 6 months. A significant correlation (r = −.73; p < .001) was detected between reductions in C-terminal telopeptide of Type I collagen and increases in femoral neck BMD. In conclusion, this intervention improved BMD in premenopausal women, with bone turnover markers potentially useful for early intervention assessment, though further research is needed.