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It is unknown how plasma leptin affects fat oxidation depending on sex in young adults. Therefore, the present cross-sectional study aimed to examine the associations of plasma leptin with resting fat oxidation (RFO), maximal fat oxidation during exercise (MFO), and insulin sensitivity, considering the different responses in men and women, and the mediating role of fatness and cardiorespiratory fitness (CRF). Sixty-five young adults (22.5 ± 4.3 years; body mass index = 25.2 ± 4.7 kg·m-2, 23 females) participated in this study. Fasting plasma glucose, insulin, and leptin were analyzed. Variables related to insulin resistance (HOMA1-IR, HOMA2-IR), secretion (HOMA-%ß), and sensitivity (HOMA-%S, QUICKI) were computed. RFO and MFO were determined through indirect calorimetry. A peak oxygen uptake (VO2peak) test was performed until exhaustion after the MFO test. The MFO was relativized to body mass (MFO-BM) and the legs' lean mass divided by the height squared (MFO-LI). In men, leptin was negatively associated with MFO-BM and positively with HOMA-%ß (p ≤ 0.02 in both). In women, leptin was positively associated with RFO and QUICKI, and negatively with MFO-BM (p < 0.05 in all). The association between leptin and MFO was mediated by CRF (p < 0.05), but not by fat mass (p > 0.05). Plasma leptin is associated with fat oxidation and insulin secretion/sensitivity, with different responses within each sex. The association between leptin and fat oxidation is mediated by cardiorespiratory fitness.

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This study aimed to analyze the influence of the peroxisome proliferator-activated receptor (PPAR)-gamma coactivator (PGC)-1 alpha (PPARGC1A) gene rs8192678 C>T polymorphism on different health-related parameters in male and female young adults. The PPARGC1A gene rs8192678 polymorphism was ascertained by polymerase chain reaction in 74 healthy adults (28 women; 22.72 ± 4.40 years) from Andalusia (Spain). Health-related variables included cardiometabolic risk, anthropometry and body composition, biochemical parameters, insulin sensitivity (QUICKI and HOMA-IR indexes), blood pressure (BP) at rest and after exercise, diet, basal metabolism, physical activity, maximal fat oxidation, and cardiorespiratory fitness. Our results showed differences by PPARGC1A gene rs8192678 C>T polymorphism in body mass (p = 0.002), body mass index (p = 0.024), lean body mass (p = 0.024), body fat (p = 0.032), waist circumference (p = 0.020), and BP recovery ratio (p < 0.001). The recessive model (CC vs. CT/TT) showed similar results but also with differences in basal metabolism (p = 0.045) and total energy expenditure (p = 0.024). A genotype*sex interaction was found in the QUICKI index (p = 0.016), with differences between CC and CT/TT in men (p = 0.049) and between men and women inside the CT/TT group (p = 0.049). Thus, the PPARGC1A gene rs8192678 C>T polymorphism is associated with body composition, basal metabolism, total energy expenditure, and BP recovery, where the CC genotype confers a protective effect. Moreover, our study highlighted sexual dimorphism in the influence of PPARGC1A gene rs8192678 C>T polymorphism on the QUICKI index.

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The present work aimed to examine the association between physical activity (PA) and sedentary behaviour with maximal fat oxidation (MFO) in young individuals. A total of 77 active adults (30 women; 22.8 ± 4.5 years) were included in this cross-sectional study in which PA and sedentary behaviour were measured using accelerometers for 7 consecutive days. PA was classified into different intensities (i.e. light, moderate, vigorous, and moderate-to-vigorous) and sedentary behaviour into sedentary time (i.e. time, number of bouts, and length of bouts) and sedentary breaks (i.e. time, number of breaks, and length of breaks). MFO was determined using a graded cycloergometer test through indirect calorimetry and relativized to lean mass (MFOLM) and lean leg mass (MFOLL). Positive associations were found for light and vigorous PA in relation with MFO, MFOLM and MFOLL, independently of cofounders (P ≤ 0.01). Moreover, a negative association was found between MFO and MFOLM and the length of sedentary bouts which was accentuated after adjusting by cardiorespiratory fitness (P ≤ 0.05). These results suggest that light and vigorous PA and sedentary behaviour are related to MFO during exercise. Despite this, further interventional studies are needed to clarify if increments of light and vigorous PA could enhance MFO in different populations.

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BACKGROUND: Due to the prevalence and incidence worldwide of type 2 diabetes, and the significant role physical activity plays in these patients, a systematic review has been conducted to find out the effects that high-intensity interval training has on inflammatory biomarkers in subjects with type 2 diabetes. This project aims to determine the effect this training modality has on inflammatory biomarkers, in addition to observing its effects on the values of body composition and determining if this is a more effective, less effective or equally effective alternative to standard aerobic or resistance training. METHODS: A search was conducted in the months of November and December 2020 on different databases: Pubmed, WoS and PEDro. A protocol for this systematic review was registered in PROSPERO (Registration number: CRD42021281186). The studies selected met the previously defined inclusion criteria, and the methodological quality of the papers used was evaluated according to the Downs and Black Checklist. RESULTS: Out of 46 studies found, seven were included. The most relevant data concerning the characteristics of the clinical trials and HIIT characteristics, the values of body composition and the biomarkers under study were extracted from each study. Moreover, the results obtained from the different studies were described. CONCLUSIONS: HIIT could have an effect on inflammatory biomarkers. There is likely to be a relationship between changes in inflammatory profile and fat loss. A controlled diet may be a good complement to reduce the inflammatory profile. Further studies are required to determine whether HIIT is a better, worse or an equivalent alternative to medium-intensity aerobic exercise to improve the inflammatory profile.

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There is controversy about the relationship between ACE I/D polymorphism and health. Seventy-four healthy adults (n = 28 women; 22.5 ± 4.2 years) participated in this cross-sectional study aimed at determining the influence of ACE I/D polymorphism, ascertained by polymerase chain reaction, on cardiometabolic risk (i.e., waist circumference, body fat, blood pressure (BP), glucose, triglycerides, and inflammatory markers), maximal fat oxidation (MFO), cardiorespiratory fitness (maximal oxygen uptake), physical activity and diet. Our results showed differences by ACE I/D polymorphism in systolic BP (DD: 116.4 ± 11.8 mmHg; ID: 116.7 ± 6.3 mmHg; II: 109.4 ± 12.3 mmHg, p = 0.035) and body fat (DD: 27.3 ± 10.8%; ID: 22.6 ± 9.7%; II: 19.3 ± 7.1%, p = 0.030). Interestingly, a genotype*sex interaction in relativized MFO by lean mass (p = 0.048) was found. The DD polymorphism had higher MFO values than ID/II polymorphisms in men (8.4 ± 3.0 vs. 6.5 ± 2.9 mg/kg/min), while the ID/II polymorphisms showed higher R-MFO values than DD polymorphism in women (6.6 ± 2.3 vs. 7.6 ± 2.6 mg/kg/min). In conclusion, ACE I/D polymorphism is apparently associated with adiposity and BP, where a protective effect can be attributed to the II genotype, but not with cardiorespiratory fitness, diet and physical activity. Moreover, our study highlighted that there is a sexual dimorphism in the influence of ACE I/D gene polymorphism on MFO.

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It is unknown whether resting fat oxidation (RFO), maximal fat oxidation (MFO) and FatMax (intensity at which MFO is reached) are related to cardiometabolic risk (CMR). Thus the aim of this study was to examine the association of RFO, MFO and FatMax with CMR. 81 healthy adults (n = 31 women; 22.72 ± 4.40 years) participated in this cross-sectional study. Glucose and triglycerides were analysed in plasma. Body composition, anthropometry, physical activity, blood pressure (BP) and heart rate measurements were taken. RFO and MFO were determined through indirect calorimetry. Maximal oxygen uptake (VO2max) test was performed until exhaustion after MFO test. The CMR cluster was created from individual CMR factors: waist circumference, body fat percentage, systolic BP, diastolic BP, blood glucose and plasma triglycerides. Groups of high and low MFO and VO2max were created. RFO was not associated with CMR (p < 0.05). FatMax, MFO and VO2max were associated with individual CMR factors as waist circumference (R2 = 0.144; R2 = 0.241; R2 = 0.285; p = 0.001; respectively) and plasma triglycerides (R2 = 0.111; p = 0.004 and R2 = 0.130; p = 0.002 and R2 = 0.093; p = 0.008; respectively) and clustered CMR factors (R2 = 0.105; p = 0.008 and R2 = 0.162; p = 0.001 and R2 = 0.239; p = 0.001; respectively). VO2max was also associated with body fat percentage (R2 = 0.105; p = 0.003) and diastolic BP (R2 = 0.083; p = 0.01), even adjusting for sex or age (p < 0.05). Groups with high level of MFO or VO2max obtained lower CMR (p = 0.001), even adjusting for sex or age (p < 0.01). FatMax, MFO and, especially, VO2max are associated with CMR, regardless of age and sex. However, RFO is not associated with CMR.

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