The present study aimed to investigate the effects of a 12-week concurrent training intervention on cardiometabolic health in obese men. Twelve obese men (42.5 ± 5.3 years old) participated in the current 12−week randomized controlled trial with a parallel group design. The participants were randomly assigned to a concurrent training group or to a no-exercise control group. Anthropometry and body composition assessment were determined by electrical bio-impedance. Blood samples were obtained and a cardiometabolic risk Z-Score was calculated. Energy metabolism-related parameters [i.e., resting metabolic rate (RMR), respiratory quotient (RQ), and substrate oxidation in both resting conditions and during exercise] were determined by indirect calorimetry. Echocardiographic studies were performed using an ultrasound system equipped with a transducer to measure cardiac function. A significant decrease of weight (Δ = −4.21 kg; i.e., primary outcome), body mass index (Δ = −1.32 kg/m2), fat mass (FM; Δ = −3.27 kg), blood pressure (BP; Δ = −10.81 mmHg), and cardiometabolic risk Z-Score (Δ = −0.39) was observed in the exercise group compared with the control group (all P < 0.05), while no significant changes were noted in waist circumference (WC), lean mass (LM), bone mineral content, glycemic and lipid profiles, liver function, nor in energy metabolism-related parameters (all P > 0.1). Moreover, a significant increment of left ventricular (LV) end diastolic diameter (Δ = −4.35 mm) was observed in the exercise group compared with the control group (P = 0.02). A 12-week concurrent training intervention is an effective strategy to induce weight and fat loss with simultaneous reductions of BP and cardiometabolic risk, and improving cardiac function in obese men.
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 (VO 2 max) 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 VO 2 max were created. RFO was not associated with CMR (p < 0.05). FatMax, MFO and VO 2 max were associated with individual CMR factors as waist circumference (R 2 = 0.144; R 2 = 0.241; R 2 = 0.285; p = 0.001; respectively) and plasma triglycerides (R 2 = 0.111; p = 0.004 and R 2 = 0.130; p = 0.002 and R 2 = 0.093; p = 0.008; respectively) and clustered CMR factors (R 2 = 0.105; p = 0.008 and R 2 = 0.162; p = 0.001 and R 2 = 0.239; p = 0.001; respectively). VO 2 max was also associated with body fat percentage (R 2 = 0.105; p = 0.003) and diastolic BP (R 2 = 0.083; p = 0.01), even adjusting for sex or age (p < 0.05). Groups with high level of MFO or VO 2 max obtained lower CMR (p = 0.001), even adjusting for sex or age (p < 0.01). FatMax, MFO and, especially, VO 2 max are associated with CMR, regardless of age and sex. However, RFO is not associated with CMR.
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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