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.

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.

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 (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). VO₂max 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 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.

Impaired fat oxidation is linked to cardiometabolic risk. Maximal fat oxidation rate (MFO) reflects metabolic flexibility and is influenced by lean mass, muscle strength, muscle quality - defined as the ratio of strength to mass - and cardiorespiratory fitness. The relationship between these factors and fat oxidation is not fully understood. The aim is to analyze the associations of lean-mass, muscle strength and quality with fat oxidation parameters in young adults, considering the mediating role of VO₂max. A cross-sectional observational study. Eighty-one adults (50 males, 31 females; age 22.8 ± 4.4, BMI 25.70 ± 5.75, lean-mass 54.19 ± 8.78, fat-mass 18.66 ± 11.32) Body composition assessment by bioimpedance determine fat and lean-mass. Indirect calorimetry at rest and exercise was used for the calculation of fat oxidation. An incremental exercise protocol in a cycle ergometer with two consecutive phases was performed. The first to determine MFO consisted of 3 min steps of 15W increments with a cadence of 60rpm. The test was stopped when RQ ≥ 1. After 5 min rest, a phase to detect VO₂max began with steps of 15W/min until exhaustion. Muscular strength was assessed by handgrip dynamometry and the standing longitudinal jump test. A strength cluster was calculated with handgrip and long jump adjusted by sex and age. Data were analyzed using multiple linear regression and mediation analyses. Total lean-mass and leg lean-mass were not associated with MFO. Long jump, relativized by lean-mass and by leg lean-mass have a standardized indirect effect on MFO of 0.50, CI: 0.32-0.70, on MFO/lean-mass 0.43, CI:0.27-0.60 and MFO/leg lean-mass 0.44, CI: 0.30-0.06, which VO₂max mediated, VO₂max/lean-mass and VO₂max/leg lean-mass, respectively (all p < 0.01). The handgrip/arm lean-mass had an indirect effect of 0.25 (CI: 0.12-0.38) on MFO/leg lean-mass, with VO₂max/leg lean-mass as the mediator (p < 0.01). The Cluster/lean-mass and Cluster/Extremities lean-mass have a standardized indirect effect on MFO/lean-mass (0.34, CI: 0.20-0.48) and MFO/leg lean-mass (0.44, CI: 0.28-0.60), mediated by VO2max/lean-mass and VO2max/leg lean-mass (p < 0.01). Muscular strength and quality have an indirect effect on MFO mediated by VO₂max. These findings suggest the importance of muscle quality on MFO.

La condición física es un conjunto de atributos físicos determinante de la capacidad de realizar un trabajo pudiendo o no estar relacionado con la salud^10,11; la capacidad cardiorrespiratoria (CCR) es un componente de esta condición utilizado como indicador de salud y de expectativa de vida, siendo objetivada a través del consumo de oxígeno máximo (VO₂ max)^12–14; corresponde a la mayor cantidad de oxígeno que una persona puede consumir, transportar y utilizar en una inspiración durante la realización de un ejercicio dinámico^15,16. Para evaluar esta variable se necesita de las máximas capacidades cardiorrespiratorias del sujeto^17,18, situación que puede resultar riesgosa en algunos casos¹⁹. En pacientes con obesidad, estas evaluaciones generalmente son submáximas y se utiliza el término consumo de oxígeno peak (VO₂ peak) para denominar la cantidad de oxígeno consumido en el momento de la detención de la prueba^15,20–22, el cual se expresa en valores absolutos (L/min) o relativos al peso corporal (ml/kg/min)²³. Uno de los aspectos poco descritos del VO₂ es su cinética, la cual consiste en la respuesta dinámica del VO₂ al comienzo de un ejercicio de carga constante durante 6 a 10 minutos, aproximadamente^24–26. Para poder describir el comportamiento de la cinética del VO₂ a carga subumbral, se utiliza la expresión matemática: VO₂ = BL + A(1- e^-(t-TD/τ)), donde VO2 = consumo de oxígeno en función del tiempo; BL = consumo de oxígeno inicial o de base; A = ganancia total del consumo de oxígeno; e = base del logaritmo natural, t = tiempo; τ = tau; TD = tiempo de retraso que precede al incremento en el VO₂ muscular²⁷.