Higher Oxygen Consumption Research Articles

Physiologic Phenotype of Cardiogenic Shock Due to End-Stage Heart Failure and Acute Myocardial Infarction: Effect of ECLS

<h3>Purpose</h3> This study (i) models and compares the pathophysiology of cardiogenic shock (CS) due to end stage heart failure (ESHF) and acute myocardial infarction (AMI) using patient data and (ii) compares the effects extracorporeal life support (ECLS) in these 2 patient groups. <h3>Methods</h3> Data from consecutive patients with CS due to ESHF and AMI were used as the basis for simulating the hemodynamics with the computational model by Burkhoff et al. ESHF is defined as diagnosis of an ischemic or non-ischemic cardiomyopathy prior to CS. The effects of right atrial (RA) to femoral artery ECLS at 3.5L/min were simulated. <h3>Results</h3> Patient with ESHF had lower ejection fraction, more mitral regurgitation and higher right atrial pressure [TABLE]. Compared to AMI, CS due to ESHF is associated with (i) lower left (LV) and right ventricular (RV) diastolic pressure-volume relation (lower ‘stiffness') [FIGURE]; (ii) lower LV and RV end-systolic elastance (Ees) and (iii) larger pressure-volume loop area (PVA) corresponding to high myocardial oxygen consumption (MVO2), (iv) lower RV efficiency (ratio of stroke work to MVO2). ECLS increased systemic blood pressure and pulmonary artery wedge pressure (PAWP) in both groups, but patients with AMI had higher relative increase in PAWP due to the steeper diastolic pressure-volume relation compared to ESHF. <h3>Conclusion</h3> The hemodynamic phenotype in CS due to ESHF differs from AMI with higher LV and RV capacitance (lower 'stiffness'), lower LV and RV Ees (contractility) and lower RV efficiency in the former. ECLS increased systemic and pulmonary artery wedge pressure, which is more marked in AMI.

SGLT2 Inhibitor-Induced Low-Grade Ketonemia Ameliorates Retinal Hypoxia in Diabetic Retinopathy-A Novel Hypothesis.

Diabetic retinopathy (DR) is a well-recognized microvascular complication of diabetes. Growing evidence suggests that, in addition to retinal vascular damage, there is significant damage to retinal neural tissue in DR. Studies reveal neuronal damage before clinically evident vascular lesions and DR is now classified as a neurovascular complication. Hyperglycemia causes retinal damage through complex metabolic pathways leading to oxidative stress, inflammation, vascular damage, capillary ischemia, and retinal tissue hypoxia. Retinal hypoxia is further worsened by high oxygen consumption in the rods. Persistent hypoxia results in increases in vascular endothelial growth factor (VEGF) and other pro-angiogenic factors leading to proliferative DR/macular edema and progressive visual impairment. Optimal glucose control has favorable effects in DR. Other treatments for DR include laser photocoagulation, which improves retinal oxygenation by destroying the high oxygen consuming rods and their replacement by low oxygen consuming glial tissue. Hypoxia is a potent stimulator of VEGF, and intravitreal anti-VEGF antibodies are effective in regressing macular edema and in some studies, retinal neovascularization. In this review, we highlight the complex pathophysiology of DR with a focus on retinal oxygen/fuel consumption and hypoxic damage to retinal neurons. We discuss potential mechanisms through which sodium-glucose cotransporter 2 (SGLT2) inhibitors improve retinal hypoxia-through ketone bodies, which are energetically as efficient as glucose and yield more ATP per molecule of oxygen consumed than fat, with less oxidative stress. Retinal benefits would occur through improved fuel energetics, less hypoxia and through the anti-inflammatory/oxidative stress effects of ketone bodies. Well-designed studies are needed to explore this hypothesis.

High Oxygen Consumption in SARS-COV2: Could the Development of Low-Cost Oxygen Rebreather Be Considered?

OPINION article Front. Physiol., 21 January 2021Sec. Respiratory Physiology and Pathophysiology Volume 11 - 2020 | https://doi.org/10.3389/fphys.2020.607913

Improved Normothermic Machine Perfusion After Short Oxygenated Hypothermic Machine Perfusion of Ischemically Injured Porcine Kidneys.

In an era where global kidney shortage has pushed the field of transplantation towards using more marginal donors, modified kidney preservation techniques are currently being reviewed. Some techniques require further optimization before implementation in full scale transplantation studies. Using a porcine donation after circulatory death kidney model, we investigated whether initial kidney hemodynamics improved during normothermic machine perfusion if this was preceded by a short period of oxygenated hypothermic machine perfusion (oxHMP) rather than static cold storage (SCS). Kidneys subjected to 75 minutes of warm ischemia were randomly assigned to either SCS (n = 4) or SCS + oxHMP (n = 4), with a total cold storage time of 240 minutes. Cold preservation was followed by 120 minutes of normothermic machine perfusion with continuous measurement of hemodynamic parameters and renal function. oxHMP preserved kidneys maintained significantly lower renal resistance throughout the normothermic machine perfusion period compared to SCS kidneys (P < 0.001), reaching lowest levels at 60 minutes with means of 0.71 ± 0.35 mm Hg/mL/min/100 g (SCS) and 0.45 ± 0.15 mm Hg/mL/min/100 g (oxHMP). Accordingly, the oxHMP group had a higher mean renal blood flow versus SCS kidneys (P < 0.001). oxHMP kidneys had higher oxygen consumption during normothermic machine perfusion compared to SCS preserved kidneys (P < 0.001). Creatinine clearance remained similar between groups (P = 0.665). Preceding oxHMP significantly improved initial normothermic machine perfusion hemodynamics and increased total oxygen consumption. With the long period of warm ischemia, immediate kidney function was not observed, reflected by the findings of low creatinine clearance in both groups.

Effect of Achyranthes Aspera Linn. Leaves Extract on Reactive Oxygen Species (ROS) in Diabetes-induced Rats by Flow cytometry and Possible Molecular Mechanism through Molecular Docking

Background::Oxidative stress is caused due to the overproduction of the reactive oxygen species (ROS) and the disturbance developed in the antioxidant potential of biochemical processes. ROS mostly form in the brain due to the high consumption of oxygen and the insufficiency of endogenous antioxidant resistance mechanisms. Cytochrome P450 2E1 has an excessive percentage of NADPH oxidase activity, which causes the production of ROS and increases oxidative stress.Objectives::We have studied the effect of ethyl acetate extract of Achyranthes Aspera (EAAA) on ROS in the brain of diabetes-induced rats. We have also investigated the possible molecular mechanism of reduction in ROS through molecular docking.Methods:To study the oxidative stress induced by ROS in diabetic rats, we estimated the ROS in rat brain through flow cytometry. The oral dose of EAAA 50mg/kg and 100 mg/kg was given to diabetesinduced rats. Results were articulated as mean ± standard deviation (SD). Data were analyzed using analysis of variance (ANOVA) followed by Bonferroni as a post hoc test. We performed molecular docking of flavonoids on CYP2E1 to study the inhibitory potential.Results::The results have shown that EAAA reduces the generation of ROS in the diabetes-induced rat in a dose-dependent manner. The oral dose of EAAA 50mg/kg and 100 mg/kg was given to the rats and the ROS generation got affected accordingly. Luteolin, quercetin, and apigenin inhibited the CYP2E1 very effectively. Luteolin formed 4 hydrogen bonds with CYP2E1, which indicated its potential inhibition. Although, luteolin and apigenin showed a very good binding affinity with the enzyme.Conclusion::From the present work, we have concluded that the ethyl acetate extract of achyrantesaspera can effectively inhibit the ROS generation in the diabetes-induced rats by inhibiting the activity of CYP2E1.

Analytical Model for Pem Fuel Cell Concentration Impedance

Analytical model for concentration/pressure (zeta) impedance of the cathode side of a PEM fuel cell is developed. The model is based on transient oxygen mass transport equations through the gas - diffusion and cathode catalyst layers. Analytical solution for zeta - impedance is derived and the relation of zeta - impedance and regular cell impedance is obtained. In the limit of high oxygen consumption in the catalyst layer, simple equations for the static point of zeta impedance are derived. These equations allow one to estimate oxygen transport coefficients of the catalyst and gas diffusion layers from the static point of zeta - spectrum. Qualitative resemblance of the model and experimental zeta - spectra is demonstrated.

Acute exposure to C60 fullerene damages pulmonary mitochondrial function and mechanics

C60 fullerene (C60) nanoparticles, a nanomaterial widely used in technology, can offer risks to humans, overcome biological barriers, and deposit onto the lungs. However, data on its putative pulmonary burden are scanty. Recently, the C60 interaction with mitochondria has been described in vitro and in vivo. We hypothesized that C60 impairs lung mechanics and mitochondrial function. Thirty-five male BALB/c mice were randomly divided into two groups intratracheally instilled with vehicle (0.9% NaCl + 1% Tween 80, CTRL) or C60 (1.0 mg/kg, FUL). Twenty-four hours after exposure, 15 FUL and 8 CTRL mice were anesthetized, paralyzed, and mechanically ventilated for the determination of lung mechanics. After euthanasia, the lungs were removed en bloc at end-expiration for histological processing. Lung tissue elastance and viscance were augmented in FUL group. Increased inflammatory cell number, alveolar collapse, septal thickening, and pulmonary edema were detected. In other six FUL and six CTRL mice, mitochondria expressed reduction in state 1 respiration [FUL = 3.0 ± 1.14 vs. CTRL = 4.46 ± 0.9 (SEM) nmol O2/min/mg protein, p = 0.0210], ATP production (FUL = 122.6 ± 18 vs. CTRL = 154.5 ± 14 μmol/100 μg protein, p = 0.0340), and higher oxygen consumption in state 4 [FUL = 12.56 ± 0.9 vs. CTRL = 8.26 ± 0.6], generation of reactive oxygen species (FUL 733.1 ± 169.32 vs. CTRL = 486.39 ± 73.1 nmol/100 μg protein, p = 0.0313) and reason ROS/ATP [FUL = 8.73 ± 2.3 vs. CTRL = 2.99 ± 0.3]. In conclusion, exposure to fullerene C60 impaired pulmonary mechanics and mitochondrial function, increased ROS concentration, and decrease ATP production.

Simulation Analysis of the System Integrating Oxy-Fuel Combustion and Char Gasification

Abstract To explore the feasibility of converting hot flue gas into valuable syngas through char gasification process, Aspen Plus is applied to evaluate the performance of the integrated system including oxy-combustion, pyrolysis, gasification, and flue gas recirculation. The impact of feedstock type (reed straw and municipal solid waste (MSW)), feeding rate (0.1–1 t/h), and flue gas recycle ratio (FGR) (10%–30%) is investigated. The economic analysis of the integrated system is also performed. The results indicate that higher oxygen consumption is required for biomass gasification to reach the same temperature as MSW gasification. The gasification temperature is 750 °C–950 °C under 10%–30% FGR. The CO + H2 content in syngas from biomass gasification is slightly higher than that from MSW gasification. For the integrated system, more natural gas (NG) can be saved and more fossil CO2 can be reduced under biomass gasification. When the feedstock input is 1 t/h, the fossil CO2 emission can be reduced by 70% when taking biomass, the CO2 reduction is double of that when taking MSW. The total OPEX cost can be 26% saved by biomass and 62% saved by MSW due to the government subsidy. If CO2 tax is considered, the advantage of biomass for saving OPEX cost will be more obvious.

Dietary Thiols: A Potential Supporting Strategy against Oxidative Stress in Heart Failure and Muscular Damage during Sports Activity.

Moderate exercise combined with proper nutrition are considered protective factors against cardiovascular disease and musculoskeletal disorders. However, physical activity is known not only to have positive effects. In fact, the achievement of a good performance requires a very high oxygen consumption, which leads to the formation of oxygen free radicals, responsible for premature cell aging and diseases such as heart failure and muscle injury. In this scenario, a primary role is played by antioxidants, in particular by natural antioxidants that can be taken through the diet. Natural antioxidants are molecules capable of counteracting oxygen free radicals without causing cellular cytotoxicity. In recent years, therefore, research has conducted numerous studies on the identification of natural micronutrients, in order to prevent or mitigate oxidative stress induced by physical activity by helping to support conventional drug therapies against heart failure and muscle damage. The aim of this review is to have an overview of how controlled physical activity and a diet rich in antioxidants can represent a “natural cure” to prevent imbalances caused by free oxygen radicals in diseases such as heart failure and muscle damage. In particular, we will focus on sulfur-containing compounds that have the ability to protect the body from oxidative stress. We will mainly focus on six natural antioxidants: glutathione, taurine, lipoic acid, sulforaphane, garlic and methylsulfonylmethane.

Longitudinal changes in sedentary behavior, physical activity and aerobic fitness over 5 years in a cohort at risk for Alzheimer’s disease

AbstractBackgroundLow levels of physical activity and aerobic fitness are established modifiable risk factors for Alzheimer’s disease and all‐cause mortality. Work from our group and others has demonstrated significant and positive cross‐sectional relationships between physical activity, aerobic fitness and indicators of brain health (e.g. biomarkers of AD, cognition). The aims of the current study were to determine 5‐year changes in sedentary behavior, physical activity and aerobic fitness in adults at risk for Alzheimer’s disease.MethodThis study enrolled fifty‐seven cognitively unimpaired adults from the Wisconsin Registry for Alzheimer’s Prevention. Participants completed 7 days of physical activity monitoring via accelerometry and a maximal exercise test at two time‐points – 5 years apart. Based on current physical activity guidelines, our chosen measures were time spent engaged in sedentary behavior and moderate‐to‐vigorous physical activity. Aerobic fitness was defined as the highest oxygen consumption (VO2peak, mL/kg/min) value recorded during the final stage of the maximal exercise test when standardized criteria were met. A repeated measures model was used to investigate whether sedentary behavior, physical activity, and aerobic fitness changed over a 5‐year period. Cohen’s d effect sizes and bivariate correlations were used to explore the magnitude of these changes and their relationships with age.ResultAt baseline, participants (mean age at baseline 63.81±6.1) spent 77.86±8.11 hours/week sedentary, engaged in 10.34±4.26 hours/week of physical activity and displayed an aerobic fitness level of 28.26 ±0.99 mL/kg/min. At follow‐up (mean age at follow‐up 68.52±6.1), we observed non‐significant increases in sedentary behavior 2.1% (d=.2; p=.09), and significant declines in physical activity 12.3% (d=.3; p=.01) and aerobic fitness 14.2% (d=1.2; p&lt;.001). Age was negatively associated with 5‐year change in physical activity (r=‐.31; p=.02) but not sedentary behavior (p=.19) or aerobic fitness (p=.80).ConclusionThis study found that physical activity and aerobic fitness significantly declined over a 5‐year period in adults at risk for Alzheimer’s disease, and this decline may accelerate with advancing age. Strategies aimed at promoting physical activity and aerobic fitness (e.g. exercise training) in mid‐late adulthood are warranted. Future studies are needed to test whether changes in sedentary behavior, physical activity, and aerobic fitness are related to brain and cognitive health.

251 Impacts of different levels of dietary zinc oxide on mitochondrial energy metabolism and oxidative stress conditions in post-weaned piglets

Abstract Zinc oxide (ZnO) is commonly added to weanling piglet diets for its documented benefits as growth promoting agent and usefulness for preventing diarrhea. We have recently reported the occurrence of mitochondrial energetic deficiencies and oxidative stress conditions in post-weaned piglets. In cells, Zn is known to be primarily located in mitochondria, where it is involved in mitochondrial function. The objective of this study was to determine the impacts of different levels of dietary ZnO on mitochondrial function and oxidative stress. One hundred twenty suckling piglets (5.65 ± 0.68 kg) were selected at d14. After weaning (d21), they were fed a basal diet supplemented with 100 mg/kg (low; L), 1000 mg/kg (medium; M) or 3000 mg/kg (high; H) of ZnO until d42 (n = 40/treatment). Piglets were sacrificed at d21, d23, d35, and d42 of age (n = 10/treatment/d) for sample collection. Mitochondrial respiration was evaluated using an extracellular flux analyzer and our results showed higher oxygen consumption rates in liver mitochondria from H group (P &amp;lt; 0.05) at d42. The cellular energy status was characterized by measuring liver adenosine 5’-triphosphate (ATP) content, and lower levels were reported in H group (P &amp;lt; 0.01) at d42. These observations were concomitant with a decrease in activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) in cytosol and mitochondria. Quantitative RT-PCR analyses revealed that expression of genes implicated in oxidative stress response such as glutathione synthase (GSS), heme oxygenase 1 (HO1) and metallothionein 3 (MT3) is increased in H group at d42 (P &amp;lt; 0.05). In plasma, GPx activity and oxidative damage to proteins (carbonyls) was higher in H group (P &amp;lt; 0.05). These findings indicate that ZnO affects mitochondrial function and oxidative stress in post-weaned piglets and provide insights to guide the prophylactic practices using high levels of dietary ZnO.

Effect of lead in the aerobic decomposition of Myriophyllum aquaticum (Vellozo) Verdecourt

Lead is a toxic element that has been used since early times and is still employed today in several industrial processes. Events as the collapse of the Fundão dam in Bento Rodrigues, district of Mariana (MG) on November 2015, significantly increase concentrations of metals above-recommended levels, including lead. In this context, this study aims to evaluate the impact of lead in the cycling rate of organic matter in the aquatic environment. Thus, the rates of aerobic decomposition of Myriophyllum aquaticum (Vell.) Verdec at different concentrations of lead (5.0, 10.0, 20.0 and 30.0 mg L-1) were measured, analyzing the dissolved oxygen consumption. Decomposition chambers filled with samples of water and M. aquaticum were incubated at 20° C in the dark for 80 days and periodically had the oxygen concentrations determined by polarography, when the concentrations were less than 2 mg L-1, the incubations were re-aerated. At the lowest concentrations (5.0 and 10.0 mg L-1) of lead the mineralization was lower, however, the reaction coefficients and the amount of oxygen consumed were equivalent to the control. At the highest concentrations (20.0 and 30.0 mg L-1) the mineralization was increased, with the reduction of reaction coefficients and higher oxygen consumption.

A threefold perspective on the role of a pockmark in benthic faunal communities and biodiversity patterns

Pockmarks are circular-shaped depressions that increase seabed heterogeneity and are characterized by discontinuous fluid emissions. To understand how environmental conditions of pockmarks affect the structure of macro- and meiofauna, we investigated two sites in a pockmark field in the northwestern Madagascar margin. In a comparative approach, we explored the community structure of the dominant taxa (Polychaeta, Nematoda and hyaline foraminifera) in each component (macro-, metazoan meiofauna and foraminifera, respectively). The investigated active pockmark showed approximately two times higher meiofauna abundance compared to in a site away from another pockmark field, but macrofauna showed the opposite trend, with almost half density at the pockmark site. However, at both sites, macro- and meiofauna showed higher richness and abundance values in the top well-oxygenated layers of the sediment than in the underlaying ones. Polychaeta and Nematoda showed lower richness in the pockmark, opposed to hyaline foraminiferans, but lower evenness in the pockmark was found for the three groups. The detection of gas flares in the water column attests of the recent activity within the pockmark. High amount of sulfur-bearing minerals (mainly pyrite) evidences a production of dissolved free sulfides (not detected at the time of sampling) by sulfate reduction process driven by organic matter degradation and anaerobic oxidation of methane. Furthermore, recent increase in sedimentation rates in the past 70 years and organic matter inputs could have led to higher organic matter degradation rates resulting in reduced conditions and a high oxygen consumption. All this together seem to act as key factors in the determination of variation in richness, abundance and community composition of macrofauna and meiofauna. Additionally, some taxa seem to be more tolerant to these extreme conditions, such as species belonging to the Nematoda genus Desmodora and the phylum Kinorhyncha, which are highly abundant in the pockmark, and hence, may be considered as potential bioindicators of pockmark activity in this area. Further studies are required for a better assessment.

Age and Sex Influence Mitochondria and Cardiac Health in Offspring Exposed to Maternal Glucolipotoxicity.

SummaryInfants of diabetic mothers are at risk of cardiomyopathy at birth and myocardial infarction in adulthood, but prevention is hindered because mechanisms remain unknown. We previously showed that maternal glucolipotoxicity increases the risk of cardiomyopathy and mortality in newborn rats through fuel-mediated mitochondrial dysfunction. Here we demonstrate ongoing cardiometabolic consequences by cross-fostering and following echocardiography, cardiomyocyte bioenergetics, mitochondria-mediated turnover, and cell death following metabolic stress in aged adults. Like humans, cardiac function improves by weaning with no apparent differences in early adulthood but declines again in aged diabetes-exposed offspring. This is preceded by impaired oxidative phosphorylation, exaggerated age-related increase in mitochondrial number, and higher oxygen consumption. Prenatally exposed male cardiomyocytes have more mitolysosomes indicating high baseline turnover; when exposed to metabolic stress, mitophagy cannot increase and cardiomyocytes have faster mitochondrial membrane potential loss and mitochondria-mediated cell death. Details highlight age- and sex-specific roles of mitochondria in developmentally programmed adult heart disease.

Experimental study on the spatial and temporal variations of temperature and indicator gases during coal spontaneous combustion

Coal spontaneous combustion is one of the main potential hazards in the process of mining. To study the spatial and temporal variations of higher-temperature area and indicator gases, an adiabatic oxidation testing system was developed to simulate the whole process of coal spontaneous combustion. The experimental results show that the entire process of coal spontaneous combustion could be divided into three stages: slow-oxidation, accelerated-oxidation and combustion stages. In the slow-oxidation stage, the higher-temperature area shifted slowly from the bottom to the top and then stayed at the top until accelerated-oxidation stage was reached; [Formula: see text] and [Formula: see text] concentration remained more or less constant as well as the oxygen concentration. In accelerated-oxidation stage, the higher-temperature area moved to the bottom rapidly and subsequently stayed approximately in the center of the coal; [Formula: see text], [Formula: see text] concentration and oxygen consumption increased sharply. In addition, the occurrence of higher-temperature area is accompanied by higher oxygen consumption. The obtained results show that higher air supply rate could shorten spontaneous combustion period and there exists a hyperbolic relationship between the temperature and time.

Principles for minimizing oxygen debt: can they translate to clinical application and improve outcomes?

Oxygen delivery is dependent on pulmonary gas exchange, cardiac output, blood oxygen-carrying capacity, and tissue oxygen extraction. Reduction in oxygen delivery or higher oxygen consumption can initiate complex protective cellular processes precipitating oxygen debt. In critically ill and potentially surgical patients, stress and consequent hormonal or metabolic changes can trigger oxygen debt which is associated with worse morbidity and mortality. Increase in oxygen delivery by augmenting cardiac output or by increasing fraction of inspired oxygen (FiO2) can help reduce oxygen debt. However, the extent of oxygen debt in an individual patient is poorly defined and difficult to measure. Furthermore, large heterogeneity in clinical trials assessing outcomes benefit of increasing oxygen delivery limits our ability to recommend goal directed fluid therapy aimed at increasing cardiac ouput or higher FiO2. To understand and prevent oxygen debt in critically ill and surgical patients, we need to develop continuous monitoring techniques to assess the balance of oxygen delivery and consumption. Furthermore, methods of increasing oxygen delivery like goal-directed fluid therapy, higher FiO2 and anemia prevention should be rigorously evaluated with focus on establishing outcomes benefit.

Impact of experimental obesity on diaphragm structure, function, and bioenergetics.

Obesity is associated with bioenergetic dysfunction of peripheral muscles; however, little is known regarding the impact of obesity on the diaphragm. We hypothesized that obesity would be associated with diaphragm dysfunction attributable to mitochondrial oxygen consumption and structural and ultrastructural changes. Wistar rat litters were culled to 3 pups to induce early postnatal overfeeding and consequent obesity. Control animals were obtained from unculled litters. From postnatal day 150, diaphragm ultrasound, computed tomography, high-resolution respirometry, immunohistochemical, biomolecular, and ultrastructural histological analyses were performed. The diaphragms of obese animals, compared with those of controls, presented changes in morphology as increased thickening fraction, diaphragm excursion, and diaphragm dome height, as well as increased mitochondrial respiratory capacity coupled to ATP synthesis and maximal respiratory capacity. Fatty acid synthase gene expression was also higher in obese animals, suggesting a source of energy for the respiratory chain. Myosin heavy chain-IIA was increased, indicating shift from glycolytic toward oxidative muscle fiber profile. Diaphragm tissue also exhibited ultrastructural changes, such as compact, round, and swollen mitochondria with fainter cristae and more lysosomal bodies. Dynamin-1 expression in the diaphragm was reduced in obese rats, suggesting decreased mitochondrial fission. Furthermore, gene expressions of peroxisome γ proliferator-activated receptor coactivator-1α and superoxide dismutase-2 were lower in obese animals than in controls, which may indicate a predisposition to oxidative injury. In conclusion, in the obesity model used herein, muscle fiber phenotype was altered in a manner likely associated with increased mitochondrial respiratory capability, suggesting respiratory adaptation to increased metabolic demand.NEW & NOTEWORTHY Obesity has been associated with peripheral muscle dysfunction; however, little is known about its impact on the diaphragm. In the current study, we found high oxygen consumption in diaphragm tissue and changes in muscle fiber phenotypes toward a more oxidative profile in experimental obesity.

Specific high-intensity intervaltraining for jiu-jitsu

Known as HIIT (High-Intensity Interval Training) or high-intensity interval training is at the top of current training. This type of training allows athletes to exercise longer in high intensity and not the other way around. The main objective of this work is to provide a tool for physical education professionals and trainers to evaluate their jiu-jitsu fighters specifically through an adaptation of interval training to jiu-jitsu, and can also obtain parameters through a targeted methodology, such as the fighter's specific endurance index test. The methodology also consists of promoting during the test, active recovery and a high cadence in the executions of movements, this recovery will also promote a higher oxygen consumption with close effort/pause, being considered as short HIIT, with values in the subjective scale of effort perception of 6 to 20, corresponding to high-intensity interval training. According to all the results obtained we can verify that it is an evaluation tool that complies with the requirements of an activity characterized as short intensity interval training, with active recovery, so it has higher caloric expenditure in the training section, as well as oxygen consumption and even a higher average heart rate in training because the subjective perception of mean effort among the subjects tested was 16 on the Borg scale. It is concluded that this proposal meets the initial objectives and will, in addition, this concept can be used for any type of physical activity and various types of sports gestures, thus being an excellent tool for teachers and technicians, and can also be used as part of a structure of physical preparation for combat modalities in several specific phases of training.

Biochanin A induces a brown-fat phenotype via improvement of mitochondrial biogenesis and activation of AMPK signaling in murine C3H10T1/2 mesenchymal stem cells.

In this study, we investigated the effect of Biochanin A (BioA), an O-methylated isoflavone on the brown-fat phenotype formation and on the associated thermogenic program including mitochondrial biogenesis and lipolysis in C3H10T1/2 MSCs. Our data demonstrates that Treatment with BioA in an adipogenic differentiation cocktail induced formation of brown-fat-like adipocytes from C3H10T1/2 MSCs without treatment with a known browning inducer (rosiglitazone or T3) at an early stage of differentiation. The formation of brown-fat-like adipocytes by BioA treatment was evidenced by upregulation of key thermogenic markers: Ucp1, Pgc1α, Prdm16, and Pparγ. BioA also increased the expression of beige (Cd137 and Fgf21) and brown (Elovl3 and Zic1)-specific markers. Additionally, BioA treatment promoted mitochondrial biogenesis, judging by the upregulation of genes; Cox8b, Cidea, Dio2, Sirt1, Opa1, and Fis1. BioA treatment increased the amount of mitochondrial DNA and its encoded proteins: oxidative phosphorylation complexes (I-V); this change was associated with high oxygen consumption by C3H10T1/2 MSCs. A small-interfering-RNA-induced gene knockdown and experiments with dorsomorphin-driven competitive inhibition revealed that BioA exerts the thermogenic action via activation of AMPK signaling. Our study shows the mechanism of BioA-induced promotion of a brown-fat phenotype. Nonetheless, clinical research is necessary to validate BioA as a brown-fat-like signature inducer.

The Impact of Ethnicity on Cardiac Adaptation.

Regular intensive exercise is associated with a plethora of electrical, structural and functional adaptations within the heart to promote a prolonged and sustained increase in cardiac output. Bradycardia, increased cardiac dimensions, enhanced ventricular filling, augmentation of stroke volume and high peak oxygen consumption are recognised features of the athlete's heart. The type and magnitude of these adaptations to physical exercise are governed by age, sex, ethnicity, sporting discipline and intensity of sport. Some athletes, particularly those of African or Afro-Caribbean (black) origin reveal changes that overlap with diseases implicated in sudden cardiac death. In such instances, erroneous interpretation has potentially serious consequences ranging from unfair disqualification to false reassurance. This article focuses on ethnic variation in the physiological cardiac adaption to exercise.