Body Size Measurements Grouped Independently of Common Clinical Measures of Metabolic Health: An Exploratory Factor Analysis.

Background: Obesity is commonly aggregated with indices of metabolic health. Proponents of body positivity approaches question whether body size is a determinant of health and well-being. Our objective was to conduct an exploratory factor analysis (EFA) to determine if body size measurements factor load with or independent of metabolic health measures.

Intramuscular diacylglycerol accumulates with acute hyperinsulinemia in insulin-resistant phenotypes.

Elevated skeletal muscle diacylglycerols (DAGs) and ceramides can impair insulin signaling, and acylcarnitines (acylCNs) reflect impaired mitochondrial fatty acid oxidation, thus, the intramuscular lipid profile is indicative of insulin resistance. Acute (i.e.

Fat and fat-free mass measurement agreement by dual-energy X-ray absorptiometry versus bioelectrical impedance analysis: Effects of posture and waist circumference.

Background: Bioelectrical impedance analysis (BIA) operates under the assumption that the conductor has a uniform cylindrical shape. However, this assumption may be violated if measures are taken in the seated position, especially in people with a high waist circumference (WC).

Aims: The aims of this research were to determine whether posture (supine, standing, and seated) and WC affect agreement between BIA and dual-energy X-ray absorptiometry (DXA) measures of fat mass (FM) and fat-free mass (FFM).

Two weeks of high-intensity interval training increases skeletal muscle mitochondrial respiration via complex-specific remodeling in sedentary humans.

Aerobic training remodels the quantity and quality (function per unit) of skeletal muscle mitochondria to promote substrate oxidation, however, there remain key gaps in understanding the underlying mechanisms during initial training adaptations. We used short-term high-intensity interval training (HIIT) to determine changes to mitochondrial respiration and regulatory pathways that occur early in remodeling. Fifteen normal-weight sedentary adults started seven sessions of HIIT over 14 days and 14 participants completed the intervention.

Impact of 4 weeks of western diet and aerobic exercise training on whole-body phenotype and skeletal muscle mitochondrial respiration in male and female mice.

High dietary fat intake induces significant whole-body and skeletal muscle adaptations in mice, including increased capacity for fat oxidation and mitochondrial biogenesis. The impact of a diet that is high in fat and simple sugars (i.e.

The Data Behind Popular Diets for Weight Loss.

Both scientific evidence and popular diet trends have sought to identify the ideal diet for weight loss with strategies focused on either restricting carbohydrates or fat. While there is a strong physiologic rationale for either carbohydrate restriction or fat restriction to achieve a calorie deficit needed for weight loss, evidence from randomized controlled trials suggest either type of diet is effective for weight loss. The level of adherence, rather than macronutrient content, is the driver of successful weight loss.

Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults.

Introduction: Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and nonlipid substrates. It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates.

Short-Term High-Fat Feeding Does Not Alter Mitochondrial Lipid Respiratory Capacity but Triggers Mitophagy Response in Skeletal Muscle of Mice.

Lipid overload of the mitochondria is linked to the development of insulin resistance in skeletal muscle which may be a contributing factor to the progression of type 2 diabetes during obesity. The targeted degradation of mitochondria through autophagy, termed mitophagy, contributes to the mitochondrial adaptive response to changes in dietary fat. Our previous work demonstrates long-term (2-4 months) consumption of a high-fat diet increases mitochondrial lipid oxidation capacity but does not alter markers of mitophagy in mice.

Skeletal Muscle ACSL Isoforms Relate to Measures of Fat Metabolism in Humans.

Introduction: Evidence from model systems implicates long-chain acyl-coenzyme A synthetase (ACSL) as key regulators of skeletal muscle fat oxidation and fat storage; however, such roles remain underexplored in humans.

Purpose: We sought to determine the protein expression of ACSL isoforms in skeletal muscle at rest and in response to acute exercise and identify relationships between skeletal muscle ACSL and measures of fat metabolism in humans.

Methods: Sedentary adults (n = 14 [4 males and 10 females], body mass index = 22.

Mitochondrial adaptations to exercise do not require Bcl2-mediated autophagy but occur with BNIP3/Parkin activation.

Understanding the mechanisms regulating mitochondrial respiratory function and adaptations to metabolic challenges, such as exercise and high dietary fat, is necessary to promote skeletal muscle health and attenuate metabolic disease. Autophagy is a constitutively active degradation pathway that promotes mitochondrial turnover and transiently increases postexercise. Recent evidence indicates Bcl2 mediates exercise-induced autophagy and skeletal muscle adaptions to training during high-fat diet.

Diet and Exercise Training Influence Skeletal Muscle Long-Chain acyl-CoA Synthetases.

Introduction: Long-chain acyl-CoA synthetases (ACSL) are implicated as regulators of oxidation and storage of fatty acids within skeletal muscle; however, to what extent diet and exercise alter skeletal muscle ACSL remains poorly understood.

Purpose: This study aimed to determine the effects of diet and exercise training on skeletal muscle ACSL and to examine relationships between ACSL1 and ACSL6 and fat oxidation and fat storage, respectively.

Methods: Male C57BL/6J mice consumed a 60% high-fat diet (HFD) for 12 wk to induce obesity compared with low-fat diet (LFD).

Treatment with Nitrate, but Not Nitrite, Lowers the Oxygen Cost of Exercise and Decreases Glycolytic Intermediates While Increasing Fatty Acid Metabolites in Exercised Zebrafish.

Background: Dietary nitrate improves exercise performance by reducing the oxygen cost of exercise, although the mechanisms responsible are not fully understood.

Objectives: We tested the hypothesis that nitrate and nitrite treatment would lower the oxygen cost of exercise by improving mitochondrial function and stimulating changes in the availability of metabolic fuels for energy production.

Methods: We treated 9-mo-old zebrafish with nitrate (sodium nitrate, 606.

Robust intrinsic differences in mitochondrial respiration and HO emission between L6 and C2C12 cells.

Rat L6 and mouse C2C12 cell lines are commonly used to investigate myocellular metabolism. Mitochondrial characteristics of these cell lines remain poorly understood despite mitochondria being implicated in the development of various metabolic diseases. To address this need, we performed high-resolution respirometry to determine rates of oxygen consumption and HO emission in suspended myoblasts during multiple substrate-uncoupler-inhibitor titration protocols.

Insulin-stimulated Rac1-GTP binding is not impaired by palmitate treatment in L6 myotubes.

Ras-related C3 botulinum toxin substrate 1 (Rac1) is required for normal insulin-stimulated glucose transport in skeletal muscle and evidence indicates Rac1 may be negatively regulated by lipids. We investigated if insulin-stimulated activation of Rac1 (i.e.

Skeletal muscle autophagy remains responsive to hyperinsulinemia and hyperglycemia at higher plasma insulin concentrations in insulin-resistant mice.

Skeletal muscle autophagy is suppressed by insulin, but it is not clear if such suppression is altered with insulin resistance. We investigated if the inhibitory action of insulin on autophagy remains intact despite insulin resistance to glucose metabolism. C57BL/6J mice consumed either a low-fat (10% fat) diet as control or high-fat (60% fat) diet for 12 weeks to induce insulin resistance.

Differential effects of vitamin C or protandim on skeletal muscle adaptation to exercise.

Maintaining proteostasis is a key mechanism for preserving cell function. Exercise-stimulated proteostasis is regulated, in part, by redox-sensitive signaling. Several studies suggest that supplementation with exogenous antioxidants blunts exercise-induced cellular adaptations, although this conclusion lacks consensus.

Remodeling of skeletal muscle mitochondrial proteome with high-fat diet involves greater changes to β-oxidation than electron transfer proteins in mice.

Excess fat intake can increase lipid oxidation and expression of mitochondrial proteins, indicating remodeling of the mitochondrial proteome. Yet intermediates of lipid oxidation also accumulate, indicating a relative insufficiency to completely oxidize lipids. We investigated remodeling of the mitochondrial proteome to determine mechanisms of changes in lipid oxidation following high-fat feeding.

Long-term rates of mitochondrial protein synthesis are increased in mouse skeletal muscle with high-fat feeding regardless of insulin-sensitizing treatment.

Skeletal muscle mitochondrial protein synthesis is regulated in part by insulin. The development of insulin resistance with diet-induced obesity may therefore contribute to impairments to protein synthesis and decreased mitochondrial respiration. Yet the impact of diet-induced obesity and insulin resistance on mitochondrial energetics is controversial, with reports varying from decreases to increases in mitochondrial respiration.

Assessment of protein synthesis in highly aerobic canine species at the onset and during exercise training.

Canis lupus familiaris, the domesticated dog, is capable of extreme endurance performance. The ability to perform sustained aerobic exercise is dependent on a well-developed mitochondrial reticulum. In this study we examined the cumulative muscle protein and DNA synthesis in groups of athletic dogs at the onset of an exercise training program and following a strenuous exercise training program.