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The time spent in sedentary behaviour represents an important public health burden. To reduce sedentary time in the general population, the simplest, most effective, and most accessible method is to decrease lying and sitting time. We aimed to compare differences on energy expenditure (EE) across lying, sitting, and standing positions; and to analyse the associations between the change on EE of changing from one position to another and anthropometric and body composition parameters in young healthy adults. A total of 55 (69% women) young healthy adults aged 21.7 ± 2.2 participated in the study. We measured EE by indirect calorimetry across lying, sitting, and standing positions following the standard procedures. The EE was significantly higher in standing than in both lying and sitting positions (mean difference: 0.121±0.292 and 0.125±0.241 kcal/min, respectively; all P<0.001), and no differences were observed between lying and sitting positions (P = 1.000). There was a negative association between the EE differences in sitting vs. standing position and lean body mass (P = 0.048), yet no associations between EE differences with the rest of the anthropometric and body composition parameters were observed in each position pair studied (all P>0.321). Our findings support the fact that increasing the time spent standing could be a simple strategy to slightly increase EE. Therefore, our results have important clinical implications including a better monitoring, characterizing, and promoting countermeasures to sedentariness through low-level physical activities. [ABSTRACT FROM AUTHOR]

Background: Exercise performed in a postprandial state does not increase 24-h fat oxidation of male and female subjects. Conversely, it has been shown in male subjects that exercise performed in a postabsorptive state increases 24-h fat oxidation compared with that in sedentary control and that with exercise trials performed after breakfast, lunch, or dinner. There is a paucity of study evaluating the effect of exercise performed in a postabsorptive state in female subjects. Method: Nine young female subjects participated in indirect calorimetry measurement over 24-h using a room-size metabolic chamber in which subjects remained sedentary or performed 60 min exercise before breakfast at 50% of . Exercise was accompanied by an increase in energy intake to ensure that subjects were in a similar state of energy balance over 24 h for the two trials. Findings: Compared with the sedentary condition, exercise performed before breakfast increased 24-h fat oxidation (519 ± 37 vs. 400 ± 41 kcal/day). Time courses of relative energy balance differed between trials with transient negative energy balance observed before breakfast. The lowest values of relative energy balance observed during the 24-h calorimetry, i.e., transient energy deficit, were greater in exercise trials than in sedentary trials. The transient deficit in carbohydrate balance was also observed before breakfast, and magnitude of the deficit was greater in exercise trial compared to that of sedentary trial. Interpretation: Under energy-balanced conditions, exercise performed in a post-absorptive state increases 24-h fat oxidation in female subjects. The effect of exercise performed before breakfast can be attributed to nutritional state: a transient deficit in energy and carbohydrate at the end of exercise. [ABSTRACT FROM AUTHOR]

The aim of the present work was to further explore the physiological roles of muscle-derived IL-6. Adult-floxed and conditional skeletal muscle IL-6 knock out male and female mice were used to study energy expenditure (indirect calorimetry at rest and during treadmill exercise, and body temperature cycle during the light phase) and energy intake (response to fast/refeeding). We also evaluated the responses to leptin and the activity of the insulin signalling pathway in skeletal muscle and liver by phosphorylation of Akt at Ser 473. The stress response was also studied. Results indicate a relevant role of muscle IL-6 in maintaining energy homeostasis, especially in males. Absence of muscle IL-6 in male mice results in lower core body temperature in the light phase, increased respiratory exchange ratio (RER) both at rest and during exercise, increased expression of TCA cycle marked gene, citrate synthase in muscle, reduced fat storage and decreased body weight and food consumption in response to leptin. In females, muscle IL-6 deficiency increases VO2 and CO2 levels similarly. Also in contrast to males, energy expenditure (EE) measured over 48h reveals a significant elevation in female mice with muscle IL-6 deficiency; moreover, they show a modified response to fasting-refeeding and to restraint stress. The present results contribute to the understanding of the role of muscle IL-6 in male and female mouse metabolism, not only during exercise but also in the basal state and in situations where energy balance is altered. [ABSTRACT FROM AUTHOR]

Wearable physical activity monitors are growing in popularity and provide the opportunity for large numbers of the public to self-monitor physical activity behaviours. The latest generation of these devices feature multiple sensors, ostensibly similar or even superior to advanced research instruments. However, little is known about the accuracy of their energy expenditure estimates. Here, we assessed their performance against criterion measurements in both controlled laboratory conditions (simulated activities of daily living and structured exercise) and over a 24 hour period in free-living conditions. Thirty men (n = 15) and women (n = 15) wore three multi-sensor consumer monitors (Microsoft Band, Apple Watch and Fitbit Charge HR), an accelerometry-only device as a comparison (Jawbone UP24) and validated research-grade multi-sensor devices (BodyMedia Core and individually calibrated Actiheart™). During discrete laboratory activities when compared against indirect calorimetry, the Apple Watch performed similarly to criterion measures. The Fitbit Charge HR was less consistent at measurement of discrete activities, but produced similar free-living estimates to the Apple Watch. Both these devices underestimated free-living energy expenditure (-394 kcal/d and -405 kcal/d, respectively; P<0.01). The multi-sensor Microsoft Band and accelerometry-only Jawbone UP24 devices underestimated most laboratory activities and substantially underestimated free-living expenditure (-1128 kcal/d and -998 kcal/d, respectively; P<0.01). None of the consumer devices were deemed equivalent to the reference method for daily energy expenditure. For all devices, there was a tendency for negative bias with greater daily energy expenditure. No consumer monitors performed as well as the research-grade devices although in some (but not all) cases, estimates were close to criterion measurements. Thus, whilst industry-led innovation has improved the accuracy of consumer monitors, these devices are not yet equivalent to the best research-grade devices or indeed equivalent to each other. We propose independent quality standards and/or accuracy ratings for consumer devices are required. [ABSTRACT FROM AUTHOR]

Background: Wrist-worn monitors claim to provide accurate measures of heart rate and energy expenditure. People wishing to lose weight use these devices to monitor energy balance, however the accuracy of these devices to measure such parameters has not been established. Aim: To determine the accuracy of four wrist-worn devices (Apple Watch, Fitbit Charge HR, Samsung Gear S and Mio Alpha) to measure heart rate and energy expenditure at rest and during exercise. Methods: Twenty-two healthy volunteers (50% female; aged 24 ± 5.6 years) completed ~1-hr protocols involving supine and seated rest, walking and running on a treadmill and cycling on an ergometer. Data from the devices collected during the protocol were compared with reference methods: electrocardiography (heart rate) and indirect calorimetry (energy expenditure). Results: None of the devices performed significantly better overall, however heart rate was consistently more accurate than energy expenditure across all four devices. Correlations between the devices and reference methods were moderate to strong for heart rate (0.67–0.95 [0.35 to 0.98]) and weak to strong for energy expenditure (0.16–0.86 [-0.25 to 0.95]). All devices underestimated both outcomes compared to reference methods. The percentage error for heart rate was small across the devices (range: 1–9%) but greater for energy expenditure (9–43%). Similarly, limits of agreement were considerably narrower for heart rate (ranging from -27.3 to 13.1 bpm) than energy expenditure (ranging from -266.7 to 65.7 kcals) across devices. Conclusion: These devices accurately measure heart rate. However, estimates of energy expenditure are poor and would have implications for people using these devices for weight loss. [ABSTRACT FROM AUTHOR]

Facioscapulohumeral muscular dystrophy (FSHD) is caused by mutations leading to ectopic expression of the transcription factor DUX4, and encompasses both muscle-related and non-muscle phenotypes. Mouse models bearing this gene represent valuable tools to investigate which pathologies are due to DUX4 expression, and how DUX4 leads to these pathologies. The iDUX4(2.7) mouse contains an X-linked doxycycline-inducible DUX4 gene that shows low level basal expression in the absence of doxycycline, leading to male lethality, generally in embryo, but always before 8 weeks of age. Here, we describe additional non-muscle phenotypes in this animal model. We find that iDUX4(2.7) female carriers are extremely hyperactive, spending large amounts of time ambulating and much less time resting. Rare 3-week old males, although hypophagic, runted and extremely fragile, are capable of high activity, but show periods of catatonic torpor in which animals appear dead and respiration is virtually absent. We also examine a non-muscle phenotype of interest to FSHD, high frequency hearing loss. We find that young iDUX4(2.7) females are significantly impaired in their ability to hear at frequencies above 8 kHz. These phenotypes make the iDUX4(2.7) mouse an attractive model in which to study non-muscle activities of DUX4. [ABSTRACT FROM AUTHOR]

The current study extends previously reported PPARα agonist WY 14,643 (30 µmol/kg/day for 4 weeks) effects on circulating amino acid concentrations in rats fed a 48% saturated fat diet. Steady-state tracer experiments were used to examine in vivo kinetic mechanisms underlying altered plasma serine, glycine and arginine levels. Urinary urea and creatinine excretion were measured to assess whole-body amino acid catabolism. WY 14,643 treated animals demonstrated reduced efficiency to convert food consumed to body weight gain while liver weight was increased compared to controls. WY 14,643 raised total amino acid concentration (38%), largely explained by glycine, serine and threonine increases. 3H-glycine, 14C-serine and 14C-arginine tracer studies revealed elevated rates of appearance (Ra) for glycine (45.5±5.8 versus 17.4±2.7 µmol/kg/min) and serine (21.0±1.4 versus 12.0±1.0) in WY 14,643 versus control. Arginine was substantially decreased (−62%) in plasma with estimated Ra reduced from 3.1±0.3 to 1.2±0.2 µmol/kg/min in control versus WY 14,643. Nitrogen excretion over 24 hours was unaltered. Hepatic arginase activity was substantially decreased by WY 14,643 treatment. In conclusion, PPARα agonism potently alters metabolism of several specific amino acids in the rat. The changes in circulating levels of serine, glycine and arginine reflected altered fluxes into the plasma rather than changes in clearance or catabolism. This suggests that PPARα has an important role in modulating serine, glycine and arginine de novo synthesis. [ABSTRACT FROM AUTHOR]

Introduction: Mitochondrial dysfunction, lipid accumulation, insulin resistance and metabolic inflexibility have been implicated in the etiology of type 2 diabetes (T2D), yet their interrelationship remains speculative. We investigated these interrelationships in a group of T2D and obese normoglycemic control subjects. Methods: 49 non-insulin dependent male T2D patients and 54 male control subjects were enrolled, and a hyperinsulinemic-euglycemic clamp and indirect calorimetry were performed. A muscle biopsy was taken and intramyocellular lipid (IMCL) was measured. In vivo mitochondrial function was measured by PCr recovery in 30 T2D patients and 31 control subjects. Results: Fasting NEFA levels were significantly elevated in T2D patients compared with controls, but IMCL was not different. Mitochondrial function in T2D patients was compromised by 12.5% (p<0.01). Whole body glucose disposal (WGD) was higher at baseline and lower after insulin stimulation. Metabolic flexibility (ΔRER) was lower in the type 2 diabetic patients (0.050±0.033 vs. 0.093±0.050, p<0.01). Mitochondrial function was the sole predictor of basal respiratory exchange ratio (RER) (R2 = 0.18, p<0.05); whereas WGD predicted both insulin-stimulated RER (R2 = 0.29, p<0.001) and metabolic flexibility (R2 = 0.40, p<0.001). Conclusions: These results indicate that defects in skeletal muscle in vivo mitochondrial function in type 2 diabetic patients are only reflected in basal substrate oxidation and highlight the importance of glucose disposal rate as a determinant of substrate utilization in response to insulin. [ABSTRACT FROM AUTHOR]