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OBJECTIVES: Traditional jumping-dance rituals performed by Maasai men involve prolonged physical exertion that may contribute significantly to overall physical activity level. We aimed to objectively quantify the metabolic intensity of jumping-dance activity and assess associations with habitual physical activity and cardiorespiratory fitness (CRF).METHODS: Twenty Maasai men (18-37 years) from rural Tanzania volunteered to participate in the study. Habitual physical activity was monitored using combined heart rate (HR) and movement sensing over 3 days, and jumping-dance engagement was self-reported. A 1-h jumping-dance session resembling a traditional ritual was organized, during which participants' vertical acceleration and HR were monitored. An incremental, submaximal 8-min step test was performed to calibrate HR to physical activity energy expenditure (PAEE) and assess CRF.RESULTS: Mean (range) habitual PAEE was 60 (37-116) kJ day -1 kg -1 , and CRF was 43 (32-54) mL O 2 min -1 kg -1 . The jumping-dance activity was performed at an absolute HR of 122 (83-169) beats·min -1 , and PAEE of 283 (84-484) J min -1 kg -1 or 42 (18-75)% when expressed relative to CRF. The total PAEE for the session was 17 (range 5-29) kJ kg -1 , ~28% of the daily total. Self-reported engagement in habitual jumping-dance frequency was 3.8 (1-7) sessions/week, with a total duration of 2.1 (0.5-6.0) h/session. CONCLUSIONS: Intensity during traditional jumping-dance activity was moderate, but on average sevenfold higher than habitual physical activity. These rituals are common, and can make a substantial contribution to overall physical activity in Maasai men, and thus be promoted as a culture-specific activity to increase energy expenditure and maintain good health in this population.

It has recently been established that myosin, the molecular motor protein, is able to exist in two conformations in relaxed skeletal muscle. These conformations are known as the super-relaxed (SRX) and disordered-relaxed (DRX) states and are finely balanced to optimize ATP consumption and skeletal muscle metabolism. Indeed, SRX myosins are thought to have a 5- to 10-fold reduction in ATP turnover compared with DRX myosins. Here, we investigated whether chronic physical activity in humans would be associated with changes in the proportions of SRX and DRX skeletal myosins. For that, we isolated muscle fibers from young men of various physical activity levels (sedentary, moderately physically active, endurance-trained, and strength-trained athletes) and ran a loaded Mant-ATP chase protocol. We observed that in moderately physically active individuals, the amount of myosin molecules in the SRX state in type II muscle fibers was significantly greater than in age-matched sedentary individuals. In parallel, we did not find any difference in the proportions of SRX and DRX myosins in myofibers between highly endurance- and strength-trained athletes. We did however observe changes in their ATP turnover time. Altogether, these results indicate that physical activity level and training type can influence the resting skeletal muscle myosin dynamics. Our findings also emphasize that environmental stimuli such as exercise have the potential to rewire the molecular metabolism of human skeletal muscle through myosin.

Maximal fat oxidation during exercise (MFO) and the intensity that elicits MFO (Fatmax) seems to show a diurnal variation in men, which favours an increased performance in the afternoon than the morning. At present, it remains unknown whether the observed MFO and Fatmax diurnal variation in men is also present in women. Therefore, the current study examined the diurnal variations of MFO and Fatmax in women. Nineteen healthy women (age: 26.9 ± 8.7 years, maximum oxygen uptake: 39.8 ± 6.5 ml/kg/min) participated in the study. MFO and Fatmax were determined by a graded exercise test in cycloergometer using a cross-over design performed on two separate daytime schedules, one conducted in the morning (8am–11am) and one in the afternoon (5pm–8pm). Stoichiometric equations were used to calculate fat oxidation rates. There were no significant differences between MFO-morning and MFO-afternoon (0.24 ± 0.10 vs. 0.23 ± 0.07 g/min, respectively; P = 0.681). Similarly, there was no significant differences between Fatmax-morning and Fatmax-afternoon (41.1 ± 4.7 vs. 42.6 ± 5.5% of maximal oxygen uptake, respectively; P = 0.305). These results persisted after controlling for fat mass percentage (all P > 0.5). In summary, the main finding of the present study was that MFO and Fatmax were similar independent of the time-of-day when the exercise test is performed in healthy women. These results have important clinical implications since they suggest that, in contrast to what was found in men, MFO and Fatmax show similar rates during the course of the day in women. Highlights MFO and Fatmax were similar during the afternoon and morning in young healthy women. Our results suggest that, in women, it does not matter when endurance exercise is performed in term of fat metabolism during exercise.

Myalgia and new-onset of type 2 diabetes have been associated with statin treatment, which both could be linked to reduced coenzyme Q10 (CoQ10) in skeletal muscle and impaired mitochondrial function. Supplementation with CoQ10 focusing on levels of CoQ10 in skeletal muscle and mitochondrial function has not been investigated in patients treated with statins. To investigate whether concomitant administration of CoQ10 with statins increases the muscle CoQ10 levels and improves the mitochondrial function, and if changes in muscle CoQ10 levels correlate with changes in the intensity of myalgia. 37 men and women in simvastatin therapy with and without myalgia were randomized to receive 400 mg CoQ10 daily or matched placebo tablets for eight weeks. Muscle CoQ10 levels, mitochondrial respiratory capacity, mitochondrial content (using citrate synthase activity as a biomarker), and production of reactive oxygen species were measured before and after CoQ10 supplementation, and intensity of myalgia was determined using the 10 cm visual analogue scale. Muscle CoQ10 content and mitochondrial function were unaltered by CoQ10 supplementation. Individual changes in muscle CoQ10 levels were not correlated with changes in intensity of myalgia. CoQ10 supplementation had no effect on muscle CoQ10 levels or mitochondrial function and did not affect symptoms of myalgia.

The aim was to investigate if acute recombinant human erythropoietin (rHuEPO) injection had an effect on mitochondrial function and if exercise would have an additive effect. Furthermore, to investigate if in vitro incubation with rHuEPO had an effect on muscle mitochondrial respiratory capacity. Eight healthy young men were recruited for this double-blinded randomized placebocontrolled crossover study. rHuEPO (400 IU/kg body wt) or saline injection was given intravenously, before an acute bout of exercise. Resting metabolic rate and fat oxidation were measured. Biopsies were obtained at baseline, 120 min after injection, and right after the acute exercise bout. Mitochondrial function (mitochondrial respiration and H2O2 emission) was measured in permeabilized skeletal muscle using high-resolution respirometry and fluorometry. Specific gene expression and enzyme activity were measured. Skeletal muscle mitochondrial respiratory capacity was measured with and without incubation with rHuEPO. Fat oxidation at rest increased after rHuEPO injection, but no difference was found in fat oxidation during exercise. Mitochondrial respiratory capacity was increased after rHuEPO injection when pyruvate was in the assay, which was not the case when saline was injected. No changes were seen in H2O2 emission after rHuEPO injection or acute exercise. Incubation of skeletal muscle fibers in vitro with rHuEPO increased mitochondrial respiratory capacity. Acute rHuEPO injection increased mitochondrial respiratory capacity when pyruvate was used in the assay. No statistical difference was found in H2O2 emission capacity, although a numerical increase was seen after rHuEPO injection. In vitro incubation of the skeletal muscle sample with rHuEPO increases mitochondrial respiratory capacity.

Introduction: Assessment of maximal oxygen consumption (VO2max) is an important clinical tool when examining both healthy and unhealthy populations, as a low VO2max is associated with cardiovascular disease and all-cause mortality. Aim: This study investigated the accuracy of a non-exercise test for assessment of VO2max using seismocardiography (SCG). Methods: 97 participants (20-45 years, 50 males) underwent a nonexercise test using SCG at rest in the supine position (SCG VO2max) and a graded exercise test to voluntary exhaustion on a cycle ergometer with indirect calorimetry (IC VO2max). An interim analysis was applied after 50 participants had completed testing (SCG VO2max 1.0) allowing for the algorithm to be modified (SCG VO2max 2.1). Results: SCG VO2max 2.1 (n=47, test set) estimation was 3.5 pm 1.8 mlcdot min{-1}cdot kg{-1} (p < 0.001) lower compared to IC VO2max, with a Pearson correlation of r=0.65 (p < 0.0001) and a standard error of estimate of 7.1 ml·min-1 ·kg-1. The coefficient of variation between tests was 8 pm 1%. Conclusion: The accuracy of VO2max assessment using SCG requires further optimization prior to clinical application, as SCG VO2max was systematically lower than IC VO2max, and only a moderate correlation together with considerable variation were observed between tests.

The effect of oral glutathione (GSH) supplementation was studied in obese subjects with and without type 2 diabetes (T2DM) on measures of glucose homeostasis and markers of oxidative stress. Twenty subjects (10 patients with T2DM and 10 obese subjects) were recruited for the study, and randomized in a double-blinded placebo-controlled manner to consume either 1000 mg GSH per day or placebo for 3 weeks. Before and after the 3 weeks insulin sensitivity was measured with the hyperinsulinemic-euglycemic clamp and a muscle biopsy was obtained to measure GSH and skeletal muscle mitochondrial hydrogen peroxide (H2O2) emission rate. Whole body insulin sensitivity increased significantly in the GSH group. Skeletal muscle GSH was numerically increased (∼19%) in the GSH group; no change was seen in GSH to glutathione disulfide ratio. Skeletal muscle mitochondrial H2O2 emission rate did not change in response to the intervention and neither did the urinary excretion of the RNA oxidation product 8-oxo-7,8-dihydroguanosine or the DNA oxidation product 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), although 8-oxodG decreased as a main effect of time. Oral GSH supplementation improves insulin sensitivity in obese subjects with and without T2DM, although it does not alter markers of oxidative stress. The study has been registered in clinicaltrials.gov (NCT02948673). Novelty: Reduced glutathione supplementation increases insulin sensitivity in obese subjects with and without T2DM. H2O2 emission rate from skeletal muscle mitochondria was not affected by GSH supplementation.