Applied Physiology, Nutrition, and Metabolism最新文献

The ability to rapidly generate muscular torque and velocity is important in specialized activities and daily tasks of living. Tendon stiffness is one factor in the neuromuscular system that influences musculoskeletal torque transmission. Previous studies have reported weak-to-moderate correlations between tendon stiffness and rate of torque development (RTD). However, these correlations have been reported only for isometric contractions, which may not be relevant to contractions involving joint rotation (i.e., dynamic). The purpose was to investigate the effect of calcaneal tendon stiffness on the dynamic RTD and rate of velocity development (RVD) in plantar flexor muscles. Young adult males (n = 13) and females (n = 2) performed prone isometric- and isotonic-mode maximal voluntary plantar flexion contractions (MVC). Ultrasound imaging was used to quantify tendon morphological characteristics to estimate Young's elastic modulus (YM). Maximal voluntary and electrically evoked (300 Hz) isometric- and isotonic-mode (at 10% and 40% MVC loads) contractions were evaluated for RTD and RVD through a 25° ankle joint range of motion. YM was correlated with isometric RTD, but only for evoked contractions (RTD_0-50 ms: r = 0.54, p = 0.02, RTD_0-200 ms: r = 0.62, p = 0.01). Conversely, YM was not correlated with dynamic RTD (voluntary: r = -0.07-0.41, p = 0.06-0.40, evoked: r = -0.2-0.3, p = 0.14-0.24) nor RVD (voluntary: r = -0.08-0.24, p = 0.27-0.40, evoked: r = 0.12-0.3, p = 0.14-0.34). These correlations would indicate that calcaneal tendon stiffness is an important factor for rapid isometric torque development, but less so for isotonic contractions. The determinants of dynamic contractile rates are more complex and warrant further study.

Patients with cystic fibrosis (CF) are at high risk of fat-soluble vitamin deficiencies, even with supplementation. The contribution of a suboptimal vitamin K status to respiratory and endocrine pathophysiology in CF has been inadequately characterized. This is a cross-sectional study in adult CF patients (≥18 years old) from the Montreal Cystic Fibrosis Cohort. Vitamin K₁ (VK1) was measured with high-performance liquid chromatography, using fasted serum samples collected during an oral glucose tolerance test (OGTT: 2 h with plasma glucose and insulin every 30 min) (n = 168). Patients were categorized according to VK1 status (suboptimal defined as <0.30 nmol/L). Suboptimal VK1 levels were observed in 66% of patients. Patients with a suboptimal VK1 status have a higher risk of colonization with Pseudomonas aeruginosa (p = 0.001), have lower body mass index (BMI) (p = 0.003), and were more likely to have exocrine pancreatic insufficiency (p = 0.002). Using an established threshold for VK1, we did show significantly reduced OGTT-derived measures of insulin secretion in patients with a VK1 status below 0.30 nmol/L (first- and second-phase area under the curve (AUC)_INS/GLU (p = 0.002 and p = 0.006), AUC_INS (p = 0.012) and AUC_INS/GLU (p = 0.004)). Subclinical vitamin K deficiency is more common than other fat-soluble vitamin deficiencies in patients with CF. We demonstrate an association between a suboptimal VK1 status and measures of insulin secretion. We highlight the potential associations of mild vitamin K deficiency with pseudomonal colonization and lower BMI, although these need to be validated in prospective studies.

This paper examines the opinion that we should aim to optimize, rather than maximize, protein intakes to avoid over-emphasizing muscle-centric protein requirements. An optimal eating approach strives to minimize amino acid oxidative waste and more efficiently stimulate postprandial muscle protein accretion. To do this, practitioners should acknowledge higher quality protein foods as better in delivering target amounts of amino acids into circulation, and the food matrix (e.g., nutrient-nutrient interactions) can be leveraged to potentiate essential amino acid incorporation into skeletal muscle protein.

Human milk is the ideal source of nutrition for infants; however, adherence to breastfeeding recommendations is suboptimal and availability of Canadian breastfeeding data are limited. Using the 2017-2018 Canadian Community Health Survey Public Use Microdata File (Maternal Experiences Module, n = 5558, weighted n = 1 669 462) we computed breastfeeding indicators and explored sociodemographic, health, and geographical predictors of breastfeeding with univariate logistic regression models. Nationally, of all participants who gave birth in the preceding 5 years, 91% initiated breastfeeding, 43% exclusively breastfed to ≥5 months and 35% to ≥6 months, 56% reported any breastfeeding at ≥6 months, and 31% reported breastfeeding at ≥12 months. Breastfeeding cessation was most commonly attributed to insufficient milk supply (25%), but reasons differed significantly by breastfeeding duration. Breastfeeding initiation, exclusivity for ≥5 months, and extended breastfeeding ≥12 months all differed by geographic region, and by most sociodemographic and health characteristics. Positive breastfeeding outcomes were highest in British Columbia, and lowest in Quebec and the Atlantic region, and generally higher if caregivers had recently immigrated to Canada, were married, were >30 years of age, were not White, were nonsmoking, had completed postsecondary education, and had an annual household income >$40 000. These disparities indicate the need for tailored, equitable approaches to breastfeeding support, and continued regional monitoring of breastfeeding outcomes.

Mechanistic target of rapamycin complex 1 (mTORC1) is a protein complex that regulates skeletal muscle protein synthesis and hypertrophy. mTORC1-mediated signaling activities are activated during denervation-induced skeletal muscle atrophy and suppressed during calorie restriction-induced atrophy. Mitochondria control the qualitative plasticity of skeletal muscles primarily through biogenesis, fusion, and fission. We recently showed that mTORC1 activation contributes toward mitochondrial homeostasis. In this study, we examined the role of mTORC1 in mitochondrial adaptation during denervation- or calorie restriction-induced skeletal muscle atrophy. Seven-week-old Institute of Cancer Research mice were subjected to 14 days of denervation or calorie restriction combined with the administration of the mTORC1 inhibitor-"rapamycin". Our results showed that although mTORC1 inhibition did not alter mitochondrial biogenesis, content and enzyme activity, it suppressed the activation of dynamin-related protein 1 (DRP1), a mitochondrial fission-related protein in denervated muscle, and reduced DRP1 expression in calorie-restricted muscle. Furthermore, calorie restriction-induced mitochondrial fragmentation was partially suppressed by mTORC1 inhibition. Taken together, our results indicate that mTORC1 activation upon denervation and inhibition upon calorie restriction contributes to qualitative changes in muscle plasticity by at least partially regulating the mitochondrial fission response.

Secondary cardiovascular disease is the main cause of mortality in congenital heart disease (CHD) patients. The cardiovascular risk could be widely prevented with adherence to a healthy lifestyle; however, clusters of lifestyle behaviors related to atherosclerosis risk factors in children and adolescents with CHD remain unclear. We aimed to describe the clusters of lifestyle behaviors of children and adolescents with CHD and to evaluate their association with atherosclerosis risk factors. We conducted a cross-sectional study on 227 children and adolescents with CHD (median age:10.02 [IQR:7.08-13.02] years). Dietary intake, physical activity (PA), and sedentary behavior (SB) were evaluated. Clusters of lifestyle behaviors were determined using a two-step cluster analysis. Atherosclerosis risk factors evaluated include body fat mass, central obesity, blood pressure, lipid parameters, glucose, C-reactive protein, and carotid intima-media thickness (cIMT). Multiple logistic regressions were used. The "unhealthy: high SB + low PA" cluster was associated with elevated body fat mass, central obesity, and elevated cIMT. Furthermore, the "unhealthy: low PA + unhealthy eating habits" cluster was associated with elevated body fat mass, central obesity, and elevated glucose. The unhealthier lifestyle behavior clusters were associated with atherosclerosis risk factors in children and adolescents with CHD. Multidisciplinary strategies to promote healthy behaviors are needed to prevent cardiovascular disease in later life.

Apnea (breath-holding) elicits co-activation of sympathetic and parasympathetic nervous systems, affecting cardiac control. In situations of autonomic co-activation (e.g., cold water immersion), cardiac arrhythmias are observed during apnea. Chronic endurance training reduces resting heart rate in part via elevation in parasympathetic tone, and has been identified as a risk factor for development of arrhythmias. However, few studies have investigated autonomic control of the heart in trained athletes during stress. Therefore, we determined whether heightened vagal tone resulting from endurance training promotes a higher incidence of arrhythmia during apnea. We assessed the heart rate, rhythm (ECG lead II), and cardiac inotropic (speckle-tracking echocardiography) response to apnea in 10 endurance trained and 7 untrained participants. Participants performed an apnea at rest and following sympathetic activation using post-exercise circulatory occlusion (PECO). All apneas were performed prior to control (CON) and following vagal block using glycopyrrolate (GLY). Trained participants had lower heart rates at rest (p = 0.03) and during apneas (p = 0.009) under CON. At rest, 3 trained participants exhibited instances of junctional rhythm and 4 trained participants developed ectopy during CON apneas, whereas 3 untrained participants developed ectopic beats only with concurrent sympathetic activation (PECO). Following GLY, no arrhythmias were noted in either group. Vagal block also revealed increased cardiac chronotropy (heart rate) and inotropy (strain rate) during apnea, demonstrating a greater sympathetic influence in the absence of parasympathetic drive. Our results highlight that endurance athletes may be more susceptible to ectopy via elevated vagal tone, whereas untrained participants may only develop ectopy through autonomic conflict.

We evaluated effects of calorie restriction (CR; consuming 65% of ad libitum (AL) intake) for 8 weeks on female wildtype (WT) and Akt substrate of 160 kDa knockout (AS160-KO) rats. Insulin-stimulated glucose uptake (ISGU) was determined in isolated epitrochlearis muscles incubated with 0, 50, 100, or 500 µU/mL insulin. Phosphorylation of key insulin signaling proteins that control ISGU (Akt and AS160) was assessed by immunoblotting (Akt phosphorylation on Threonine-308, pAkt^Thr308 and Serine-473, pAkt^Ser473; AS160 phosphorylation on Serine-588, pAS160^Ser588, and Threonine-642, pAS160^Thr642). Abundance of proteins that regulate ISGU (GLUT4 glucose transporter protein and hexokinase II) was also determined by immunoblotting. The major results were as follows: (i) WT-CR versus WT-AL rats had greater ISGU with 100 and 500 µU/mL insulin; (ii) CR versus WT-AL rats had greater GLUT4 protein abundance; (iii) WT-CR versus WT-AL rats had greater pAkt^Thr308 with 500 µU/mL insulin; (iv) WT-CR versus WT-AL rats did not differ for pAkt^Ser473, pAS160^Ser588, or pAS160^Thr642 at any insulin concentration; (v) AS160-KO versus WT rats with each diet had lower ISGU at each insulin concentration, but not lower pAkt on either phosphosite; (vi) AS160-KO versus WT rats had lower muscle GLUT4 abundance regardless of diet; and (vii) AS160-KO-CR versus AS160-KO-AL rats did not differ for ISGU, GLUT4 abundance, pAkt on either phosphosite, or pAS160 on either phosphosite. These novel results demonstrated that AS160 expression, but not greater pAS160 on key phosphosites, was essential for the CR-induced increases in muscle ISGU and GLUT4 abundance of female rats.

Acute exercise can result in temporary decrease in endothelial functions, which may represent a transient period of risk. Numerous mechanisms underpinning these responses included release of extracellular vesicles (EVs) derived from apoptotic or activated endothelial cells and platelets. This study aims to compare the time course of endothelial responses to moderate-intensity continuous exercise (MICE) and high-intensity interval exercise (HIIE) and the associations with EV release. Eighteen young healthy males (age: 22.6 ± 3.7 years, BMI: 25.6 ± 2.5 m²/kg, and VO_2peak: 38.6 ± 6.5 mL/kg/min) completed two randomly assigned exercises: HIIE (10 × 1 min-@-90% heart rate reserve (HRR) and 1 min passive recovery) and MICE (30 min-@-70% HRR) on a cycle ergometer. Flow-mediated dilation (FMD) was used to assess endothelial function and blood samples were collected to evaluate endothelial cell-derived EV (CD62E⁺) and platelet-derived EV (CD41a⁺), 10, 60, and 120 min before and after exercise. There were similar increases but different time courses (P = 0.017) in FMD (increased 10 min post-HIIE, P < 0.0001 and 60 min post-MICE, P = 0.038). CD62E⁺ remained unchanged (P = 0.530), whereas overall CD41a⁺ release was reduced 60 min post-exercise (P = 0.040). FMD was not associated with EV absolute release or change (P > 0.05). Acute exercise resulted in similar improvements, but different time course in FMD following either exercise. Whilst EVs were not associated with FMD, the reduction in platelet-derived EVs may represent a protective mechanism following acute exercise.