Amy E. Mendham

A 12-week sports-based exercise programme for inactive Indigenous Australian men improved clinical risk factors associated with type 2 diabetes mellitus

OBJECTIVES This study assessed the effect of a 12-week sports-based exercise intervention on glucose regulation, anthropometry and inflammatory markers associated with the prevalence of type 2 diabetes mellitus (T2DM) in Indigenous Australian men. DESIGN Twenty-six inactive Indigenous Australian men (48.6±6.6 years) were randomized into exercise (n=16) or control (n=10)conditions. METHODS Training included ∼2-3 days/week for 12 weeks of sports and gym exercises in a group environment, whilst control participants maintained normal activity and dietary patterns. Pre- and post-intervention testing included: anthropometry, peak aerobic capacity, fasting blood chemistry of inflammatory cytokines, adiponectin, leptin, cholesterol, glucose, insulin and C-peptide. An oral glucose tolerance test measured glucose, insulin and C-peptide 30, 60, 90 and 120min post 75g glucose ingestion. RESULTS The exercise condition decreased insulin area under the curve (25±22%), increased estimated insulin sensitivity (35±62%) and decreased insulin resistance (9±35%; p<0.05), compared with control (p>0.05). The exercise condition decreased in body mass index, waist circumference and waist to hip ratio (p<0.05), compared to control (p>0.05). Leptin decreased in the exercise group, with no changes for adiponectin (p>0.05) or inflammatory markers (p>0.05) in either condition. Aerobic fitness variables showed significant increases in peak oxygen consumption for the exercise condition compared to no change in control (p>0.05). CONCLUSIONS Findings indicate positive clinical outcomes in metabolic, anthropometric and aerobic fitness variables. This study provides evidence for sport and group-based activities leading to improved clinical risk factors associated with T2DM development in clinically obese Indigenous Australian men.

Rugby-Specific Small-Sided Games Training Is an Effective Alternative to Stationary Cycling at Reducing Clinical Risk Factors Associated with the Development of Type 2 Diabetes: A Randomized, Controlled Trial

Introduction The present study investigated whether rugby small-sided games (SSG) could be an effective alternative to continuous stationary cycling (CYC) training at reducing clinical risk factors associated with the development of type 2 diabetes mellitus (T2DM). Methods Thirty-three middle-aged (48.6±6.6y), inactive men were randomized into a CYC (n=11), SSG (n=11), or control (CON, n=11) group. Participants trained 3d.wk-1 for 8 weeks, while control participants maintained normal activity and dietary patterns. Exercise duration was matched between groups, which involved CYC or SSG (four quarters, interspersed with 2-min passive recovery). Both training programs were designed to induce similar internal loads of maximal heart rate (~80-85%HRmax) and rating of perceived exertion. Pre- and post-intervention testing included dual-energy x-ray absorptiometry scan, graded exercise test, fasting 2h oral glucose tolerance test and resting muscle biopsy. Western blotting was used to assess the content of skeletal muscle proteins associated with mitochondrial biogenesis and glucose regulation. Results Both CYC and SSG increased VO2 at 80%HRmax, and reduced glycated haemoglobin, glucose area under the curve (AUC; SSG, -2.3±2.4; CYC -2.2±1.6 mmol.L1(120min)1; p<0.05), and total body fat-mass (SSG -2.6±0.9%; CYC -2.9±1.1%), compared to no change in CON (p<0.05). SSG reduced insulin AUC (-30.4±40.7 µlU.mL1(120min)1; p<0.05) and increased total body fat-free mass (1.1±1.2kg; p<0.05), with no change in CYC or CON (P>0.05). There were no differences within or between conditions for protein content of peroxisome proliferator-activated receptor gamma coactivator-1α, sirtuin-1, p53, glucose transporter-4, protein kinase AKT/PKB, myocyte enhancer factor 2A, mitochondrial transcription factor, nuclear respiratory factor (NRF)-1, NRF-2 or mitochondrial complexes I-V (p>0.05). Conclusion Rugby small-sided games is an effective alternative to continuous cycling for improving metabolic risk-factors associated with the prevention of T2DM. Despite such positive adaptations in clinical risk factors, there were no changes in the content of skeletal muscle proteins associated with glucose regulation and mitochondrial biogenesis. Trial Registration Australian New Zealand Clinical Trial Registry ACTRN12613000874718

Greater Effect of East versus West Travel on Jet Lag, Sleep, and Team Sport Performance

Purpose This study aimed to determine the recovery timeline of sleep, subjective jet lag and fatigue, and team sport physical performance after east and west long-haul travel. Methods Ten physically trained men underwent testing at 0900 h and 1700 h local time on four consecutive days 2 wk before outbound travel (BASE), and the first 4 d after 21 h of outbound (WEST) and return (EAST) air travel across eight time zones between Australia and Qatar. Data collection included performance (countermovement jump, 20-m sprint, and Yo-Yo intermittent recovery level 1 [YYIR1] test) and perceptual (jet lag, motivation, perceived exertion, and physical feeling) measures. In addition, sleep was measured via wrist activity monitors and self-report diaries throughout the aforementioned data collection periods. Results Compared with the corresponding day at BASE, the reduction in YYIR1 distance after EAST was significantly different from the increase in WEST on day 1 after travel (P < 0.001). On day 2, significantly slower 20-m sprint times were detected in EAST compared with WEST (P = 0.03), with large effect sizes (ES) also indicating a greater reduction in YYIR1 distance in EAST compared with WEST (d = 1.06). Mean sleep onset and offset were significantly later and mean time in bed and sleep duration were significantly reduced across the 4 d in EAST compared with BASE and WEST (P < 0.05). Lastly, mean jet lag, fatigue, and motivation ratings across the 4 d were significantly worse in EAST compared with BASE and WEST (P < 0.05) and WEST compared with BASE (P < 0.05). Conclusions Long-haul transmeridian travel can impede team sport physical performance. Specifically, east travel has a greater detrimental effect on sleep, subjective jet lag, fatigue, and motivation. Consequently, maximal and intermittent sprint performance is also reduced after east travel, particularly within 72 h after arrival.

Measurement of β-oxidation capacity of biological samples by respirometry: a review of principles and substrates.

Oxidation of fatty acids is a major source of energy in the heart, liver, and skeletal muscle. It can be measured accurately using respirometry in isolated mitochondria, intact cells, and permeabilized cells or tissues. This technique directly measures the rate of oxygen consumption or flux at various respiratory states when appropriate substrates, uncouplers, and inhibitors are used. Acylcarnitines such as palmitoylcarnitine or octanoylcarnitine are the commonly used substrates. The β-oxidation pathway is prone to feedforward inhibition resulting from accumulation of short-chain acyl-CoA and depletion of CoA, but inclusion of malate or carnitine prevents accumulation of these intermediaries and CoA depletion.

Review of a causal role of fructose-containing sugars in myocardial susceptibility to ischemia/reperfusion injury

In 2012, the World Health Organization Global Status Report on noncommunicable diseases showed that 7.4 million deaths were due to ischemic heart disease. Consequently, cardiovascular disease is a significant health burden, especially when partnered with comorbidities such as obesity, metabolic syndrome, and type 2 diabetes mellitus. Of note, these diseases can all be induced or exacerbated by diet. Carbohydrates, in particular, fructose and glucose, generally form the largest part of the human diet. Accumulating evidence from animal studies suggests that if large amounts of fructose are consumed either in isolation or in combination with glucose (fructose-containing sugars), myocardial susceptibility to ischemia/reperfusion (I/R) injury increases. However, the underlying mechanisms that predisposes the myocardium to I/R injury in the fructose model are not elucidated, and no single mechanistic pathway has been described. Based on all available data on this topic, this review describes previously investigated mechanisms and highlights 3 main mechanistic pathways whereby fructose has shown to increase myocardial susceptibility to I/R injury. These pathways include (1) increased reactive oxygen species, resulting in reduced nitric oxide synthase and coronary flow; (2) elevated plasma fatty acids and insulin, leading to increased cardiac triglyceride content and lipotoxicity; and (3) disrupted myocardial calcium handling/homeostasis. Moreover, we highlight various factors that should be taken into account when the fructose animal model is used, such as rat strain, treatment periods, and doses. We argue that failure to do so would result in erratic inferences drawn from the existing body of evidence on fructose animal models.

Differences in the acute inflammatory and glucose regulatory responses between small-sided games and cycling in sedentary, middle-aged men

OBJECTIVES This study compared the acute inflammatory and glucose regulatory response within and between rugby specific small-sided games and stationary cycling in sedentary, middle-aged Caucasian men. DESIGN Nine middle-aged, sedentary men who were free from disease participated in 2 × 40 min exercise conditions (stationary cycling and small-sided games) in a randomised, cross-over design. METHODS Heart rate and Rating of Perceived Exertion were collected during each bout. Venous blood was collected at fasting, 0, 30, 60 and 240 min post-exercise for measurement of glucose, insulin, cortisol and inflammatory markers including tumour necrosis factor-α, interleukin-1 β, interleukin-6, interleukin-1 receptor agonist and C-reactive protein. RESULTS No significant differences existed between conditions for heart rate and Rating of Perceived Exertion (p > 0.05). Interleukin-6 was increased immediately post-exercise in both conditions (p < 0.05), but greater in small-sided games at 240 min post-exercise compared with stationary cycling (p < 0.05). Glucose was lower in small-sided games than stationary cycling at 30 and 240 min post-exercise (p < 0.05). Interleukin-1 receptor agonist, insulin and cortisol showed an exercise-induced increase (p < 0.05), with no significant differences between conditions (p > 0.05). Results for C-reactive protein, tumour necrosis factor-α and interleukin-1 β showed no significant exercise-induced changes within or between conditions (p > 0.05). CONCLUSIONS Both small-sided games and stationary cycling conditions were sufficient to stimulate an acute anti-inflammatory response as indicated by the post-exercise elevation of interleukin-6, interleukin-1 receptor agonist and cortisol. The novel findings are that an acute bout of small-sided games bout is capable of maintaining an elevated post-exercise interleukin-6 response and lowered blood glucose concentration, compared with intensity- and duration-matched stationary cycling condition.

Similar mitochondrial signaling responses to a single bout of continuous or small-sided-games-based exercise in sedentary men

This study assessed the mitochondrial related signaling responses to a single bout of noncontact, modified football (touch rugby), played as small-sided games (SSG), or cycling (CYC) exercise in sedentary, obese, middle-aged men. In a randomized, crossover design, nine middle-aged, sedentary, obese men completed two, 40-min exercise conditions (CYC and SSG) separated by a 21-day recovery period. Heart rate (HR) and ratings of perceived exertion (RPE) were collected during each bout. Needle biopsies from the vastus lateralis muscle were collected at rest and 30 and 240 min postexercise for analysis of protein content and phosphorylation (PGC-1α, SIRT1, p53, p53Ser15, AMPK, AMPKThr172, CAMKII, CAMKIIThr286, p38MAPK, and p38MAPKThr180/Tyr182) and mRNA expression (PGC-1α, p53, NRF1, NRF2, Tfam, and cytochrome c). A main effect of time effect for both conditions was evident for HR, RPE, and blood lactate (P < 0.05), with no condition by time interaction (P > 0.05). Both conditions increased PGC1-α protein and mRNA expression at 240 min (P < 0.05). AMPKThr172 increased 30 min post CYC (P < 0.05), with no change in SSG (P > 0.05). CYC increased p53 protein content at 240 min to a greater extent than SSG (P < 0.05). mRNA expression of NRF2 decreased in both conditions (P < 0.05). No condition by time interactions were evident for mRNA expression of Tfam, NRF1, cytochrome c, and p53. The similar PGC-1α response between intensity-matched conditions suggests both conditions are of similar benefit for stimulating mitochondrial biogenesis. Differences between conditions regarding fluctuation in exercise intensity and type of muscle contraction may explain the increase of p53 and AMPK within CYC and not SSG (noncontact, modified football).

Differences in post-exercise inflammatory and glucose regulatory response between sedentary indigenous australian and caucasian men completing a single bout of cycling

This study compared the acute inflammatory and glucose responses following aerobic exercise in sedentary Indigenous Australian and Caucasian men, matched for fitness and body composition.

Exercise intervention alters HDL subclass distribution and function in obese women

BackgroundObesity is associated with a change in high-density lipoprotein (HDL) function and subclass. Exercise training reduces cardiovascular risk in obese patients. We aimed to explore the effect of an exercise training stimulus on HDL functionality and subclass in obese women.MethodsThirty-two obese black South African women were randomly assigned to exercise (combined aerobic and resistance exercise) or control (no exercise) conditions for 12-weeks. Pre- and post-testing included venous blood sampling for analysis of lipid profile and HDL functionality, by measuring cellular cholesterol efflux capacity, reduction in endothelial vascular cell adhesion molecule (VCAM) expression (anti-inflammatory function), paraoxonase (PON) (antioxidative function) and platelet activating factor acetylhydrolase (PAF-AH) activities (anti-thrombotic function). PON-1 and PAF-AH expression were determined in serum and in isolated HDL using Western blotting. Levels of large, intermediate and small HDL subclasses were measured using the Lipoprint® system.ResultsExercise training resulted in a decrease in body mass index (− 1.0 ± 0.5% vs + 1.2 ± 0.6%, p = 0.010), PON activity (− 8.7 ± 2.4% vs + 1.1 ± 3.0%, p = 0.021), PAF-AH serum expression (− 22.1 ± 8.0% vs + 16.9 ± 9.8, p = 0.002), and the distribution of small HDL subclasses (− 10.1 ± 5.4% vs + 15.7 ± 6.6%, p = 0.004) compared to controls. Exercise did not alter HDL cellular cholesterol efflux capacity and anti-inflammatory function.ConclusionsThese results demonstrate the potential for exercise training to modify HDL subclass distribution and HDL function in obese women.Trial registrationClinical trials number: PACTR201711002789113.

The Acute Exercise-Induced Inflammatory Response: A Comparison of Young-Adult Smokers and Nonsmokers

Purpose: This study examined postexercise inflammatory and leukocyte responses in smokers and nonsmokers, as well as the effects of cigarette smoking on the acute postexercise inflammatory and leukocyte response in habitual smokers. Method: Eleven recreationally active male smokers and 11 nonsmokers matched for age and aerobic fitness were familiarized and underwent baseline fitness testing. Participants then completed 40 min of cycling at 50% peak aerobic workload. Smokers performed 2 randomized exercise sessions, including an acute postexercise smoking condition (2 cigarettes in 15 min of 12 mg tar and 1 mg nicotine) and a no-smoking condition, while nonsmokers performed 1 exercise session without smoking. Venous blood was obtained preexercise and postexercise for analysis of interleukin (IL)-6, IL-1 receptor antagonist (ra), tumor necrosis factor-alpha (TNF-α), and c-reactive protein (CRP). Results: No differences existed between groups for resting CRP (d = 0.25–0.46; p = .374–.617). Despite no baseline difference (d = 0.03–0.07; p = .141–.70), exercise-induced increases were observed for IL-1 ra in smokers (d = 0.50; p = .024–.033), which was not observed in the never-smoker group. No between-group difference was observed for IL-6 across all points (d = 0.09–0.5; p = .102–.728); however, all groups observed significant within-group change (d = 0.27–1.09; p = .001–.042). Further, TNF-α for smokers smoking was elevated above both smokers not smoking and nonsmokers at baseline and across the protocol (d = 1.20–1.80; d = 0.20–1.0; p = .001–.035). Additionally, a marked postexercise increase in leukocyte and neutrophil concentrations was evident in smokers smoking compared with nonsmokers and smokers not smoking as indicated by a moderate-to-large effect size (d = 0.72; d = 0.78). Conclusion: Consequently, male smokers exhibit an altered postexercise proinflammatory profile compared with age- and fitness-matched nonsmokers.