PL-009 Not just a one HIIT wonder: two popular HIIT protocols elicit similar health benefits in a controlled but real world environment

Objective Currently 40% of the UK do not meet the physical activity guidelines with a ‘lack of time’ the most commonly cited barrier to sufficient physical activity. In laboratory based training interventions, high intensity interval training (HIT) offers a time-efficient alternative to moderate intensity continuous training (MICT) but its success requires expensive specialised cycle ergometers and vigorous encouragement from the researchers. To investigate whether two popular HIT protocols, performed using readily available cycle ergometers and without encouragement, can improve aerobic exercise capacity, arterial stiffness and body composition. Methods Eighty-two sedentary males (n=26) and females (n=56) aged 18-65 participated in the study (28±1 y, BMI 25±0.4 kg.m-2). In a randomised cross-over design, participants completed either 6 weeks of 30HIT (4-8x30s sprint with 120s active recovery) or 60HIT (6-10x60s sprint with 60s active recovery). Training sessions were completed on a Wattbike, 3 times per week. VO2peak, body composition (DXA scan), blood glucose (oral glucose tolerance test (OGTT)) and arterial stiffness (pulse wave velocity (PWV)) were assessed pre and post each 6-week training phase, with 4-6 weeks washout period between interventions. Results VO2peakincreased post intervention in 30HIT (36±1 to 39±1 ml.min-1.kg-1) and 60HIT (36±1 to 39±1 ml.min-1.kg-1) (P<0.001), with no difference between intervention group (P=0.208). Body fat percentage decreased pre to post training in both conditions (P=0.001). PWV decreased in 30HIT (2%) and 60HIT (4%) (P<0.005). During the OGTT, there was a trend towards decreasing area under the curve pre to post (P=0.083). When normalized to Watt maxthe participants producing a higher mean power output improved their VO2peakmore than those producing a low MPO (P<0.05). Following further analysis this was only true in 60HIT (P<0.05). Conclusions Both 30HIT and 60HIT could be effective real world strategies to improve aerobic capacity, body composition, arterial stiffness and insulin sensitivity. Improvements were seen even though the time spent sprinting was less in 30HIT (4mins compared to 10mins in 60HIT). In addition, how the 30HIT protocol is executed does not seem to have an effect on physiological outcomes. This suggests 30HIT may be a more applicable training intervention in the real world

Insulin Resistance in the Offspring of Parents with Type 2 Diabetes

Wagenmakers discusses the paper by Petersen and colleagues on insulin resistance in young lean individuals and its association with reduced phosphate transport into muscle cells and impaired mitochondrial energy generation in muscle

PL-001 Home-Based High-Intensity Interval Training Improves Muscle Capillarisation and eNOS/NAD(P)Hoxidase Protein Ratio in Obese Individuals with Elevated Cardiovascular Disease Risk

Objective Obesity and inactivity lead to structural and functional muscle microvascular impairments associated with development of chronic disease. This study is the first to investigate the effect of a novel home-based high-intensity interval training (HIT) (Home-HT) intervention in obese individuals with elevated cardiovascular disease (CVD) risk on capillarisation and muscle microvascular eNOS/NAD(P)Hoxidase ratio. Comparisons were made with home-based moderate-intensity continuous training (Home-MICT) and supervised laboratory-based low-volume HIT (Lab-HIT) as control groups. Methods Thirty-two sedentary obese adults (age 36±2 years; BMI 34.3±0.8 kg∙m-2; O2peak24.6±1.0 ml∙kg-1∙min-1) were allocated to 12 weeks of Home-HIT (n=9), Home-MICT (n=13) or Lab-HIT (n=10). Muscle biopsies were taken pre- and post-training to assess specifically in the endothelial layer of muscle arterioles and capillaries the protein content of eNOS, serine1177phosphorylated eNOS, NOX2 and p47phox, and various capillarisation measures using quantitative immunofluorescence microscopy. Results All interventions induced comparable increases in total eNOS content in terminal arterioles and capillaries (P<0.001). There was no change in ser1177phosphorylated eNOS (arterioles P=0.802; capillaries P=0.311), but eNOS ser1177/eNOS ratio significantly decreased following training in arterioles and capillaries (P<0.001). Training decreased NOX2 content (arterioles P<0.001; capillaries P<0.001), but there was no change in p47phoxcontent (arterioles P=0.101; capillaries P=0.345). All measures of capillarisation increased (P<0.05). These adaptations occurred alongside increased O2peak(P<0.001) and whole-body insulin sensitivity (P=0.033). There were no significant differences between training programmes. Conclusions The training effects of Home-HIT on skeletal muscle microvascular adaptations are comparable to those of traditional training methods, with the advantage that Home-HIT reduces barriers to exercise in obese individuals with elevated CVD risk

Decreased Aerobic Exercise Capacity After Long-Term Remission From Cushing Syndrome: Exploration of Mechanisms.

BACKGROUND: Although major improvements are achieved after cure of Cushing syndrome (CS), fatigue and decreased quality of life persist. This is the first study to measure aerobic exercise capacity in patients in remission of CS for more than 4 years in comparison with matched controls, and to investigate whether the reduction in exercise capacity is related to alterations in muscle tissue. METHODS: Seventeen patients were included. A control individual, matched for sex, estrogen status, age, body mass index, smoking, ethnicity, and physical activity level was recruited for each patient. Maximal aerobic capacity (VO2peak) was assessed during incremental bicycle exercise to exhaustion. In 8 individually matched patients and controls, a percutaneous muscle biopsy was obtained and measures were made of cross-sectional areas, capillarization, and oxphos complex IV (COXIV) protein content as an indicator of mitochondrial content. Furthermore, protein content of endothelial nitric oxide synthase (eNOS) and eNOS phosphorylated on serine1177 and of the NAD(P)H-oxidase subunits NOX2, p47phox, and p67phox were measured in the microvascular endothelial layer. FINDINGS: Patients showed a lower mean VO2peak (SD) (28.0 [7.0] vs 34.8 [7.9] ml O2/kg bw/min, P < .01), maximal workload (SD) (176 [49] vs 212 [67] watt, P = .01), and oxygen pulse (SD) (12.0 [3.7] vs 14.8 [4.2] ml/beat, P < .01) at VO2peak. No differences were seen in muscle fiber type-specific cross-sectional area, capillarization measures, mitochondrial content, and protein content of eNOS, eNOS-P-ser1177, NOX2, p47phox, and p67phox. INTERPRETATION: Because differences in muscle fiber and microvascular outcome measures are not statistically significant, we hypothesize that cardiac dysfunction, seen in active CS, persists during remission and limits blood supply to muscles

Passive Heat Therapy in Sedentary Humans Increases Skeletal Muscle Capillarisation and eNOS Content but Not Mitochondrial Density or GLUT4 Content.

Passive heat therapy (PHT) has been proposed as an alternative intervention to traditional moderate intensity continous training (MICT) in individuals who are unable or unwilling to exercise. This study aimed to make the first comparison of the effect of PHT and MICT on 1) skeletal muscle capillarisation and endothelial specific eNOS content and 2) mitochondrial density, GLUT4 and IMTG content. Twenty young sedentary males (21±1years, BMI 25±1kg.m-2) were allocated to either 6 weeks of PHT (n=10; 40-50min at 40°C in a heat chamber, 3x/wk) or MICT (n=10; time matched cycling at ~65% VO2peak). Muscle biopsies were taken from the vastus lateralis muscle pre- and post-training. Immunofluorescence microscopy was used to assess changes in skeletal muscle mitochondrial density, GLUT4 and IMTG content, capillarisation and endothelial specific eNOS content. VO2peak and whole body insulin sensitivity were also assessed. PHT and MICT both increased capillary density and capillary-fibre perimeter exchange index (P<0.05), and endothelial specific eNOS content (P<0.05). However, unlike MICT (P<0.05) PHT did not increase mitochondrial density (P=0.443), GLUT4 (P=0.217) or IMTG content (P=0.957). Both intervention improved aerobic capacity and whole body insulin sensitivity (P<0.05). 6 weeks PHT in young sedentary males increases skeletal muscle capillarisation and eNOS content to a similar extent as MICT, however, unlike MICT PHT does not affect skeletal muscle mitochondrial density, GLUT4 or IMTG content

PL-017 High-fat overfeeding increases intramuscular triglyceride content and perilipin protein expression in human skeletal muscle

Objective High-fat high-calorie diets can induce whole body insulin resistance (IR) whilst increasing stores of intramuscular triglyceride (IMTG) contained within lipid droplets (LD). Perilipin (PLIN) proteins assist in IMTG storage. Synaptosomal-associated protein (SNAP23) may support LD growth and also direct IMTG-derived fatty acids (FA) to mitochondria for β-oxidation. The objectives of this study were: 1) to test the hypothesis that 7 days of high-fat overfeeding increases IMTG content to prevent lipid induced muscle IR and 2) identify changes in PLINs, SNAP23 and mitochondria content and colocalisation of PLINs with LD, and SNAP23 with LD and mitochondria. Methods Muscle biopsies were obtained from thevastus lateralisof thirteen healthy individuals (age: 23±1years, BMI: 24.4±0.7kg.m-2) before (0min) and during (30min) an oral glucose tolerance test (OGTT), pre and post 7-days consuming a high-fat (65% energy) high-calorie (+50% kcal) diet. IMTG, PLIN2, PLIN3, PLIN5, SNAP23 and mitochondria content were measured using (semi)-quantitative confocal immunofluorescence microscopy. PLIN2, PLIN3 and PLIN5 colocalisation to LD was measured using object-based colocalisation analyses. Pearson’s correlation coefficient quantified colocalisation between SNAP23 and plasma membrane (PM), mitochondria and LD. Phosphorylation of intermediates of the muscle insulin-signalling cascade (Akt and AS160) were measured at 0 and 30 min of the OGTT before and after the dietary intervention. Results Following overfeeding phosphorylation of Akt and AS160 in muscle was not impaired during the OGTT, however Matsuda index of whole-body insulin sensitivity decreased (-23%; P &lt; 0.01). IMTG content increased in type I fibres (+100%; P &lt; 0.001) due to both an increase in LD number (+43%; P &lt; 0.001) and size (+44%; P&lt; 0.001). Of the PLINs investigated, only PLIN3 content increased (+50%;P &lt; 0.01) exclusively in type I fibres. PLIN2-associated LD increased (+80%; P &lt; 0.01) in type I fibres only, whereas PLIN3 and PLIN5-associated LD were unaltered. SNAP23 and mitochondria content did not change, nor did the colocalisation of SNAP23 with the PM, mitochondria or LD. Conclusions Our data confirm the hypothesis that following high-fat overfeeding IMTG stores increased whilst activation of key muscle insulin signalling components were maintained. The increase in IMTG stores is likely supported by the concurrent increase in total PLIN3 content and a redistribution of existing stores of PLIN2 to the expanded LD pool in type I fibres. To confirm if increased IMTG storage protects muscle from IR future research should determine whether meal-derived FAs are directed to IMTG rather than ceramides and diacylglycerol

The effect of different training modes on skeletal muscle microvascular density and endothelial enzymes controlling NO availability

It is becoming increasingly apparent that a high vasodilator response of the skeletal muscle microvasculature to insulin and exercise is of critical importance for adequate muscle perfusion and long-term microvascular and muscle metabolic health. Previous research has shown that a sedentary lifestyle, obesity, and ageing lead to impairments in the vasodilator response, while a physically active lifestyle keeps both microvascular density and vasodilator response high. To investigate the molecular mechanisms behind these impairments and the benefits of exercise training interventions, our laboratory has recently developed quantitative immunofluorescence microscopy methods to measure protein content of eNOS and NAD(P)Hoxidase specifically in the endothelial layer of capillaries and arterioles of human skeletal muscle. As eNOS produces NO and NAD(P)Hoxidase superoxide anions (quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity. The novel methods show that endurance training (ET) and high intensity interval training (HIT) generally regarded as a time efficient alternative to ET, increase eNOS protein content and the eNOS/NADP(H) oxidase protein ratio in previously sedentary lean and obese young men. Resistance exercise training had smaller but qualitatively similar effects. Western blot data of other laboratories suggest that endurance exercise training leads to similar changes in sedentary elderly men. Future research will be required to investigate the relative importance of other sources and tissues in the balance between NO and O2- production seen by the vascular smooth muscle layer of terminal arterioles