Excessive sitting time is a risk factor for cardiovascular disease mortality and morbidity independent of physical activity. This aim of this study was to evaluate the impact of a sit-stand workstation on sitting time, and vascular, metabolic and musculoskeletal outcomes in office workers, and to investigate workstation acceptability and feasibility. A two-arm, parallel-group, individually randomised controlled trial was conducted in one organisation. Participants were asymptomatic full-time office workers aged ≥18 years. Each participant in the intervention arm had a sit-stand workstation installed on their workplace desk for 8 weeks. Participants in the control arm received no intervention. The primary outcome was workplace sitting time, assessed at 0, 4 and 8 weeks by an ecological momentary assessment diary. Secondary behavioural, cardiometabolic and musculoskeletal outcomes were assessed. Acceptability and feasibility were assessed via questionnaire and interview. ANCOVA and magnitude-based inferences examined intervention effects relative to controls at 4 and 8 weeks. Participants and researchers were not blind to group allocation. Forty-seven participants were randomised (intervention n = 26; control n = 21). Relative to the control group at 8 weeks, the intervention group had a beneficial decrease in sitting time (−80.2 min/8-h workday (95 % CI = −129.0, −31.4); p = 0.002), increase in standing time (72.9 min/8-h workday (21.2, 124.6); p = 0.007) and decrease in total cholesterol (−0.40 mmol/L (−0.79, −0.003); p = 0.049). No harmful changes in musculoskeletal discomfort/pain were observed relative to controls, and beneficial changes in flow-mediated dilation and diastolic blood pressure were observed. Most participants self-reported that the workstation was easy to use and their work-related productivity did not decrease when using the device. Factors that negatively influenced workstation use were workstation design, the social environment, work tasks and habits. Short-term use of a feasible sit-stand workstation reduced daily sitting time and led to beneficial improvements in cardiometabolic risk parameters in asymptomatic office workers. These findings imply that if the observed use of the sit-stand workstations continued over a longer duration, sit-stand workstations may have important ramifications for the prevention and reduction of cardiometabolic risk in a large proportion of the working population. ClinicalTrials.gov NCT02496507 .

Key points: Reduced carbohydrate (CHO) availability before and after exercise may augment endurance training‐induced adaptations of human skeletal muscle, as mediated via modulation of cell signalling pathways. However, it is not known whether such responses are mediated by CHO restriction, energy restriction or a combination of both. In recovery from a twice per day training protocol where muscle glycogen concentration is maintained within 200–350 mmol kg⁻¹ dry weight (dw), we demonstrate that acute post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate potent cell signalling pathways that regulate hallmark adaptations associated with endurance training. In contrast, consuming CHO before, during and after an acute training session attenuated markers of bone resorption, effects that are independent of energy availability. Whilst the enhanced muscle adaptations associated with CHO restriction may be regulated by absolute muscle glycogen concentration, the acute within‐day fluctuations in CHO availability inherent to twice per day training may have chronic implications for bone turnover. We examined the effects of post‐exercise carbohydrate (CHO) and energy availability (EA) on potent skeletal muscle cell signalling pathways (regulating mitochondrial biogenesis and lipid metabolism) and indicators of bone metabolism. In a repeated measures design, nine males completed a morning (AM) and afternoon (PM) high‐intensity interval (HIT) (8 × 5 min at 85% ) running protocol (interspersed by 3.5 h) under dietary conditions of (1) high CHO availability (HCHO: CHO ∼12 g kg⁻¹, EA∼ 60 kcal kg⁻¹ fat free mass (FFM)), (2) reduced CHO but high fat availability (LCHF: CHO ∼3 (⁻¹, EA∼ 60 kcal kg⁻¹ FFM) or (3), reduced CHO and reduced energy availability (LCAL: CHO ∼3 g kg⁻¹, EA∼ 20 kcal kg⁻¹ FFM). Muscle glycogen was reduced to ∼200 mmol kg⁻¹ dw in all trials immediately post PM HIT (P < 0.01) and remained lower at 17 h (171, 194 and 316 mmol kg⁻¹ dw) post PM HIT in LCHF and LCAL (P < 0.001) compared to HCHO. Exercise induced comparable p38MAPK phosphorylation (P < 0.05) immediately post PM HIT and similar mRNA expression (all P < 0.05) of PGC‐1α, p53 and CPT1 mRNA in HCHO, LCHF and LCAL. Post‐exercise circulating βCTX was lower in HCHO (P < 0.05) compared to LCHF and LCAL whereas exercise‐induced increases in IL‐6 were larger in LCAL (P < 0.05) compared to LCHF and HCHO. In conditions where glycogen concentration is maintained within 200–350 mmol kg⁻¹ dw, we conclude post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate cell signalling pathways that regulate hallmark adaptations associated with endurance training. In contrast, consuming CHO before, during and after HIT running attenuates bone resorption, effects that are independent of energy availability and circulating IL‐6.

AIMS To investigate whether 1) six weeks of high-intensity interval training (HIT) induces similar improvements in cardio-metabolic health markers as moderate-intensity continuous training (MICT) in people with type 1 diabetes, and 2) whether HIT abolishes acute reductions in plasma glucose observed following MICT sessions. METHODS Fourteen sedentary individuals with type 1 diabetes (n=7 per group) completed six weeks of HIT or MICT 3 times per week. Pre- and post-training measurements were made of 24h interstitial glucose profiles (using continuous glucose monitors (CGMS)) and cardio-metabolic health markers ($V˙$O_2peak, blood lipid profile and aortic pulse wave velocity; aPWV). Capillary blood glucose concentrations were assessed before and after exercise sessions throughout the training programme to investigate changes in blood glucose during exercise in the fed state. RESULTS Six weeks of HIT or MICT increased $V˙$O_2peak by 14% and 15%, respectively (P<0.001), and aPWV by 12% (P0.05). In the fed state, the mean change in capillary blood glucose concentration during the HIT sessions was -0.2±0.5 mmol/L, whereas blood glucose change was -5.5±0.4 mmol/L during MICT. CONCLUSIONS Six weeks of HIT improved $V˙$O_2peak and aortic PWV to a similar extent as MICT. The finding that blood glucose remained stable during HIT in the fed state, but consistently fell during MICT, suggests that HIT may be the preferred training mode for some people with type 1 diabetes.

Purpose New Zealand blackcurrant (NZBC) extract has previously been shown to increase fat oxidation during prolonged exercise, but this observation is limited to males. We examined whether NZBC intake also increases fat oxidation during prolonged exercise in females, and whether this was related to greater concentrations of circulating fatty acids. Methods In a randomised, crossover, double-blind design, 16 endurance-trained females (age: 28 ± 8 years, BMI: 21.3 ± 2.1 kg·m⁻², VO_2max: 43.7 ± 1.1 ml·kg⁻¹·min⁻¹) ingested 600 mg·day⁻¹ NZBC extract (CurraNZ^™) or placebo (600 mg·day⁻¹ microcrystalline cellulose) for 7 days. On day 7, participants performed 120 min cycling at 65% VO_2max, using online expired air sampling with blood samples collected at baseline and at 15 min intervals throughout exercise for analysis of glucose, NEFA and glycerol. Results NZBC extract increased mean fat oxidation by 27% during 120 min moderate-intensity cycling compared to placebo (P = 0.042), and mean carbohydrate oxidation tended to be lower (P = 0.063). Pre-exercise, plasma NEFA (P = 0.034) and glycerol (P = 0.051) concentrations were greater following NZBC intake, although there was no difference between conditions in the exercise-induced increase in plasma NEFA and glycerol concentrations (P > 0.05). Mean fat oxidation during exercise was moderately associated with pre-exercise plasma NEFA concentrations (r = 0.45, P = 0.016). Conclusions Intake of NZBC extract for 7 days elevated resting concentrations of plasma NEFA and glycerol, indicative of higher lipolytic rates, and this may underpin the observed increase in fat oxidation during prolonged cycling in endurance-trained females.

Aims To compare the effect of a bout of high-intensity interval training (HIT) with a bout of moderate-intensity continuous training (MICT) on glucose concentrations over the subsequent 24h period. METHODS Fourteen people with type 1 diabetes (duration of type 1 diabetes 8.2±1.4 years), all on basal-bolus regimen, completed a randomised, counterbalanced, crossover study. Continuous glucose monitoring was used to assess glycaemic control following a single bout of HIT (6 x 1min intervals) and 30 mins of moderate-intensity continuous training (MICT) on separate days, compared to a non-exercise control day (CON). Exercise was undertaken following an overnight fast with omission of short-acting insulin. Capillary blood glucose samples were recorded pre and post-exercise to assess the acute changes in glycaemia during HIT and MICT. RESULTS There was no difference in the incidence of or percentage time spent in hypoglycaemia, hyperglycaemia or target glucose range over the 24h and nocturnal period (24:00-06:00h) between CON, HIT and MICT (P>0.05). Blood glucose concentrations were not significantly (P=0.49) different from pre to post-exercise with HIT (+0.39±0.42 mmol/L) or MICT (-0.39±0.66 mmol/L), with no difference between exercise modes (P=1.00). CONCLUSIONS HIT or 30 mins of MICT can be carried out after an overnight fast with no increased risk of hypoglycaemia or hyperglycaemia, and provided the pre-exercise glucose concentration is 7-14 mmol/L, no additional carbohydrate ingestion is necessary to undertake these exercises. As HIT is a time-efficient form of exercise, the efficacy and safety of long-term HIT should now be explored.