Background There is no consensus on reporting non-mortality trauma complications in a graded manner. The Clavien-Dindo scale of complications was originally for elective surgery, and requires adaptation to provide meaningful data for trauma patients. In particular the original score does not account for those treated without surgery. We report an adapted Clavien-Dindo in trauma (ACDiT) scale and apply it to patients managed operatively and non-operatively. Methods A combined prospective and retrospective international multi-center observational study was undertaken to apply the ACDiT scale to 484 trauma patients at 3 university teaching hospitals (Birmingham, England (n=303); Houston, Texas (n=113); and Glasgow, Scotland (n=68)). These included both intensive care (ICU) and non-ICU managed patients. The Clavien-Dindo scoring system was adapted for trauma patients based on consensus amongst an international collaboration of trauma specialists at these sites. Data included whether initial patients were managed operatively or non-operatively. Complication grades were compared to hospital-free and ICU-free days as other outcome measures of patient morbidity. Results 217/484 (44.8%) patients experienced complications, of whom 61/217 (28.1%) died (Grade V). The remainder consisted of grades I (n=20), II (n=60), III (n=24) and IV (n=52). There was a strong association between higher ACDiT grade category and lower number of hospital-free and ICU-free days (p<0.01). Eighty-eight patients with complications did not require surgery, validating the score’s usefulness in patients managed non-operatively. Conclusions The ACDiT scale can be used to grade the severity of post-trauma complications in patients managed both operatively and non-operatively. It provides clinically meaningful data for morbidity and mortality meetings and other quality improvement exercises.

Purpose Dietary nitrate (NO 3 − ) has repeatedly been shown to improve endurance and intermittent, high-intensity events in temperate conditions. However, the ergogenic effects of dietary NO 3 − on intermittent exercise performance in hot conditions have yet to be investigated. Methods In a randomised, counterbalanced, double-blind crossover study, 12 recreationally trained males ingested a nitrate-rich beetroot juice shot (BRJ) (6.2 mmol NO 3 − ) or a nitrate-depleted placebo (PLA) (< 0.004 mmol NO 3 − ) 3 h prior to an intermittent sprint test (IST) in temperate (22 °C, 35% RH) and hot conditions (30 °C, 70% RH). The cycle ergometer IST consisted of twenty maximal 6 s sprints interspersed by 114 s of active recovery. Work done, power output, heart rate and RPE were measured throughout; tympanic temperature was measured prior to and upon completion. Results There were no significant effects of supplement on sprint performance in either temperate or hot, humid conditions ( p > 0.05). There was a reduced peak (BRJ: 659 ± 100W vs. PLA: 693 ± 139W; p = 0.056) and mean power (BRJ: 543 ± 29W vs. PLA: 575 ± 38W; p = 0.081) following BRJ compared to PLA in the hot and humid condition, but this was not statistically significant. There was no effect of supplement on total work done irrespective of environmental condition. However, ~ 75% of participants experienced performance decreases following BRJ in the hot and humid environment. No differences were observed between trials for tympanic temperature measured at the conclusion of the exercise trial. Conclusion In conclusion, an acute dose of inorganic dietary NO 3 − does not improve repeated-sprint performance in either temperate, or hot and humid conditions.

PurposeElevated postprandial glycaemia [PPG] increases the risk of cardiometabolic complications in insulin-resistant, centrally obese individuals. Therefore, strategies that improve PPG are of importance for this population. Consuming large doses of whey protein [WP] before meals reduces PPG by delaying gastric emptying and stimulating the secretion of the incretin peptides, glucose-dependent insulinotropic polypeptide [GIP] and glucagon-like peptide 1 [GLP-1]. It is unclear if these effects are observed after smaller amounts of WP and what impact central adiposity has on these gastrointestinal processes.MethodsIn a randomised-crossover design, 12 lean and 12 centrally obese adult males performed two 240 min mixed-meal tests, ~5–10 d apart. After an overnight fast, participants consumed a novel, ready-to-drink WP shot (15 g) or volume-matched water (100 ml; PLA) 10 min before a mixed-nutrient meal. Gastric emptying was estimated by oral acetaminophen absorbance. Interval blood samples were collected to measure glucose, insulin, GIP, GLP-1, and acetaminophen.ResultsWP reduced PPG area under the curve [AUC0–60] by 13 and 18.2% in the centrally obese and lean cohorts, respectively (both p &lt;0.001). In both groups, the reduction in PPG was accompanied by a two-three-fold increase in GLP-1 and delayed gastric emptying. Despite similar GLP-1 responses during PLA, GLP-1 secretion during the WP trial was ~27% lower in centrally obese individuals compared to lean (p = 0.001). In lean participants, WP increased the GLP-1ACTIVE/TOTAL ratio comparative to PLA (p = 0.004), indicative of reduced GLP-1 degradation. Conversely, no treatment effects for GLP-1ACTIVE/TOTAL were seen in obese subjects.ConclusionPre-meal ingestion of a novel, ready-to-drink WP shot containing just 15 g of dietary protein reduced PPG in lean and centrally obese males. However, an attenuated GLP-1 response to mealtime WP and increased incretin degradation might impact the efficacy of nutritional strategies utilising the actions of GLP-1 to regulate PPG in centrally obese populations. Whether these defects are caused by an individual’s insulin resistance, their obese state, or other obesity-related ailments needs further investigation.Clinical Trial RegistrationISRCTN.com, identifier [ISRCTN95281775]. https://www.isrctn.com/.

To investigate the impact of residual b-cell function on continuous glucose monitoring (CGM) outcomes following acute exercise in people with type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS Thirty participants with T1D for ‡3 years were recruited. First, participants wore a blinded CGM unit for 7 days of free-living data capture. Second, a 3-h mixed-meal test assessed stimulated C-peptide and glucagon. Peak C-peptide was used to allocate participants into undetectable (Cpep und <3 pmol/L), low (Cpep low 3-200 pmol/L), or high (Cpep high >200 pmol/L) C-peptide groups. Finally, participants completed 45 min of incline treadmill walking at 60% VO 2peak followed by a further 48-h CGM capture. RESULTS CGM parameters were comparable across groups during the free-living observation week.In the 12-and 24-h postexercise periods (12 h and 24 h), the Cpep high group had a significantly greater amount of time spent with glucose 3

Mitigating postprandial hyperglycaemic excursions may be effective in not only enhancing glycaemic control for people with type 2 diabetes but also reducing the onset of diabetes-related complications. However, there are growing concerns over the long-term efficacy of anti-hyperglycaemic pharmacotherapies, which coupled with their rising financial costs, underlines the need for further non-pharmaceutical treatments to regulate postprandial glycaemic excursions. One promising strategy that acutely improves postprandial glycaemia for people with type 2 diabetes is through the provision of mealtime whey protein, owing to the slowing of gastric emptying and increased secretion of insulin and the incretin peptides. The magnitude of this effect appears greater when whey protein is consumed before, rather than with, a meal. Herein, this dietary tool may offer a simple and inexpensive strategy in the management of postprandial hyperglycaemia for people with type 2 diabetes. However, there are insufficient long-term studies that have investigated the use of mealtime whey protein as a treatment option for individuals with type 2 diabetes. The methodological approaches applied in acute studies and outcomes reported may also not portray what is achievable long-term in practice. Therefore, studies are needed to refine the application of this mealtime strategy to maximize its clinical potential to treat hyperglycaemia and to apply these long-term to address key components of successful diabetes care. This review discusses evidence surrounding the provision of mealtime whey protein to treat postprandial hyperglycaemia in individuals with type 2 diabetes and highlights areas to help facilitate its clinical application.

Exercise mobilizes angiogenic cells, which stimulate vascular repair. However, limited research suggests exercise-induced increase of endothelial progenitor cell (EPCs) is completely lacking in type 1 diabetes (T1D). Clarification, along with investigating how T1D influences exercise-induced increases of other angiogenic cells (hematopoietic progenitor cells; HPCs) and cell surface expression of chemokine receptor 4 (CXCR4) and 7 (CXCR7), is needed. Thirty T1D patients and 30 matched non-diabetes controls completed 45 min of incline walking. Circulating HPCs (CD34+, CD34+CD45dim) and EPCs (CD34+VEGFR2+, CD34+CD45dimVEGFR2+), and subsequent expression of CXCR4 and CXCR7, were enumerated by flow cytometry at rest and post-exercise. Counts of HPCs, EPCs and expression of CXCR4 and CXCR7 were significantly lower at rest in the T1D group. In both groups, exercise increased circulating angiogenic cells. However, increases was largely attenuated in the T1D group, up to 55% lower, with CD34+ (331 ± 437 Δcells/mL vs. 734 ± 876 Δcells/mL p = 0.048), CD34+VEGFR2+ (171 ± 342 Δcells/mL vs. 303 ± 267 Δcells/mL, p = 0.006) and CD34+VEGFR2+CXCR4+ (126 ± 242 Δcells/mL vs. 218 ± 217 Δcells/mL, p = 0.040) significantly lower. Exercise-induced increases of angiogenic cells is possible in T1D patients, albeit attenuated compared to controls. Decreased mobilization likely results in reduced migration to, and repair of, vascular damage, potentially limiting the cardiovascular benefits of exercise.Trial registration: ISRCTN63739203.

IntroductionExercise acutely alters markers of bone resorption and formation. As risk of fracture is increased in patients with type 1 diabetes, understanding if exercise-induced bone turnover is affected within this population is prudent. We assessed bone turnover responses to acute exercise in individuals with long-duration type 1 diabetes and matched controls.Research design and methodsParticipants with type 1 diabetes (n=15; age: 38.7±13.3; glycosylated hemoglobin: 60.5±6.7 mmol/mol; diabetes duration: 19.3±11.4 years) and age-matched, fitness-matched, and body mass index-matched controls (n=15) completed 45 min of incline walking (60% peak oxygen uptake). Blood samples were collected at baseline and immediately, 30 min, and 60 min postexercise. Markers of bone resorption (β-C-terminal cross-linked telopeptide of type 1 collagen, β-CTx) and formation (procollagen type-1 amino-terminal propeptide, P1NP), parathyroid hormone (PTH), phosphate, and calcium (albumin-adjusted and ionized) were measured. Data (mean±SD) were analyzed by a mixed-model analysis of variance.ResultsBaseline concentrations of P1NP and β-CTx were comparable between participants with type 1 diabetes and controls. P1NP did not change with exercise (p=0.20) but β-CTx decreased (p<0.001) in both groups, but less so in participants with type 1 diabetes compared with controls (−9.2±3.7%; p=0.02). PTH and phosphate increased immediately postexercise in both groups; only PTH was raised at 30 min postexercise (p<0.001), with no between-group differences (p>0.39). Participants with type 1 diabetes had reduced albumin and ionized calcium at all sample points (p<0.01).ConclusionsFollowing exercise, participants with type 1 diabetes displayed similar time-course changes in markers of bone formation and associated metabolites, but an attenuated suppression in bone resorption. The reduced albumin and ionized calcium may have implications for future bone health. Further investigation of the interactions between type 1 diabetes, differing modalities and intensities of exercise, and bone health is warranted.

Aims: Exercise can disrupt glycemia in individuals with type 1 diabetes (T1D). A large inter-individual variability in the glucose responses to exercise exists. It is not known how residual beta-cell function in long duration T1D influences glycaemia around exercise. Methods: Individuals with T1D completed a postprandial urine C-peptide creatinine ratio test (UCPCR), and 25 participants (M/F 14/11, 39.4±12.4 years, HbA1c 58.8±9.3 mmol/mol-1, BMI 25.6±4.0 kg/m2, diabetes duration 21.4±13.7 years) with a range of UCPCR were recruited. Participants were split into undetectable, microsecretors and clinically significant C-peptide groups (&lt;0.001, 0.001-0.2 and &gt;0.2 nmol/mmol, respectively). After a maximum exercise test, participants attended the second visit whereby they completed 45 minutes of walking at 60%VO2peak. Participants then left the laboratory, with the remainder of the trial under free-living control. Blinded continuous glucose monitoring (CGM) was captured for 12 hours before exercise and for 3 days afterwards. Data (mean±SD) were analysed by one way ANOVA with significance accepted at p ≤0.05. Results: CGM data were successfully captured for 22/25 participants. In the 12 hours prior to exercise, there was no significant differences in CGM between groups. In the first 12 hours post-exercise, the clinical C-peptide group spent significantly more time (83.7±23.2%) in time in euglycemia (3.9-10 mmol/l) compared to the microsecretors (38.8±16.9%, p =0.002) and undetectable participants (40.5±23.3%, p =0.005). The clinical group had lower post exercise SD (1.95±1.26) than the microsecretors (3.56±1.09 p =0.045) and tended to be lower than the undetectable (3.54±1.10 p =0.07). Conclusion: Residual beta-cell function may offer protection against exercise induced dysglycemia. C-peptide could potentially be a method of stratifying the amount of exercise related support patients need to manage glucose around exercise. Disclosure G.S. Taylor: None. K. Smith: None. J. Scragg: None. A. Bashir: None. R.A. Oram: Other Relationship; Self; Randox Laboratories Ltd. T.J. McDonald: None. E.J. Stevenson: None. J.A. Shaw: Advisory Panel; Self; Sanofi. Other Relationship; Self; Novo Nordisk A/S. D.J. West: Research Support; Self; Arla Foods Ingredients, Dexcom, Inc. Funding Diabetes Research & Wellness Foundation