Dan West

A combined insulin reduction and carbohydrate feeding strategy 30 min before running best preserves blood glucose concentration after exercise through improved fuel oxidation in type 1 diabetes mellitus

Abstract In this study, we examined the glycaemic and fuel oxidation responses to alterations in the timing of a low glycaemic index carbohydrate and 75% reduced insulin dose, prior to running, in type 1 diabetes individuals. After carbohydrate (75 g isomaltulose) and insulin administration, the seven participants rested for 30 min, 60 min, 90 min or 120 min (conditions 30MIN, 60MIN, 90MIN, and 120MIN, respectively) before completing 45 min of running at 70% peak oxygen uptake. Carbohydrate and lipid oxidation rates were monitored during exercise and blood glucose and insulin were measured before and for 3 h after exercise. Data were analysed using repeated-measures analysis of variance. Pre-exercise blood glucose concentrations were lower for 30MIN compared with 120MIN (P < 0.05), but insulin concentrations were similar. Exercising carbohydrate and lipid oxidation rates were lower and greater, respectively, for 30MIN compared with 120MIN (P < 0.05). The drop in blood glucose during exercise was less for 30MIN (3.7 mmol · l−1, s[xbar] = 0.4) compared with 120MIN (6.4 mmol · l−1, s[xbar] = 0.3) (P = 0.02). For 60 min post-exercise, blood glucose concentrations were higher for 30MIN compared with 120MIN (P < 0.05). There were no cases of hypoglycaemia in the 30MIN condition, one case in the 60MIN condition, two in the 90MIN condition, and five in the 120MIN condition. In conclusion, a low glycaemic index carbohydrate and reduced insulin dose administered 30 min before running improves pre- and post-exercise blood glucose responses in type 1 diabetes.

Blood glucose responses to reductions in pre-exercise rapid-acting insulin for 24 h after running in individuals with type 1 diabetes

Abstract In this study, we examined pre-exercise insulin reductions on consequent metabolic and dietary patterns for 24 h after running in individuals with type 1 diabetes. Seven participants self-administered their Full rapid-acting insulin dose or 75%, 50% or 25% of it, immediately before consuming a 1.12-MJ meal. After 2 h, participants completed 45 min of running at 70% peak oxygen uptake ([Vdot]O2peak). Blood glucose and insulin were measured for 2 h before and 3 h after exercise. Blood glucose, diet, and administered insulin were self-recorded for 24 h after exercise. Data were analysed using repeated-measures analysis of variance. Pre-exercise peak insulin concentrations were greatest with the Full dose and consequently elicited the lowest blood glucose concentrations (P < 0.05). Blood glucose decreased under all conditions with exercise, with the fall with the Full dose (−6.1 mmol · l−1, sx = 0.4) greater than with 25% insulin (−3.2 mmol · l−1, sx = 0.4; P < 0.05). There was little change in blood glucose from 0 to 3 h post-exercise under all conditions (P > 0.05). Blood glucose at 3 h post-exercise was greatest with the 25% dose. Over the next 21 h, blood glucose area under the curve was greater with the 25% dose compared with all other trials despite consuming less energy and fewer carbohydrates (P < 0.05). A 75% reduction to pre-exercise insulin results in the greatest preservation of blood glucose, and a reduced dietary intake, for 24 h after running in individuals with type 1 diabetes.

Impact of pre-exercise rapid-acting insulin reductions on ketogenesis following running in Type 1 diabetes

Diabet. Med. 28, 218–222 (2011)

Heart rate prescribed walking training improves cardiorespiratory fitness but not glycaemic control in people with type 2 diabetes

Abstract In this study, we examined the effects of a supervised, heart rate intensity prescribed walking training programme on cardiorespiratory fitness and glycaemic control in people with type 2 diabetes mellitus. After receiving local ethics approval, 27 individuals (21 males, 6 females) with type 2 diabetes were randomly assigned to an experimental (“walking”) or control group. Participants completed a Balke-Ware test to determine peak heart rate, peak oxygen consumption ([Vdot]O2peak), and peak gradient. The walking group then completed a 7-week (four sessions a week) supervised, heart rate prescribed walking training programme, whereas the control group continued daily life. After training, participants completed another Balke-Ware test. Fasting blood glucose and glycosylated haemoglobin were measured at rest. The results showed that walking training elicited 80% (s = 2) of peak heart rate and a rating of perceived exertion of 11 (s = 1). Peak heart rate and [Vdot]O2peak were higher in the walking than in the control group after training (P < 0.05). Based on the peak gradient before training, the respiratory exchange ratio was significantly lower (P < 0.05) and there was a strong trend for [Vdot]O2 (P = 0.09) and heart rate (P = 0.09) to be lower after training at the same gradient in the walking compared with the control group. These improvements increased walking peak gradient by 5 min (s = 4 min) compared with the control (P < 0.05). There was no change in fasting blood glucose or glycosylated haemoglobin after training. Despite no change in glycaemic control, heart rate prescribed walking improved peak and sub-maximal cardiorespiratory responses. The beneficial adaptations support the use of heart rate monitoring during walking in people with type 2 diabetes mellitus.

The influence of a carbohydrate and whey protein based breakfast on metabolic and appetite parameters following a second meal

Whey protein consumption may improve metabolic health outcomes by influencing glucose metabolism, appetite and consequently energy balance. Ingestion of whey has been shown to amplify insulin secretion in comparison with other proteins and this insulinotrophic property may be beneficial in reducing postprandial hyperglycaemia which, in the long term, is a significant risk factor for type 2 diabetes. The aim of the present study was to investigate the effect of adding whey protein to a carbohydrate breakfast on postprandial metabolism and appetite responses following a subsequent standard meal. Healthy male participants (n= 10; age 24(2) y, mass 79·7(3·8) kg, BMI 24·5 (2·1) kg/m) performed three trials in a randomised and counter-balanced fashion, consuming either a carbohydrate breakfast (CHO) (1800 kJ, 86% energy from carbohydrate) with or without the addition of 20 g of whey protein isolate (CHO+WP), or omitting breakfast (NB). At 180 minutes post-breakfast participants consumed a standardised pasta based lunch meal (3427 kJ, 49%, 37% and 14% energy from carbohydrate, fat and protein respectively) and remained at rest for a further 180 minutes. Throughout, regular venous blood samples were collected for the determination of blood glucose, plasma insulin and plasma triglyceride. Visual analogue scales captured subjective appetite responses throughout the study protocol. Blood glucose concentrations increased similarly after both breakfast meals (peak; CHO: 6·44(0·34) vs CHO+WP: 5·50(0·17) mmol/l, p> 0·05), with no change observed under NB (p> 0·05). Post breakfast insulinaemia was greater after CHO+WP than CHO (time averaged AUC; CHO: 154·7(18·5) vs CHO+WP: 193·1(26·3), p= 0·033), while similar triglyceride responses were observed between all three trials (p> 0·05). Following a subsequent meal there were no differences across all trials in glycaemia (CHO: 3·99(0·15) vs CHO+WP: 4·14(0·13) vs NB: 4·13(0·96) mmol/l, p> 0·05) or insulinaemia (CHO: 136·9(15·7) vs CHO+WP: 130·7(18·8) vs NB: 110·8(18·6) pmol/l, p> 0·05). Triglyceride concentrations were similarly elevated following lunch in CHO and CHO+WP (AUC; CHO: 0·99(0·11) vs CHO+WP: 1·16(0·16) mmol/l, p= 0·327), both remaining significantly higher than NB (0·82(0·10) mmol/l, p> 0·05). There were no differences in sensations of fullness (AUC; CHO: 45(5) vs CHO+WP: 48(4) mm, p> 0·05) or hunger (CHO: 54(4) vs CHO+WP: 49(4) mm, p> 0·05) between CHO and CHO+WP across the entire trial period (360 minutes). The addition of whey protein to a carbohydrate-based breakfast increased the insulinaemic response to that meal, however it did not subsequently influence metabolic or appetite responses following a second meal. Omitting breakfast consumption induced comparable glycaemic, insulinaemic and appetite responses to subsequent feeding.

Exercise-induced hyperglycaemia in the absence of diabetes

Physical activity influences glucose uptake, transport and disposal [1]. Moderate exercise (VO2max < 60%) is associated with an increase in glucagon relative to insulin to maintain euglycaemia [2,3]. However, intense exercise (VO2max > 80%) results in an eightfold increase in hepatic glucose output while glucose utilization may increase only threefold [4,5]. Exercise stimulates the translocation of Glut-4 in skeletal muscle to facilitateglucoseuptake [6]. Increasedcatecholamineproduction is a major regulator of hepatic glucose output with intense exercise [4,7,8]. In health, insulin secretion increases during the recovery period following intense exercise to normalize plasma glucose. This response is impaired in diabetes and accounts for worsening hyperglycaemia during exercise [4,7,9]. We describe exercise-induced hyperglycaemia in a healthy woman without diabetes, who has provided written consent for publication of this case. A 53-year-old woman (weight 66 kg, height 1.7 m, VO2 peak 47 ml ⁄ kg ⁄ min) with a family history of Type 2 diabetes presented with high blood glucose levels following competitive running of 40–48 km ⁄ week. She felt ‘unwell’ after runs, which prompted her to check blood glucose levels as a friend suggested that she may have hypoglycaemia. Glucose values ranged between 11.2 and 16.1 mmol ⁄ l after 16-km runs. She had a fasting glucose of 4.0 mmol ⁄ l and HbA1c 5.9%. During a 75-g oral glucose tolerance test fasting glucose was 5.2 mmol ⁄ l and the 2-h value was 4.4 mmol ⁄ l. Renal and liver function, urinary catecholamines, fasting gut hormones, glutamic acid decarboxylase and islet cell antibodies, and an overnight dexamethasone suppression test were unremarkable. Locally shehadundergoneanexercise tolerance test, runningat12 km ⁄ h on a treadmill for a period of 45 min. Plasma glucose increased from a basal value of 5.0 to 13.5 mmol ⁄ l with exercise. This was associated with an expected increase in plasma insulin (9.0 to 33.1 mU ⁄ l) and C-peptide (595 to 1316 pmol ⁄ l) and a reduction in plasma glucagon (26.0 to 13.0 pmol ⁄ l). She was invited to attend for further assessment in our exercise laboratory. Initially, her anaerobic threshold of exercise was determined by a running exercise treadmill test (rest to 13 km ⁄ h) with measurements of lactate, glucose and VO2. Lactate increased slightly but linearly up to 11 km ⁄ h and then exponentially as the anaerobic contribution increased at greater speed. Therefore, 11 km ⁄ h was determined as the anaerobic threshold. She then attended for further treadmill tests to assess the metabolic and counterregulatory hormonal response to exercise 1 km ⁄ h above and below the anaerobic threshold of 11 km ⁄ h. The glucose and lactate responses are shown in Figure 1. The lactate and glucose increases were greater with the 12 km ⁄ h exercise. Of note, the peak glucose level was 11.5 mmol ⁄ l, observed 10 min after exercise, indicating it was related to anaerobic metabolism. Therefore, there is evidence of exercise-induced hyperglycaemia following the high-intensity run (12 km ⁄ h) compared with the primarily oxidative, low-intensity run (10 km ⁄ h). The hormonal responses to these exercise challenges were also examined. The peak noradrenaline concentration was almost twofold higher in the12 km ⁄ hcomparedwith the10 km ⁄ hexercise (5580 ng ⁄ l vs. 2908 ng ⁄ l) and returned to basal 20 min post exercise. With respect to cortisol, the low-intensity run did not change serum levels (100 nmol ⁄ l); however, with high intensity, cortisol levels increased and reached a peak 20 min post exercise (cortisol > 800 nmol ⁄ l). We describe a subject without diabetes who experienced hyperglycaemia during anaerobic exercise as identified by the increasing levels of plasma lactate. Increases in plasma noradrenaline and cortisol were observed with intense exercise consistent with catecholamine-mediated hepatic glucose production [5]. With respect to insulin, in healthy subjects post-exercise levels typically increase, leading to facilitated glucose uptake and replenishment of muscle and hepatic glycogen stores. This usually corresponds to a rapid decrease in catecholamine release [4,7]. In the exercise test before referral, there was a clear increase in plasma insulin and C-peptide post exercise, which is in keeping with the above observations, and consistent with previous literature in healthy subjects [5]. This suggests the subject might be resistant to the increased insulin and restoration of the post-exercise glucose to a normal level is slow. A weakness of the current exercise regimes was that endogenous insulin, C-peptide and glucagon were not measured during the