Effects of acute caffeine supplementation on reducing exercise-associated hypoglycaemia in individuals with Type 1 diabetes mellitus.

AIM: To determine the effects of acute caffeine ingestion on glycaemia during moderate to vigorous intensity aerobic exercise and in recovery in individuals with Type 1 diabetes. METHODS: A total of 13 patients with Type 1 diabetes [eight women, five men: mean ± sd age 25.9 ± 8.8 years, BMI 71.9 ± 11.0 kg, maximal oxygen consumption 46.6 ± 12.7 ml/kg/min, body fat 19.9 ± 7.2%, duration of diabetes 14.4 ± 10.1 years and HbA1c 55 ± 8 mmol/mol (7.4 ± 0.8%)] were recruited. Participants ingested capsules that contained gelatin or pure caffeine (6.0 mg/kg body mass) and performed afternoon exercise for 45 min at 60% maximal oxygen consumption on two separate visits with only circulating basal insulin levels. RESULTS: The main finding was that a single caffeine dose attenuates the drop in glycaemia by 1.8 ± 2.8 mmol/l compared with placebo intake during exercise (P=0.056). Continuous glucose monitoring data, however, showed that caffeine was associated with elevated glycaemia at bedtime after exercise, compared with placebo, but lower glucose concentrations in the early morning the next day. CONCLUSIONS: Caffeine intake should be considered as another strategy that may modestly attenuate hypoglycaemia in individuals with Type 1 diabetes during exercise, but should be taken with precautionary measures as it may increase the risk of late-onset hypoglycaemia.

Diabetes, trekking and high altitude: recognizing and preparing for the risks.

Although regular physical activity is encouraged for individuals with diabetes, exercise at high altitude increases risk for a number of potential complications. This review highlights our current understanding of the key physiological and clinical issues that accompany high-altitude travel and proposes basic clinical strategies to help overcome obstacles faced by trekkers with Type 1 or Type 2 diabetes. Although individuals with diabetes have adaptations to the hypoxia of high altitude (increased ventilation, heart rate, blood pressure and hormonal responses), elevated counter-regulatory hormones can impair glycaemic control, particularly if mountain sickness occurs. Moreover, high-altitude-induced anorexia and increased energy expenditure can predispose individuals to dysglycaemia unless careful adjustments in medication are performed. Frequent blood glucose monitoring is imperative, and results must be interpreted with caution because capillary blood glucose meter results may be less accurate at high elevations and low temperatures. It is also important to undergo pre-travel screening to rule out possible contraindications owing to chronic diabetes complications and make well-informed decisions about risks. Despite the risks, healthy, physically fit and well-prepared individuals with Type 1 or Type 2 diabetes who are capable of advanced self-management can be encouraged to participate in these activities and attain their summit goals. Moreover, trekking at high altitude can serve as an effective means to engage in physical activity and to increase confidence with fundamental diabetes self-management skills.

The effect of puberty on fat oxidation rates during exercise in overweight and normal-weight girls.

Excess weight is often associated with insulin resistance (IR) and may disrupt fat oxidation during exercise. This effect is further modified by puberty. While studies have shown that maximal fat oxidation rates (FOR) during exercise decrease with puberty in normal-weight (NW) and overweight (OW) boys, the effect of puberty in NW and OW girls is unclear. Thirty-three NW and OW girls ages 8-18 yr old completed a peak aerobic capacity test on a cycle ergometer. FOR were calculated during progressive submaximal exercise. Body composition and Tanner stage were determined. For each participant, a best-fit polynomial curve was constructed using fat oxidation vs. exercise intensity to estimate max FOR. In a subset of the girls, IR derived from an oral glucose tolerance test (n = 20), and leptin and adiponectin levels (n = 11) were assessed in relation to FOR. NW pre-early pubertal girls had higher max FOR [6.9 ± 1.4 mg·kg fat free mass (FFM)(-1)·min(-1)] than NW mid-late pubertal girls (2.2 ± 0.9 mg·kg FFM(-1)·min(-1)) (P = 0.002), OW pre-early pubertal girls (3.8 ± 2.1 mg·kg FFM(-1)·min(-1)), and OW mid-late pubertal girls (3.3 ± 0.9 mg·kg FFM(-1)·min(-1)) (P < 0.05). Bivariable analyses showed positive associations between FOR with homeostatic model assessment of IR (P = 0.001), leptin (P < 0.001), and leptin-to-adiponectin ratio (P = 0.001), independent of percent body fat. Max FOR decreased in NW girls during mid-late puberty; however, this decrease associated with puberty was blunted in OW girls due to lower FOR in pre-early puberty. The presence of IR due to obesity potentially masks the effect of puberty on FOR during exercise in girls.

Acute high-intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes.

High-volume endurance exercise (END) improves glycaemic control in type 2 diabetes (T2D) but many individuals cite 'lack of time' as a barrier to regular participation. High-intensity interval training (HIT) is a time-efficient method to induce physiological adaptations similar to END, but little is known regarding the effect of HIT in T2D. Using continuous glucose monitoring (CGM), we examined the 24-h blood glucose response to one session of HIT consisting of 10 × 60 s cycling efforts at ~90% maximal heart rate, interspersed with 60 s rest. Seven adults with T2D underwent CGM for 24-h on two occasions under standard dietary conditions: following acute HIT and on a non-exercise control day (CTL). HIT reduced hyperglycaemia measured as proportion of time spent above 10 mmol/l (HIT: 4.5 ± 4.4 vs. CTL: 15.2 ± 12.3%, p = 0.04). Postprandial hyperglycaemia, measured as the sum of post-meal areas under the glucose curve, was also lower after HIT vs. CTL (728 ± 331 vs. 1142 ± 556 mmol/l·9 h, p = 0.01). These findings highlight the potential for HIT to improve glycaemic control in T2D.

The joint association of physical activity and glycaemic control in predicting cardiovascular death and all-cause mortality in the US population.

AIMS/HYPOTHESIS: The aim of this study was to examine the joint association of physical activity and glycaemic control as measured by HbA(1c) on all-cause and cardiovascular disease (CVD) mortality risk. METHODS: The sample included 10,352 adults from the Third National Health and Nutrition Examination Survey (NHANES III) Linked Mortality Public-use File (follow-up 13.4 ± 3.9 years; 2,463 deaths). Physical activity was assessed by questionnaire and classified into inactive and active categories based on self-reported frequency of leisure-time activity. HbA(1c) was categorised to reflect the American Diabetes Association diagnostic and treatment guidelines. RESULTS: Being physically active was associated with a decreased risk of all-cause (HR 0.74 [95% CI 0.67, 0.81]) and CVD (HR 0.71 [95% CI 0.62, 0.82]) mortality, whereas higher levels of HbA(1c) were associated with an increased mortality risk. HbA(1c) ≥ 7% (53 mmol/mol) was associated with the highest risk for all-cause (HR 1.54 [95% CI 1.30, 1.82]) and CVD (HR 1.93 [95% CI 1.52, 2.45]) mortality. Across all categories of HbA(1c), active individuals were not at increased risk for all-cause mortality compared with inactive individuals with normal glycaemic control. Similar findings were observed for CVD mortality, except that active individuals with HbA(1c) ≥ 7% (53 mmol/mol) were still at increased risk for CVD mortality. However, their risk for CVD death was substantially lower than the risk for their inactive counterparts (HR 1.38 [95% CI 1.03, 1.84] vs HR 1.98 [95% CI 1.34, 2.92]). CONCLUSIONS/INTERPRETATION: Physical activity is associated with lower all-cause and CVD mortality risk for individuals across all levels of glycaemic control. Therefore, engaging in a physically active lifestyle and achieving normal levels of glycaemic control may both be important for the prevention of early mortality.

Voluntary physical activity and leucine correct impairments in muscle protein synthesis in partially pancreatectomised rats.

AIMS/HYPOTHESIS: Poorly controlled type 1 diabetes mellitus can cause reduced skeletal muscle mass and weakness during adolescence, which may affect long-term management of the disease. The aim of this study was to determine whether regular voluntary physical activity and leucine feeding restore rates of protein synthesis and deficits in skeletal muscle mass in a young, hypoinsulinaemic/hyperglycaemic rat model of diabetes. METHODS: Four-week-old male Sprague-Dawley rats were partially pancreatectomised (Px) to induce hypoinsulinaemia/hyperglycaemia and housed with/without access to running wheels for 3 weeks (n = 12-14/group). Sham surgery rats (shams) served as sedentary controls (n = 18). Protein synthesis and markers of protein anabolism were assessed in the fasted state and following leucine gavage. Fibre type and cross-sectional areas of the gastrocnemius muscle were measured using a metachromatic ATPase stain. RESULTS: Compared with sedentary behaviour, regular activity lowered fasting glycaemia and reduced fed hyperglycaemia in Px rats. Active-Px rats, which ran 2.2 ± 0.71 km/night, displayed greater muscle mass and fibre areas similar to shams, while sedentary-Px rats displayed a 20-30% loss in muscle fibre areas. Muscle protein synthesis (basal and in response to leucine gavage) was impaired in sedentary-Px (by ~65%), but not in active-Px rats, when compared with shams. Following leucine gavage, the phosphorylation status of eIF4E binding protein 1 (4E-BP1) and ribosomal S6 kinase 1 (S6K1), markers of mammalian target of rapamycin complex 1 (mTORC1) signalling, increased in shams (by two- and ninefold, respectively) and in active-Px (1.5- and fourfold, respectively) rats, but not in sedentary-Px rats. CONCLUSION/INTERPRETATION: Moderate physical activity in young Px rats normalises impairments in skeletal muscle growth and protein synthesis. These findings illustrate the critical compensatory role that modest physical activity and targeted nutrition can have on skeletal muscle growth during periods of hypoinsulinaemia in adolescent diabetes.

Continuous moderate-intensity exercise with or without intermittent high-intensity work: effects on acute and late glycaemia in athletes with Type 1 diabetes mellitus.

AIMS: Individuals with Type 1 diabetes mellitus are susceptible to hypoglycaemia during and after continuous moderate-intensity exercise, but hyperglycaemia during intermittent high-intensity exercise. The combination of both forms of exercise may have a moderating effect on glycaemia in recovery. The aims of this study were to compare the physiological responses and associated glycaemic changes to continuous moderate-intensity exercise vs. continuous moderate-intensity exercise + intermittent high-intensity exercise in athletes with Type 1 diabetes. METHODS: Interstitial glucose levels were measured in a blinded fashion in 11 trained athletes with Type 1 diabetes during two sedentary days and during 2 days in which 45 min of afternoon continuous moderate-intensity exercise occurred either with or without intermittent high-intensity exercise. The total amount of work performed and the duration of exercise was identical between sessions. RESULTS: During exercise, heart rate, respiratory exchange ratio, oxygen utilization, ventilation and blood lactate levels were higher during continuous moderate-intensity + intermittent high-intensity exercise vs. continuous moderate-intensity exercise (all P < 0.05). Despite these marked cardiorespiratory differences between trials, there was no difference in the reduction of interstitial glucose or plasma glucose levels between the exercise trials. Nocturnal glucose levels were higher in continuous moderate-intensity + intermittent high-intensity exercise and in sedentary vs. continuous moderate-intensity exercise (P < 0.05). Compared with continuous moderate-intensity exercise alone, continuous moderate-intensity + intermittent high-intensity exercise was associated with less post-exercise hypoglycaemia (5.2 vs. 1.5% of the time spent with glucose < 4.0 mmol/l) and more post-exercise hyperglycaemia (33.8 vs. 20.4% of time > 11.0 mmol/l). CONCLUSIONS: Although the decreases in glucose level during continuous moderate-intensity exercise and continuous moderate-intensity + intermittent high-intensity exercise are similar, the latter form of exercise protects against nocturnal hypoglycaemia in athletes with Type 1 diabetes.

Exercise and diabetes.

Diet and exercise form the foundation of a healthy lifestyle. These are especially important for people living with diabetes mellitus, as they are the most practical non-pharmacological means by which patients may significantly improve their blood glucose levels. Exercise increases insulin sensitivity (both short and long term), lowers blood sugar levels, reduces body fat and improves cardiovascular (CV) function. Because of this, exercise offers enormous benefit to patients with diabetes. Blood glucose levels can significantly drop during and after physical activities, due to the increased utilisation of glucose as a fuel during exercise and the up-regulation of glucose transport into working muscles. Therefore, patients (especially those with type 1 diabetes) must account for the effects of exercise and adjust their medications and nutrition accordingly. Improvements in real-time continuous glucose monitoring and optimisation of basal insulin dosing may offer significant benefit to preventing hypoglycaemia in patients with type 1 diabetes who regularly exercise. Diverse exercise programmes and devices can also assist patients in monitoring their activities as well as motivating them to achieve their exercise goals. For patients with type 1 diabetes, questions such as how much, how long, how strenuous and what kind of exercise must be addressed in order for healthcare professionals to offer maximum benefit to their patients. Additionally, since patients with type 2 diabetes often have other significant co-morbidities such as obesity and CV disease, care providers must evaluate each patient's risk factors before designing an exercise programme. Several publications in the last year have addressed these issues and may serve as a valuable resource to provide safe and effective recommendations to patients and their healthcare providers. To be included in the Exercise and Diabetes chapter for the 2010 YEARBOOK, we reviewed leading peer-reviewed manuscripts that were published in the period July 2009 to June 2010. PubMed was used in the initial screening of articles.

Exercise equipment and diabetes.

Regular exercise is one of the most powerful treatments for the prevention and treatment of insulin resistance and type 2 diabetes mellitus. Exercise is also beneficial for those living with type 1 diabetes although challenges exist with its prescription as it can promote both hyperglycaemia and hypoglycaemia and motivating patients is always a challenge. Nonetheless, promoting regular exercise should be the cornerstone of all healthcare professionals working with these patients. In this year's review on exercise and exercise equipment, we highlight 10 publications that focus on topics ranging from exercise adherence to fuel metabolism. We also highlight some new innovative tools that facilitate exercise participation and evaluation.

Fat oxidation rate and the exercise intensity that elicits maximal fat oxidation decreases with pubertal status in young male subjects.

The range of exercise intensities that elicit high fat oxidation rates (FOR) in youth and the influence of pubertal status on peak FOR are unknown. In a longitudinal design, we compared FOR over a range of exercise intensities in a small cohort of developing prepubertal male subjects. Five boys all at Tanner stage 1 (ages 11-12 yr) and nine men (ages 20-26 yr) underwent an incremental cycle ergometry test to volitional exhaustion. FOR curves were determined from indirect calorimetry during the final 30 s of each increment. The same protocol was duplicated annually in the boys as they progressed through puberty. The peak FOR was considerably higher (P<0.05) in boys at Tanner 1 (8.6+/-1.5 mg.kg lean body mass(-1).min(-1)) (mean+/-SD) compared with men (4.2+/-1.1 mg.kg lean body mass(-1).min(-1)). FOR dropped as boys developed through puberty (Tanner 2/3 peak rate=7.6+/-0.6 mg.kg lean body mass(-1).min(-1); Tanner 4 peak rate=5.4+/-1.8 mg.kg lean body mass(-1).min(-1), main effect of Tanner stage; P<0.05) to the levels found in men (not significant). The exercise intensity that elicited peak FOR was higher in the boys at Tanner 1 [56+/-6% peak aerobic power (VO2 peak)] than in men (31+/-4% VO2 peak) (P<0.001). This value tended to decrease by Tanner stage 4 (45+/-10% VO2 peak, main effect of Tanner stage; P=0.06). We conclude that, compared with men, prepubertal boys have higher relative FOR throughout a wide range of exercise intensities and that FOR drops as boys develop through puberty.

Slower conduction velocity and motor unit discharge frequency are associated with muscle fatigue during isometric exercise in type 1 diabetes mellitus.

Type 1 diabetes mellitus (T1DM) is associated with a peripheral neuropathy that reduces nerve conduction velocity. This may impair high motor-unit discharge frequencies (MUDF), decrease muscle activation, and curtail the ability to sustain repetitive contractile tasks. We examined (1) whether MUDF, the contractile properties of the knee extensors, and the conduction velocity of persons with T1DM differed from controls; (2) whether persons with T1DM can maintain adequate MUDF during a fatigue protocol; and (3) the relationship between these parameters and impaired glycemic control. We studied male and female subjects with T1DM and controls matched for age, height, weight, and gender. Single motor unit recordings were made from vastus lateralis during maximal and submaximal contractions and during a fatigue protocol. Glycemic control was assessed from blood glucose concentration and glycosylated hemoglobin (HbA1c). Control femoral conduction velocities were comparable to literature values and those of the T1DM subjects were slower. These values correlated with plasma glucose and HbA1c. T1DM subjects fatigued 45% sooner than controls, and time to fatigue and conduction velocity were correlated (r = 0.54, P < 0.05). Discharge frequencies tended to be slower during 50% maximal voluntary contractile force in the T1DM subjects at task failure. Persons with T1DM had slower conduction velocities and lower MUDF than their controls, which apparently leads to impaired activation of muscle and decreased endurance during isometric fatigue.

Physical activity, sport, and pediatric diabetes.

The benefits derived from regular physical activity include improved cardiovascular fitness, increased lean mass, improved blood lipid profile, enhanced psychosocial well-being, and decreased body adiposity. The benefits for children with diabetes may also include blood glucose control and enhanced insulin sensitivity. However, for these children, engagement in vigorous physical activity and sport must be properly controlled through modifications in insulin therapy and nutritional intake so that the benefits of exercise outweigh the risks. The following review describes the various physiological and metabolic factors which occur both during exercise and during sport while describing specific recommendations to control glucose excursions by proper insulin management and diet.

Off seasonal and pre-seasonal assessment of circulating energy sources during prolonged running at the anaerobic threshold in competitive triathletes.

OBJECTIVES: To compare changes in circulating energy sources during prolonged exercise in off season (OS) and pre-season (PS) training of triathletes. METHODS: Nine athletes of the Swiss national triathlon team (three female, mean (SD) age 28.7 (4.9) years, height 169.8 (6.0) cm, weight 57.0 (6.2) kg, VO(2)max 66.5 (5.3) ml/min/kg; six male, mean (SD) age 24.0 (4.1) years, height 181.4 (6.9) cm, weight 73.5 (6.0) kg, VO(2)max 75.9 (4.9) ml/min/kg) were tested twice (2.5 months apart) during a 25 km aerobic capacity test run at the end of the OS and just before the season. The average training load during the OS was 9.9 h/week, and this increased to 14.4 h/week in the PS. With heart rates as reference, exercise intensity during the aerobic capacity test was 97.0 (4.9)% of the anaerobic threshold and 91.2 (4.5)% of VO(2)max. Blood samples were collected before, during, and after the aerobic capacity test. Samples were collected every 5 km during three minute rest intervals. RESULTS: Blood was analysed for triglyceride (TG), free fatty acids, cholesterol, high density lipoprotein cholesterol, glucose, insulin, lactate, and changes in plasma volume. A two factor (season by distance) repeated measures analysis of variance revealed an increase in capacity for prolonged exercise in the PS by a decrease in running intensity during the aerobic capacity test (% of speed at 2.0 mmol/l lactate threshold, p = 0.008), an increase in running speed at the anaerobic threshold (p = 0.003) and at 4.0 and 2.0 mmol/l (p<0.001) of the lactate threshold. A significant season by distance interaction was found for TG (p<0.001). TG concentrations peaked at 5 km and decreased logarithmically throughout the OS (1.48 (0.34) to 0.86 (0.20) mmol/l) and PS (1.90 (0.31) to 0.73 (0.18) mmol/l) tests. From the OS to the PS, there was an increase in the difference in TG at 5-15 km with a concomitant increase at 2.0 mmol/l of the lactate threshold. The peak TG concentrations at 5 km followed by a logarithmic decrease suggest that TG may also provide circulating energy. A greater logarithmic decrease in TG occurred in the PS than in the OS, indicating a higher rate of use. There was an increase in the difference in TG at 5-15 km similar to the increase in the speed at 2.0 mmol/l of the lactate threshold between the two seasons. Glucose, insulin, lactate, and free fatty acids were similar in the two seasons. CONCLUSION: Free fatty acid and TG concentrations were much higher than expected, and the two training seasons showed significantly different patterns of TG concentration during prolonged running. These responses may be related to aerobic capacity of prolonged exercise.

Diabetes and the hypothalamo-pituitary-adrenal (HPA) axis.

Patients and animals with poorly controlled or uncontrolled diabetes present with diurnal hypersecretion of glucocorticoids and altered regulation of the hypothalamo-pituitary-adrenocortical (HPA) axis. Although some of these changes are reversed with insulin replacement therapy, neuroendocrine function is not always restored to normal, even with rigorous glycemic control. In addition, stress responsiveness is also impaired in diabetes and this has important implications in the way patients with diabetes cope with many stress challenges, including the metabolic challenge of insulin-induced hypoglycemia. HPA dysregulation in diabetes appears to involve complex interactions between impaired glucocorticoid negative feedback sensitivity and factors such as hypoinsulinemia, hyperglycemia and/or hypoleptinemia, that may increase central drive of the axis. This review examines some of the evidence indicating hyperactivation of the HPA axis in patients with diabetes. Using the streptozotocin-diabetic rat as a model of type-1 diabetes, we will focus on elucidating some of the mechanisms underlying HPA dysregulation in diabetes. Hyperactivation of the HPA axis in diabetes is associated with increased expression of hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal mineralocorticoid receptor (MR) mRNA. Although insulin replacement restores ACTH and corticosterone levels to normal, likely through glucocorticoid-mediated suppression of ACTH secretion, CRH and MR mRNA expression remain elevated. A better understanding of these mechanisms may be important in developing new treatment modalities for patients with diabetes mellitus.

Mechanisms of impaired hypothalamic-pituitary-adrenal (HPA) function in diabetes: reduced counterregulatory responsiveness to hypoglycaemia.

In summary, our data suggest that in uncontrolled diabetes, increased HPA activity is caused by increased central drive at or above the level of the PVN. Insulin treatment only restores HPA activity at and below the pituitary level, presumably by GC-mediated suppression of ACTH secretion. We hypothesize that the defective HPA response to hypoglycaemia is at least in part due to a lack of a decrease in MR mRNA in response to hypoglycaemia, and diminished sensitivity of the pituitary and adrenal gland to stimulation. Interestingly, insulin treatment restores the HPA response, but not the defective epinephrine response. Therefore, defective epinephrine responses are not linked to defective HPA responses. Similarly, antecedent hypoglycaemia specifically impairs epinephrine responses, but not HPA responses to hypoglycaemia. These studies have revealed some of the mechanisms of impaired HPA function in diabetes and its impaired responsiveness to hypoglycaemia. Further investigations are essential for understanding poor counterregulation in insulin-treated diabetes and may lead to new strategies for preventing hypoglycaemia.

Substrate utilization during exercise with glucose and glucose plus fructose ingestion in boys ages 10--14 yr.

We measured substrate utilization during exercise performed with water (W), exogenous glucose (G), and exogenous fructose plus glucose (FG) ingestion in boys age 10-14 yr. Subjects (n = 12) cycled for 90 min at 55% maximal O(2) uptake while ingesting either W (25 ml/kg), 6% G (1.5 g/kg), or 3% F plus 3% G (1.5 g/kg). Fat oxidation increased during exercise in all trials but was higher in the W (0.28 +/- 0.023 g/min) than in the G (0.24 +/- 0.023 g/min) and FG (0.25 +/- 0.029 g/min) trials (P = 0.04). Conversely, total carbohydrate (CHO) oxidation decreased in all trials and was lower in the W (0.63 +/- 0.05 g/min) than in the G (0.78 +/- 0.051 g/min) and FG (0.74 +/- 0.056 g/min) trials (P = 0.009). Exogenous CHO oxidation, as determined by expired (13)CO(2), reached a maximum of 0.36 +/- 0.032 and 0.31 +/- 0.030 g/min at 90 min in G and FG, respectively (P = 0.04). Plasma insulin levels decrease during exercise in all trials but were twofold higher in G than in W and FG (P < 0.001). Plasma glucose levels decreased transiently after the onset of exercise in all trials and then returned to preexercise values in the W and FG (approximately 4.5 mmol/l) trials but were elevated by approximately 1.0 mmol/l in the G trial (P < 0.001). Plasma lactate concentrations decreased after the onset of exercise in all trials but were lower by approximately 0.5 mmol/l in W than in G and FG (P = 0.02). Thus, in boys exercising at a moderate intensity, the oxidation rate of G plus F is slightly less than G alone, but both spare endogenous CHO and fat to a similar extent. In addition, compared with flavored W, the ingestion of G alone and of G plus F delays exhaustion at 90% peak power by approximately 25 and 40%, respectively, after 90 min of moderate-intensity exercise.

Glucose ingestion and substrate utilization during exercise in boys with IDDM.

This study was intended to compare exogenous [(13)C]glucose (Glu(exo)) oxidation in boys with insulin-dependent diabetes mellitus (IDDM) and healthy boys of similar age, weight, and maximal O(2) uptake. In a control trial with water intake (CT) and in a (13)C-enriched glucose trial (GT), subjects cycled for 60 min (58.8 +/- 0.9% maximal O(2) uptake) while the utilization of total glucose, total fat, and Glu(exo) was assessed. In CT, total glucose was 84.7 +/- 9.2 vs. 91.3 +/- 6.6 g/60 min (not significantly different) and total fat was 13.3 +/- 2.2 vs. 11.1 +/- 1.7 g/60 min (not significantly different) in IDDM vs. healthy boys, respectively. In GT, Glu(exo) was 10.4 +/- 1.7 vs. 14.8 +/- 1.1 g/60 min, corresponding to 9.0 +/- 1.0 vs. 12.4 +/- 0.5% of the total energy supply in IDDM and healthy boys, respectively (P < 0.05). Endogenous glucose was spared in both groups by 12.6 +/- 3.5% (P < 0.05). Blood glucose and plasma insulin concentrations were two- to threefold higher in IDDM vs. healthy boys in both trials. In conclusion, Glu(exo) is impaired in exercising boys with IDDM, even when plasma insulin levels are elevated.

Perceived exertion with glucose ingestion in adolescent males with IDDM.

PURPOSE: The rating of perceived exertion (RPE) is an indicator of exercise effort in adolescents that may be influenced by certain pediatric conditions. The purpose of this study was to determine the influence of insulin-dependent diabetes mellitus (IDDM) and glucose intake on RPE. METHODS: Eight male adolescents with IDDM and eight healthy controls of similar age, weight, and VO2peak cycled for 60 min at 60%VO2peak on two occasions spaced 1-4 wk apart. During a control trial (CT), subjects drank water, and in a glucose trial (GT), glucose at a rate of approximately 1.5 g x kg(-1) x h(-1). Heart rate, ventilation, and RPE (Borg 6-20 scale) were assessed at 5, 25, 35, and 55 min and blood glucose and lactate levels before and at 30 and 60 min. RESULTS: RPE in both trials was 15-25% higher in IDDM versus healthy subjects (F = 8.83; df = 1,14; eta-squared = 0.39; P = 0.01). In CT, it increased from 10.6 +/- 0.4 at 5 min to 15.2 +/- 0.6 at 55 min in IDDM and from 9.3 +/- 0.9 at 5 min to 13.0 +/- 0.8 at 55 min in healthy adolescents. In GT, RPE increased similarly to CT in the IDDM group but was 1-2 points lower in the healthy group. Blood glucose levels were 4.8 +/- 1.8 mmol x L(-1) and 1.8 +/- 0.4 mmol x L(-1) higher by the end of exercise in GT than in CT for the IDDM and healthy groups, respectively. There were no differences in heart rate, ventilation, or lactate levels between the groups or trials. CONCLUSIONS: For exercise performed at a similar moderate intensity, RPE in IDDM is higher by 2-3 points than in controls. Compared with water, glucose intake is associated with lower RPE in healthy, but not in IDDM, adolescents.

Substrate utilization in boys during exercise with [13C]-glucose ingestion.

The influence of glucose ingestion on substrate utilization during prolonged exercise in children and adolescents is currently unknown. In the present study we determined the effect of intermittent exogenous glucose (GLUexo) ingestion on substrate utilization during prolonged exercise, in adolescent boys ages 13 17 years. Healthy untrained volunteers performed four 30-min exercise bouts on a cycle ergometer, separated by 5-min rest periods (approximately equal to 60% maximum O2 consumption), on two occasions spaced 1-4 weeks apart. Two trials were performed, a control trial (CT), in which subjects ingested water intermittently during the exercise, and a glucose trial (GT), in which subjects ingested a 13C-enriched GLUexo drink (approximately egual to glucose kg body mass(-1)), also intermittently during the exercise. Total free fatty acids (FATtotal), glucose (GLUtotal) and carbohydrate (CHOtotal) oxidation was determined from indirect calorimetry, while GLUexo oxidation was calculated from the 13C/12C ratio in expired air after 5-10 min and 25-30 min of exercise in each bout. Heart rate and rating of perceived exertion (RPE) were determined at the same time intervals. The oxidation of CHOtotal was 169.1 (12.9) g x 120 min(-1) and 203.1 (15.9) g x 120 min(-1) (P < 0.01) and that of FATtotal was 31.0 (4.2) g x 120 min(-1) and 17.1 (2.5) g x 120 min(-1) (P < 0.01) in CT and GT, respectively. GLUexo oxidation in GT was 57.8 (4.3) g x 120 min(-1), or 34.2 (2.2)% of that ingested. Endogenous glucose oxidation was 169.1 (12.9) g x 120 min(-1) and 145.3 (11.9) g x 120 min(-1) (P < 0.01) in CT and GT, respectively. Insulin and glucose concentrations were higher in GT than in CT by 226% and 37%, respectively (both P < 0.05). Free fatty acids and glycerol concentrations were lower in GT than in CT, by 27% and 79%, respectively (both P < 0.05). Heart rate was similar between trials, but RPE was lower in GT vs CT at both 115 and 135 min. Thus, under these experimental conditions, GLUexo intake spares endogenous carbohydrate and fat by 16% and 45%, respectively, contributes to approximately 25% of the total energy demand of exercise, and lowers the RPE.