Maximal lipid oxidation in patients with type 2 diabetes is normal and shows an adequate increase in response to aerobic training (original) (raw)
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High Oxidative Capacity Due to Chronic Exercise Training Attenuates Lipid-Induced Insulin Resistance
Diabetes, 2012
Fat accumulation in skeletal muscle combined with low mitochondrial oxidative capacity is associated with insulin resistance (IR). Endurance-trained athletes, characterized by a high oxidative capacity, have elevated intramyocellular lipids, yet are highly insulin sensitive. We tested the hypothesis that a high oxidative capacity could attenuate lipid-induced IR. Nine endurance-trained (age = 23.4 6 0.9 years; BMI = 21.2 6 0.6 kg/m 2 ) and 10 untrained subjects (age = 21.9 6 0.9 years; BMI = 22.8 6 0.6 kg/m 2 ) were included and underwent a clamp with either infusion of glycerol or intralipid. Muscle biopsies were taken to perform high-resolution respirometry and protein phosphorylation/expression. Trained subjects had ;32% higher mitochondrial capacity and ;22% higher insulin sensitivity (P , 0.05 for both). Lipid infusion reduced insulin-stimulated glucose uptake by 63% in untrained subjects (P , 0.05), whereas this effect was blunted in trained subjects (29%, P , 0.05). In untrained subjects, lipid infusion reduced oxidative and nonoxidative glucose disposal (NOGD), whereas trained subjects were completely protected against lipid-induced reduction in NOGD, supported by dephosphorylation of glycogen synthase. We conclude that chronic exercise training attenuates lipid-induced IR and specifically attenuates the lipid-induced reduction in NOGD. Signaling data support the notion that high glucose uptake in trained subjects is maintained by shuttling glucose toward storage as glycogen. Diabetes 61: [2472][2473][2474][2475][2476][2477][2478] 2012 F at accumulation in skeletal muscle strongly associates with the development of muscle insulin resistance (IR), the main risk factor in the development of type 2 diabetes (T2D). Indeed, elevated intramyocellular triglycerides (IMTGs) are associated with obesity and T2D (1-6). However, the question of why triglycerides accumulate in skeletal muscle has not been answered yet. In recent years, mitochondrial dysfunction has received large attention as a putative candidate underlying IMTG accumulation and thereby the development of IR. Several studies showed compromised in vivo and ex vivo mitochondrial function as a contributor to the development of IR and T2D (7-11). Studies have indicated that intrinsic mitochondrial function (i.e., respiratory capacity per mitochondria) (10-12) as well as mitochondrial content is reduced in T2D and in first-degree relatives. However, whether mitochondrial function and content are important in the prevention of lipid-induced muscular fat accumulation and IR has not been firmly established.
Background: Aerobic exercise is recommended for glycemic and weight control in type 2 diabetes (T2D), but exercise intensity that increase post-exercise fat oxidation has not been established yet. It is expected that high-intensity exercise induce higher absolute oxidations and rates of oxidation of CHO (during) and fat (after) in normoglycemic, but in hyperglycemic it is unclear. Aim: To compare the effects of exercise intensity on CHO and fat oxidation during and after exercise in individuals with T2D. Methods: Eleven persons with T2D, randomly underwent three experimental sessions 72 hours apart: 1) 20 minute of high-intensity exercise (120% of lactate threshold (LT) – 120%LT), 2) 20 minute of moderate intensity exercise (80% of LT – 80%LT), and 3) 20 minute of control session (CON) – no exercise was performed and the individuals remained seated during the whole time. Percentages of CHO and fat contribution and CHO and fat oxidation rate (mg/min) were analyzed during and after sessions. Results: The rate of CHO oxidation during exercise was significantly higher during 120%LT in relation to 80%LT and CON (18.2 ± 5.6 vs. 9.5 ± 2.7 vs. 1.1 ± 0.4 mg • min −1), the absolute rate of fat oxidation was significantly higher in 120%LT compared to 80%LT and CON during exercise (13.5 ± 3.3, 9.5 ± 2.2, and 0.7 ± 0.2 mg • min −1 , respectively, p < 0.05). During the post-exercise oxygen consumption recovery period, only the 120%LT had higher fat oxidation (94.5% vs. 68.1%, p < 0.05), when compared to CON. Both exercise sessions equally elicited a lowered glycaemia during the post-exercise period, but CHO oxidation was lower after 120%LT than CON (0.1 ± 0.2 vs. 0.9 ± 0.5 mg • min −1 , p < 0.05). Conclusions: Higher intensity elicited an elevated CHO oxidation rate during exercise and a higher percentage of fat utilization during the post-exercise recovery period compared to moderate-intensity exercise and control sessions. Relevance for patients: High-intensity aerobic exercise, even of short duration, may benefit individuals with T2D on the substrate oxidation related to the body fat. Exercise can be an important tool for the prevention and management of T2D due to its effects on carbohydrate and fat metabolism, reduction of body fat, and control of blood glucose.
Diabetes & …, 2008
Aim.-We investigated whether or not, in type 2 diabetic (T2D) patients, an individualized training effect on whole-body lipid oxidation would be associated with changes in muscle oxidative capacity. Methods.-Eleven T2D patients participated in the study. Whole-body lipid oxidation during exercise was assessed by indirect calorimetry during graded exercise. Blood samples for measuring blood glucose and free fatty acids during exercise, and muscle oxidative capacity measured from skeletal muscle biopsy (mitochondrial respiration and citrate synthase activity), were investigated in the patients before and after a 10-week individualized training program targeted at LIPOX max , corresponding to the power at which the highest rate of lipids is oxidized (lipid oxidation at LIPOX max). Results.-Training induced both a shift to a higher-power intensity of LIPOX max (+9.1 ± 4.2 W; P < 0.05) and an improvement of lipid oxidation at LIPOX max (+51.27 ± 17.93 mg min −1 ; P < 0.05). The improvement in lipid oxidation was correlated with training-induced improvement in mitochondrial respiration (r = 0.78; P < 0.01) and citrate synthase activity (r = 0.63; P < 0.05). Conclusion.-This study shows that a moderate training protocol targeted at the LIPOX max in T2D patients improves their ability to oxidize lipids during exercise, and that this improvement is associated with enhanced muscle oxidative capacity.
Polish Annals of Medicine, 2012
Introduction: The worldwide epidemic of obesity is due to the imbalance between physical activity and dietary energy intake. This is a major contributor to various diseases including type 2 diabetes, dyslipidemia, coronary heart disease, hypertension, sleep apnea, and some kinds of cancer. In obese individuals disturbances in glucose and lipid oxidation are observed, which probably could be improved upon after exercise training. However, the influence of exercise performed by obese individuals on their glucose and lipid metabolism is not clearly understood. Aim: This study examined whether the intervention of aerobic exercise influences the rates of lipid and glucose oxidation at rest and after an insulin-stimulated state in obese women. Materials and methods: We examined five obese (BMI430 kg/m 2) females without diabetes, aged 31-62, who participated in a 12-week program of aerobic exercise (5 days/week, 30 min/day). Insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp (EHC) technique and whole-body lipid and glucose oxidation rates were measured by indirect calorimetry (IC) using the ventilated hood technique. EHC and IC were performed before and after the 12-week exercise program. Results and discussion: During our investigation, the measurements of body weight, BMI, waist and hip circumferences, body fat (%), fat-free mass (kg), insulin sensitivity, rates of lipid and glucose oxidation, non-oxidative glucose metabolism and increase in the respiratory exchange ratio were taken before and after the exercise intervention. However, the statistical evaluation did not show any significant differences between corresponding results taken before and after the training program. We observed that fat mass decreased and insulin sensitivity increased in three subjects; whereas, in two cases we did not observe any changes after the aerobic training program. Conclusions: The results obtained indicated that a 12-week aerobic training program was not sufficient to improve insulin sensitivity and substrate metabolism in each obese
2014
The contribution of fat oxidation to energy production during exercise is influenced by intensity of exercise. The aim of this study was to assess the relationship between the highest value of fat oxidation rate (FATmax) and the oxygen uptake (VO2) in sedentary type 2 diabetes (T2D) patients vs healthy sedentary subjects. Sedentary T2D patients and healthy sedentary subjects were evaluated to a graded exercise test, and oxygen uptake and fat oxidation rate were detected. Data show that in T2D patients fat oxidation rate is not impaired and the positive linear correlation between FATmax and both VO2 and VO2max suggests that even in T2D patients the muscle oxidative capacity might increase in response to aerobic training.
Asian Journal of Sports Medicine
Background: As part of type 2 diabetes mellitus (T2DM) lifestyle management, exercise programs must be demonstrably effective and safe. Objectives: A randomized controlled trial (RCT) was used to evaluate the results of glycemic control and oxidative stress of a new T2DM management exercise program in a training facility setting. Methods: The study participants were randomly allocated into either an experimental (EXP) group who participated in the new training program or a control (CTR) group who participated in continuous cardiorespiratory exercise. Each participant's glycemic control (glycated hemoglobin A, HbA1c), fitness level (maximum oxygen uptake, VO2max), and oxidative stress (malondialdehyde, MDA and superoxide dismutase, SOD) were measured before and after the training program. The 12-week training program combined high-intensity interval training (HIIT) three times a week with resistance training (RT) twice a week while gradually increasing the intensity. The HIIT element was comprised of one minute of high-intensity exercise and four minutes of low-intensity exercise. The RT element was comprised of nine exercises for the core, upper extremities, and lower extremities. Results: The 42 T2DM patients who participated in this RCT were 35-64 years old. The HbA1c level of the EXP group decreased (∆ =-0.43 ± 1.01%), although not significantly. The VO2max was higher in the EXP group (38.13 ± 5.93 mL/kg/min) than in the CTR group (32.09 ± 5.24 mL/kg/min, P = 0.004). The overall oxidative stress decreased in the EXP group (MDA level ∆ =-0.14 ± 0.39 nm/mL) when compared to the CTR group (MDA level ∆ = 0.18 ± 0.26 nm/mL, P = 0.011), and the SOD level significantly increased more in the EXP group [median ∆ = 0.47 U/mL (interquartile range = 0.08-0.74 U/mL)] when compared to the CTR group (∆ = 0.14 ± 0.35 U/mL, P = 0.036). The EXP group's composite effects score was significantly higher (8.72 ± 1.27) than the CTR group's score (7.20 ± 1.08, P = 0.001). Conclusions: The combined HIIT and RT exercise program was not significantly improving glycemic control, however it lowered oxidative stress.
Muscle Oxidative Capacity Is a Better Predictor of Insulin Sensitivity than Lipid Status
The Journal of Clinical Endocrinology & Metabolism, 2003
We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TG m ) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O 2 uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TG m were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P < 0.05) than in OLD, YOUNG, and TRAINED. TG m was elevated in TYPE 2 compared with all other groups (P < 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P < 0.01), whereas -hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r ؍ 0.71, P < 0.001; -hydroxyacyl CoA dehydrogenase, r ؍ 0.61, P ؍ 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P < 0.05). In conclusion, despite markedly elevated skeletal muscle TG m in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TG m concentration or long-chain fatty acyl CoA content. (J Clin Endocrinol Metab 88: 5444 -5451, 2003)
Metabolic Effects of Aerobic Training and Resistance Training in Type 2 Diabetic Subjects
Diabetes Care, 2012
OBJECTIVE To assess differences between the effects of aerobic and resistance training on HbA1c (primary outcome) and several metabolic risk factors in subjects with type 2 diabetes, and to identify predictors of exercise-induced metabolic improvement. RESEARCH DESIGN AND METHODS Type 2 diabetic patients (n = 40) were randomly assigned to aerobic training or resistance training. Before and after 4 months of intervention, metabolic phenotypes (including HbA1c, glucose clamp–measured insulin sensitivity, and oral glucose tolerance test–assessed β-cell function), body composition by dual-energy X-ray absorptiometry, visceral (VAT) and subcutaneous (SAT) adipose tissue by magnetic resonance imaging, cardiorespiratory fitness, and muscular strength were measured. RESULTS After training, increase in peak oxygen consumption (VO2peak) was greater in the aerobic group (time-by-group interaction P = 0.045), whereas increase in strength was greater in the resistance group (time-by-group intera...