Substrate oxidation during exercise: Type 2 diabetes is associated with a decrease in lipid oxidation and an earlier shift towards carbohydrate utilization

CHU de Montpellier, Service central de Physiologie Clinique, Unité d'Exploration Métabolique (CERAMM), Hôpital Lapeyronie, 34000 Montpellier, France.
Diabetes & Metabolism (Impact Factor: 3.27). 01/2007; 32(6):604-10. DOI: 10.1016/S1262-3636(07)70315-4
Source: PubMed


Exercise is a recommended treatment for type 2 diabetes but the actual pattern of metabolic adaptation to exercise in this disease is poorly known and not taken in account in the protocols used. Metabolic defects involved in the pathways of substrate oxidation were described in type 2 diabetes. We hypothesized that type 2 diabetes, regardless of age, gender, training status and weight, could influence by its own the balance of substrates at exercise.
30 sedentary type 2 diabetic subjects and 38 sedentary matched control subjects were recruited. We used exercise calorimetry to determine lipid and carbohydrate oxidation rates. We calculated two parameters quantifying the balance of substrates induced by increasing exercise intensity: the maximal lipid oxidation point (PLipoxMax) and the Crossover point (COP), intensity from which the part of carbohydrate utilization providing energy becomes predominant on lipid oxidation.
Lipid oxidation was lower in the diabetic group, independent of exercise intensity. PLipoxMax and COP were lower in the diabetic group [PLipoxMax=25.3+/-1.4% vs. 36.6+/-1.7% %Wmax (P<0.0001)] - COP =24.2+/-2.2% vs. 38.8+/-1.9% %Wmax (P<0.0001).
Type 2 diabetes is associated with a decrease in lipid oxidation at exercise and a shift towards a predominance of carbohydrate oxidation for exercise intensities lower than in control subjects. Taking into account these alterations could provide a basis for personalizing training intensity.

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    • "MFO is an index obtained at low to moderate exercise intensities (ranging from 33 to 65% VO 2 max) 10—14 during a submaximal graded exercise. Several studies have reported a reduced MFO in obese people [15] and in people with T2DM [16] and metabolic syndrome [17]. Therefore, these studies have suggested that MFO and insulin resistance may be strongly related. "
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    ABSTRACT: Introduction: The hallmark features of obesity include insulin resistance and an impaired ability to oxidize lipids. As compared to exercise training, it remains relatively unclear if diet-induced weight loss can also induce fat metabolism. This study was undertaken to examine the effects of diet-induced weight loss on fat metabolism during a single session of exercise in middle-aged obese men. Methods: Fifteen obese men who were otherwise healthy (average age of 53.5 ± 6.9 yr and average body mass index of 27.8 ± 1.6 kg/m(2)) participated in a 12-wk weight loss program primarily consisting of dietary modification. Maximal fat oxidation (MFO) rates, MFO per lean body mass (MFOLBM) and insulin resistance (HOMA-IR) were measured before and after the program. Participants performed a 24-min graded exercise test on a cycle ergometer, with 15-W increments every 4 min. Expired gas analysis was performed by indirect calorimetry, and nonprotein respiratory quotient equations were used to calculate fat oxidation rates. Results: The weight (-8.3 ± 3.8 kg), fat mass (-4.5 ± 1.9 kg), and lean body mass (-3.8 ± 2.4 kg) (P < 0.001 for all measurements) of the participants were decreased at the end of the 12-wk program. The MFO tended to increase by 19% (P = 0.08) and MFOLBM significantly increased by 28.8% (P = 0.02). Although insulin resistance also significantly decreased by 49% (P < 0.001), changes in fat oxidation variables did not correlate with changes in insulin resistance. Conclusion: Diet-induced weight loss improves fat metabolism with the improvement in insulin resistance.:
    Full-text · Article · Apr 2012 · Obesity Research & Clinical Practice
    • "Submaximal steady-state cycle ergometer tests are commonly used to assess two important metabolic indices: the crossover point (COP), the intensity of effort at which energy is derived more from carbohydrate (CHO) than from fat metabolism [1]; and the point of maximal fat oxidation (LIPOX max ) [2]. Such data are of particular interest in patients with metabolic defects, such as obesity [3] [4] [5] and type 2 diabetes [6] [7], but may also be useful when prescribing exercise and developing individualized training programmes for healthy subjects [8] [9]. The corresponding intensities of effort can be expressed as either heart rate or power output values [10] [11]. "
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    ABSTRACT: Our study aimed to assess the influence of protocol on the crossover point and maximal fat-oxidation (LIPOX(max)) values in sedentary, but otherwise healthy, young men. Maximal oxygen intake was assessed in 23 subjects, using a progressive maximal cycle ergometer test. Twelve sedentary males (aged 20.5±1.0 years) whose directly measured maximal aerobic power (MAP) values were lower than their theoretical maximal values (tMAP) were selected from this group. These individuals performed, in random sequence, three submaximal graded exercise tests, separated by three-day intervals; work rates were based on the tMAP in one test and on MAP in the remaining two. The third test was used to assess the reliability of data. Heart rate, respiratory parameters, blood lactate, the crossover point and LIPOX(max) values were measured during each of these tests. The crossover point and LIPOX(max) values were significantly lower when the testing protocol was based on tMAP rather than on MAP (P<0.001). Respiratory exchange ratios were significantly lower with MAP than with tMAP at 30, 40, 50 and 60% of maximal aerobic power (P<0.01). At the crossover point, lactate and 5-min postexercise oxygen consumption (EPOC(5 min)) values were significantly higher using tMAP rather than MAP (P<0.001). During the first 5 min of recovery, EPOC(5 min) and blood lactate were significantly correlated (r=0.89; P<0.001). Our data show that, to assess the crossover point and LIPOX(max) values for research purposes, the protocol must be based on the measured MAP rather than on a theoretical value. Such a determination should improve individualization of training for initially sedentary subjects.
    No preview · Article · Sep 2011 · Diabetes & Metabolism
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    • "Using the laws of Wishnofsky, calculated predicted weight changes and actual weight changes may be different. Because diabetes patients had lower lipid oxidation than healthy subjects who used the same weight management program during exercise [36] and insulin increases body weight [37], an actual body weight decrease is more common than a lower expected weight. Therefore, we infer that further studies are required to determine the energy deficit suitable for producing a 1 kg weight loss in Korean patients. "
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    ABSTRACT: The purpose of this study was to evaluate the usefulness of an accelerometer in predicting body weight (BW) change during a lifestyle intervention and to find out whether exercise or overall physical activity is associated with change in insulin sensitivity and body composition. A total of 49 overweight (body mass index [BMI] ≥ 23 kg/m(2)) women with diabetes were enrolled and performed lifestyle intervention while monitoring BW, total energy expenditure (TEE) and physical activity energy expenditure (PAEE) using an accelerometer, and energy intake (EI) using a three-day dietary record at baseline and every 2 weeks for 12 weeks. We assessed body composition using bioimpedance analysis and compared the actual BW change to the predicted BW change, which was calculated from the energy deficit (ED) between EI and TEE (ED = EI-TEE). Mean age was 57.2 years, duration of diabetes was 8.0 years, and BMI was 27.8 kg/m(2). There was no significant difference between EI and TEE at baseline. For 12 weeks, the ED was 474.0 kcal·day(-1), which was significantly correlated with BW change (-3.1 kg) (r = 0.725, P < 0.001). However, the actual BW change was 50% lower than the predicted BW change. Both TEE and PAEE correlated with change in K(ITT) (r = 0.334, P = 0.019; r = 0.358, P = 0.012, respectively), BMI (r = -0.395, P = 0.005; r = -0.347, P = 0.015, respectively), and fat mass (r = -0.383, P = 0.007; r = -0.395, P = 0.005, respectively), but only TEE correlated with fat free mass change (r = -0.314, P = 0.030). The accelerometer appears to be a useful tool for measuring TEE under free-living conditions for both short- and long-term periods.
    Full-text · Article · Dec 2010 · Korean Diabetes Journal
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