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      Four weeks of electrical stimulation improves glucose tolerance in a sedentary overweight or obese Hispanic population

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          Abstract

          Introduction/purpose

          Most US adults (54%) do not meet the minimum exercise recommendations by the American College of Sports Medicine. Neuromuscular electrical stimulation (NMES) is a novel alternate strategy to induce muscle contraction. However, the effectiveness of NMES to improve insulin sensitivity and energy expenditure is unclear. The purpose of this study was to investigate the effects of 4 weeks of NMES on glucose tolerance in a sedentary overweight or obese population.

          Methods

          Participants ( n  = 10; age: 36.8 ± 3.8 years; BMI = 32 ± 1.3 kg/m 2) were randomized into either control or NMES group. All participants received bilateral quadriceps stimulation (12 sessions; 30 min/session; three times/week at 50 Hz and 300 µs pulse width) altering pulse amplitude to either provide low-intensity sensory level (control; tingling sensation) or at high-intensity neuromuscular level (NMES; maximum tolerable levels with visible muscle contraction). Glucose tolerance was assessed by a 3-h oral glucose tolerance test (OGTT), and substrate utilization was measured by indirect calorimetry and body composition via dual X-ray absorptiometry at baseline and after 4 weeks of NMES intervention.

          Results

          Control and NMES groups had comparable fasting blood glucose, glucose tolerance, substrate utilization, and muscle mass at baseline. Four weeks of NMES resulted in a significant improvement in glucose tolerance measured by OGTT, whereas no change was observed in the control group. There was no change in substrate utilization and muscle mass in both control and NMES groups.

          Conclusion

          NMES is a novel and effective strategy to improve glucose tolerance in an at-risk overweight or obese sedentary population.

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          Most cited references44

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          A new predictive equation for resting energy expenditure in healthy individuals.

          A predictive equation for resting energy expenditure (REE) was derived from data from 498 healthy subjects, including females (n = 247) and males (n = 251), aged 19-78 y (45 +/- 14 y, mean +/- SD). Normal-weight (n = 264) and obese (n = 234) individuals were studied and REE was measured by indirect calorimetry. Multiple-regression analyses were employed to drive relationships between REE and weight, height, and age for both men and women (R2 = 0.71): REE = 9.99 x weight + 6.25 x height - 4.92 x age + 166 x sex (males, 1; females, 0) - 161. Simplification of this formula and separation by sex did not affect its predictive value: REE (males) = 10 x weight (kg) + 6.25 x height (cm) - 5 x age (y) + 5; REE (females) = 10 x weight (kg) + 6.25 x height (cm) - 5 x age (y) - 161. The inclusion of relative body weight and body-weight distribution did not significantly improve the predictive value of these equations. The Harris-Benedict Equations derived in 1919 overestimated measured REE by 5% (p less than 0.01). Fat-free mass (FFM) was the best single predictor of REE (R2 = 0.64): REE = 19.7 x FFM + 413. Weight also was closely correlated with REE (R2 = 0.56): REE = 15.1 x weight + 371.
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            Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss.

            The current study was undertaken to investigate fatty acid metabolism by skeletal muscle to examine potential mechanisms that could lead to increased muscle triglyceride in obesity. Sixteen lean and 40 obese research volunteers had leg balance measurement of glucose and free fatty acid (FFA) uptake (fractional extraction of [9,10 (3)H]oleate) and indirect calorimetry across the leg to determine substrate oxidation during fasting and insulin-stimulated conditions. Muscle obtained by percutaneous biopsy had lower carnitine palmitoyl transferase (CPT) activity and oxidative enzyme activity in obesity (P < 0.05). During fasting conditions, obese subjects had an elevated leg respiratory quotient (RQ, 0.83 +/- 0.02 vs. 0.90 +/- 0.01; P < 0.01) and reduced fat oxidation but similar FFA uptake across the leg. During insulin infusions, fat oxidation by leg tissues was suppressed in lean but not obese subjects; rates of FFA uptake were similar. Fasting values for leg RQ correlated with insulin sensitivity (r = -0.57, P < 0.001). Thirty-two of the obese subjects were restudied after weight loss (WL, -14.0 +/- 0.9 kg); insulin sensitivity and insulin suppression of fat oxidation improved (P < 0.01), but fasting leg RQ (0.90 +/- 0.02 vs. 0.90 +/- 0.02, pre-WL vs. post-WL) and muscle CPT activity did not change. The findings suggest that triglyceride accumulation in skeletal muscle in obesity derives from reduced capacity for fat oxidation and that inflexibility in regulating fat oxidation, more than fatty acid uptake, is related to insulin resistance.
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              Evidence for 5' AMP-activated protein kinase mediation of the effect of muscle contraction on glucose transport.

              The intracellular signaling proteins that lead to exercise-stimulated glucose transport in skeletal muscle have not been identified, although it is clear that there are separate signaling mechanisms for exercise- and insulin-stimulated glucose transport. We have hypothesized that the 5'AMP-activated protein kinase (AMPK) functions as a signaling intermediary in exercise-stimulated glucose uptake. This hypothesis was based on recent studies showing the following: 1) muscle contraction increases AMPK activity and 2) perfusion of rat hindlimb skeletal muscles with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a compound that results in increased AMPK activity, increased insulin-stimulated glucose uptake. In the current study, isolated rat epitrochlearis muscles were treated to contract in vitro (via electrical stimulation for 10 min) and/or incubated in the absence or presence of AICAR (2 mmol/l), insulin (1 micromol/l), or wortmannin (100 nmol/l). Both contraction and AICAR significantly increased AMPK activity, while the enzyme was not activated by insulin. AICAR, contraction, and insulin all increased 3-O-methylglucose (3MG) transport by threefold to fivefold above basal. The phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin completely blocked insulin-stimulated transport, but did not inhibit AICAR- or contraction-stimulated transport. The increase in glucose transport with the combination of maximal AICAR plus maximal insulin treatments was partially additive, suggesting that these stimuli increase glucose transport by different mechanisms. In contrast, there was no additive effect on glucose transport with the combination of AICAR plus contraction. These data suggest that AICAR and contraction stimulate glucose transport by a similar insulin-independent signaling mechanism and are consistent with the hypothesis that AMPK is involved in exercise-stimulated glucose uptake.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                10 January 2022
                01 February 2022
                : 11
                : 2
                : e210533
                Affiliations
                [1 ]Metabolic, Nutrition, and Exercise Research (MiNER) Laboratory, Department of Kinesiology, University of Texas at El Paso, El Paso, Texas , USA
                [2 ]Institute for Health and Sport (IHES) , Victoria University, Melbourne, Victoria, Australia
                [3 ]Australian Institute for Musculoskeletal Science (AIMSS) , Victoria University, Melbourne, Victoria, Australia
                [4 ]Department of Pathology , University of Massachusetts Medical School, Worcester, Massachusetts, USA
                Author notes
                Correspondence should be addressed to S Bajpeyi: sbajpeyi@ 123456utep.edu
                Author information
                http://orcid.org/0000-0002-8762-4865
                http://orcid.org/0000-0002-5336-8330
                Article
                EC-21-0533
                10.1530/EC-21-0533
                8859936
                35007207
                6e05bc4a-7845-4afc-b780-c0e380724d4d
                © The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 31 December 2021
                : 10 January 2022
                Categories
                Research

                nmes,insulin resistance,glycemic control
                nmes, insulin resistance, glycemic control

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