Effects of neuromuscular electrical stimulation on energy expenditure and postprandial metabolism in healthy men

2021 ◽  
Author(s):  
Yung-Chih Chen ◽  
Russell G Davies ◽  
Aaron Hengist ◽  
Harriet A Carroll ◽  
Oliver J Perkin ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Energy Expenditure ◽  
Neuromuscular Electrical Stimulation ◽  
Metabolic Health ◽  
Carbohydrate Oxidation ◽  
Metabolic Effects ◽  
Whole Body ◽  
Healthy Men ◽  
Potential Strategy ◽  
Postprandial Insulin

It is unclear whether NeuroMuscular Electrical Stimulation (NMES) has meaningful metabolic effects when users have the opportunity to self-select the intensity to one that can be comfortably tolerated. Nine healthy men aged 28 ± 9 y (mean ± SD) with a body mass index 22.3 ± 2.3 kg/m2 completed 3 trials involving a 2-h oral glucose tolerance test whilst, in a randomized counterbalanced order, (1) sitting motionless (SIT), (2) standing motionless (STAND); and (3) sitting motionless with NMES of quadriceps and calves at a self-selected tolerable intensity. Mean (95% confidence interval [CI]) total energy expenditure was greater in the NMES trial (221 [180–262] kcal/2 h) and STAND trial (178 [164–191] kcal/2 h) than during SIT (159 [150–167] kcal/2 h) (both, p < 0.05). This was primarily driven by an increase in carbohydrate oxidation in the NMES and STAND trials compared to SIT (p < 0.05). Postprandial insulin iAUC was lower in both NMES and STAND compared to SIT (16.4 [7.7–25.1], 17 [7–27] & 22.6 [10.8–34.4] nmol·120 min/L, respectively; both, p < 0.05). Compared with sitting, both NMES and STAND increased energy expenditure and whole-body carbohydrate oxidation and reduced postprandial insulin concentrations in healthy men, with more-pronounced effects seen with NMES. Self-selected NMES is a potential strategy to improve metabolic health. This trial is registered at ClinicalTrials.gov (ID: NCT04389736). Novelty • NMES at a comfortable intensity enhances energy expenditure & carbohydrate oxidation and reduces postprandial insulinemia. • Thus, self-selected NMES represents a potential strategy to improve metabolic health.

Electrical stimulation of human lower extremities enhances energy consumption, carbohydrate oxidation, and whole body glucose uptake

2004 ◽  
Vol 96 (3) ◽  
pp. 911-916 ◽  
Author(s):  
Taku Hamada ◽  
Tatsuya Hayashi ◽  
Tetsuya Kimura ◽  
Kazuwa Nakao ◽  
Toshio Moritani
Keyword(s):  
Electrical Stimulation ◽  
Energy Consumption ◽  
Oxygen Uptake ◽  
Glucose Uptake ◽  
Lower Extremities ◽  
Carbohydrate Oxidation ◽  
Triceps Surae ◽  
Metabolic Effects ◽  
Whole Body ◽  
Euglycemic Clamp

Our laboratory has recently demonstrated that low-frequency electrical stimulation (ES) of quadriceps muscles alone significantly enhanced glucose disposal rate (GDR) during euglycemic clamp (Hamada T, Sasaki H, Hayashi T, Moritani T, and Nakao K. J Appl Physiol 94: 2107–2112, 2003). The present study is further follow-up to examine the acute metabolic effects of ES to lower extremities compared with voluntary cycle exercise (VE) at identical intensity. In eight male subjects lying in the supine position, both lower leg (tibialis anterior and triceps surae) and thigh (quadriceps and hamstrings) muscles were sequentially stimulated to cocontract in an isometric manner at 20 Hz with a 1-s on-off duty cycle for 20 min. Despite small elevation of oxygen uptake by 7.3 ± 0.3 ml·kg-1·min-1 during ES, the blood lactate concentration was significantly increased by 3.2 ± 0.3 mmol/l in initial period (5 min) after the onset of the ES ( P < 0.01), whereas VE showed no such changes at identical oxygen uptake (7.5 ± 0.3 ml·kg-1·min-1). ES also induced enhanced whole body carbohydrate oxidation as shown by the significantly higher respiratory gas exchange ratio than with VE ( P < 0.01). These data indicated increased anaerobic glycolysis by ES. Furthermore, whole body glucose uptake determined by GDR during euglycemic clamp demonstrated a significant increase during and after the cessation of ES for at least 90 min ( P < 0.01). This post-ES effect was significantly greater than that of the post-VE period ( P < 0.01). These results suggest that ES can substantially enhance energy consumption, carbohydrate oxidation, and whole body glucose uptake at low intensity of exercise. Percutaneous ES may become a therapeutic utility to enhance glucose metabolism in humans.

scholarly journals Effects of whole-body neuromuscular electrical stimulation device on hemodynamics, arrhythmia, and sublingual microcirculation

2021 ◽  
Author(s):  
Megumi Hoshiai ◽  
Kaori Ochiai ◽  
Yuma Tamura ◽  
Tomoki Tsurumi ◽  
Masato Terashima ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Blood Glucose ◽  
Blood Lactate ◽  
Neuromuscular Electrical Stimulation ◽  
Whole Body ◽  
Left Ventricular Ejection ◽  
Sublingual Microcirculation ◽  
Blood Fluidity ◽  
Lactate Levels ◽  
Blood Lactate Levels

AbstractNeuromuscular electrical stimulation has been used to treat cardiovascular diseases and other types of muscular dysfunction. A novel whole-body neuromuscular electrical stimulation (WB-NMES) wearable device may be beneficial when combined with voluntary exercises. This study aimed to investigate the safety and effects of the WB-NMES on hemodynamics, arrhythmia, and sublingual microcirculation. The study included 19 healthy Japanese volunteers, aged 22–33 years, who were not using any medication. Electrocardiogram (ECG), echocardiography, and blood sampling were conducted before a 20-min WB-NMES session and at 0 and 10 min after termination of WB-NMES. Their tolerable maximum intensity was recorded using numeric rating scale. Arrhythmia was not detected during neuromuscular electrical stimulation or during 10 min of recovery. Blood pressure, heart rate, left ventricular ejection fraction, and diastolic function remained unchanged; however, mild mitral regurgitation was transiently observed during WB-NMES in a single male participant. A decrease in blood glucose and an increase in blood lactate levels were observed, but no changes in blood fluidity, sublingual microcirculation, blood levels of noradrenaline, or oxidative stress were shown. WB-NMES is safe and effective for decreasing blood glucose and increasing blood lactate levels without changing the blood fluidity or microcirculation in healthy people.

Influence of fasting on carbohydrate and fat metabolism during rest and exercise in men

1988 ◽  
Vol 64 (5) ◽  
pp. 1923-1929 ◽  
Author(s):  
J. J. Knapik ◽  
C. N. Meredith ◽  
B. H. Jones ◽  
L. Suek ◽  
V. R. Young ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Ketone Bodies ◽  
Carbohydrate Oxidation ◽  
Metabolic Effects ◽  
Whole Body ◽  
Time To Exhaustion ◽  
Carbohydrate Utilization ◽  
Insulin Levels ◽  
Glucose Flux

Metabolic effects of an overnight fast (postabsorptive state, PA) or a 3.5-day fast (fasted state, F) were compared in eight healthy young men at rest and during exercise to exhaustion at 45% maximum O2 uptake. Glucose rate of appearance (Ra) and disappearance (Rd) were calculated from plasma glucose enrichment during a primed, continuous infusion of [6,6–2H]glucose. Serum substrates and insulin levels were measured and glycogen content of the vastus lateralis was determined in biopsies taken before and after exercise. At rest, whole-body glucose flux (determined by the deuterated tracer) and carbohydrate oxidation (determined from respiratory exchange ratio) were lower in F than PA, but muscle glycogen levels were similar. During exercise, glucose flux, whole-body carbohydrate oxidation, and the rate of muscle glycogen utilization were significantly lower during the fast. In the PA state, glucose Ra and Rd increased together throughout exercise. However, in the F state Ra exceeded Rd during the 1st h of exercise, causing an increase in plasma glucose to levels similar to those of the PA state. The increase in glucose flux was markedly less throughout F exercise. Lower carbohydrate utilization in the F state was accompanied by higher circulating fatty acids and ketone bodies, lower plasma insulin levels, and the maintenance of physical performance reflected by similar time to exhaustion.

scholarly journals Neuronal Protein Tyrosine Phosphatase 1B Deficiency Results in Inhibition of Hypothalamic AMPK and Isoform-Specific Activation of AMPK in Peripheral Tissues

2009 ◽  
Vol 29 (16) ◽  
pp. 4563-4573 ◽  
Author(s):  
Bingzhong Xue ◽  
Thomas Pulinilkunnil ◽  
Incoronata Murano ◽  
Kendra K. Bence ◽  
Huamei He ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Target Genes ◽  
Fiber Type ◽  
Metabolic Effects ◽  
Whole Body ◽  
Acid Oxidation ◽  
Peripheral Tissues ◽  
Leptin Sensitivity ◽  
Brown Adipose ◽  
Ampk Activity

ABSTRACT PTP1B−/− mice are resistant to diet-induced obesity due to leptin hypersensitivity and consequent increased energy expenditure. We aimed to determine the cellular mechanisms underlying this metabolic state. AMPK is an important mediator of leptin's metabolic effects. We find that α1 and α2 AMPK activity are elevated and acetyl-coenzyme A carboxylase activity is decreased in the muscle and brown adipose tissue (BAT) of PTP1B−/− mice. The effects of PTP1B deficiency on α2, but not α1, AMPK activity in BAT and muscle are neuronally mediated, as they are present in neuron- but not muscle-specific PTP1B−/− mice. In addition, AMPK activity is decreased in the hypothalamic nuclei of neuronal and whole-body PTP1B−/− mice, accompanied by alterations in neuropeptide expression that are indicative of enhanced leptin sensitivity. Furthermore, AMPK target genes regulating mitochondrial biogenesis, fatty acid oxidation, and energy expenditure are induced with PTP1B inhibition, resulting in increased mitochondrial content in BAT and conversion to a more oxidative muscle fiber type. Thus, neuronal PTP1B inhibition results in decreased hypothalamic AMPK activity, isoform-specific AMPK activation in peripheral tissues, and downstream gene expression changes that promote leanness and increased energy expenditure. Therefore, the mechanism by which PTP1B regulates adiposity and leptin sensitivity likely involves the coordinated regulation of AMPK in hypothalamus and peripheral tissues.

scholarly journals Natural Phenolic Compounds Targeting The AMPK Activation For Metabolic Health

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Khoa D.A Nguyen ◽  
Khanh V Doan ◽  
Keyword(s):  
Phenolic Compounds ◽  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Antioxidant Property ◽  
Metabolic Health ◽  
Metabolic Effects ◽  
Whole Body ◽  
Ampk Activation ◽  
Ampk Signaling ◽  
Natural Phenolic Compounds

AMP-activated protein kinase (AMPK) is a cellular energy sensor which plays a crucial role in regulation of whole-body energy homeostasis. Activation of AMPK signaling results in favorable effects on mitochondrial function, autophagy, glucose/lipid metabolism, and insulin sensitivity, making it an important therapeutic target in treatment/prevention of metabolic disorders and cancer. Recently, pharmacological studies of natural phenolic compounds indicated that the benefits on metabolic health of these phytochemicals are not only related to their protogenic antioxidant property but also to their AMPK-activating potential. Due to their diverse structures, identification of phenolic compound molecules which have potential to target the AMPK activation for beneficial metabolic effects may be promising in order to develop novel therapeutics in the prevention and/or treatment of metabolic disorders. In this minireview, we summarize beneficial metabolic outcomes of AMPK activation and discuss the capability of natural polyphenols to activate the AMPK pathway focusing on the phenolic acids as potential lead compounds.

scholarly journals Microcirculatory and Metabolic Responses during Voluntary Cycle Ergometer Exercise with a Whole-Body Neuromuscular Electrical Stimulation Device

2021 ◽  
Vol 11 (24) ◽  
pp. 12048
Author(s):  
Kaori Ochiai ◽  
Yuma Tamura ◽  
Masato Terashima ◽  
Tomoki Tsurumi ◽  
Takanori Yasu
Keyword(s):  
Electrical Stimulation ◽  
Neuromuscular Electrical Stimulation ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Oxygen Intake ◽  
Exercise Programs ◽  
Cycle Ergometer Exercise ◽  
Blood Fluidity ◽  
Ergometer Exercise

Vigorous exercise increases blood viscosity and may pose a risk of cardiovascular events in patients with cardiovascular diseases. We recently reported that single-use of novel whole-body neuromuscular electrical stimulation (WB-NMES) can be safely applied in healthy subjects without adversely affecting blood fluidity. We performed a crossover study to explore the effectiveness and safety of a hybrid exercise with ergo-bicycle and WB-NMES; 15 healthy volunteers, aged 23–41 years, participated in this study. No arrhythmias were detected during the hybrid exercise and 20 min recovery, and although blood fluidity was transiently exacerbated immediately after both the exercise programs, in vivo parameters in the sublingual and nailfold microcirculation remained unchanged. There was a significant decrease in blood glucose and increase in lactic acid levels immediately after both exercise programs. Even with the same workload as the cycle ergometer exercise, the oxygen intake during the hybrid exercise remained higher than that during the cycle ergometer exercise alone (p < 0.05, r = 0.79, power = 0.81). Both the hybrid and voluntary cycle ergometer exercises transiently exacerbated blood fluidity ex vivo; however, microvascular flow was not adversely affected in vivo.

Carbohydrate Oxidation: Do We Eat Ourselves or Our Food?

1988 ◽  
Vol 33 (1) ◽  
pp. 203-204 ◽  
Author(s):  
S. Melville ◽  
M.A. McNurlan ◽  
B. A. McGaw ◽  
K.C. McHardy ◽  
L.M. Fearns ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Energy Intake ◽  
Carbohydrate Oxidation ◽  
Whole Body ◽  
Fed State ◽  
Energy Needs

In post-absorptive man, energy is derived solely from oxidation of body stores, mainly by oxidation of fat rather than glycogen.1 Eating changes this pattern so that carbohydrate (CHO) oxidation predominates.1 If during feeding energy intake exceeds energy expenditure, the energy needs of the whole body can in theory be met entirely from the diet. However, it is not clear whether the CHO utilised in the fed state does come directly from the absorbed diet, or whether some continues to be removed from body stores.

scholarly journals MGAT2 deficiency and vertical sleeve gastrectomy have independent metabolic effects in the mouse

2014 ◽  
Vol 307 (11) ◽  
pp. E1065-E1072 ◽  
Author(s):  
Joram D. Mul ◽  
Denovan P. Begg ◽  
April M. Haller ◽  
Josh W. Pressler ◽  
Joyce Sorrell ◽  
...  
Keyword(s):  
Body Weight ◽  
Sleeve Gastrectomy ◽  
Glucose Metabolism ◽  
Energy Expenditure ◽  
Lipid Synthesis ◽  
Metabolic Effects ◽  
Whole Body ◽  
Vertical Sleeve Gastrectomy ◽  
Beneficial Effects ◽  
Reduced Body

Vertical sleeve gastrectomy (VSG) is currently one of the most effective treatments for obesity. Despite recent developments, the underlying mechanisms that contribute to the metabolic improvements following bariatric surgery remain unresolved. VSG reduces postprandial intestinal triglyceride (TG) production, but whether the effects of VSG on intestinal metabolism are related to metabolic outcomes has yet to be established. The lipid synthesis enzyme acyl CoA:monoacylglycerol acyltransferase-2 ( Mogat2; MGAT2) plays a crucial role in the assimilation of dietary fat in the intestine and in regulation of adiposity stores as well. Given the phenotypic similarities between VSG-operated and MGAT2-deficient animals, we reasoned that this enzyme could also have a key role in mediating the metabolic benefits of VSG. However, VSG reduced body weight and fat mass and improved glucose metabolism similarly in whole body MGAT2-deficient ( Mogat2−/−) mice and wild-type littermates. Furthermore, along with an increase in energy expenditure, surgically naive Mogat2−/− mice had altered macronutrient preference, shifting preference away from fat and toward carbohydrates, and increased locomotor activity. Collectively, these data suggest that the beneficial effects of VSG on body weight and glucose metabolism are independent of MGAT2 activity and rather that they are separate from the effects of MGAT2 deficiency. Because MGAT2 inhibitors are proposed as a pharmacotherapeutic option for obesity, our data suggest that, in addition to increasing energy expenditure, shifting macronutrient preference away from fat could be another important mechanism by which these compounds could contribute to weight loss.

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