Purpose.-Physical inactivity is associated with disruptions in glucose metabolism and energy balance, whereas energy restriction may blunt these adverse manifestations. During hypocaloric feeding, higher-protein intake maintains lean mass which is an important component of metabolic health. This study determined whether mild energy restriction preserves glycemic control during physical inactivity and whether this preservation is more effectively achieved with a higher-protein diet.Methods.-Ten adults (24±1 year) consumed a control (64% carbohydrate, 20% fat, 16% protein) and higher-protein diet (50% carbohydrate, 20% fat, 30% protein) during two ten-day inactivity periods (>10,000→~5,000 steps/day) in a randomized cross-over design. Energy intake was decreased by ~400 kcal/d to account for reduced energy expenditure associated with inactivity. A subset of subjects (n=5) completed ten days of inactivity while consuming 35% excess of their basal energy requirements, which served as a positive control condition (overfeeding+inactivity).Results.-Daily steps were decreased from 12,154±308 to 4,275±269 steps/day (P<0.05) which was accompanied by reduced VO 2 max (−1.8±0.7 ml/kg/min, P<0.05), independent of diet conditions. No disruptions in fasting or postprandial glucose, insulin, and nonesterified fatty acids in response to 75-g of oral glucose were observed following inactivity for both diet conditions (P>0.05). Overfeeding+inactivity increased body weight, body fat, HOMA-IR, and 2-hour postprandial glucose and insulin concentrations (P<0.05), despite no changes in lipid concentrations.
ObjectiveStudies have shown that fidgeting augments metabolic demand and increases blood flow to the moving limbs, whereas prolonged sitting suppresses these factors and exacerbates postprandial glucose excursions. Therefore, the hypothesis of this study was that leg fidgeting during prolonged sitting would improve postprandial glycemic control.MethodsAdults with obesity (n = 20) participated in a randomized crossover trial in which blood glucose and insulin concentrations were measured during a 3‐hour sitting period following the ingestion of a glucose load (75 g). During sitting, participants either remained stationary or intermittently fidgeted both legs (2.5 minutes off and 2.5 minutes on). Accelerometer counts, oxygen consumption, and popliteal‐artery blood flow were also measured during the sitting period.ResultsAs expected, fidgeting increased accelerometer counts (P < 0.01), oxygen consumption (P < 0.01), and blood flow through the popliteal artery (P < 0.05). Notably, fidgeting lowered both glucose (P < 0.01) and insulin (P < 0.05) total area under the curve (AUC) and glucose incremental AUC (P < 0.05). Additionally, there was a strong negative correlation between fidgeting‐induced increases in blood flow and reduced postprandial glucose AUC within the first hour (r = −0.569, P < 0.01).ConclusionsLeg fidgeting is a simple, light‐intensity physical activity that enhances limb blood flow and can be incorporated during prolonged sitting to improve postprandial glycemic control in people with obesity.
During exercise, there is coordination between various hormonal systems to ensure glucoregulation. This study examined if hypoglycemia occurs during moderate-intensity exercise in non-obese and obese individuals with and without type 2 diabetes (T2D). Eighteen non-obese, 18 obese, and 10 obese with T2D completed 2 study days that included a meal at 1,800 h followed by rest (NOEX) or exercise (PMEX; 45 min/55% of VO 2 max 2 h post meal). Glucose, insulin, and glucagon concentrations were measured throughout this 5.5 h period. Subjects with T2D had elevated glucose responses to the meal on both study days, compared to non-obese and obese subjects ( P < 0.05). During evening exercise (PMEX), subjects with T2D had a greater drop in glucose concentration (−98.4 ± 13.3 mg/dL) compared to obese (−44.8 ± 7.1 mg/dL) and non-obese (−39.3 ± 6.1 mg/dL; P < 0.01) subjects. Glucose levels decreased more so in females than males in both conditions ( P < 0.01). Nadir glucose levels <70 mg/dL were observed in 33 subjects during NOEX and 39 subjects during PMEX. Obese males had a larger exercise-induced insulin drop than obese females ( P = 0.01). During PMEX, peak glucagon concentrations were elevated compared to NOEX ( P < 0.001). Male participants with T2D had an increased glucagon response during NOEX and PMEX compared to females ( P < 0.01). In conclusion, in individuals with varying glucose tolerance, there is a dramatic drop in glucose levels during moderate-intensity exercise, despite appropriate insulin concentrations prior to exercise, and glucagon levels rising during exercise. Moderate-intensity exercise can result in low glucose concentrations (<60 mg/dL), and yet many of these individuals will be asymptomatic.
Background Insulin‐stimulated peripheral and cerebrovascular vasodilation are consistently observed in preclinical animal models. Hyperinsulinemia also has profound vasodilatory effects within the skeletal muscle vasculature in healthy young adults; however, the magnitude of insulin‐stimulated cerebrovascular vasodilation in humans remains unclear. We hypothesized insulin‐stimulated vasodilation would be observed in both the peripheral and cerebral circulations in healthy young adults. Methods Middle cerebral artery velocity (MCAv) was measured with transcranial Doppler ultrasound in 9 healthy young adults (4M/5F, 28±2 yrs, 24±1 kg/m2) at baseline and following a 60‐min hyperinsulinemic (40 mU/m2 body surface area/min), euglycemic infusion. Femoral artery diameter and mean blood velocity were measured by Doppler ultrasound to determine femoral artery blood flow (FBF). Mean arterial blood pressure (MABP) was measured continuously by finger photoplethysmography. Cerebrovascular conductance index (CVCi = MCAv/MABP x 100) and femoral vascular conductance (FVC = FBF/MABP x 100) were calculated. Results Intravenous insulin infusion resulted in an increase in plasma insulin (5±1 to 41±2 µIU/mL, p<0.01) with blood glucose maintained at baseline levels (75±2 to 72±4 mg/dL, p=0.48). MABP was maintained throughout the infusion protocol (85±3 to 88±3 mmHg, p=0.21). There was a significant increase in FBF (134±24 to 184±30 mL/min, p=0.05) and FVC (153±22 to 211±31 mL/min/100 mmHg, p=0.04) during hyperinsulinemia. In contrast, there was no effect of hyperinsulinemia on MCAv (54±3 to 51±3 cm/s, p=0.28) or CVCi (65±5 to 58±3 AU, p=0.14). There was no association between insulin‐stimulated peripheral and cerebrovascular vasodilation (R=‐0.421, p=0.26). Conclusions Hyperinsulinemia in healthy young adults elicits peripheral vasodilation. Contrary to our hypothesis, following a 60‐minute systemic intravenous insulin infusion there is no change in MCAv or CVCi in healthy young adults. These data indicate the cerebral and peripheral vasculature are differentially regulated during hyperinsulinemia.
BackgroundReduced physical activity is generally associated with disruptions in glucose metabolism and increased accumulation of adiposity. However, whether these adverse effects of physical inactivity manifest when individuals are maintained in energy balance is unknown. Thus, this study examined whether weight maintenance diets prevent physical inactivity‐induced metabolic dysfunction in healthy active adults.DesignTen lean young adults (24±1 year; 25±1 kg/m2) consumed a control (64% carbohydrate, 20% fat, 16% protein) and higher‐protein diet (50% carbohydrate, 20% fat, 30% protein) during ten days of reduced ambulatory activity (>10,000 → ~5,000 steps/day) in a randomized cross‐over design. To mimic the typical Western lifestyle, a subset of male subjects (n=5) completed a 3rd ten‐day physical inactivity trial while consuming 35% excess of their basal energy requirements.ResultsDuring inactivity, daily steps and activity‐associated energy expenditure were decreased by ~65% (P<0.05) and this led to a reduction in maximal aerobic capacity (−1.8±0.7 ml/kg/min, P=0.004), independent of diet conditions. Fat free mass tended to decrease following inactivity (P=0.06), despite no change in body fat percentage or fat mass. Fasting glucose, but not fasting insulin levels, were lowered by physical inactivity, with no differences between diet conditions. Both diets prevented physical inactivity‐induced disruptions in postprandial glucose, insulin, and nonesterified fatty acids in response to a 75‐g oral glucose load (AUC, P>0.05). Overfeeding + physical inactivity increased body weight, body fat percentage, and fat mass (P>0.05). Moreover, fasting glucose, insulin, and 2‐hour postprandial glucose and insulin levels were significantly elevated (P<0.05). Surrogate markers of insulin sensitivity (QUICKI) and insulin resistance (HOMA‐IR) were decreased and increased, respectively after overfeeding + inactivity, despite no changes in blood lipid concentrations.ConclusionsMetabolic disruptions associated with physical inactivity are absent in healthy subjects consuming weight maintenance diets. These findings suggest that small changes in feeding behavior aimed at preventing weight gain is a viable strategy to protect against inactivity‐induced metabolic dysfunction.Support or Funding InformationAmerican Egg Board (#00050021 to NCW; JAK, sponsor)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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