Influence Of Glucose Ingestion Research Articles

Endocrine responses and food intake in fasted individuals under the influence of glucose ingestion.

IntroductionDifferent metabolic conditions can affect what and how much we eat. Hormones of glucose metabolism and adipokines such as adiponectin take part in the control of these decisions and energy balance of the body. However, a comprehensive understanding of how these endocrine and metabolic factors influence food intake has not been reached. We hypothesised that the amount of food a person consumes differs substantially after a fasting period even after the energy deficit was partially removed by glucose ingestion and endocrine signals like insulin and C-peptide indicated a high glucose metabolic status. Furthermore, the macronutrient composition of the consumed food and a possible association with adiponectin under the influence of glucose ingestion was assessed.MethodsIn a within-subject design, 24 healthy males participated in both a fasting (42 h) and control (non-fasting) condition. A total of 20 blood samples from each subject were collected during each condition to assess serum levels of adiponectin, insulin, C-peptide, cortisol and ACTH. At the end of each condition food intake was measured with an ad libitum buffet after the acute energy deficit was compensated using a carbohydrate-rich drink.ResultsThe total amount of caloric intake and single macronutrients was higher after the fasting intervention after replenishment with glucose. All recorded hormone levels, except for adiponectin, were significantly different for at least one of the study intervals. The relative proportions of the macronutrient composition of the consumed food were stable in both conditions under the influence of glucose ingestion. In the non-fasting condition, the relative amount of protein intake correlated with adiponectin levels during the experiment.Discussion and conclusionAn anabolic glucose metabolism after glucose ingestion following a fasting intervention did not even out energy ingestion compared to a control group with regular food intake and glucose ingestion. Anorexigenic hormones like insulin in this context were not able despite higher levels than in the control condition to ameliorate the drive for food intake to normal or near normal levels. Relative macronutrient intake remains stable under these varying metabolic conditions and glucose influence. Serum adiponectin levels showed a positive association with the relative protein intake in the non-fasting condition under the influence of glucose although adiponectin levels overall did not differ in between the conditions.

Investigating the influence of a glucose drink on emotional memory

The ingestion of a glucose drink has been shown to reliably facilitate declarative memory. However, it remains unclear as to how circulatory levels of glucose influences memory for emotional material, with contradictory findings reported in the literature. Emotional material evokes a natural memory advantage, with measurable increases in circulatory glucose levels being observed in response to emotional words (in the absence of glucose administration). Increased glucose levels (naturally occurring or through an intervention) however, have not been shown to reliably facilitate emotional material. This randomised, placebo-controlled, crossover design, was employed to further investigate the influence of glucose ingestion on memory for emotional words in healthy adults (N = 29; age: 18–49 years). This population is most susceptible to glucose facilitation during more cognitively demanding tasks. A dual task manipulation (alternating hand movement sequences) was introduced during the encoding phase. The glucose drink did not influence memory for emotional words in this study. A main effect of emotion was found, with memory for emotional words (positive and negative) being greater than for neutral words, both at immediate and delayed recall. The results contrast with similar research, which has previously observed improved memory for only negative items. It may be that the memory measures utilised in this study were not sensitive enough to detect any subtle changes to memory induced by a glucose load. Differential physiological responses were observed in response to drink type. Heart rate was found to decrease upon presentation of negative words, following placebo but not glucose. The mechanism underlying this effect is unclear.

Viewpoint: Are there valid concerns for completing a marathon at 39 weeks of pregnancy?

recently, widespread media attention has been given to Amber Danielle Miller, a 27-yr-old woman (163 cm tall), who, at 39 wk of pregnancy, gave birth following her completion of the Chicago Marathon on October 9, 2011 ([17][1], [19][2], [21][3]). She completed the Marathon in 6 h, 25 min, and 50 s

SIRT1, AMP-activated protein kinase phosphorylation and downstream kinases in response to a single bout of sprint exercise: influence of glucose ingestion

This study was designed to examine potential in vivo mechanisms of AMP-activated protein kinase (AMPK) phosphorylation inhibition and its downstream signaling consequences during the recovery period after a single bout of sprint exercise. Sprint exercise induces Thr(172)-AMPK phosphorylation and increased PGC-1alpha mRNA, by an unknown mechanism. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before exercising to inhibit AMPKalpha phosphorylation. Exercise elicited different patterns of Ser(221)-ACCbeta, Ser(473)-Akt and Thr(642)-AS160 phosphorylation, during the recovery period after glucose ingestion. Thirty minutes after the control sprint, Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation was reduced by 33% coinciding with increased Thr(172)-AMPKalpha phosphorylation (both, P < 0.05). Glucose abolished the 30-min Thr(172)-AMPKalpha phosphorylation. Ser(221)-ACCbeta phosphorylation was elevated immediately following and 30 min after exercise in C and G, implying a dissociation between Thr(172)-AMPKalpha and Ser(221)-ACCbeta phosphorylation. Two hours after the sprint, PGC-1alpha protein expression remained unchanged while SIRT1 (its upstream deacetylase) was increased. Glucose ingestion abolished the SIRT1 response without any significant effect on PGC-1alpha protein expression. In conclusion, glucose ingestion prior to a sprint exercise profoundly affects Thr(172)-AMPKalpha phosphorylation and its downstream signaling during the recovery period.

Influence of glucose ingestion by humans during recovery from exercise on substrate utilization during subsequent exercise in a warm environment. Bilzon, J. L., Murphy, J. L., Allsopp, A. J., Wootton, S. A., and Williams, C. Eur. J. Appl. Physiol., 87(4-5): 318-326, 2002.(Abstracts of foreign literature)

Influence of glucose ingestion by humans during recovery from exercise on substrate utilization during subsequent exercise in a warm environment. Bilzon, J. L., Murphy, J. L., Allsopp, A. J., Wootton, S. A., and Williams, C. Eur. J. Appl. Physiol., 87(4-5): 318-326, 2002.(Abstracts of foreign literature)

Influence of glucose ingestion by humans during recovery from exercise on substrate utilisation during subsequent exercise in a warm environment.

Carbohydrate (CHO) ingestion during short-term recovery from prolonged running has been shown to increase the capacity for subsequent exercise in a warm environment. The aim of this study was to examine the effects of the amount of glucose given during recovery on substrate storage and utilisation during recovery and subsequent exercise in a warm environment. A group of 11 healthy male volunteers took part in two experiments in a controlled warm environment (35 degrees C, 40% relative humidity), 1 week apart. On each occasion the subjects completed two treadmill runs (T1 and T2) at a speed equivalent to 60% of maximal oxygen uptake, for 90 min, until they were fatigued, or until aural temperature (T(aur)) reached 39 degrees C. The two runs were separated by a 4 h recovery period (REC), during which subjects consumed 55 g of naturally enriched [U-(13)C]-glucose in the form of a 7.5% carbohydrate-electrolyte solution (CES, mass of solution 667 g) immediately after T1. The subjects then consumed either: the same quantity of CES, or an equivalent volume of an electrolyte placebo, at 60, 120 and 180 min during REC, providing a total of 220 g (C220) or 55 g (C55) of [U-(13)C]-glucose, respectively. Expired gases were collected at 15 min intervals during exercise and 60 min intervals during REC, for determination of total CHO and fat oxidation by indirect respiratory calorimetry, and orally ingested [U-(13)C]-glucose oxidation, estimated from the (13)C:(12)C ratio of expired CO(2). Substrate metabolism did not differ between conditions during T1. Despite the fact that total CHO (P < 0.05) and ingested glucose oxidation (P < 0.01) were greater during REC of the C220 condition, glycogen synthesis was estimated to be approximately fivefold greater (P < 0.01) than in the C55 condition. During T2 the rate of total CHO oxidation was higher (P < 0.01) and total fat oxidation lower (P < 0.01) at all times during the C220 compared to the C55 condition. The greater CHO oxidation during C220 appeared to be met from ingested sources, as the rate of [U-(13)C]-glucose oxidation was greater (P < 0.01) at all times during T2, compared to C55. Whilst more of the ingested substrate remained unoxidised on completion of T2 during C220, exercise duration was similar in the two experimental conditions, and was limited by thermoregulatory incapacity (T(aur) > 39 degrees C) rather than substrate availability per se.

β-hydroxy-β-methylbutyrate (HMB) kinetics and the influence of glucose ingestion in humans

The dietary supplement, β-hydroxy-β-methylbutyrate (HMB), has been shown to decrease muscle proteolysis during the stress of exercise and disease. The aim of this investigation was to determine the time course kinetics of HMB and to determine whether oral glucose ingestion alters the kinetics. In Study 1, eight males (32 ± 10 yrs) participated in two randomize trials: 1) oral ingestion of 1g of HMB with water in capsule form (HMB), and 2) placebo. Blood samples were obtained prior to ingestion of treatment and at 30, 60, 90, 120, 150, and 180 min for the measurement of plasma HMB. Additional blood samples were obtained at 6, 9, and 12 hr. Urine was collected prior to ingestion and at 3, 6, 9, and 12 h for the measurement of urinary HMB. In Study 2, eight males (25 ± 6 yrs) followed the same study design and testing procedure as for Study 1. Treatments were 1) modified glucose tolerance test (75 g glucose) (GLU), 2) oral ingestion of 3 g of HMB with water (HMB), and 3) ingestion of 3 g of HMB with 75 g of glucose (HMB+GLU). Blood samples were analyzed for insulin, glucose, and HMB. Additional blood samples were obtained at 24h and 36h for the measurement of HMB. Additional urine samples were collected at 24h and 36h. In Study 1, plasma HMB peaked at 120 nmol/ml at 2.0 ± 0.4 hr in HMB trial. Half-life was 2.37 ± 0.1 hr. Following the consumption of 1g of HMB, ∼14% of the HMB consumed accumulated in the urine. In Study 2, plasma glucose and insulin levels were significantly greater in GLU and HMB+GLU treated subjects compared to HMB treated subject at minutes 30, 60 and 90. Plasma HMB peaked at 487.9 ± 19.0 nmol/ml at 1.0 ± 0.1 hr in the HMB treated subjects and at 352.1 ± 15.3 nmol/ml at 1.94 ± 0.2 hr when subjects consumed HMB+GLU. The time to reach peak was different (P <0.001) between HMB and HMB+GLU. The plasma HMB half-life was less (P = 0.08) 2.38 ± 0.1 hr in HMB trial compared to 2.69 ± 0.2 hr in HMB+GLU trial. Area under the plasma HMB curve during the first 3 hr was less (P = 0.002) in the HMB+GLU trial compared to the HMB trial. From 3 h through 36 h the area under the HMB curve tended to be less (P = 0.106) for the HMB+GLU compared to the HMB alone. HMB accumulation in the urine as well as the area under the curve were similar with both HMB (94875.8 ± 15159.5 nmol/36 hrs) and HMB+GLU (80678.2 ± 3863.1 nmol/36 hrs). The percentage of the HMB dose that accumulates in the urine was 27% for HMB+GLU and 29% for HMB alone. In conclusion, HMB plasma levels peak within 60 to 120 min depending on the amount of HMB consumed and whether glucose is consumed with HMB. The plasma half-life is ∼2.5 hr. Plasma HMB reaches baseline levels at ∼9 hr following ingestion. However, 70 to 85% of the ingested oral HMB is retained in the body for further metabolism.

Influence of glucose ingestion on fuel-hormone response during prolonged exercise.

Healthy subjects were studied at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. At 90 min of exercise 200 g glucose were ingested. A control group was studied during prolonged exercise without glucose administration. Glucose ingestion was followed by a 35% rise in arterial glucose, a 60-70% fall in arterial FFA and glycerol and a two- to threefold rise in arterial insulin. Plasma glucagon, which rose fourfold in controls, failed to rise in the glucose-fed subjects. Glucose uptake by the exercising legs was twofold greater than in controls, accounting for 60% of leg oxygen consumption. Splanchnic glucose output rose rapidly after glucose ingestion to values twice those observed in controls. However, splanchnic uptake of gluconeogenic precursors (lactate, pyruvate and glycerol) fell by 70-100%. Total splanchnic glucose escape after glucose ingestion was 84 +/- 5 g representing 42% of the ingested load. It is concluded that glucose ingestion during prolonged exercise results in a) augmented uptake and oxidation of glucose by the exercising legs, b) diminished lipolysis, c) augmented splanchnic glucose escape in association with decreased hepatic gluconeogenesis, d) retention of half of the ingested glucose within the splanchnic bed, and e) reversal of exercise-induced stimulation of glucagon secretion.

Electrocardiographic Effects of Glucose Ingestion

To assess the influence of glucose ingestion on resting and exercise electrocardiograms, 35 subjects were tested after ingestion of a glucose solution and a placebo on separate days. Graded submaximal exercise tests (GXTs) were performed to 90% predicted maximal heart rate. Computer-processed ECGs taken at rest showed a decrease in T-wave amplitude, more ST-segment depression, increased R-wave amplitude, and increased heart rate after glucose. Minnesota code classifications of these same ECGs were more abnormal after glucose. Computer-processed exercise ECGs showed a decrease in T-wave area after glucose ingestion during and after exercise. ST-segment area showed the most variability at one minute after exercise. Three subjects had normal exercise ECGs after placebo and abnormal ECGs after glucose ingestion (ST area >7.5μv/sec). Both resting and exercise ECGs should be made fasting to avoid this significant source of variability.