Resting Blood Glucose Research Articles

High or Low Body Fat Deposition in the Presence of a Normal Oral Sugar Test is Not Associated With Postthaw Semen Parameters in Stallions

This study compared the postthaw semen parameters of stallions with high and low body condition score (BCS) and evaluated associations between body morphometric parameters and postthaw semen parameters. Twenty stallions were split into Low BCS (BCS<7, n = 11) and High BCS (BCS ≥7, n = 9) groups, and underwent a complete morphometric analysis (e.g., neck scores and circumference, crest neck height, body weight, and height), and subcutaneous body fat thickness (SFT) at the tail head, withers, shoulders, and retroperitoneal space. A fasted oral sugar test (OST) was conducted on all stallions. One ejaculate from each stallion was frozen with a commercial egg yolk-based extender. Postthaw sperm motility parameters, plasma membrane integrity, mitochondrial membrane potential, hydrogen peroxide and intracellular superoxide production, and lipid peroxidation were analyzed for all stallions. The circumference at 25% and 50% of the neck’s length were larger for High-BCS stallions (P < .05). There were no differences between groups for the neck crest height (P > .05). Stallions with High BCS had greater SFT at the tail head than stallions with Low BCS (P < .05); however, there were no differences between groups in the SFT at the shoulders and withers (P > .05). All stallions had resting blood glucose below the cutoff for equine metabolic syndrome. There were no differences between groups for resting glucose concentrations or for a peak at 30 or 60 minutes after initiation of the OST (P > .05). There were no differences in sperm parameters between groups (P > .05). Collectively, the findings of the present study suggest that High BCS or Low BCS in the presence of normal OST do not explain post-thaw semen parameters.

Effect of Tibial Nerve Stimulation on Menopause‐associated Symptoms in Ovariectomized Rats

Human menopause transition and post‐menopausal syndrome, driven by reduced ovarian activity which reduces estrogen levels, are associated with an increased risk for symptoms including but not limited to sexual dysfunction, osteoporosis, and metabolic disease. Current treatments (both hormonal and non‐hormonal) are limited in efficacy and may have adverse consequences, so investigation for additional treatment options are necessary. Previous studies have demonstrated that tibial nerve stimulation or electro‐acupuncture are minimally invasive treatments that increase vaginal blood flow and serum estrogen in the rat model. In this study we examined the effects of biweekly tibial nerve stimulation (0.2 ms pulse width, 20 Hz, 2× motor threshold) under ketamine‐xylazine anesthesia in female ovariectomized (OVX) Sprague Dawley rats on various measurements that can change in association with menopause (serum estradiol, resting blood glucose, vaginal blood perfusion, uterine weight/histology, and bone density) either at weekly time‐points or during a terminal necropsy. Rats were split into three groups (n = 10 per group): 1) intact + no stimulation, 2) OVX + no stimulation, and 3) OVX + stimulation. Although preliminary data has not shown significant differences between treatment groups, data collection is ongoing and trends are expected after weeks of stimulation. The results of this study will examine the effects of tibial nerve stimulation on various menopause associated symptoms, and help guide recommendations for future studies and treatments.

Aerobic exercise training at maximal fat oxidation intensity improves body composition, glycemic control, and physical capacity in older people with type 2 diabetes

BackgroundAerobic training has been used as one of the common treatments for type 2 diabetes; however, further research on the individualized exercise program with the optimal intensity is still necessary. The purpose of this study was to investigate the effects of supervised exercise training at the maximal fat oxidation (FATmax) intensity on body composition, glycemic control, lipid profile, and physical capacity in older people with type 2 diabetes. MethodsTwenty-four women and 25 men with type 2 diabetes, aged 60–69 years. The exercise groups trained at the individualized FATmax intensity for 1 h/day for 3 days/week over 16 weeks. No dietary intervention was introduced during the experimental period. Whole body fat, abdominal fat, oral glucose tolerance test, lipid profile, and physical capacity were measured before and after the interventions. ResultsFATmax intensity was at 41.3 ± 3.2% VO2max for women and 46.1 ± 10.3% VO2max for men. Exercise groups obtained significant improvements in body composition, with a special decrease in abdominal obesity; decreased resting blood glucose concentration and HbA1c; and increased VO2max, walking ability, and lower body strength, compared to the non-exercising controls. Daily energy intake and medication remained unchanged for all participants during the experimental period. ConclusionBeside the improvements in the laboratory variables, the individualized FATmax training can also benefit daily physical capacity of older people with type 2 diabetes.

Acute Effects of an "Energy Drink" on Short-Term Maximal Performance, Reaction Times, Psychological and Physiological Parameters: Insights from a Randomized Double-Blind, Placebo-Controlled, Counterbalanced Crossover Trial.

The current study examined the relationships between the effects of consuming a caffeine-containing “energy drink” upon (i) short-term maximal performance, (ii) reaction times, and (iii) psychological factors (i.e., mood state, ratings of perceived exertion (RPE), and affective load) and on physiological parameters (i.e., blood pressure and blood glucose). A randomized, double-blind, placebo-controlled, counterbalanced crossover design was implemented in this study. Nineteen male physical-education students (age: 21.2 ± 1.2 years; height: 1.76 ± 0.08 m; body-mass: 76.6 ± 12.6 kg) performed two test sessions: after drinking the “Red Bull’ beverage (RB) and after drinking a placebo (PL). One hour after ingestion of each drink, resting blood glucose and blood pressure were measured and the participants completed the Profile of Mood States questionnaire. Then, after a 5-min warm-up, simple visual reaction time and handgrip force were measured, and the 30-s Wingate test was performed. Immediately after these tests, the RPE, blood glucose, and blood pressure were measured, and the affective load was calculated. Differences between treatments were assessed using two-way repeated measures analyses of variance and paired t-tests, as appropriate. Relationships between the test variables were assessed using Bland–Altman correlations. Significant (i) improvements in peak and mean power output, handgrip force, pre- and post-exercise blood glucose, blood pressure, and vigor and (ii) reductions in reaction times, depression, confusion, fatigue, anger, anxiety, RPE, and affective load scores were observed after RB compared to PL. There were significant correlations of (i) physical performances and reaction times with (ii) RPE, affective load, and pre- and post-exercise blood glucose levels. Gains in peak and mean power were significantly correlated with reductions in fatigue, anxiety (peak power only), and anger (mean power only). The reduction of reaction times was significantly correlated with decreases in confusion and anger and with increases in vigor. Handgrip force and reaction times were significantly correlated with pre- and post-exercise blood pressures. We conclude that RB ingestion has a positive effect on physical performance and reaction times. This effect is related to ergogenic responses in both psychological (i.e., RPE, affective load, and mood state) and physiological (i.e., blood glucose and blood pressure) domains.

Effect of Chronic Vagal Nerve Stimulation on Glucose Tolerance in Conscious Rats

Previously, we demonstrated that cervical vagal nerve stimulation (VNS) inhibits insulin secretion and markedly increases resting blood glucose levels in anesthetized rats. Based on these findings, we hypothesized that chronic cervical VNS induces impaired glucose tolerance in conscious rats.All animal experiments were approved by the Institutional Animal Care and Use Committee of The University of Iowa. Rats were chronically instrumented with telemetric blood pressure sensors inserted into the aorta through the femoral artery and right‐sided cervical vagal nerve stimulators. Three and six days following surgery, repeated glucose tolerance tests (1.5 g dextrose/kg BW, i.p.) were performed after overnight fasting with the vagal nerve stimulators on or off (sham stimulation) in randomized order. VNS (3V, 5Hz, 1ms pulse duration, 1h on 1h off) or sham stimulation was started on the day before the glucose tolerance test. The stimulators were switched to a continuous stimulation mode (instead of 1 h on, 1 h off) for the entire duration of the glucose tolerance tests (2–3 hours) and switched off thereafter. Effectiveness of VNS was confirmed in all animals by the heart rate response to VNS (assessed through the telemetric blood pressure sensors).The study is still ongoing at the time of this writing. Preliminary results from three animals that completed the study so far indicate that baseline blood glucose levels were elevated in animals that received overnight VNS (168±16 mg/dL, n=3) compared to sham stimulated animals (123±15 mg/dL, n=3, P=0.11). The maximal increase in blood glucose levels during the oral glucose tolerance tests (time point 30 min) was greater in rats with VNS (+412±23 mg/dL, n=3) compared to sham stimulated animals (+233±41 mg/dL, n=3, P=0.11). Furthermore, two‐way Analysis of Variance revealed that glucose levels were significantly elevated throughout the 120 min of the glucose tolerance tests in rats with VNS compared to sham‐stimulated animals (P&lt;0.01).These preliminary results suggest that cervical VNS impairs glucose tolerance in conscious rats. It remains to be determined if human patients treated with VNS are at greater risk to develop type 2 diabetes.Support or Funding InformationSupported by a pilot grant from the University of Iowa Hospitals and Clinics Center for Hypertension Research and the German Research Foundation.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Myostatin inhibition therapy for insulin-deficient type 1 diabetes.

While Type 1 Diabetes Mellitus (T1DM) is characterized by hypoinsulinemia and hyperglycemia, persons with T1DM also develop insulin resistance. Recent studies have demonstrated that insulin resistance in T1DM is a primary mediator of the micro and macrovascular complications that invariably develop in this chronic disease. Myostatin acts to attenuate muscle growth and has been demonstrated to be elevated in streptozotocin-induced diabetic models. We hypothesized that a reduction in mRNA expression of myostatin within a genetic T1DM mouse model would improve skeletal muscle health, resulting in a larger, more insulin sensitive muscle mass. To that end, Akita diabetic mice were crossed with MyostatinLn/Ln mice to ultimately generate a novel mouse line. Our data support the hypothesis that decreased skeletal muscle expression of myostatin mRNA prevented the loss of muscle mass observed in T1DM. Furthermore, reductions in myostatin mRNA increased Glut1 and Glut4 protein expression and glucose uptake in response to an insulin tolerance test (ITT). These positive changes lead to significant reductions in resting blood glucose levels as well as pronounced reductions in associated diabetic symptoms, even in the absence of exogenous insulin. Taken together, this study provides a foundation for considering myostatin inhibition as an adjuvant therapy in T1DM as a means to improve insulin sensitivity and blood glucose management.

Myostatin Inhibition as an Adjuvant Therapy in Type 1 Diabetes Mellitus

While Type 1 Diabetes Mellitus (T1DM) is characterized by hypoinsulinemia and hyperglycemia, persons with T1DM also develop insulin resistance and recent studies have demonstrated that insulin resistance is a primary mediator of the micro and macrovascular complications that invariably develop in this chronic disease. Therefore, we hypothesized that a reduction in circulating myostatin (a TGF‐beta family member known to regulate muscle mass) in a T1DM mouse model would improve skeletal muscle health, resulting in an increased insulin sensitivity and a reduction in blood glucose. To that end, we crossed Akita diabetic mice with the MyostatinLn/Ln mouse line (which displays a ~60% reduction in myostatin levels) to generate a novel mouse line (MyostatinLn/Ln; Akita+/−). Our data support the hypothesis that reducing circulating myostatin levels prevented the loss of skeletal muscle mass observed in T1DM, as well as significantly increasing Glut1 and Glut4 transporter densities with the end result being an increased glucose uptake in response to an insulin tolerance test (ITT). These positive changes in T1DM skeletal muscle health resulted in significant reductions in resting blood glucose levels and other diabetic symptoms (hyperphagia, polydypsia), even in the absence of exogenous insulin. Taken together, these studies provide a foundation for considering pharmacological myostatin inhibitors as an adjuvant therapy in T1DM as a means to delay the development of diabetic complications.Support or Funding InformationThis work is funded by a grant from Natural Sciences and Engineering Research Council of Canada to TJH

Skeletal muscle glucose uptake during treadmill exercise in neuronal nitric oxide synthase-μ knockout mice.

Nitric oxide influences intramuscular signaling that affects skeletal muscle glucose uptake during exercise. The role of the main NO-producing enzyme isoform activated during skeletal muscle contraction, neuronal nitric oxide synthase-μ (nNOSμ), in modulating glucose uptake has not been investigated in a physiological exercise model. In this study, conscious and unrestrained chronically catheterized nNOSμ(+/+) and nNOSμ(-/-) mice either remained at rest or ran on a treadmill at 17 m/min for 30 min. Both groups of mice demonstrated similar exercise capacity during a maximal exercise test to exhaustion (17.7 ± 0.6 vs. 15.9 ± 0.9 min for nNOSμ(+/+) and nNOSμ(-/-), respectively, P > 0.05). Resting and exercise blood glucose levels were comparable between the genotypes. Very low levels of NOS activity were detected in skeletal muscle from nNOSμ(-/-) mice, and exercise increased NOS activity only in nNOSμ(+/+) mice (4.4 ± 0.3 to 5.2 ± 0.4 pmol·mg(-1)·min(-1), P < 0.05). Exercise significantly increased glucose uptake in gastrocnemius muscle (5- to 7-fold) and, surprisingly, more so in nNOSμ(-/-) than in nNOSμ(+/+) mice (P < 0.05). This is in parallel with a greater increase in AMPK phosphorylation during exercise in nNOSμ(-/-) mice. In conclusion, nNOSμ is not essential for skeletal muscle glucose uptake during exercise, and the higher skeletal muscle glucose uptake during exercise in nNOSμ(-/-) mice may be due to compensatory increases in AMPK activation.

Effects of Acute Exercise on Plasma Apelin and Blood Glucose in Healthy Young Subjects

Apelin has been reported to enhance glucose uptake but most studies have examined apelin in diabetics and obese individuals. There are few studies that have reported apelin levels in plasma from apparently healthy individuals. However, no study has examined the acute effects of exercise on apelin and its response to glucose concentration in apparently healthy young subjects. PURPOSE: To determine plasma apelin concentration and its response to blood glucose following two acute exercise bouts and a glucose load. METHODS: Apparently healthy male (N=7) and female (N=5) subjects (22.8 3.0 yrs), nonsmokers and not on any medications that would alter metabolism. Subjects reported at 7-9 A.M. after an overnight fast, rested > 30 min and then completed the three conditions in a randomized order: VO2 max (MX) (6.9 ± 1.1 min); 30-min 70-75% VO2max (SM); and 54g glucose feeding (GF). Blood was drawn at four time points ([1] pre, [2] immediately post ex or 30 min post GF, [3]1 hr post and [4] 24 hrs post) and immediately centrifuged and plasma stored in aliquots at -80°C until assayed. Blood glucose was measured immediately using a glucose meter (Bayer Contour) and plasma apelin (Apelin-12 Elisa, Phoenix Pharmaceuticals) was measured in duplicate. RMANOVA was used to assess differences across time and between conditions. RESULTS: Resting blood glucose (77.1 ± 10.7 mg/dl) was not different across treatments. Apelin at rest was significantly higher for MX (.64 ± .36 ng/ml) compared to GF (.45 ± .22 ng/ml) (p=0.05) but not with SM (.54 ± .36 ng/ml). Blood glucose increased immediately after MX (109.2± 17.8 mg/dl) and GF (106.7± 20.9 mg/dl) p=0.05 and returned to normal 1 hr post treatment. The SM exercise did not alter glucose over time (80 ± 6.6 mg/dl). Apelin was not significantly changed with either MX or SM over time. However, apelin was elevated 1 hr post GF (.58 ± .23 ng/ml) and 24 hr post GF (.58 ± .32 ng/ml) (p=0.03) compared to rest. CONCLUSION: GF elevated apelin concentration both 1hr and 24hr post treatment, however the exercise did not significantly alter apelin. The MX exercise demonstrated a similar increase in glucose compared to the GF but did not alter apelin which suggests that other factors may have influenced the apelin response. We intend to examine the insulin response and insulin sensitivity as it relates to apelin concentration.

Blood Glucose Control Using a Novel Continuous Blood Glucose Monitor and Repetitive Intravenous Insulin Boluses: Exploiting Natural Insulin Pulsatility as a Principle for a Future Artificial Pancreas

The aim of this study was to construct a glucose regulatory algorithm by employing the natural pulsatile pattern of insulin secretion and the oscillatory pattern of resting blood glucose levels and further to regulate the blood glucose level in diabetic pigs by this method. We developed a control algorithm based on repetitive intravenous bolus injections of insulin and combined this with an intravascular blood glucose monitor. Four anesthetized pigs were used in the study. The animals developed a mildly diabetic state from streptozotocin pretreatment. They were steadily brought within the blood glucose target range of 4.5–6.0 mmol/L in 21 to 121 min and kept within that range for 128 to 238 min (hypoglycemic values varied from 2.9 to 51.1 min). The study confirmed our hypotheses regarding the feasibility of this new principle for blood glucose control, and the algorithm was constantly improved during the study to produce the best results in the last animals. The main obstacles were the drift of the IvS-1 sensor and problems with the calibration procedure, which calls for an improvement in the sensor stability before this method can be applied fully in new studies in animals and humans.

Disruption to Recovery Metabolism in the Fence LizardSceloporus occidentalisInfected with the Malarial ParasitePlasmodium mexicanum

Abstract Western Fence Lizards, Sceloporus occidentalis, are frequently parasitized by the malaria-causing protozoan Plasmodium mexicanum, reducing hemoglobin concentrations, increasing reliance on anaerobic metabolism, and elevating the cost of recovery. We examined the influence of malarial infections in Fence Lizards on aerobic capacity, blood metabolites, and cardiopulmonary activity following activity (<2 min of maximal activity) on a treadmill at 35.0 ± 1.0°C. Aerobic capacity was determined from resting and maximal oxygen uptake. Blood glucose and lactate were measured before activity and at 15 min intervals during 60 min of recovery. Heart rate and ventilation rate were determined from electrocardiograph tracings. Maximal aerobic capacity was over 35% higher in uninfected lizards compared to both malaria-infected lizards and anemic-uninfected animals. Malarial infection decreased lizard resting blood glucose levels, yet induced hyperglycemia during recovery; blood glucose levels were elevated by a...

Sun-Dried Raisins are a Cost-Effective Alternative to Sports Jelly Beans in Prolonged Cycling

The purpose of this study was to examine the effects of a natural carbohydrate (CHO) source in the form of sun-dried raisins (SDRs) vs. Sports Jelly Beans™ (SJBs) on endurance performance in trained cyclists and triathletes. Ten healthy men (18-33 years) completed 1 water-only acclimatization exercise trial and 2 randomized exercise trials administered in a crossover fashion. Each trial consisted of a 120-minute constant-intensity glycogen depletion period followed by a 10-km time trial (TT). During each experimental trial, participants consumed isocaloric amounts of SDRs or SJBs in 20-minute intervals. Measurements included time to complete 10-km TT, power output during 10-km TT, blood glucose levels and respiratory exchange ratio during glycogen depletion period, rate of perceived exertion (RPE), 'flow' questionnaire responses, and a hedonic (i.e., pleasantness) sensory acceptance test. There were no significant differences in endurance performance for TT time (SDRs vs. SJBs, 17.3 ± 0.4 vs. 17.3 ± 0.4 seconds) or power (229.3 ± 13.0 vs. 232.0 ± 13.6 W), resting blood glucose levels (5.8 ± 04 mmol·L(-1) for SDRs and 5.4 ± 0.2 mmol·L(-1) for SJBs), RPE, or flow experiences between SDR and SJB trials. However, the mean sensory acceptance scores were significantly higher for the SDRs compared to the SJBs (50.7 ± 1.7 vs. 44.3 ± 2.7). Consuming SDRs or SJBs during 120 minutes of intense cycling results in similar subsequent TT performances and are equally effective in maintaining blood glucose levels during exercise. Therefore, SDRs are a natural, pleasant, cost-effective CHO alternative to commercial SJBs that can be used during moderate- to high-intensity endurance exercise.

Effect of type 2 diabetes on plasma kallikrein activity after physical exercise and its relationship to post-exercise hypotension

Aim The present study was undertaken to determine the effects of type 2 diabetes (T2D) on plasma kallikrein activity (PKA) and postexercise hypotension (PEH). Methods Ten T2D patients (age: 53.6 ± 1.3 years; body mass index: 30.6 ± 1.0 kg/m 2; resting blood glucose: 157.8 ± 40.2 mg dL −1) and 10 non-diabetic (ND) volunteers (age: 47.5 ± 1.0 years; body mass index: 28.3 ± 0.9 kg/m 2; resting blood glucose: 91.2 ± 10.5 mg dL −1) underwent two experimental sessions, consisting of 20 min of rest plus 20 min of exercise (EXE) at an intensity corresponding to 90% of their lactate threshold (90LT) and a non-exercise control (CON) session. Blood pressure (BP; Microlife BP 3AC1-1 monitor) and PKA were measured during rest and every 15 min for 135 min of the postexercise recovery period (RP). Results During the RP, the ND individuals presented with PEH at 30, 45 and 120 min ( P < 0.05) while, in the T2D patients, PEH was not observed at any time. PKA increased at 15 min postexercise in the ND ( P < 0.05), but not in the T2D patients. Conclusion T2D individuals have a lower PKA response to exercise, which probably suppresses its hypotensive effect, thus reinforcing the possible role of PKA on PEH.

Exogenous glucose oxidation is reduced with carbohydrate feeding during exercise after starvation

Lean healthy individuals are characterized by the ability to rapidly adapt metabolism to acute changes in substrate availability and metabolic rate. However, in glucose-intolerance/insulin-resistant conditions, such as that induced by starvation, the flexibility of tissues to rapidly respond to change in substrate availability is diminished. We asked whether the conundrum of increased glucose demand by the contracting skeletal muscle during prolonged exercise and the glucose intolerance of starvation would result in the obstruction of oxidative disposal of ingested 13C-labeled glucose during exercise. Seven lean, healthy, physically active individuals (2 women, 5 men) completed a randomized crossover study comparing the effects of the normal-fed condition vs a 67-hour water-only fast on the metabolic response to carbohydrate ingestion during 80 minutes of exercise at 56% of maximum oxygen uptake. Compared with the normal condition, fasting resulted in a large overall increase in the rate of fat oxidation (mean effect, 71%; 95% confidence limit, ±22%) and moderate reductions in both exogenous (−54%, ±10%) and endogenous (−40%, ±19%) glucose oxidation rates during exercise. Over the course of exercise, fat oxidation was impermeable to change in the fasting condition, but increased moderately (33%, ±19%) in the normal condition. These changes were associated with a large increase in plasma free fatty-acid concentration (120%, ±64%) and a moderate increase in blood lactate concentration (58%, ±50%). In contrast, large reductions in resting blood glucose (−21%, ±14%) and moderate reductions in plasma insulin concentrations (−47%, ±26%) were observed in the fast condition; but this effect was reversed for glucose (30%, ± 24%) and negated for insulin by the end of exercise. To conclude, a 67-hour fast leads to an impermeable increase in fat oxidation, suppression of both exogenous and endogenous carbohydrate oxidation, and a metabolic response consistent with resistance to contraction-induced exogenous glucose uptake and oxidation.

A One-Year Home-Based Lifestyle Intervention is Effective in Improving Glycemic Control in Patients with Type 2 Diabetes

PURPOSE: Supervised exercise training improves glycemic control in patients with type 2 diabetes. Available resources currently limit the widespread application of supervised exercise training for patients with type 2 diabetes meaning that more practical and economical solutions need to be developed. The aims of this study were to determine the effects of a one-year predominantly home-based lifestyle intervention on glycemic control in patients with type 2 diabetes and investigate the characteristics of patients who respond better to the training. METHODS: A randomized controlled trial was conducted in 176 patients with type 2 diabetes. The lifestyle intervention (n=88) comprised individualized and gym-based exercise training for one month followed by dietary advice and home-based training monitored by telephone exercise counselling for 11 months. Control subjects (n=88) received usual care. Glycemic control (HbA1c, blood glucose), body composition, insulin sensitivity (insulin, QUICKI) and VO2max were assessed at baseline and one year. RESULTS: Compared to controls, the intervention group showed significant (p<0.05) changes in BMI (-1.9kg/m2), waist circumference (-2.8cm), percentage fat mass (-2%), resting blood glucose (-1.1mmol/L), HbA1c (-0.7%), insulin sensitivity (+6%) and VO2max (+2.2ml/kg/min). The improvement in HbA1c was significantly (p<0.05) correlated to baseline VO2max (r=0.27), change in waist circumference (r=0.31) and change in VO2max (r= -0.19). Furthermore change in HbA1c was significantly (p<0.05) independently predicted by baseline VO2max (β=0.26, p<0.01) and change in waist circumference (β=0.26, p=0.02). ROC analysis revealed that patients with a baseline VO2max of less than 21.5ml/kg/min (AUC=0.65, p<0.01) would benefit more from the intervention. CONCLUSION: A one-year, predominantly home-based lifestyle intervention improved glycemic control, body composition and cardiorespiratory fitness in patients with type 2 diabetes compared to usual care. Patients with low levels of cardiorespiratory fitness could be prioritised for treatment.

Gender Differences in Response to Exercise Following a Low Carbohydrate Diet

Low carbohydrate diets (LCD) have gained significant popularity yet lack comprehensive research as to their effectiveness on substrate utilization and exercise performance. PURPOSE: to determine the effect of LCD on substrate utilization and exercise performance, and to identify any gender differences in these responses. METHODS: Sixteen moderately trained subjects (8 men, 8 women) volunteered. Subjects completed a 40 min glycogen-lowering treadmill run at 70% VO2max followed by 3 d of either a LCD (15% CHO, 60% FAT, 25% PRO) or normal mixed diet (55% CHO, 25% FAT, 20% PRO; NM) in a single-blind, counterbalanced, crossover design. Upon completion of the diet and after an overnight fast, they ran for 30 min at 70% VO2max (steady state; SS) followed immediately by a one mile time trial (TT). VO2, HR and RPE were measured throughout exercise. Fingertip blood samples were drawn pre-exercise and immediately after SS and TT. Data were analyzed using a 2 (diet, repeated) × 2 (gender) ANOVA. RESULTS: RER values were significantly lower (P<0.05) at rest and during SS and TT following LCD. Resting blood glucose was significantly lower (P<0.01) following LCD (4.6±0.2 mmol.L−1) vs NM (5.3±0.2 mmol.L−1). Lactate was significantly lower (P<0.01) following LCD (6.0±0.6 mmol.L−1) vs NM (7.8±0.6 mmol.L−1) during TT, while glycerol was significantly higher (P<0.01) during both SS and TT. TT performance was significantly longer (P<0.01) in LCD (493.3±24.9 s) than NM (456.4±20.9 s). A significant dietx gender interaction occurred during TT (P<0.01) such that men's RPE was higher in LCD (17.5±0.4) vs NM (15.9±0.4) whereas the women's was slightly lower (16.0±0.4 and 16.2±0.4, respectively). RPE was significantly higher following LCD during SS (P<0.01). In both SS and TT, CHO oxidation was significantly lower following LCD (P<0.01) and values for men were significantly greater than women (P<0.01). CONCLUSIONS: Short-term LCD resulted in a shift toward greater fat oxidation and impaired running performance. Additionally, men but not women perceived TT performance to be more effortful following LCD.

Oxidative stress impairs cardiac chemoreflexes in diabetic rats.

We investigated the effects of diabetes mellitus and antioxidant treatment on the sensory and reflex function of cardiac chemosensory nerves in rats. Diabetes was induced by streptozotocin (STZ; 85 mg/kg ip). Subgroups of sham- and STZ-treated rats were chronically treated with an antioxidant, vitamin E (60 mg/kg per os daily, started 2 days before STZ). Animals were studied 6-8 wk after STZ injection. We measured renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MABP), and cardiac vagal and sympathetic afferent activities in response to stimulation of chemosensitive sensory nerves in the heart by epicardial application of capsaicin (Caps) and bradykinin (BK). In cardiac sympathetic-denervated rats, Caps and BK (1-10.0 microg) evoked a vagal afferent mediated reflex depression of RSNA and MABP, which was significantly blunted in STZ-treated rats (P < 0.05). In vagal-denervated rats, Caps and BK (1-10.0 microg) evoked a sympathetic afferent-mediated reflex elevation of RSNA and MABP, which also was significantly blunted in STZ-treated rats (P < 0.05). Chronic vitamin E treatment effectively prevented these cardiac chemoreflex defects in STZ-treated rats without altering resting blood glucose or hemodynamics. STZ-treated rats with insulin replacement did not exhibit impaired cardiac chemoreflexes. In afferent studies, Caps and BK (0.1 g-10.0 microg) increased cardiac vagal and sympathetic afferent nerve activity in a dose-dependent manner in sham-treated rats. These responses were significantly blunted in STZ-treated rats. Vitamin E prevented the impairment of afferent discharge to chemical stimulation in STZ rats. The following were concluded: STZ-induced, insulin-dependent diabetes in rats extensively impairs the sensory and reflex properties of cardiac chemosensitive nerve endings, and these disturbances can be prevented by chronic treatment with vitamin E. These results suggest that oxidative stress plays an important role in the neuropathy of this autonomic reflex in diabetes.

Insulin Receptor Substrate-2 Is Not Necessary for Insulin- and Exercise-stimulated Glucose Transport in Skeletal Muscle

Insulin receptor substrate-2-deficient (IRS2(-/-)) mice develop type 2 diabetes. The purpose of this study was to determine whether there is a defect in basal, insulin-, and exercise-stimulated glucose transport in the skeletal muscle of these animals. IRS2(-/-) and wild-type (WT) mice (male, 8-10 weeks) exercised on a treadmill for 1 h or remained sedentary. 2-Deoxyglucose (2DG) uptake was measured in isolated soleus muscles incubated in vitro in the presence or absence of insulin. Resting blood glucose concentration in IRS2(-/-) mice (10.3 mM) was higher than WT animals (4.1 mM), but there was a wide range among the IRS2(-/-) mice (3-25 mM). Therefore, IRS2(-/-) mice were divided into two subgroups based on blood glucose concentrations (IRS2(-/-)L < 7.2 mM, IRS2(-/-)H > 7.2 mM). Only IRS2(-/-)H had lower basal, exercise-, and submaximally insulin-stimulated 2DG uptake, while maximal insulin-stimulated 2DG uptake was similar among the three groups. The ED(50) for insulin to stimulate 2DG uptake above basal in IRS2(-/-)H was higher than WT and IRS2(-/-)L mice, suggesting insulin resistance in the skeletal muscle from the IRS2(-/-) mice with high blood glucose concentrations. Furthermore, resting blood glucose concentrations from all groups were negatively correlated to submaximally insulin-stimulated 2DG uptake (r(2) = 0.33, p < 0.01). Muscle GLUT4 content was significantly lower in IRS2(-/-)H mice compared with WT and IRS2(-/-)L mice. These results demonstrate that the IRS2 protein in muscle is not necessary for insulin- or exercise-stimulated glucose transport, suggesting that the onset of diabetes in the IRS2(-/-) mice is not due to a defect in skeletal muscle glucose transport; hyperglycemia may cause insulin resistance in the muscle of IRS2(-/-) mice.

Plasma glucose levels predict the disrupting effects of adrenoceptor antagonists on enhancement of memory storage

Adrenoceptor antagonists block the enhancement of memory storage produced by epinephrine injection, but not that produced by glucose injection. The present experiment determined whether adrenoceptor antagonists modify resting blood glucose levels or the magnitude of epinephrine-, glucose-, and footshock-induced increases in circulating glucose levels in a manner related to these previously observed effects on memory. The α- and β-adrenoceptor antagonists, phenoxybenzamine and propranolol, respectively, were injected in rats 30 min prior to administration of epinephrine, glucose, or footshock. Plasma glucose levels were sampled during the next 30 min. Epinephrine-induced increases in plasma glucose levels were potentiated by phenoxybenzamine and were attenuated and delayed by propranolol. The adrenoceptor antagonists did not alter resting plasma glucose levels, or the increases in plasma glucose levels resulting from glucose injection or footshock. These findings suggest that phenoxybenzamine and propranolol alter blood glucose responses to epinephrine injection in a manner which may contribute to attenuation of epinephrine-induced enhancement of memory storage with peripheral injections of adrenoceptor antagonists.

Training improves glucose homeostasis in rats during exercise via glucose production

The effects of endurance training (running 1 h/day at 35 m/min, 10% grade) on glucose homeostasis during exercise (running 20 m/min) was studied in 30-h fasted rats. Primed-continuous infusion of [6-3H]- and [U-14C]glucose were employed to assess rates of appearance (Ra), disappearance (Rd), and apparent recycling. Training resulted in a 65% increase in skeletal muscle succinate dehydrogenase (SDH) activity but did not significantly influence body weight. Resting blood glucose concentrations were not significantly different between controls, 5.01 +/- 0.19 mM, and trained animals, 4.86 +/- 0.16 mM. Exercise resulted in a more rapid decline in blood glucose levels for control animals, reaching a value of 2.35 +/- 0.39 mM at 60 min, compared with 3.69 +/- 0.47 mM for trained animals. Glucose Ra was not significantly different between groups at rest, and rose for both groups during exercise. However, for controls Ra plateaued between 15 and 60 min of exercise at 11.03 +/- 0.73 mumol.100 g-1.min-1, whereas trained animals demonstrated a continuous rise to 17.13 +/- 1.18 mumol.100 g-1.min-1. Glucose Rd values were not significantly different between groups during the first 30 min of exercise but were significantly higher for trained animals during the final 30 min. As a result of the higher glucose Ra, trained animals demonstrated a smaller mean difference between Ra and Rd during exercise when compared with controls, -0.27 +/- 0.14 vs. -0.96 +/- 0.17 mumol.100 g-1.min-1. Trained animals further demonstrated significantly higher rates of glucose carbon recycling during the final 30 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)