Rationale and design of a randomized controlled trial examining oral administration of bisphenol A on hepatic glucose production and skeletal muscle insulin sensitivity in adults.

Previous observational studies have shown that the endocrine disrupting chemical bisphenol A (BPA) is associated with type 2 diabetes, but few studies have examined direct effects of BPA on human health. The purpose of this study is to determine whether orally administered BPA at the US Environmental Protection Agency (EPA) safe dose of 50 µg/kg body weight has an adverse effect on hepatic glucose production and skeletal muscle insulin sensitivity. Forty, non-habitually active, healthy adults of normal weight will be enrolled. Participants will begin with a 2-day baseline energy balance diet low in bisphenols in which urine and blood will be collected, and standard tests performed to assess the primary outcome measures of hepatic glucose production (via [6,6-2H] glucose infusion) and skeletal muscle insulin sensitivity (via euglycemic hyperinsulinemic clamp technique). Secondary outcome measures are fasting hormones/endocrine factors (insulin, glucose, C-peptide, Pro-insulin, adiponectin, 17-beta-estradiol, free fatty acids) related to the pathogenesis of type 2 diabetes. Participants will then be randomly assigned to a 4-day energy balance diet plus oral administration of BPA at 50 µg/kg body weight (Diet + BPA) or 4-day energy balance diet plus oral administration of placebo (Diet + No BPA); all outcome measures will be reassessed after 4 days. Findings from this study will provide a framework for other studies in this area, and provide much needed experimental evidence using gold standard measures as to whether oral BPA administration over several days poses any risk of type 2 diabetes.

Ripple Effect of Lifestyle Interventions During Pregnancy on Untreated Partners' Weight.

OBJECTIVE: Weight-loss interventions have a positive "ripple effect" on untreated partners' weight, but ripple effects in pregnancy are unknown. The objective of this study was to determine whether prenatal lifestyle interventions that reduce gestational weight gain in pregnant women have a positive ripple effect on untreated partners' weight. METHODS: Two clinical trials with the same outcome measures randomly assigned pregnant women to a lifestyle intervention or usual care. Untreated partners were randomly assigned according to their pregnant partner's group allocation and were assessed at study entry (~13 weeks' gestation), 35 weeks' gestation, and 6 and 12 months after delivery. RESULTS: A total of 122 partners (100% male, 23% Hispanic, 82% married, and 48% with obesity) were randomly assigned to the intervention (n = 59) or usual care (n = 63). There was no intervention or intervention-by-time interaction effect on partner weight (P = 0.795). Partner weight changes were not statistically significant (P = 0.120) from study entry to 35 weeks' gestation (mean 0.19 kg; 95% CI: -0.73 to 1.24) or to 12 months after delivery (mean 0.82 kg; 95% CI: -0.26 to 1.91). CONCLUSIONS: There was no evidence of a ripple effect on partner weight. In a self-selected sample, partners of pregnant women appeared not to experience sympathy weight gain.

Randomized controlled clinical trial of behavioral lifestyle intervention with partial meal replacement to reduce excessive gestational weight gain.

Background: Behavioral lifestyle interventions during pregnancy can prevent excessive gestational weight gain (GWG) in women with normal weight; however, effective interventions to reduce GWG in ethnically diverse women with obesity are lacking. Objective: A randomized controlled trial was conducted to test whether a behavioral lifestyle intervention with partial meal replacement reduces GWG rate in Hispanic and non-Hispanic women with overweight or obesity relative to enhanced usual care. Design: Participants (n = 257) were recruited in San Luis Obispo, California, and Providence, Rhode Island, between November 2012 and May 2016. Participants were pregnant (mean ± SD: 13.6 ± 1.8 wk of gestation) with overweight or obesity and had a mean age of 30.3 y; 41.6% of participants were Hispanic. Women were randomly assigned within site and by ethnicity to enhanced usual care (n = 128) or to a behavioral lifestyle intervention with partial meal replacement (n = 129). The primary outcome was GWG per week of observation. Secondary outcomes were proportions exceeding Institute of Medicine (IOM) guidelines for total GWG, changes in weight-control behaviors and cardiovascular disease risk factors, and incidence of pregnancy complications. Study retention was 99.6% (256 of 257). Results: The intervention compared with usual care resulted in less mean ± SD weekly GWG (0.33 ± 0.25 compared with 0.39 ± 0.23 kg/wk; P = 0.02) and total GWG (9.4 ± 6.9 compared with 11.2 ± 7.0 kg; P = 0.03) and reduced the proportion of women who exceeded IOM guidelines for total GWG (41.1% compared with 53.9%; P = 0.03). No significant group × time × demographic subgroup (ethnicity, BMI, age, parity, and income) interactions were observed. Among intervention participants, greater meal replacement intake was related to reduced GWG rate (ß = -0.07; 95% CI:-0.12, -0.03; P = 0.002). The intervention compared with usual care increased weight-control strategies (P < 0.0001) and cognitive restraint (P < 0.0001) and reduced triglycerides (P = 0.03). Conclusion: Prenatal behavioral intervention with partial meal replacement significantly reduced GWG in Hispanic and non-Hispanic women with overweight or obesity. This trial was registered at www.clinicaltrials.gov as NCT01545934.

Effects of maternal lifestyle intervention during pregnancy on untreated partner weight: Results from fit for delivery study.

OBJECTIVE: To test the hypothesis that untreated partners of pregnant women receiving a prenatal lifestyle intervention (vs. standard care) would lose more weight during pregnancy and postpartum. METHODS: Fit for Delivery was a study of 401 pregnant women with overweight/obesity (OW/OB) and normal weight (NW) randomized to prenatal lifestyle intervention or standard care. Mother's self-report of partners' weight was obtained at study entry (<16 weeks gestation), 30 weeks gestation, and 6 and 12 months postpartum. RESULTS: At study entry, 157 of 200 (78%) of intervention mothers and 144 of 201 (72%) of standard care mothers reported having a partner. In intent-to-treat analyses, there was no significant treatment × time effects on partner weight (P = 0.67). In secondary analyses, partners of OW/OB intervention women lost weight from study entry to 6 and 12 months postpartum (-0.5 ± 9.5 kg, -1.0 ± 9.3 kg; P < 0.05), while partners of standard care women gained weight during the same time frame (+2.5 ± 6.7 kg, +2.9 ± 7.4 kg; P < 0.05); adjusting for partner study entry BMI removed these effects. CONCLUSIONS: Lifestyle intervention delivered to pregnant women did not significantly reduce weight of untreated partners. Future research is needed to test prenatal interventions that engage partners and use objective measures of weight.

Effects of combined creatine and sodium bicarbonate supplementation on repeated sprint performance in trained men.

Creatine and sodium bicarbonate supplementation independently increase exercise performance, but it remains unclear whether combining these 2 supplements is more beneficial on exercise performance. The purpose of this study was to evaluate the impact of combining creatine monohydrate and sodium bicarbonate supplementation on exercise performance. Thirteen healthy, trained men (21.1 ± 0.6 years, 23.5 ± 0.5 kg·m(-2), 66.7 ± 5.7 ml·(kg·m)(-1) completed 3 conditions in a double-blinded, crossover fashion: (a) Placebo (Pl; 20 g maltodextrin + 0.5 g·kg(-1) maltodextrin), (b) Creatine (Cr; 20 g + 0.5 g·kg(-1) maltodextrin), and (c) Creatine plus sodium bicarbonate (Cr + Sb; 20 g + 0.5 g·kg(-1) sodium bicarbonate). Each condition consisted of supplementation for 2 days followed by a 3-week washout. Peak power, mean power, relative peak power, and bicarbonate concentrations were assessed during six 10-second repeated Wingate sprint tests on a cycle ergometer with a 60-second rest period between each sprint. Compared with Pl, relative peak power was significantly higher in Cr (4%) and Cr + Sb (7%). Relative peak power was significantly lower in sprints 4-6, compared with that in sprint 1, in both Pl and Cr. However, in Cr + Sb, sprint 6 was the only sprint significantly lower compared with sprint 1. Pre-Wingate bicarbonate concentrations were significantly higher in Cr + Sb (10%), compared with in Pl and Cr, and mean concentrations remained higher after sprint 6, although not significantly. Combining creatine and sodium bicarbonate supplementation increased peak and mean power and had the greatest attenuation of decline in relative peak power over the 6 repeated sprints. These data suggest that combining these 2 supplements may be advantageous for athletes participating in high-intensity, intermittent exercise.

Aerobic exercise reduces neuronal responses in food reward brain regions.

Acute exercise suppresses ad libitum energy intake, but little is known about the effects of exercise on food reward brain regions. After an overnight fast, 30 (17 men, 13 women), healthy, habitually active (age = 22.2 ± 0.7 yr, body mass index = 23.6 ± 0.4 kg/m(2), Vo(2peak) = 44.2 ± 1.5 ml·kg(-1)·min(-1)) individuals completed 60 min of exercise on a cycle ergometer or 60 min of rest (no-exercise) in a counterbalanced, crossover fashion. After each condition, blood oxygen level-dependent responses to high-energy food, low-energy food, and control visual cues, were measured by functional magnetic resonance imaging. Exercise, compared with no-exercise, significantly (P < 0.005) reduced the neuronal response to food (high and low food) cues vs. control cues in the insula (-0.37 ± 0.13 vs. +0.07 ± 0.18%), putamen (-0.39 ± 0.10 vs. -0.10 ± 0.09%), and rolandic operculum (-0.37 ± 0.17 vs. 0.17 ± 0.12%). Exercise alone significantly (P < 0.005) reduced the neuronal response to high food vs. control and low food vs. control cues in the inferior orbitofrontal cortex (-0.94 ± 0.33%), insula (-0.37 ± 0.13%), and putamen (-0.41 ± 0.10%). No-exercise alone significantly (P < 0.005) reduced the neuronal response to high vs. control and low vs. control cues in the middle (-0.47 ± 0.15%) and inferior occipital gyrus (-1.00 ± 0.23%). Exercise reduced neuronal responses in brain regions consistent with reduced pleasure of food, reduced incentive motivation to eat, and reduced anticipation and consumption of food. Reduced neuronal response in these food reward brain regions after exercise is in line with the paradigm that acute exercise suppresses subsequent energy intake.

Metformin's effect on exercise and postexercise substrate oxidation.

Exercise and metformin may prevent or delay Type 2 diabetes by, in part, raising the capacity for fat oxidation. Whether the addition of metformin has additive effects on fat oxidation during and after exercise is unknown. Therefore, the purpose of this study was to evaluate the effect of metformin on substrate oxidation during and after exercise. Using a double-blind, counter-balanced crossover design, substrate oxidation was assessed by indirect calorimetry in 15 individuals taking metformin (2,000 mg/d) and placebo for 8-10 d. Measurements were made during cycle exercise at 5 submaximal cycle workloads, starting at 30% peak work (W(peak)) and increasing by 10% every 8 min to 70% W(peak). Substrate oxidation was also measured for 50 min postexercise. Differences between conditions were assessed using analysis of variance with repeated measures, and values are reported as M + or - SE. During exercise, fat oxidation (0.19 + or - 0.03 vs. 0.15 + or - 0.01 g/min, p < .01) and percentage of energy from fat (32% + or - 3% vs. 28% + or - 3%, p < .01) were higher with metformin than with placebo. Postexercise, metformin slightly lowered fat oxidation (0.12 + or - 0.02 to 0.10 + or - 0.02 g/min, p < .01) compared with placebo. There was an inverse relationship between postexercise fat oxidation and the rate of fat oxidation during exercise (r = -.68, p < .05). In healthy individuals, metformin has opposing actions on fat oxidation during and after exercise. Whether the same effects are evident in insulin-resistant individuals remains to be determined.

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals.

Results from the Diabetes Prevention Program highlight the effectiveness of metformin or regular physical activity in the prevention of type 2 diabetes. Independently, metformin and exercise increase insulin sensitivity, but they have not been studied in combination. To assess the combined effects, insulin-resistant subjects (n = 9) matched for weight, body fat, and aerobic fitness were studied before any treatment (B), after 2-3 wk of 2,000 mg/day metformin (MET), and after metformin plus 40 min of exercise at 65% Vo(2peak) (MET + Ex). A second group (n = 7) was studied at baseline and after an identical bout of exercise with no metformin (Ex). Biopsies of the vastus lateralis were taken at B, after MET, immediately after MET + Ex (group 1), or immediately after Ex (group 2). Insulin sensitivity was assessed 4 h postexercise with a euglycemic hyperinsulinemic (40 mU.m(2).min(-1)) clamp enriched with [6,6-(2)H]glucose. Insulin sensitivity was 54% higher after Ex (P < 0.01), but there was no change with Met + Ex. Skeletal muscle AMPKalpha2 activity was elevated threefold (P < 0.01) after Ex, but there was no increase with MET + Ex. These findings suggest that the combination of short-term metformin treatment and an acute bout of exercise does not enhance insulin sensitivity, and the addition of metformin may attenuate the well-documented effects of exercise alone.

Physical activity and hormonal regulation of appetite: sex differences and weight control.

Physical activity is an important contributor to regulation of energy balance and body composition. In this article, we separate the impact of exercise from the confounding influence of energy imbalance and highlight sex differences in hormonal and appetite responses to physical activity. The evolving story may influence our thinking regarding the use of physical activity to manage body composition.

Effects of exercise on energy-regulating hormones and appetite in men and women.

When previously sedentary men and women follow exercise training programs with ad libitum feeding, men lose body fat, but women do not. The purpose of this study was to evaluate whether this observation could be related to sex differences in the way energy-regulating hormones and appetite perception respond to exercise. Eighteen (9 men, 9 women) overweight/obese individuals completed four bouts of exercise with energy added to the baseline diet to maintain energy balance (BAL), and four bouts without energy added to induce energy deficit (DEF). Concentrations of acylated ghrelin, insulin, and leptin, as well as appetite ratings were measured in response to a meal after a no-exercise baseline and both exercise conditions. In men, acylated ghrelin area under the curve (AUC) was not different between conditions. In women, acylated ghrelin AUC was higher after DEF (+32%) and BAL (+25%), and the change from baseline was higher than men (P < 0.05). In men, insulin AUC was reduced (-17%) after DEF (P < 0.05), but not BAL. In women, insulin AUC was lower (P < 0.05) after DEF (-28%) and BAL (-15%). Leptin concentrations were not different across conditions in either sex. In men, but not in women, appetite was inhibited after BAL relative to DEF. The results indicate that, in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained. The data are consistent with the paradigm that mechanisms to maintain body fat are more effective in women.

Impact of metformin on peak aerobic capacity.

Individually, exercise and the drug metformin have been shown to prevent or delay type 2 diabetes. Metformin mildly inhibits complex I of the electron transport system and may impact aerobic capacity in people exercising while taking metformin. The purpose of the study was to evaluate the effects of metformin on maximal aerobic capacity in healthy individuals without mitochondrial dysfunction. Seventeen healthy, normal-weight men (n=11) and women (n=6) participated in a double-blind, placebo-controlled, cross-over design. Peak aerobic capacity was measured twice using a continuous, incrementally graded protocol; once after 7-9 d of metformin (final dose=2000 mg/d) and once with placebo, with 1 week between tests. The order of the conditions was counterbalanced. Peak oxygen uptake (VO2 peak), heart rate (HR), ventilation (VE), respiratory exchange ratio (RER), rating of perceived exertion (RPE), and test duration were compared across conditions using paired t tests with the R statistical program. VO2 peak (-2.7%), peak heart rate (-2.0%), peak ventilation (-6.2%), peak RER (-3.0%), and exercise duration (-4.1%) were all reduced slightly, but significantly, with metformin (all p<0.05). There was no effect of metformin on RPE or ventilatory breakpoint. Correlations between the decrement in VO2 peak and any of the other outcome variables were weak (r2<0.20) and not significant. Short-term treatment with metformin has statistically significant, but physiologically subtle, effects that reduce key outcomes related to maximal exercise capacity. Whether this small but consistent effect is manifested in people with insulin resistance or diabetes who already have some degree of mitochondrial dysfunction remains to be determined.

Effects of short-term exercise and energy surplus on hormones related to regulation of energy balance.

Energy surplus raises circulating concentrations of leptin and insulin while lowering plasma ghrelin. Exercise has the opposite effects. The purpose of this study was to determine whether exercise counters the hormonal effects of energy surplus independent of changes in energy balance. To do that, we assessed plasma concentrations of leptin, insulin, and ghrelin at baseline, after overfeeding, and after overfeeding plus exercise. Baseline (B) leptin and insulin concentrations and ghrelin area under the curve were measured during an oral glucose challenge in 9 healthy, active subjects (6 male, 3 female) after 2 days in energy balance without exercise. Measurements were repeated after subjects were overfed by +3213 +/- 849 kJ/d for 3 more sedentary days (OF). In the third condition, the same net energy surplus (+3125 +/- 933 kJ/d) was generated for 24 hours by doubling the overfeeding (+6284 +/- 1669 kJ/d) and countering it with a bout of exercise (expenditure = 3063 +/- 803 kJ); and measurements were made the next day (OF + EX). Compared with B, leptin went up (5.8 +/- 8.2 to 7.6 +/- 10.6 ng/mL) after OF, but was not significantly higher after OF + EX (7.1 +/- 10.2 ng/mL). Compared with B, insulin was +36% and +43% higher after OF and OF + EX, respectively. In contrast, ghrelin area under the curve did not change after OF but was significantly lower (-14%) than B or OF after OF + EX (indicating greater suppression). These data suggest that the effect of short-term exercise on fasting leptin and insulin depends on energy balance but the ghrelin response may be partially mediated by effects of exercise independent of energy balance.

Contributions of working muscle to whole body lipid metabolism are altered by exercise intensity and training.

To evaluate the contribution of working muscle to whole body lipid oxidation, we examined the effects of exercise intensity and endurance training (9 wk, 5 days/wk, 1 h, 75% Vo(2 peak)) on whole body and leg free fatty acid (FFA) kinetics in eight male subjects (26 +/- 1 yr, means +/- SE). Two pretraining trials [45 and 65% Vo(2 max) (45UT, 65UT)] and two posttraining trials [65% of pretraining Vo(2 peak) (ABT), and 65% of posttraining Vo(2 peak) (RLT)] were performed using [1-(13)C]palmitate infusion and femoral arteriovenous sampling. Training increased Vo(2 peak) by 15% (45.2 +/- 1.2 to 52.0 +/- 1.8 ml.kg(-1).min(-1), P < 0.05). Muscle FFA fractional extraction was lower during exercise (EX) compared with rest regardless of workload or training status ( approximately 20 vs. 48%, P < 0.05). Two-leg net FFA balance increased from net release at rest ( approximately -36 micromol/min) to net uptake during EX for 45UT (179 +/- 75), ABT (236 +/- 63), and RLT (136 +/- 110) (P < 0.05), but not 65UT (51 +/- 127). Leg FFA tracer measured uptake was higher during EX than rest for all trials and greater during posttraining in RLT (716 +/- 173 micromol/min) compared with pretraining (45UT 450 +/- 80, 65UT 461 +/- 72, P < 0.05). Leg muscle lipid oxidation increased with training in ABT (730 +/- 163 micromol/min) vs. 65UT (187 +/- 94, P < 0.05). Leg muscle lipid oxidation represented approximately 62 and 30% of whole body lipid oxidation at lower and higher relative intensities, respectively. In summary, training can increase working muscle tracer measured FFA uptake and lipid oxidation for a given power output, but both before and after training the association between whole body and leg lipid metabolism is reduced as exercise intensity increases.

Changes in ventilatory threshold at high altitude: effect of antioxidants.

PURPOSE: To investigate the effects of prolonged hypoxia and antioxidant supplementation on ventilatory threshold (VT) during high-altitude (HA) exposure (4300 m). METHODS: Sixteen physically fit males (25 +/- 5 yr; 77.8 +/- 8.5 kg) performed an incremental test to maximal exertion on a cycle ergometer at sea level (SL). Subjects were then matched on VO2peak, ventilatory chemosensitivity, and body mass and assigned to either a placebo (PL) or antioxidant (AO) supplement group in a randomized, double-blind manner. PL or AO (12 mg of beta-carotene, 180 mg of alpha-tocopherol acetate, 500 mg of ascorbic acid, 100 mug of selenium, and 30 mg of zinc daily) were taken 21 d prior to and for 14 d at HA. During HA, subjects participated in an exercise program designed to achieve an energy deficit of approximately 1400 kcal.d(-1). VT was reassessed on the second and ninth days at HA (HA2, HA9). RESULTS: Peak power output (Wpeak) and VO2peak decreased (28%) in both groups upon acute altitude exposure (HA2) and were unchanged with acclimatization and exercise (HA9). Power output at VT (WVT) decreased from SL to HA2 by 41% in PL, but only 32% in AO (P < 0.05). WVT increased in PL only during acclimatization (P < 0.05) and matched AO at HA9. Similar results were found when VT was expressed in terms of % Wpeak and % VO2peak. CONCLUSIONS: VT decreases upon acute HA exposure but improves with acclimatization. Prior AO supplementation improves VT upon acute, but not chronic altitude exposure.

Endurance training has little effect on active muscle free fatty acid, lipoprotein cholesterol, or triglyceride net balances.

We evaluated the hypothesis that net leg total FFA, LDL-C, and TG uptake and HDL-C release during moderate-intensity cycling exercise would be increased following endurance training. Eight sedentary men (26 +/- 1 yr, 77.4 +/- 3.7 kg) were studied in the postprandial state during 90 min of rest and 60 min of exercise twice before (45% and 65% V(O2 peak)) and twice after 9 wk of endurance training (55% and 65% posttraining V(O2 peak)). Measurements across an exercising leg were taken to be a surrogate for active skeletal muscle. To determine limb lipid exchange, femoral arterial and venous blood samples drawn simultaneously at rest and during exercise were analyzed for total and individual FFA (e.g., palmitate, oleate), LDL-C, HDL-C, and TG concentrations, and limb blood flow was determined by thermodilution. The transition from rest to exercise resulted in a shift from net leg total FFA release (-44 +/- 16 micromol/min) to uptake (193 +/- 49 micromol/min) that was unaffected by either exercise intensity or endurance training. The relative net leg release and uptake of individual FFA closely resembled their relative abundances in the plasma with approximately 21 and 41% of net leg total FFA uptake during exercise accounted for by palmitate and oleate, respectively. Endurance training resulted in significant changes in arterial concentrations of HDL-C (49 +/- 5 vs. 52 +/- 5 mg/dl, pre vs. post) and LDL-C (82 +/- 9 vs. 76 +/- 9 mg/dl, pre vs. post), but there was no net TG or LDL-C uptake or HDL-C release across the resting or active leg before or after endurance training. In conclusion, endurance training favorably affects blood lipoprotein profiles, even in young, healthy normolipidemic men, but muscle contractions per se have little effect on net leg LDL-C, or TG uptake or HDL-C release during moderate-intensity cycling exercise. Therefore, the favorable effects of physical activity on the lipid profiles of young, healthy normolipidemic men in the postprandial state are not attributable to changes in HDL-C or LDL-C exchange across active skeletal muscle.

Cytokine responses at high altitude: effects of exercise and antioxidants at 4300 m.

PURPOSE: This study tested the hypothesis that antioxidant supplementation would attenuate plasma cytokine (IL-6, tumor necrosis factor (TNF)-alpha), and C-reactive protein (CRP) concentrations at rest and in response to exercise at 4300-m elevation. METHODS: A total of 17 recreationally trained men were matched and assigned to an antioxidant (N = 9) or placebo (N = 8) group in a double-blinded fashion. At sea level (SL), energy expenditure was controlled and subjects were weight stable. Then, 3 wk before and throughout high altitude (HA), an antioxidant supplement (10,000 IU beta-carotene, 200 IU alpha-tocopherol acetate, 250 mg ascorbic acid, 50 microg selenium, 15 mg zinc) or placebo was given twice daily. At HA, energy expenditure increased approximately 750 kcal.d(-1) and energy intake decreased approximately 550 kcal.d, resulting in a caloric deficit of approximately 1200-1500 kcal.d(-1). At SL and HA day 1 (HA1) and day HA13, subjects exercised at 55% of VO2peak until they expended approximately 1500 kcal. Blood samples were taken at rest, end of exercise, and 2, 4, and 20 h after exercise. RESULTS: No differences were seen between groups in plasma IL-6, CRP, or TNF-alpha at rest or in response to exercise. For both groups, plasma IL-6 concentration was significantly higher at the end of exercise, 2, 4, and 20 h after exercise at HA1 compared with SL and HA13. Plasma CRP concentration was significantly elevated 20 h postexercise for both groups on HA1 compared to SL and HA13. TNF-alpha did not differ at rest or in response to exercise. CONCLUSION: Plasma IL-6 and CRP concentrations were elevated following exercise at high altitude on day 1, and antioxidant supplementation did not attenuate the rise in plasma IL-6 and CRP concentrations associated with hypoxia, exercise, and caloric deficit.

Interactions between energy surplus and short-term exercise on glucose and insulin responses in healthy people with induced, mild insulin insensitivity.

Short-term exercise can enhance insulin action, but the effect may be negated by the opposing action of energy surplus. The purpose of this investigation was to test the hypothesis that a single exercise bout would increase insulin action, even when opposed by a concurrent energy surplus. After 2 days in energy balance without exercise, baseline glucose and insulin areas under the curve and the insulin sensitivity index (C-ISI) were measured during an oral glucose tolerance test in 9 healthy, habitually active subjects (6 males, 3 females). A state of relative insulin insensitivity was then induced by systematic overfeeding (OF) to generate a daily energy surplus of 768 +/- 203 kcal/d for 3 days, and the oral glucose tolerance test was repeated. In the following 24 hours, the OF was increased approximately 2-fold (+6284 +/- 1669 kJ/d) and subjects performed a single bout of exercise (expenditure = 3063 +/- 803 kJ) to maintain the same energy surplus (+3125 +/- 933 kJ/d; OF and exercise) as OF. After OF, fasting insulin tended to be higher (+36%, P = .099), insulin AUC rose by 38% (P = .002), and C-ISI declined from 6.6 +/- 3.1 to 4.6 +/- 1.8 (P = .007) compared with baseline. After OF and exercise, fasting insulin remained elevated (+43% compared with baseline; P = .043) and C-ISI rose only slightly (4.6 +/- 1.8 to 5.2 +/- 2.3; P = .058), but insulin AUC declined by 20% (P = .048) compared with OF. A single exercise bout, opposed by a concurrent energy surplus, decreased the insulin response to a glucose challenge, but only partially restored the insulin AUC to baseline and had no impact on C-ISI or fasting insulin concentrations.

Effects of heat removal through the hand on metabolism and performance during cycling exercise in the heat.

OBJECTIVE: This two-part study tested the hypotheses that the use of a new cooling device, purported to extract heat from the body core through the palm of the hand, would (a) attenuate core temperature rise during submaximal exercise in the heat, thereby suppressing exercise-associated metabolic changes, and (b) facilitate a higher sustained workload, thus shortening the completion time of a time-trial performance test. METHODS: In Study 1, 8 male triathletes (age 27.9 +/- 2.0 yrs, mass 77.2 +/- 3.1 kg, VO2peak 59.0 +/- 4.1 ml x min(-1) x kg(-1)) cycled for 1 hr at the same absolute workload (approximately 60% VO2peak) in a heated room (31.9 +/- 0.1 degrees C, 24 +/- 1% humidity) on two occasions counterbalanced for cooling (C) or noncooling (NC). In Study 2, 8 similar subjects (age 26.9 +/- 2.0 yrs, mass 75.2 +/- 3.7 kg, VO2peak 54.1 +/- 3.1 ml x min(-1) x kg(-1)) performed two 30-km cycling time-trial performance tests under the same conditions (C(T), NC(T)). RESULTS: In Study 1, cooling attenuated the rise in tympanic temperature (T(TY)) (1.2 +/- 0.2 vs. 1.8 +/- 0.2 degrees C; p < 0.01) and lowered mean oxygen consumption (VO2, 2.4 +/- 0.1 vs. 2.7 +/- 0.1 L x min(-1); p < 0.05) and blood lactate (1.7 +/- 0.2 vs. 2.2 +/- 0.2 mmol x L(-1); p < 0.01) during exercise. There were no significant differences in respiratory exchange ratio (RER), blood glucose, heart rate (HR), face temperature (T(F)), or back temperature (T(B)) between NC and C. In Study 2, time to complete 30 km was 6 +/- 1% less with cooling than without cooling (60.9 +/- 2.0 vs. 64.9 +/- 2.6 min; p < 0.01). During the last 20% of C(T), subjects sustained a workload that was 14 +/- 5% (p = 0.06) higher than NC(T) at the same T(TY) and HR. CONCLUSIONS: Heat extraction through the hand during cycle ergometer exercise in the heat can (a) lower T(TY), lactate concentration, and VO2 during a submaximal set-workload test and (b) reduce the time it takes to complete a 30-km time-trial test.

Antioxidant supplementation does not attenuate oxidative stress at high altitude.

INTRODUCTION: Hypobaric hypoxia and heightened metabolic rate increase free radical production. PURPOSE: We tested the hypothesis that antioxidant supplementation would reduce oxidative stress associated with increased energy expenditure (negative energy balance) at high altitude (HA 4300 m). METHODS: For 12 d at sea level (SL), 18 active men were fed a weight-stabilizing diet. Testing included fasting blood and 24-h urine samples to assess antioxidant status [plasma alpha-tocopherol, beta-carotene, lipid hydroperoxides (LPO), and urinary 8-hydroxydeoxyguanosine (8-OHdG)] and a prolonged submaximal (55% Vo2peak) oxidative stress index test (OSI) to evaluate exercise-induced oxidative stress (plasma LPO, whole blood reduced and oxidized glutathione, glutathione peroxidase, and urinary 8-OHdG). Subjects were then matched and randomly assigned to either a placebo or antioxidant supplement group for a double-blinded trial. Supplementation (20,000 IU of beta-carotene, 400 IU alpha-tocopherol acetate, 500 mg ascorbic acid, 100 microg selenium, and 30 mg zinc, or placebo) was begun 3 wk prior to and throughout a 14-d HA intervention. At HA, subjects' daily energy intake and expenditure were adjusted to achieve a caloric deficit of approximately 1400 kcal. Fasting blood and 24-h urine samples were collected throughout HA and the OSI test was repeated on HA day 1 and day 13. RESULTS: Resting LPO concentrations increased and urinary 8-OHdG concentrations decreased over HA with no effect of supplementation. Prolonged submaximal exercise was not associated with increased concentrations of oxidative stress markers at SL or HA. CONCLUSIONS: Antioxidant supplementation did not significantly affect markers of oxidative stress associated with increased energy expenditure at HA.

Foot cooling reduces exercise-induced hyperthermia in men with spinal cord injury.

UNLABELLED: The number of individuals with spinal cord injury (SCI) participating in sports at recreational and elite levels is on the rise. However, loss of autonomic nervous system function below the lesion can compromise thermoregulatory capacity and increase the risk of heat stress relative to able-bodied (AB) individuals. PURPOSE: To test the hypotheses that exercise in a heated environment would increase tympanic temperature (TTY) more in individuals with SCI than AB individuals, and that foot cooling using a new device would attenuate the rise in TTY during exercise in both groups. METHODS: Six subjects with SCI (lesions C5-T5) and six AB controls were tested in a heated environment (means +/- SEM, temperature = 31.8 +/- 0.2 degrees C, humidity = 26 +/- 1%) for 45 min at 66% +/- 5 of arm cranking VO2peak and 30 min of recovery on two separate occasions with foot cooling (FC) or no foot cooling (NC) in randomized order. RESULTS: During exercise and recovery in both trials, SCI TTY was elevated above baseline (P < 0.001) but more so in the NC versus FC trial (1.6 +/- 0.2 degrees C vs 1.0 +/- 0.2 degrees C, respectively, P < 0.005). Within the AB group, TTY was elevated above baseline for both trials (P < 0.001) with peak increases of 0.5 +/- 0.2 degrees C and 0.3 +/- 0.2 degrees C for NC and FC, respectively. TTY, face, and back temperature were higher in both SCI trials compared with AB trials (P < 0.05). Heart rate during exercise and recovery was lower in the SCI FC versus SCI NC (P < 0.05). CONCLUSION: These results suggest that extraction of heat through the foot may provide an effective way to manipulate tympanic temperature in individuals with SCI, especially during exercise in the heat.