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Mia K. Newlin, Sara Williams, Tim McNamara, Harold Tjalsma, Dorine W. Swinkels and Emily M. Haymes

Purpose:

To investigate the effects of acute exercise on serum hepcidin and iron (sFe) in active women. Changes in interleukin-6 (IL-6), hepcidin, ferritin, and sFe in response to 2 different exercise durations were compared.

Methods:

Twelve women age 19–32 yr performed 2 treadmill runs (60 and 120 min) at 65% of VO2max. Blood samples were obtained before, immediately after, and 3, 6, 9, and 24 hr after exercise. Two-way repeatedmeasures ANOVA was conducted to examine changes in measured variables. Significance was accepted at p < .05.

Results:

Significant effects for trial were observed for hepcidin (60 min: 1.15 ± 0.48 nmol/L; 120 min: 2.28 ± 1.44 nmol/L) and for time, with hepcidin significantly increased 3 hr postexercise in both trials (60 min: 3 hr – 1.99 ± 2.00 nmol/L; 120 min: 3 hr – 4.60 ± 4.61 nmol/L). Significant main effects for time occurred for sFe, ferritin, and IL-6. sFe was significantly decreased 9 hr postexercise compared with 3 and 24 hr postexercise. IL-6 was significantly increased immediately postexercise.

Conclusions:

Both runs resulted in significant increases in hepcidin 3 hr after exercise. Increases in hepcidin were preceded by significant increases in IL-6 immediately postexercise and followed by significant decreases in sFe 9 hr postexercise. It was concluded that endurance exercise increases the production of hepcidin, which affects sFe. The 2-hr exercise bout stimulated greater changes in serum hepcidin than the 1-hr bout.

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Richard J. Bloomer, Bradford Cole and Kelsey H. Fisher-Wellman

High-kilocalorie feedings induce oxidative stress. Acute exercise has the potential to attenuate postprandial oxidative stress. No study has determined whether there are racial differences in postprandial oxidative stress with and without a preceding bout of acute exercise.

Purpose:

To investigate the impact of acute exercise on blood oxidative- stress biomarkers, triglycerides (TAG), and glucose in African American (AA) and White (W) women.

Methods:

10 AA (age 29 ± 3 yr, body-mass index [BMI] 31 ± 3 kg/m2) and 10 W (age 30 ± 2 yr, BMI 30 ± 3 kg/m2) women consumed a meal of 1.2 g of fat and carbohydrate and 0.25 g of protein per kilogram body mass, on 2 occasions—with and without a session of aerobic exercise 15 min preceding the meal (45 min cycling at 65% heart-rate reserve)—in a random-order crossover design. Blood samples were collected premeal (fasted), and at 1, 2, 4, and 6 hr postmeal and assayed for TAG, glucose, xanthine oxidase activity, hydrogen peroxide (H2O2), and malondialdehyde (MDA). Area under the curve (AUC) was calculated for each variable.

Results:

AUC was lower for AA compared with W for both the exercise and the no exercise conditions for H2O2, MDA, and TAG (p < .01). However, acute exercise had no effect on decreasing the AUC for any variable in either AA or W women (p > .05).

Conclusions:

Postprandial lipemia and oxidative stress are lower in AA than in W overweight/obese women. However, acute exercise, performed at the intensity and duration in the current study, does not influence postprandial lipemia or oxidative stress in AA or W women.

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Kent C. Hansen and Dale A. Schoeller

Objective:

Increasing fat content in an isocaloric diet is associated with positive fat imbalance. Exercise attenuates this process, and the authors hypothesized the attenuation was a result of altered postprandial lipid trafficking.

Design:

To investigate the effects of prior exercise and nutritional state on the metabolic fate of dietary fat, a study was designed with 4 treatment arms. Energy-balance modifications (fed or fasted) ± exercise were followed by postexercise feeding of 1-14C oleic acid to Sprague-Dawley rats. Fed rats were fed 6 hr before treatment, whereas fasted rats were fasted for 15 hr before treatment with the primary variable being exercise.

Measurements:

14C content of gastrointestinal tract, plasma, breath, muscle (soleus, vastus lateralis [VL], and extensor digitorum longus), liver, and adipose tissue (retroperitoneal and epididymal) was measured at 5 time points postdose (1, 2, 4, 8, and 24 hr).

Results:

Compared with matched unexercised controls, fed rats undergoing acute exercise significantly increased recovery of 14C in breath (p = .005) and plasma (p = .001), and trends of increasing 14C recovery occurred in VL (p = .07) and soleus (p = .06). Acute exercise significantly increased recovery of 14C in breath (p = .003), VL (p = .04), and soleus (p = .03) in the fasted study. Acute exercise significantly decreased the trafficking of dietary tracer into adipose tissue in only the fed study (p < .0001).

Conclusion:

Although the effect of acute exercise on trafficking dietary fat away from adipose tissue was greater in the fed group than in the fasted, acute exercise had beneficial effects on adipose tissue’s collecting dietary fat when fed or fasted.

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Zekine Lappalainen, Jani Lappalainen, David E. Laaksonen, Niku K.J Oksala, Savita Khanna, Chandan K. Sen and Mustafa Atalay

Thioredoxin (TRX) is a protein disulfide reductase that plays an important role in many thiol-dependent cellular reductive processes, antioxidant protection, and signal transduction. Moreover, TRX reduces and maintains the function of many proteins during oxidative stress, which is increased in diabetes. The authors recently reported that diabetes impairs brain redox status and TRX response to exercise training. As a continuation of their studies, they hypothesized that alpha-lipoic acid, a natural thiol antioxidant, has a favorable effect on the brain TRX and glutathione (GSH) system in diabetes. Streptozotocin-induced diabetes was used as a chronic model and exhaustive exercise as an acute model for disrupted redox balance. Half the diabetic and nondiabetic animals were subjected to a bout of exhaustive exercise after 8 wk with or without lipoic acid and analyzed for key thiol antioxidants. Lipoic acid neither altered diabetes-induced oxidative stress as assessed by the increased ratio of oxidized to total GSH nor had any impact on the antioxidant protein response to exercise. However, lipoic acid increased mRNA of TRX-interacting protein, an inhibitor of TRX-1, and glutaredoxin-1 in diabetes. Exercise increased TRX-1 mRNA in both diabetic and nondiabetic animals but had no effect on TRX-1 protein. Cytosolic superoxide dismutase mRNA was only increased in diabetes, whereas exercise increased the protein levels in nondiabetic animals. The findings suggest that exhaustive exercise induces mRNA of TRX-1 in the brain and that lipoic acid cannot prevent diabetes-induced disturbances in GSH homeostasis. Because lipoic acid increased TRX-interacting protein transcription in diabetes, high doses may impair TRX-1 homeostasis.

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Roger G. Bounds, Steven E. Martin, Peter W. Grandjean, Barbara C. O’Brien, Cindi Inman and Stephen F. Crouse

To test the effect of diet on the short-term lipid response to exercise, fourteen moderately trained (VO2max: 50.2 ± 6.7 ml/kg/min), healthy men (mean age: 28 ± 4 years) were alternately fed a high fat (60±6.7% fat) and a high carbohydrate (63 ± 3.2% carbohydrate) isoenergetic diet for 2 weeks in a randomized crossover design. During the last 4 days of the treatments, fasting total cholesterol, triglyceride. HDL-cholesterol, and HDL3-cholesterol were measured the day before, and again immediately, 24 hr. and 48 hr after exercise (4190 kJ, 70% VO2max). LDL-cholesterol and HDL2-cholesterol were calculated. Lipid concentrations were adjusted for plasma volume changes after exercise. A 2 (diet) × 4 (time) ANOVA with repeated measures revealed no significant interaction between the diet and exercise treatments. Furthermore, diet alone did not influence lipid concentrations in these trained men. Exercise resulted in an increase in HDL-C (10.7%) and HDL3-C (8.5%) concentrations and a concomitant fall in triglyceride (-25%) and total cholesterol (-3.5%). Thus, we conclude that diet composition does not affect the short-term changes in blood lipids and lipoproteins that accompany a single session of aerobic exercise in moderately trained men.

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Alaaddine El-Chab and Miriam E. Clegg

to the results and hence reduce their reproducibility ( Brouns et al., 2005 ). Therefore, the aim of this study was to investigate the effect of acute exercise (walking and cycling) prior to testing on the intraindividual variability of blood glucose and insulin responses. We hypothesized that

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Joel B. Mitchell, James R. Rowe, Meena Shah, James J. Barbee, Austen M Watkins, Chad Stephens and Steve Simmons

To examine the effect of prior exercise on the postprandial lipid response to a high-carbohydrate meal in normal-weight (NW = BMI h25) and overweight (OW = BMI ≥25) women (age 18–25), 10 NW and 10 OW participants completed 2 conditions separated by 1 month. In the morning, the day after control (CT = no exercise) or exercise conditions (EX = 60 min cycling at 60% VO2peak), participants consumed a high-carbohydrate meal (80% CHO, 15% protein, 5% fat; 75 kJ/kg BM) followed by 6 hr of hourly blood sampling. Blood was analyzed for triglycerides (TG), blood glucose (BG), and insulin (IN). TG levels over the 6-hr period were lower in NW than OW (p = .021) and lower in EX than in CT (p = .006). Area under the curve (AUC) for TG was lower in NW than OW (p = .016) and EX than CT (p = .003). There were nonsignificant tendencies for reduced BG over time (p = .053) and AUC (p = .083), and IN AUC was lower in EX than in CT (p = .040) for both groups and lower in NW than in OW (p = .039). Prior exercise improved TG levels after a high-carbohydrate meal in both groups, and OW women demonstrated a greater postprandial lipemic response than NW regardless of condition. There were tendencies for improved glucose removal with prior exercise in NW vs. OW. Acute exercise can improve postprandial TG responses and might also improve postprandial BG and IN after a large meal in NW and OW young women.

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Daniel G. Syrotuik, Kirsten L. MacFadyen, Vicki J. Harber and Gordon J. Bell

To examine the effects of elk velvet antler supplementation (EVA) combined with training on resting and exercise-stimulated hormonal response, male (n = 25) and female (n = 21) rowers ingested either E VA (560 mg/d) or placebo (PL) during 10 wk of training. VO2max, 2000 m rowing time, leg and bench press strength were determined before and after 5 and 10 wk of training. Serum hormone levels were measured prior to and 5 and 60 min after a simulated 2000 m rowing race. VO2max and strength increased and 2000 m times decreased similarly (P < 0.05) with training. There was no significant difference between the EVA and PL group for any hormonal response. Testosterone (males only) and growth hormone (both genders) were higher 5 min after the simulated race (P < 0.05) but returned to baseline at 60 min. Cortisol was higher 5 and 60 min compared to rest (both genders) (P < 0.05) and was higher 60 min post-exercise following 5 and 10 wk of training. It appears that 10 wk of EVA supplementation does not significantly improve rowing performance nor alter hormonal responses at rest or after acute exercise than training alone.

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Alfredo Córdova, Antoni Sureda, María L. Albina, Victoria Linares, Montse Bellés and Domènec J. Sánchez

The aim was to determine the levels and activities of the oxidative stress markers in erythrocytes, plasma, and urine after a flat cyclist stage. Eight voluntary male professional trained-cyclists participated in the study. Exercise significantly increased erythrocyte, leukocyte, platelet, and reticulocyte counts. The exercise induced significant increases in the erythrocyte activities of catalase (19.8%) and glutathione reductase (19.2%), while glutathione peroxidase activity decreased significantly (29.3%). Erythrocyte GSSG concentration was significantly increased after exercise (21.4%), whereas GSH was significantly diminished (20.4%). Erythrocyte malondialdehyde levels evidenced a significant decrease 3 h after finishing the stage (44.3%). Plasma malondialdehyde, GSH and GSSG levels significantly decreased after 3 hr recovery (26.8%, 48.6%, and 31.1%, respectively). The exercise significantly increased the F2-isoprostane concentration in urine from 359 ± 71 pg/mg creatinine to 686 ± 139 pg/mg creatinine. In conclusion, a flat cycling stage induced changes in oxidative stress markers in erythrocytes, plasma, and urine of professional cyclists. Urine F2-isoprostane is a more useful biomarker for assessing the effects of acute exercise than the traditional malondialdehyde measurement.

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Jonathan M. Peake

Ascorbic acid or vitamin C is involved in a number of biochemical pathways that are important to exercise metabolism and the health of exercising individuals. This review reports the results of studies investigating the requirement for vitamin C with exercise on the basis of dietary vitamin C intakes, the response to supplementation and alterations in plasma, serum, and leukocyte ascorbic acid concentration following both acute exercise and regular training. The possible physiological significance of changes in ascorbic acid with exercise is also addressed. Exercise generally causes a transient increase in circulating ascorbic acid in the hours following exercise, but a decline below pre-exercise levels occurs in the days after prolonged exercise. These changes could be associated with increased exercise-induced oxidative stress. On the basis of alterations in the concentration of ascorbic acid within the blood, it remains unclear if regular exercise increases the metabolism of vitamin C. However, the similar dietary intakes and responses to supplementation between athletes and nonathletes suggest that regular exercise does not increase the requirement for vitamin C in athletes. Two novel hypotheses are put forward to explain recent findings of attenuated levels of cortisol postexercise following supplementation with high doses of vitamin C.