Search Results

You are looking at 1 - 10 of 52 items for :

Clear All
Restricted access

Yu-Qian Liu, Yan-Zhong Chang, Bin Zhao, Hai-Tao Wang and Xiang-Lin Duan

Some athletes are diagnosed as suffering from sports anemia because of iron deficiency, but the regulatory mechanism remains poorly understood. It is reported that hepcidin may provide a way to illuminate the regulatory mechanism of exercise-associated anemia. Here the authors investigate the hepcidin-involved iron absorption in exercise-associated anemia. Twelve male Wistar rats (300 ± 10 g) were randomly divided into 2 groups, 6 in a control group (CG) and 6 in an exercise group (EG, 5 wk treadmill exercise of different intensities with progressive loading). Serum samples were analyzed for circulating levels of IL-6 by means of enzyme-linked immunosorbent assay (ELISA). The expression of hepatic hepcidin mRNA was examined by real-time polymerase chain reaction analysis. The protein levels of divalent metal transporter 1 (DMT1), ferroportin1 (FPN1), and heme-carrier protein 1 (HCP1) of duodenum epithelium were examined by Western blot. The results showed that the amount of iron and ferritin in serum were lower in EG than in CG (p < .05). The levels of IL-6 and white blood cells were greater in EG than in CG (p < .01). The expression of DMT1, HCP1, and FPN1 was significantly lower in EG than in CG (p < .01). The mRNA expressions of hepatic hepcidin and hemojuvelin in skeletal muscle were remarkably higher in EG than in CG. The data indicated that inflammation was induced by strenuous exercise, and as a result, the transcriptional level of the hepatic hepcidin gene was increased, which further inhibited the expression of iron-absorption proteins and led to exercise-associated anemia.

Restricted access

YoonMyung Kim

visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), hepatic lipid content, IMAT, and IMCL ( 26 , 30 ). Therefore, the use of these imaging techniques in clinical research settings allows to investigate and develop an effective prevention and treatment strategy for reductions in depot

Restricted access

Abbass Ghanbari-Niaki, Rozita Fathi, Sayed Alireza Hossaini Kakhak, Zhara Farshidi, Sara Barmaki, Fatemeh Rahbarizadeh and Robert R. Kraemer

Agouti-related protein (AGRP) is an orexigenic peptide secreted from the arcuate nucleus (ARC) of the hypothalamus. AGRP increases food intake and plays a role in energy balance, adiposity, weight gain, and growth-hormone release. The objective of the current study was to examine the effects of running exercise on resting hepatic, fundus, and pancreas AGRP mRNA expression, as well as liver glycogen and ATP contents, using a rat model. Twenty adult male Wistar rats (12–14 wk old, 200–220 g) were randomly assigned to control (n = 10) and training (n = 10) groups. The training group was exercised for 8 wk on a motor-driven treadmill (26 m/min, 0% grade, 60 min, 5 d/wk). Twenty-four hours before sacrifice the rats were further divided into fed control (FEC), fed trained (FET), fasted control (FAC), and fasted trained (FAT) groups. The liver, fundus, and pancreas were excised and frozen in liquid nitrogen for later analysis. Results demonstrated that 8 wk of treadmill exercise reduced hepatic but not fundus and pancreatic AGRP expression and enhanced glycogen and ATP concentrations (p < .001) in trained-rat liver, whereas fasting lowered liver glycogen and ATP levels and increased hepatic AGRP mRNA expression in nonexercising controls. Data indicate that both treadmill-exercise-induced decrease and fast-induced increase in rat liver AGRP expression might depend on liver glycogen content as an important source for energy provision.

Restricted access

Paul D. Loprinzi

Objective:

Examine the association between objectively-measured moderate-to-vigorous physical activity (MVPA) and engagement in self-reported muscle strengthening activities (MSA) with alanine aminotransferase (ALT) and gamma-glutamyltransferase (GGT), and in turn, how each of these parameters associate with of all-cause mortality.

Methods:

Data from the 2003–2006 NHANES were employed, with follow-up through December 31, 2011 (N = 5030; 20+ yrs). Physical activity was assessed via accelerometry; MSA was assessed via survey; and ALT and GGT were assessed via a blood sample. Linear regression and Cox proportional hazard models were used.

Results:

MVPA (βadjusted = 0.15; 95% CI: –0.45 to 0.76; P = .60) was not associated with ALT, but MSA was (β adjusted = –0.31; 95% CI: –0.56 to –0.05; P = .02). With regard to GGT, MSA was not significant (β adjusted = –0.12; 95% CI: –0.71 to 0.47; P = .67), nor was MVPA (β adjusted = –1.10; 95% CI: –2.20 to 0.06; P = .06). Higher ALT levels were associated with increased allcause mortality risk (HRadjusted = 1.05; 95% CI: 1.02 to 1.06; P < .001).

Conclusion:

Physical activity is favorably associated with markers of hepatic inflammation, and higher levels of markers of hepatic inflammation are associated with increased mortality risk. These findings suggest that physical activity may help protect against premature mortality through its influence on liver pathology.

Restricted access

Hyun-Tae Kim

We investigated the effect of long-term treatment (6 wk) with selenium and vitamin E, in combination with aerobic exercise training, on malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), and glutathione peroxi-dase (GPx) in STZ-induced diabetic rats. The rats were assigned randomly to one of three treatment groups (n = 12 per group): 1) exercise group (EX), 2) selenium/vitamin E/exercise group (SVE), and 3) selenium/vitamin E group (SV). To estimate the acute effect of exercise, a 30-min endurance exercise was used. The MDA concentration was significantly lower in the SVE. The ox-LDL was significantly lower in the SVE and SV. The hepatic concentrations of selenium and vitamin E were significantly higher in the SVE. These results indicate that the increase in MDA is mildly attenuated in rats that were aerobically trained. Moreover, the joint administration of selenium and vitamin E with or without exercise training reduces the levels of ox-LDL.

Restricted access

Wendy Hens, Jan Taeymans, Justien Cornelis, Jan Gielen, Luc Van Gaal and Dirk Vissers

Background:

Reduction of ectopic fat accumulation plays an important role in the prevention of insulin resistance in people with overweight or obesity. This systematic review and meta-analysis summarizes the current evidence for the use of noninvasive weight loss interventions (exercise or diet) on ectopic fat.

Methods:

A systematic literature search was performed according to the PRISMA statement. Clinical trials in PubMed, PEDro, and the Cochrane database were searched.

Results:

All 33 included studies described the effect of lifestyle interventions on ectopic fat storage in internal organs (liver, heart, and pancreas) and intramyocellular lipids (IMCL), hereby including 1146, 157, 87, and 336 participants. Overall, a significant decrease of ectopic fat was found in liver (−0.53 Hedges’ g, P < .001), heart (−0.72 Hedges’ g, P < .001) and pancreas (–0.55 Hedges’ g, P = .098) respectively. A trend toward decrease in IMCL was also observed. Meta-regression indicated a dose-response relationship between BMI reduction and decreased hepatic adiposity. Exercise alone decreased ectopic fat but the effect was greater when combined with diet.

Conclusions:

Lifestyle interventions can reduce ectopic fat accumulation in the internal organs of overweight and obese adults. The results on IMCL should be interpreted with care, keeping the ‘athlete’s paradox’ in mind.

Restricted access

Darlene A. Sedlock, Man-Gyoon Lee, Michael G. Flynn, Kyung-Shin Park and Gary H. Kamimori

Literature examining the effects of aerobic exercise training on excess postexercise oxygen consumption (EPOC) is sparse. In this study, 9 male participants (19–32 yr) trained (EX) for 12 wk, and 10 in a control group (CON) maintained normal activity. VO2max, rectal temperature (Tre), epinephrine, norepinephrine, free fatty acids (FFA), insulin, glucose, blood lactate (BLA), and EPOC were measured before (PRE) and after (POST) the intervention. EPOC at PRE was measured for 120 min after 30 min of treadmill running at 70% VO2max. EX completed 2 EPOC trials at POST, i.e., at the same absolute (ABS) and relative (REL) intensity; 1 EPOC test for CON served as both the ABS and REL trial because no significant change in VO2max was noted. During the ABS trial, total EPOC decreased significantly (p < .01) from PRE (39.4 ± 3.6 kcal) to POST (31.7 ± 2.2 kcal). Tre, epinephrine, insulin, glucose, and BLA at end-exercise or during recovery were significantly lower and FFA significantly higher after training. Training did not significantly affect EPOC during the REL trial; however, epinephrine was significantly lower, and norepinephrine and FFA, significantly higher, at endexercise after training. Results indicate that EPOC varies as a function of relative rather than absolute metabolic stress and that training improves the efficiency of metabolic regulation during recovery from exercise. Mechanisms for the decreased magnitude of EPOC in the ABS trial include decreases in BLA, Tre, and perhaps epinephrine-mediated hepatic glucose production and insulin-mediated glucose uptake.

Restricted access

Exercise Training and Meal Form on Diet-Induced Thermogenesis in College-Age Men Lance Ratcliff * Sareen S. Gropper * B. Douglas White * David M. Shannon * Kevin W. Huggins * 2 2011 21 21 1 1 11 11 18 18 10.1123/ijsnem.21.1.11 Does Hepatic Hepcidin Play an Important Role in Exercise

Restricted access

Edward A. Gray, Thomas A. Green, James A. Betts and Javier T. Gonzalez

 al., 2000 ; Coyle et al., 1986 ), commonly attributed to a reduction in hepatic glucose output due to liver glycogen depletion ( Gonzalez & Betts, 2018 ). In contrast, in all treatments in the present experiments, blood glucose concentrations rose at exhaustion. This could be explained by the high

Open access

Christopher C. Webster, Kathryn M. van Boom, Nur Armino, Kate Larmuth, Timothy D. Noakes, James A. Smith and Tertius A. Kohn

 ± 5 .24  Weight (kg) 78 ± 9 74 ± 8 .41  BMI (kg/m 2 ) 23.6 ± 1.8 23.4 ± 2.0 .76  VO 2 max (ml/min/kg) 61 ± 5 63 ± 8 .61  PPO (W/kg) 4.8 ± 0.4 5.0 ± 0.4 .34 Metabolic parameters      Endogenous glucose production (mg/kg/min) 1.6 ± 0.2 2.0 ± 0.3 .004  Hepatic insulin sensitivity index 15.6 ± 3.9 10