Journal of Exercise Nutrition & Biochemistry最新文献

Purpose: Chronic stress affects the neuronal architecture of hippocampal subfields including the Cornu Ammonis 1 (CA1) region, which governs long-term memory. Exercise exerts a beneficial effect on memory improvement via hippocampal AMP-activated protein kinase (AMPK) activation. However, the relationship between the two phenomena is poorly understood. This study used animal and cell culture experimental systems to investigate whether chronic stress-induced impairment of memory consolidation and maladaptation of the neuronal architecture in the hippocampal CA1 area is prevented by regular exercise through AMPK activation.

Methods: Mice underwent four weeks of treadmill running with or without a 6h/21d-restraint stress regimen, along with treatment with Compound C. Memory consolidation was assessed using the Morris Water Maze (MWM). Dendritic rearrangement of hippocampal CA1 neurons was evaluated using the Golgi-Cox stain and Sholl analysis. Additionally, the primary hippocampal culture system was adopted for in vitro experiments.

Results: Chronic stress-induced failure of memory retention and reduction in AMPK activation were ameliorated by the exercise regimen. Chronic stress- or repeated corticosterone (CORT)- provoked malformation of the neuronal architecture was also suppressed by both exercise and treatment with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR).

Conclusion: Chronic stress causes dendritic retraction among dorsal hippocampal CA1 neurons via the downregulation of AMPK activation, thereby leading to failure of memory retention. In contrast, regular exercise protects against chronic stress-evoked defects in memory consolidation and changes in neuronal morphology in the dorsal hippocampal CA1 area via mild activation of AMPK.

Purpose: Although it is known that exercise induces angiogenesis, a clear mechanism has remained elusive due to various experimental limitations. This review presents the current status of angiogenesis-related experiments and future directions of experimentation in relation to exercise, aging, and cancer.

Methods: We conducted a PubMed search of the available literature to identify reported exercise related changes of angiogenic factors obtained in vitro using C2C12 cells and endothelial cells, and in vivo using animal experiments and in clinical studies.

Results: Exercise induced angiogenesis under normal conditions. Aging decreased angiogenic factors and increased during exercise. On the other hand, in cancer, the results indicate that angiogenic factors tend to increase in general, and that the effects of exercise need to be studied more. The exact mechanism remains unclear.

Conclusion: The effect of exercise on angiogenesis appears positive. Both resistance and aerobic exercise have positive effects, but many evidences suggest that the effects are more pronounced with aerobic exercise. Further research on the precise mechanism(s) is necessary. It is expected that these studies will include models of aging and cancer.

Purpose: The purpose of this study was to determine whether ginseng berry extract improves blood circulation by regulating vasodilator expression in exposed to tumor necrosis factor alpha (TNF-α)-exposed endothelial cells and muscle cells.

Methods: Nitric oxide (NO) and cGMP levels in human umbilical vein endothelial cells (HUVECs) and A7r5 cells exposed to ginseng berry extract were investigated. Based on the in vitro results, healthy participants were treated with ginseng berry extract for 4 weeks and then a non-invasive vascular screening device was used to confirm the improvement of blood circulation.

Results: When TNF-α-treated cells were exposed to the ginseng berry extract, the expression levels of endothelial nitric oxide synthase (eNOS), NO, and cGMP were recovered to almost normal levels. In addition, TNF-ɑ-induced overexpression of vascular cell adhesion molecule 1 (VCAM-1), intracellular adhesion molecule 1 (ICAM-1), e-selectin, and p-selectin was lowered by ginseng berry extract. The ginseng berry extract significantly increased ankle brachial pressure index compared to placebo (p < 0.05).

Conclusion: This study confirmed that the intake of ginseng berry extract improved blood circulation and therefore, its intake would be helpful for people having problems with blood circulation.

Purpose: The aim of the study was to determine the effects of dietary CoQ10 on serum biochemical parameters, lipid peroxidation, and HSP expression in the liver and slow-twitch muscles (soleus and gastronemius deep portion) of exercise-trained rats.

Methods: A total of 42 Wistar albino rats were divided into six groups: 1) Control, 2) Coenzyme Q10 (CoQ10), 3) Chronic Exercise (CE), 4) CE + CoQ10, 5) Acute Exercise (AE), and 6) AE + CoQ10. The rats were subjected to the running test 5 days a week for 6 weeks after which CoQ10 was administered via the diet. AE (running on the treadmill until the rats were exhausted) was done on the last day.

Results: The results showed no significant difference in serum glucose and liver functions in any of the groups. However, CoQ10 and exercise treatment were found to lower cholesterol and triglyceride levels. Serum and muscle malondialdehyde (MDA) levels were found to be lower in the CE and CE + CoQ10 groups compared to the control group. The highest levels of HSP60, HSP70, and HSP90 in liver and muscle were found in the AE group, and the lowest levels were found in CE + CoQ10 group. CoQ10 supplementation reduced HSP expression in both CE- and AE-trained rats (P < 0.05).

Conclusion: The results showed that CoQ10 supplementation could reduce MDA levels, protect against oxidative damage, and regulate HSP expression in CE- and AE-trained rats. CE and CoQ10 were shown to reduce oxidative stress synergistically.

Purpose: To investigate the effect of treadmill running on D2R deficiency related susceptibility to high fat diet (HFD )-induced obesity and its metabolic complications.

Methods: D2R-/- and +/- mice were obtained by backcrossing D2R+/- heterozygotes on wild type (WT) littermates (C57BL/6J background) for >10 generations. Mice were randomly assigned to 1) WT mice with standard chow (SC) (WT+SC); 2) WT mice with high-fat diet (WT+HFD); 3) WT mice with high-fat diet plus exercise (WT+HFD+EX), 4) heterozygous (HET) D2R mice with SC (HET+SC); 5) heterozygous D2R mice with HFD (HET+HFD); and 6) heterozygous D2R mice with HFD plus exercise (HET+HFD+EX). In addition, mice assigned to EX groups were subjected to running on a motor-driven rodent treadmill with a frequency of 5 days per week.

Results: After a 10-week HFD treatment, HET D2R (+/-) mice exhibited significantly higher values for hepatic steatosis (p<0.001), areas under the curves (AUCs) for the glucose tolerance test (GTT) and the insulin tolerance test (ITT) (p<0.001 & p<0.001 respectively), serum leptin (p=0.005) and total cholesterol (TC ) (p=0.009), in conjunction with decreased locomotor activity (p=0.031), compared to HET mice exposed to standard chow. However, these HFD-induced elevations in hepatic steatosis (p<0.001), AUCs for GTT and ITT (p=0.032 & p=0.018, respectively), serum leptin (p=0.038) and TC (p=0.038) were significantly alleviated after 10 weeks of treadmill running.

Conclusion: The current findings of the study provide experimental evidence of treadmill running as an effective and non-pharmacologic strategy to treat the susceptibility of brain D2R deficiency to HFD-induced obesity and metabolic disorders.

Purpose: Declining muscle strength and function are hallmarks of the aging process. This study aimed to determine sex-related differences in myosin heavy chain (MHC) isoforms and muscle mass, strength, and quality with aging.

Methods: This cross-sectional study recruited 53 healthy participants (32 men, 21 women) aged 20-85 years who were divided into four groups: young men (n=17, YM, 29.23±4.51), older men (n=15, OM, 71.87±3.42), young women (n=11, YW, 29.64±4.88), and older women (n=10, OW, 68.1±1.91). Body composition and muscle strength and quality were analyzed. Muscle specimens were obtained from the vastus lateralis in all participants to analyze the type of MHC isoforms.

Results: Men showed a greater age-related decline in skeletal muscle mass (18.6%, p<0.01), lean body mass (10.1%, p<0.05), grip strength (35.3%, p<0.001), isometric strength (29.6%, p<0.001), isotonic power (42.5%, p<0.001), isokinetic strength (up to 44.3%, p<0.001), and muscle quality (up to 24.8%, p<0.01). In contrast, women had significantly lower isometric strength (24.2%, p<0.05), isotonic power (36.5%, p<0.01), and upper-body muscle quality (24.7%, p<0.001) with aging. In addition, the proportion of MHC IIa was significantly lower in OM (p<0.05) and OW (p<0.05) than in YM and YW, respectively. However, the proportion of MHC I was significantly higher in OM (p<0.01) than in YM but was high in both YW and OW. MHC I and MHC IIa negatively and positively correlated, respectively, with muscle strength and function.

Conclusion: These results indicate the existence of sex-related differences in muscle mass, strength, and quality and MHC isoform composition with increasing age. The effects on muscle strength and function with aging were significant in men, but not in women. Higher and lower proportions of MHC I and MHC IIa fibers, respectively, were inversely associated with muscle strength and quality. In particular, Korean YW showed lower muscle strength and quality, and the proportion of MHC isoforms was similar to that in the muscles of OW.

Purpose: Chronic stress can lead to mood-related psychomotor behaviors such as despair. Decreased hippocampal neurogenesis has been observed in patients with depression and in animal models of depression. Exercise enhances the population of the new born cells in the dentate gyrus (DG). A few studies have demonstrated that creatine has antidepressant effects in humans. However, the mechanism underpinning these effects is poorly understood. Therefore, we examined whether regular exercise and/or creatine was closely associated with the activity of the Wnt/GSK3β/β-catenin pathway in the hippocampal DG.

Methods: Mice were subjected to 4 weeks of chronic mild stress starting a week prior to the start of a 4-week protocol of treadmill running and creatine supplementation. Tail suspension (TST) and forced swimming tests (FST) were carried out 2 days after the final treadmill running session. Immunohistochemical and western blot analyses were conducted to evaluate hippocampal neurogenesis, GSK3β activity, and nuclear β-catenin protein levels in the DG. Furthermore, Wnt signaling antagonism in the DG using stereotaxic injection was performed.

Results: Chronic mild stress-induced increase in immobility in the TST and FST were restored by treadmill running and/or creatine supplementation. The number of Ki-67+ and doublecortin (DCX)+ cells were decreased by chronic stress, and this decline was reversed by the exercise and supplement regimen, along with the changes in GSK3β activity and nuclear β-catenin protein levels in the DG. Local antagonism of DG Wnt signaling caused an increase in immobility even 5 days after injection with C59.

Conclusion: Regular exercise combined with creatine supplementation had a greater effect on hippocampal neurogenesis via the Wnt/GSK3β/β-catenin pathway activation compared with each treatment in chronic mild stress-induced behavioral depression.

Purpose: Yacon, Smallanthus sonchifolius, has anti-hypertensive, anti-inflammatory, and anti-cancer potential. However, its neuroprotective and anti-neuroinflammatory effects are unknown. Moreover, activation of microglia has been considered a mechanism in the development of Alzheimer's disease. Therefore, the aim of this study was to determine the neuroprotective effects of an ethanolic yacon leaf extract (YLE) on lipopolysaccharide (LPS)-induced neuroinflammation in vitro and in vivo.

Methods: The viability of microglial BV2 cells was tested with 2,3-bis[2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolim-5-carboxanilide. The production of nitric oxide (NO) was determined by the Griess reagent. mRNA expression and protein levels of inflammatory mediators were evaluated by the real-time polymerase chain reaction and immunohistochemistry, respectively. In addition, we performed histological analysis in mice treated with an intraperitoneal injection of LPS (250 μg/kg).

Results: Our results showed that treatment with YLE significantly reduced NO production in LPS-stimulated BV2 cells. YLE also decreased mRNA levels of the inflammatory factors tumor necrosis factor alpha, inducible nitric oxide synthase, cyclooxygenase-2, and interleukin-1 beta. In vivo, YLE (40 mg/kg daily for seven days) significantly diminished LPS-induced tissue damage in the dentate gyrus and cornu amonis regions of the hippocampus by regulating the levels of inflammatory factors.

Conclusion: Our findings support the protective effects of YLE against the development of neurodegeneration.

Purpose: To determine the effects of exercise-induced muscle damage, we examined irisin responses during level running (LR), with less muscle damage, and downhill running (DHR), with greater muscle damage under equivalent exercise duration and oxygen consumption (⩒O2) conditions.

Methods: Fifteen healthy men (age: 21.6 ± 2.0 y, height: 170 ± 1.3 cm, weight: 64.8 ± 2.7 kg) were randomly assigned to either the LR group (n = 8) or the DHR group (n = 7). Subjects in the LR group performed treadmill running at 70% of maximum oxygen uptake (⩒O2max) for 30 min on a 0% gradient. In contrast, subjects in the DHR group performed the same exercise on a -10% gradient. Blood samples were collected before exercise, immediately after exercise, and 1, 3, and 24 h after exercise.

Results: No significant interaction (group × time) or main effect of group or time was observed for changes in plasma irisin concentrations over time (P > 0.05). However, the area under the curve of plasma irisin concentrations during a 3-h post-exercise period was significantly greater in the DHR (239,197 ± 8,166 ng/mL) group than in the LR (92,293 ± 8,755 ng/ml) group (P < 0.05). The blood lactate, serum cortisol, myoglobin, and plasma interleukin-6 concentrations were significantly higher in the DHR group than in the LR group after exercise (P < 0.05 for all variables).

Conclusion: DHR associated with marked muscle damage promoted a greater increase in exercise-induced irisin did LR after the same duration under identical VO2 conditions.

Purpose: Myogenic progenitors play a critical role in injury-induced myofiber regeneration. The purpose of this study was to characterize the effects of oleate and L-carnitine on the overall behavior of proliferating myogenic progenitors (myoblasts) and its link to the mitochondrial biogenic process.

Methods: C2C12 myoblasts were cultured either with no treatment, oleate, L-carnitine, or their mixture. Proliferating myoblasts were investigated under a phase-contrast microscope. Myonuclei and myosin heavy chain were stained with DAPI and MF20 antibody, respectively, in differentiated myotubes and visualized under florescence microscopy. Mitochondrial biogenic markers and porin were assessed by qRT-PCR or immunoblotting.

Results: Increased proliferation rate was observed in myoblasts conditioned with oleate or a mixture of oleate and L-carnitine in contrast to that in non-treated (NT) and L-carnitine-treated myoblasts. Myoblast viability was not statistically different among all tested groups. Fusion index and myotube width were greater in oleate- or L-carnitine-conditioned myotubes than those in NT myotubes, with the greatest effect seen in myotubes conditioned with the mixture. The gene expressions of Pgc1-α, Nrf1, and Tfam were the greatest in myotubes conditioned with the mixture, whereas the level of Ncor1 expression was lower compared to those of the other groups. Protein level of porin was the greatest in myotubes conditioned with the mixture, followed by that of individually treated myotubes with oleate and L-carnitine.

Conclusion: These results provide a critical piece of cellular evidence that combined treatment of oleate and L-carnitine could serve as a potential therapeutic strategy to facilitate biological activation of myogenic progenitors.