scholarly journals Dietary Cucumis melo reduces markers of muscle and articular inflammation following high-intensity exercise in horses

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Jennifer L MacNicol ◽  
Michael Ivan Lindinger ◽  
Michael I Lindinger ◽  
Anna Kate Shoveller ◽  
John P Cant ◽  
...  

We evaluated the antioxidative and anti-inflammatory potential of daily oral supplementation with a proprietary powdered Cucumis melo pulp (CMP) on exercise-induced markers of articular and muscular oxidative stress and inflammation in 12 horses. Horses performed a high-intensity exercise test immediately prior to, and then following, 3 weeks of daily supplementation of 1 g powdered CMP (CMP; n=8). Controls (Co; n=8) underwent the same exercise and sampling regime but were not supplemented. Blood and synovial fluid (SF) samples were taken 24 h prior to exercise (BL), and at 1 and 24 h following exercise. Plasma and SF were analysed for prostaglandin E2 (PGE2), total antioxidant status (TAS), nitrite and superoxide dismutase (SOD) activity. SF was analysed for glycosaminoglycans (GAG), and plasma was analysed for thiobarbituric acid reactive substances (TBARS). Comparisons were made using repeated measures with the initial exercise test as a covariate. There was an increase in SF SOD activity in the CMP group. Compared to Co at 1 h, CMP reduced nitrite and GAG in SF, as well as maintained plasma TAS and lymphocyte levels. At 24 h, plasma PGE2 and creatine kinase were lower in horses receiving CMP. Three weeks of supplementation with CMP reduced markers of articular and skeletal muscle oxidative stress and inflammation in response to high-intensity exercise in horses. Nutritive antioxidants may provide a useful adjunct to the daily nutrition plan of horses undergoing regular exercise training and competition.

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Xue Geng ◽  
Zhihui Li ◽  
Lin Zhang ◽  
Chenggang Zhang

Objective Exercise-induced oxidative stress is due to the massive increase in free radicals caused by strenuous exercise, which exceeds the ability of self-clearing. It is one of the main causes of sports injury and sports fatigue. Eliminating excessive production of free radicals is the key to alleviating exercise induced oxidative damage. Therefore, the purpose of this study is to study the effect of hydrogen on exercise-induced oxidative damage, to explore its possible mechanism and to explore the best dose of hydrogen with different concentrations. Methods 40 male SD rats (200±20g) were randomly divided into five groups(n=8):sedentary, exercise control, low concentration hydrogen with exercise(H1), medium concentration hydrogen with exercise(H2), high concentration hydrogen with exercise(H3). The rats performed high-intensity exercise for 4 weeks, except the sedentary. rats that with Low, medium and high concentration hydrogen were placed in a hydrogen atmosphere with a concentration of 0.5%, 1% and 1.5% for 1 h immediately after each exercise (keeping the concentration of oxygen and nitrogen in the environment the same as those in the air). The rats were weighed weekly during the experiment. The next day after 4 weeks of training, the samples were collected, and the contents of total superoxide dismutase (T-SOD), catalase (CAT), total antioxidant capacity (T- AOC) and malondialdehyde (MDA) were determined respectively. Results The weight of exercise control was significantly lower than sedentary in the third and fourth weeks of exercise (P<0.05). Compared to sedentary rats, there was no significant difference in the weight of rats between H1, H2 and H3 group. The contents of T-AOC, CAT and T-SOD in exercise control were significantly higher than those in sedentary (P<0.05). The content of CAT in H2 group was significantly decreased compared with exercise control (P<0.01). Compared with exercise control, the T-AOC and T-SOD in the H2 group showed a downward trend but no statistical difference (P>0.05), there was no significant difference between the above indexes, compared with sedentary. In addition, there was no difference in T-SOD and CAT content between H1 group and exercise control; Compared with exercise control, there was no significant difference in T-SOD, T-AOC and CAT in H3 group. At the MDA level, each exercise group increased significantly compared with the sedentary (P<0.05), and the MDA levels in the H1, H2, and H3 groups were decreased compared with the exercise control, but there was no statistical difference. Conclusions It can be seen from the above results that different concentrations of hydrogen intervention can improve the weight loss of rats after intensive exercise. More importantly, the dosage and effect of 1% concentration of hydrogen is easier to remove the excessive radicals produced by intense exercise in the body, avoid the aggravation of oxidative stress, and have very good therapeutic effect. It provides a theoretical basis for the further study of the application of hydrogen in exercise oxidative damage. 


2002 ◽  
Vol 30 (2) ◽  
pp. 280-285 ◽  
Author(s):  
C. E. Cooper ◽  
N. B. J. Vollaard ◽  
T. Choueiri ◽  
M. T. Wilson

This article reviews the role of free radicals in causing oxidative stress during exercise. High intensity exercise induces oxidative stress and although there is no evidence that this affects sporting performance in the short term, it may have longer term health consequences. The mechanisms of exercise-induced oxidative stress are not well understood. Mitochondria are sometimes considered to be the main source of free radicals, but in vitro studies suggest they may play a more minor role than was first thought. There is a growing acceptance of the importance of haem proteins in inducing oxidative stress. The release of metmyoglobin from damaged muscle is known to cause renal failure in exercise rhabdomyolysis. Furthermore, levels of methaemoglobin increase during high intensity exercise, while levels of antioxidants, such as reduced glutathione, decrease. We suggest that the free-radical-mediated damage caused by the interaction of metmyoglobin and methaemoglobin with peroxides may be an important source of oxidative stress during exercise.


2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Mallikarjuna Korivi ◽  
Chun-Tai Chen ◽  
Szu-Hsien Yu ◽  
Weibing Ye ◽  
I-Shiung Cheng ◽  
...  

We investigated the effect of chronic seaweed (Gracilaria asiatica) supplementation on maximal carrying capacity, muscle mass, and oxidative stress in rats following high-intensity resistance exercise (RE). Forty Sprague-Daley rats were equally categorized into control, exercise, seaweed, and exercise plus seaweed (ES) groups. Rats in respective groups performed RE (once per 2 days) or received seaweed (250 mg/kg bodyweight, orally) for 10 weeks. Results showed that seaweed consumption in combination with RE significantly (p < 0.05) increased maximal weight carrying capacity compared to RE alone. FHL muscle mass was significantly higher in both exercise and ES groups. Notably, high-intensity RE-induced lipid peroxidation, as evidenced by elevated thiobarbituric acid reactive substances (TBARS) in muscle, was substantially diminished (p < 0.05) by seaweed treatment. This antioxidative effect of seaweed was further represented by augmented superoxide dismutase activity and glutathione levels in seaweed groups. We noticed increased insulin concentrations and HOMA-IR, while the fasting blood glucose levels remained stable in seaweed and ES groups. Our findings conclude that seaweed in combination with RE enhanced maximal carrying strength and attenuated oxidative stress through improved antioxidant capacity. Seaweed could be a potential nutritional supplement to boost performance and to prevent exercise-induced muscle damage.


Biology ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1272
Author(s):  
Yining Lu ◽  
Huw D. Wiltshire ◽  
Julien S. Baker ◽  
Qiaojun Wang

Participation in exercise promotes health. High intensity exercise (HIE) has become increasingly popular among the general population, however, its effects on exercise-induced oxidative stress and antioxidant status in untrained humans is not clear. The aim of this systematic review was to investigate the influence of HIE on oxidative stress and antioxidant status in untrained humans. Web of Science, PubMed, MEDLINE, and Scopus were searched until March 2021. A methodological quality assessment valuation/estimation was additionally carried out in the final sample of studies. Following the PRISMA selection process, 21 studies were finally included. There was strong evidence that acute oxidative stress following the cessation of HIE exists when compared to resting states. The HIE-induced oxidative stress is transient and is most likely restored to normal levels within 24 h due to the stimulated endogenous antioxidant system whose response was lagging and lasting. Physically active humans had better antioxidant systems and suffered less oxidative stress after HIE. A physically active lifestyle was considered to enhance antioxidant capacity. For untrained humans, HIE with intensities above 70% VO2max are proposed for initial exercise levels based on the findings reported here.


2020 ◽  
Vol 245 (14) ◽  
pp. 1260-1267
Author(s):  
Sylwia Dzięgielewska-Gęsiak ◽  
Dorota Stołtny ◽  
Alicja Brożek ◽  
Małgorzata Muc-Wierzgoń ◽  
Ewa Wysocka

Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r =  0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.


Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen ◽  
Mustapha Muzaimi ◽  
Mummedy Swamy ◽  
Mohd Asnizam Asari ◽  
...  

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property.


2018 ◽  
Vol 52 (8) ◽  
pp. 850-855 ◽  
Author(s):  
Vinícius Rodrigues de Araujo ◽  
Patrícia Lisboa ◽  
Gabriel Boaventura ◽  
Fabiele Caramez ◽  
Luciane Pires ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.


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