High prevalence of muscle weakness and probable sarcopenia in patients with inflammatory bowel disease.

BACKGROUND: This study aimed to determine the prevalence of probable sarcopenia and sarcopenia in patients with inflammatory bowel disease (IBD) by using the European Working Group on Sarcopenia in Older People (EWGSOP2) diagnostic criteria. METHODS: Sarcopenia was assessed by using the sequential four-step algorithm. (1) Find: Sarcopenia risk by simple clinical symptom index (strength, assistance walking, rise from a chair, climb stairs, and falls [SARC-F questionnaire]). (2) Assess: Probable sarcopenia by low muscle strength on handgrip. (3) Confirm: Confirmed sarcopenia by low appendicular skeletal muscle mass on bioimpedance analysis. (4) Severity: Severe sarcopenia by low 4-m gait speed test. RESULTS: A total of 129 adult patients with IBD younger than 65 years and 50 age- and sex-matched healthy control (HC) participants were included to the study. Handgrip strength, gait speed, and SARC-F scores were significantly lower in patients with IBD than in the HCs (P = 0.032, <0.0001, and <0.0001, respectively). Based on the EWGSOP2 definition, 17.8% of patients with IBD had probable sarcopenia, and six patients had confirmed sarcopenia. According to the ethnicity-based population thresholds, 34.9% of patients with IBD had probable sarcopenia, and two patients had confirmed sarcopenia. Corticosteroid use within the past year was identified as an independent risk factor for low muscle strength (P = 0.012; odds ratio, 4.133), along with advanced age and disease activity. CONCLUSION: One-third of the patients younger than 65 years with IBD had probable sarcopenia, defined as low muscle strength, whereas the incidence of confirmed sarcopenia remained relatively low.

Weekend warrior exercise model for protection from chronic mild stress­induced depression and ongoing cognitive impairment.

We aim to investigate the role and biological mechanisms of the weekend warrior (WW) exercise model on depression­induced rats in comparison to the continuous exercise (CE) model. Sedentary, WW, and CE rats were subjected to chronic mild stress (CMS) procedure. CMS and exercise protocols continued for six weeks. Anhedonia was evaluated by sucrose preference, depressive behavior by Porsolt, cognitive functions by object recognition and passive avoidance, and anxiety levels by open field and elevated plus maze. After behavioral assessments, brain tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, superoxide dismutase and catalase activities and GSH content, tumor necrosis factor­α (TNF­α), interleukin­6 (IL­6), IL­1ß, cortisol and brain­derived neurotrophic factor levels and histological damage was assessed. CMS­induced depression­like outcomes with increases in anhedonia and decreases in cognitive measures that are rescued with both exercise models. The increased immobilization time in the Porsolt test was decreased with only WW. Exercise also normalized the suppression of antioxidant capacity and MPO increase induced by CMS in both exercise models. MDA levels also declined with both exercise models. Anxiety­like behavior, cortisol levels, and histological damage scores were exacerbated with depression and improved by both exercise models. TNF­α levels were depleted with both exercise models, and IL­6 only with WW. WW was as protective as CE in CMS­induced depression­like cognitive and behavioral changes via suppressing inflammatory processes and improving antioxidant capacity.

Protective effect of exercise and sildenafil on acute stress and cognitive function.

INTRODUCTION: There are contradictory results about the effects of exercise and sildenafil on cognitive functions. AIM: To investigate the effects of sildenafil pretreatment and chronic exercise on anxiety and cognitive functions. METHOD: Wistar rats (n=42) were divided as sedentary and exercise groups. A moderate-intensity swimming exercise was performed for 6 weeks, 5 days/week, 1h/day. Some of the rats were administered orogastrically with sildenafil (25mg/kg/day) either acutely or chronically. Exposure to cat odor was used for induction of stress. The level of anxiety was evaluated by elevated plus maze test, while object recognition test was used to determine cognitive functions. Brain tissues were removed for the measurement of myeloperoxidase (MPO), malondialdehyde (MDA), nitric oxide levels, lucigenin-enhanced chemiluminescence, and for histological analysis. RESULTS: Increased MPO and MDA levels in sedentary-stressed rats were decreased with sildenafil applications. Chronic exercise inhibited the increase in MPO levels. Increased nitric oxide and lucigenin chemiluminescence levels in sedentary-stressed rats, were diminished with chronic sildenafil pretreatment. The time spent in the open arms of the plus maze was declined in sedentary-stressed rats, while chronic sildenafil pretreatment increased the time back to that in non-stressed rats. Acute sildenafil application to exercised rats prolonged the time spent in open arms as compared to non-treated exercise group. The time spent with the novel object, which was decreased in sedentary-stressed rats, was increased with sildenafil pretreatment. Our results suggest that sildenafil pretreatment or exercise exerts a protective effect against acute stress and improves cognitive functions by decreasing oxidative damage.

Ameliorative effect of chronic moderate exercise in smoke exposed or nicotine applied rats from acute stress.

INTRODUCTION: Physical activity has been found to be related with many health benefits. Our aim was to investigate the effect of chronic moderate exercise from acute stress on nicotine and cigarette smoke exposed rats. METHODS: Male Sprague Dawley rats (200-250g, n = 48) were divided into 6 groups as non-exercised, exercised, smoke exposed, smoke exposed and exercised, nicotine applied, and nicotine applied and exercised. Nicotine bitartarate was applied intraperitoneally (0.1mg/kg/day) for 5 weeks, and cigarette smoke was exposed in a ventilated chamber. After 1 week of nicotine application or smoke exposure, moderate exercise training protocol was applied to exercise groups. At the end of the experiments, acute stress induction was made to all groups by electric foot shock. Holeboard tests were performed before and after the experiments. Biochemical and histological analyses were performed in lung, liver, colon, stomach, and gastrocnemius tissues. RESULTS: Malondialdehyde levels were increased in all tissues of smoke exposed group (p < .05-.01) except gastrocnemius tissue compared to non-exercised group and were decreased with exercise (p < .05-.001). Myeloperoxidase levels were increased in lung, liver and colon tissues of smoke exposed group (p < .05-.001) and liver and colon tissues of nicotine applied rats (p < .01-.001) and decrease with exercise in liver and colon tissues of both smoke exposed or nicotine applied groups (p < .05-.01). In all tissue samples, increased histological injury scores (p < .05-.001) decreased significantly with exercise (p < .01-.001). CONCLUSION: Biochemical parameters and histological scoring indicated increased tissue injury due to nicotine application and cigarette smoke exposure and exercise training ameliorated these effects in most of the tissues of acute stress induced rats.

The involvement of nitric oxide and endothelin-1 in exercise-induced bronchospasm in young soccer players.

OBJECTIVES: To investigate the levels of nitric oxide (NO) and endothelin-1 (ET-1) in soccer players with exercise-induced bronchospasm (EIB), to test whether these endogenous vasoactive molecules are involved in the development of EIB, and to examine the possible participation of reactive oxygen metabolites in these alterations. DESIGN: Observational study. SETTING: Football club. PARTICIPANTS: Forty-three soccer players (N = 43) aged 16 to 22 years performed maximal exercise test on a treadmill by using Bruce protocol. INTERVENTIONS: Respiratory function tests were evaluated before and after exercise tests. Participants were grouped as control (n = 35) or EIB (n = 8) groups according to the respiratory function test results. MAIN OUTCOME MEASURES: Endothelin-1 (ET-1), nitric oxide (NO), carbonyl, malondialdehyde, and glutathione levels were determined from the blood samples taken before and after exercise tests. RESULTS: In the control group, significant decreases in plasma ET-1 and serum NO levels were determined after exercise. On the other hand, plasma malondialdehyde and carbonyl levels were significantly decreased, whereas glutathione levels were significantly increased after exercise. In the EIB group, blood levels of NO, ET-1, carbonyl, and malondialdehyde after exercise were found to be significantly increased compared with pre-exercise levels. CONCLUSIONS: These findings demonstrate that in young soccer players, EIB is associated with elevated serum NO and plasma ET-1 levels. Moreover, significant increases in lipid peroxidation and protein oxidation and decreases in antioxidant sulfhydryl (RSH) content indicate a significant compromise in the blood antioxidant status and the presence of systemic oxidative stress in young athletes with EIB.

Diet-supported aerobic exercise reduces blood endothelin-1 and nitric oxide levels in individuals with impaired glucose tolerance.

BACKGROUND: Impaired glucose tolerance (IGT) forms an intermediate stage in the natural history of diabetes mellitus. Insulin-resistant states might be associated with dysfunction of the vascular endothelium. OBJECTIVES: To determine the effects of chronic exercise and a low-calorie diet on plasma nitric oxide (NO) and endothelin-1 (ET-1) levels in patients with IGT and to elucidate the relationship between the oxidant stress markers and NO/ET-1 levels of blood before and after exercise. METHODS: Patients with IGT (n = 14) participated in a regular exercise program and exercised for 40 minutes each day, 3 days a week for 12 weeks. Physiological, anthropometric, and biochemical measurements were performed before, during the 6th week, and at the end of the program. RESULTS: There was a significant reduction in body mass index, body fat content, systolic and diastolic blood pressures, as well as NO and ET-1 concentrations after 12 weeks of exercise and diet program. Exercise training significantly elevated subjects' maximum oxygen consumption, whereas the resting metabolic rates of the patients did not change. The formation of thiobarbituric acid reactive substances were significantly reduced, whereas sulfhydryl groups were significantly increased on the 6th week (P < .05) and at the end of program (P < .01). CONCLUSION: Our results demonstrate that exercise, along with low-calorie diet, induced reductions in the plasma of both ET-1 and NO. Beneficial effects were observed on anthropometric measurements and plasma oxidant stress markers, indicating weight loss associated with exercise training and calorie restriction may effectively improve endothelial dysfunction in patients with IGT.

Stress-induced multiple organ damage in rats is ameliorated by the antioxidant and anxiolytic effects of regular exercise.

Our aim was to investigate the effects of moderate load, regular swimming exercise on stress-induced anxiety, and associated oxidative organ injury. Male Sprague-Dawley rats (n = 48) were either kept sedentary or submitted to swimming exercise for 8 weeks. Rats were then divided as non-stressed, acute stress, and chronic stress groups. After acute or chronic stress (electric foot shocks) applications, rats were placed on a holeboard and the exploratory behavior was recorded to assess the anxiety. Rats were decapitated after the stress application. Acute and chronic stress induction led to increased serum cortisol levels as compared to non-stressed groups. Plasma aspartate aminotransferase levels that were elevated in sedentary rats with both stress exposures were lower in trained rats. Malondialdehyde levels and myeloperoxidase activity were increased in the cardiac muscle, liver, stomach, and brain of the stressed rats with a concomitant reduction in the glutathione levels, while stress-induced changes in malondialdehyde, myeloperoxidase, and glutathione levels were reversed in the trained animals. Exercise, which led to increased malondialdehyde and reduced glutathione levels in the skeletal muscle of the non-stressed rats, also protected against stress-induced oxidative damage. Regular exercise with its anxiolytic and antioxidant effects ameliorates stress-induced oxidative organ damage by a neutrophil-dependent mechanism.

Estrogen protects against oxidative multiorgan damage in rats with chronic renal failure.

The impact of sex dimorphism on chronic renal failure (CRF)-induced oxidative multiorgan damage and the effects of estradiol (E(2)) loss and E(2) supplementation on the progress of CRF were studied. Sprague-Dawley rats underwent 5/6 nephrectomy (CRF), and a group of female rats had bilateral ovariectomy (OVX), while the sham-operated rats had no nephrectomy or OVX. Rats received either estradiol propionate (50 microg/kg/day) or vehicle for six weeks. Serum BUN levels were elevated in both male and female CRF groups treated with vehicle, while creatinine level was not significantly changed in the female CRF group. CRF-induced elevation in serum TNF-alpha of male rats was abolished when the animals were treated with E(2), while OVX exaggerated TNF-alpha response. In OVX and male rats with CRF, E(2) treatment reversed the malondialdehyde elevations in all the studied tissues (kidney, heart, lung, ileum, brain, liver, and gastrocnemius muscle), while depletion of glutathione in these tissues was prevented by E(2) treatment. Similarly, increased levels of myeloperoxidase activity, lucigenin chemiluminescence, and collagen in most of the tissues were reversed by E(2) treatment. The findings show that the extent of tissue injuries was relatively less in females, while ovariectomy exacerbated all the indices of oxidative injury. Moreover, the administration of E(2), with its potent anti-oxidant and anti-inflammatory effects, markedly improved CRF-induced systemic inflammatory outcomes in both male and female rats by depressing tissue neutrophil infiltration and modulating the release of inflammatory cytokines.

Ghrelin ameliorates pancreaticobiliary inflammation and associated remote organ injury in rats.

The present study was designed to evaluate whether ghrelin could reduce organ injury and systemic inflammation induced by pancreaticobiliary obstruction. In Sprague-Dawley rats, either the bile duct (BDL) or common pancreaticobiliary duct (PBDL) was ligated or a sham operation was applied. BDL or PBDL rats received either ghrelin (10ng/kg) or saline intraperitoneally immediately before the surgery and once a day until the rats were decapitated at 72h. The pancreas, liver, lung and kidney were removed for the histological analysis, and for the determination of malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase activity (MPO). MDA and MPO levels in all the tissues, which were elevated in PBDL group (p<0.05-0.001), were reversed back to control levels in ghrelin-treated rats. In BDL group, elevations in hepatic MDA and MPO levels (p<0.001) were also abolished by ghrelin treatment. In contrast to saline-treated group with severe pancreatic damage, ghrelin-treated rats demonstrated a moderate pancreatic and hepatic destruction accompanied with reduced pulmonary and renal damages. The results illustrate that ghrelin protects the hepatic and pancreatic tissues, as well as remote organs against oxidative injury, by a neutrophil-dependent mechanism.

Colitis-induced oxidative damage of the colon and skeletal muscle is ameliorated by regular exercise in rats: the anxiolytic role of exercise.

Epidemiological studies have shown that exercise protects the gastrointestinal tract, reducing the risk of diverticulosis, gastrointestinal haemorrhage and inflammatory bowel disease, while many digestive complaints occurring during exercise are attributed to the adverse effects of exercise on the colon. In order to assess the effects of regular exercise on the pathogenesis of colitis, Sprague-Dawley rats of both sexes were either kept sedentary or given exercise on a running wheel (0.4 km h(-1), 30 min for 3 days week(-1)). At the end of 6 weeks, under anaesthesia, either saline or acetic acid (4%, 1 ml) was given intracolonically. Holeboard tests were performed for the evaluation of anxiety at 24 h before and 48 h after induction of colitis. Increased 'freezing time' in the colitis-induced sedentary group, representing increased anxiety, was reduced in the exercised colitis group (P < 0.05). On the third day following the colonic instillation, the rats were decapitated under brief ether anesthesia and the distal 8 cm of the colons were removed. In the sedentary colitis group, macroscopic and microscopic damage scores, malondialdehyde level and myeloperoxidase activity were increased when compared to the control group (P < 0.01-0.001), while exercise prior to colitis reduced all the measurements with respect to sedentary colitis group (P < 0.05-0.001). The results demonstrate that low-intensity, repetitive exercise protects against oxidative colonic injury, and that this appears to involve the anxiolytic effect of exercise, suggesting that exercise may have a therapeutic value in reducing stress-related exacerbation of colitis.