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Thyroid hormones are critical for healthy brain functions at every stage of life. Hypothyroidism can cause severe cognitive dysfunction in patients who do not receive adequate treatment. Although thyroid hormone replacement alleviates cognitive decline in hypothyroid patients, there are studies showing that there is no complete recovery. The aim of this study was to investigate the effects of high-intensity interval training (HIIT) in hypothyroid rats on spatial and recognition memory, neuroinflammation, amyloid-beta load and compare these effects with T3 replacement. Hypothyroidism was induced and maintained by administration of 6-n-propyl-2-thiouracil (PTU) with their drinking water to 6-weeks-old male Sprague-Dawley rats for 7 weeks. The animals exercised in the treadmill according to the HIIT protocol for four weeks. T3 was injected intraperitoneally daily during the last two weeks of the study. All animals performed in the elevated plus maze test, Morris water maze test, novel object recognition test, and rotarod motor performance test in the last week of the study and then the animals were sacrificed. Amyloid beta (1-42) and TNFα levels were measured in the prefrontal cortex and hippocampus by ELISA. Anxiety-like behaviors did not significantly differ between groups. T3 replacement with or without HIIT increased motor performance in PTU-treated rats. HIIT and/or T3 replacement increased the exercise performance. HIIT and/or T3 replacement alleviated spatial and recognition memory impairments and normalized TNFα and amyloid-beta levels in the hippocampus in hypothyroid rats. In summary, regular physical exercise may have potential benefits in preserving cognitive functions in hypothyroid patients., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to disclose., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Objectives: Nasal continuous positive airway pressure (nCPAP) treatment is the gold standard treatment for obstructive sleep apnea syndrome (OSAS). In this study, we aimed to show that the pulmonary functions, exercise limitation on the cardiopulmonary exercise test (CPET), and the health-related quality of life can be improved after a short treatment period by nCPAP., Materials and Methods: Our case group with severe obstructive sleep apnea (OSA) performed incremental CPET before and after 8 weeks of nCPAP treatment. All the subjects also underwent physical examination, body composition analysis, simple spirometric measurements, maximal inspiratory pressure (PImax)-maximal expiratory pressure (PEmax), and lung volume tests before and after nCPAP treatment., Results: Thirty-one patients (4 female, 27 male) completed the study. The mean age of the patients was 53.41 ± 1.46 years. Sixteen had at least one comorbidity. In addition, 17 of the subjects were ex-smokers. After nCPAP treatment for 8 weeks, higher PImax-PEmax (p< 0.05), peak oxygen uptake (p= 0.001), workpeak (p= 0.000), maximal heart rates (p= 0.000), and short form-36 scores (p< 0.05) were observed. nCPAP treatment helped control the blood pressure (p= 0.005). There was no significant change in body composition analysis, spirometric parameters, and lung volumes., Conclusion: In a short time period, nCPAP can improve exercise capacity, respiratory muscle strength, and the health-related quality of life scores and help control blood pressure., Competing Interests: Conflict of Interest: No conflict of interest was declared by the authors.

Background: Eccentric exercise is defined as a type of exercise in which the muscle produces power by extending. In contrast to isometric and concentric exercises, eccentric muscle activity is much more effective mechanically; however, it may expose the muscle to soreness. Delayed-Onset Muscle Soreness (DOMS) emerges a couple of hours after an eccentric activity, especially in individuals who are not used to this kind of exercise, and causes a temporary decrease in muscle performance, joint movement angle and muscle power, and also a temporary increase in the blood creatine kinase (CK) activity., Aims: This study investigates the effect of DOMS on the upper extremities motor performance by conducting an eccentric exercise load on the elbow flexor muscles., Study Design: Cross sectional study., Methods: The study included 10 wheelchair basketball players. First, the participants underwent blood CK activity, positioning sense, muscle pain, shooting performance measurements tests at the base, and after 30 minutes and 24 and 48 hours. Then, one week later, the one-repetition-maximums of biceps curls were determined in order to define the intensity of the eccentric exercise. An eccentric exercise protocol which would cause DOMS was applied to all players. All tests were replaced with acute exhaustive eccentric exercise; the same tests were repeated in the same order after the exercise. Blood CK activity was measured by taking an earlobe capillary blood sample. The muscle pain level was measured by using a Visual Analogue Scale (VAS). Positioning sense loss was assessed via goniometer at 30º, 60° and 90° degrees horizontally., Results: The study found a statistically significant increase in blood CK activity and positioning sense loss, and a decrease in the pressure-pain threshold, as well as the shooting percentages in the exercise group when compared with the control., Conclusion: These findings suggest that DOMS negatively affects the upper extremities motor performance of wheelchair basketball players at least 48 hours after eccentric exercise.

Maternal exercise during pregnancy has been suggested to exert beneficial effects on brain functions of the offspring. Leptin is an adipocytokine which is secreted from adipose tissues and has positive effects on learning, memory, and synaptic plasticity. In this study, pregnant rats were moderately exercised and we observed the effects of this aerobic exercise on their prepubertal and adult offsprings' spatial learning, hippocampal neurogenesis, and expression of leptin. All the pups whose mothers exercised during pregnancy learned the platform earlier and spent longer time in the target quadrant. Their thigmotaxis times were shorter than those measured in the control group. It is shown that hippocampal CA1, CA3 neuron numbers increased in both prepubertal and adult pups, in addition that GD neuron numbers increased in adult pups. Leptin receptor expression significantly increased in the prepubertal male, adult male, and adult female pups. In our study, maternal running during pregnancy resulted in significant increase in the expression of leptin receptor but not in prepubertal female pups, enhanced hippocampal cell survival, and improved learning memory capability in prepubertal and adult rat pups, as compared to the control group. In conclusion, maternal exercise during pregnancy may regulate spatial plasticity in the hippocampus of the offspring by increasing the expression of leptin.

The aim of this study was to identify possible relationships between biochemical- superoxide dismutase (SOD), glutathione peroxidase (GPx), thiobarbituric acid reactive substances (TBARS) of mussels (Mytilus galloprovincialis) and chemical (Hg, Cd, Pb, Cr, Cu, Zn, Mn and Fe) contaminants from relatively clean area (Middle Bay) and heavily polluted area (Inner Bay) of the Izmir Bay. Sampling of mussels was performed in the beginning of May 2004. Mussel digestive glands have been used for biochemical assays. Trace metal content was determined by atomic absorption spectrophotometer using standard procedures. Metal contents in mussels collected at polluted site increased compared to the middle part of the bay. While there was a positive correlation between metals and SOD enzyme activity, there was a negative correlation between metals and GPx enzyme activity. An increase was observed in SOD enzyme activity and a decrease of GPx enzyme activity at the inner part of the bay.

The purposes of this study were to investigate the effects of strenuous exercise on apoptosis of the gastrocnemius and soleus muscle fibers and clarify the role of oxidative metabolism in the strenuous exercise-induced apoptosis. The experiment was designed with 49 (n = 49) male, 24-week-old, L. Wistar albino rats. Strenuous exercise model was applied to 42 (n = 42) rats and seven (n = 7) rats served as rested controls. All rats were randomly assigned to one of the following groups (n = 7): rested control (C), immediately after exercise (0 h) and 3, 6, 12, 24, and 48 h after exercise. Apoptotic nuclei were shown by single stranded DNA (ssDNA) determination. Oxidative damage in mitochondrial fractions of the muscle tissues was evaluated by malondialdehyde (MDA) levels and reduced/oxidized glutathione (GSH/GSSG) ratios. Caspase-9, -8 and -3 activities and the level of cytochrome c (Cyt c) were measured in the cytosolic fractions of muscle tissues to follow mitochondrial-dependent (intrinsic) or ligand-mediated death receptor (extrinsic) pathways of apoptosis. Plasma interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were also determined. Based on our results, apoptosis is significantly triggered in muscle fibers by strenuous exercise (P < 0.05). Apoptosis in the soleus muscle tissues mostly depends on the intrinsic pathway and may be triggered by increased oxidative stress. In contrast, extrinsic pathway of apoptosis was predominant in the gastrocnemius muscle and increases of TNF-alpha and IL-6 may play a significant role.

Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. However, there is little information regarding whether or not exhaustive exercise could generate oxidative stress in brain and the findings are conflicting. The aim of this study was to investigate the effects of exhaustive exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, prefrontal cortex and striatum. Additionally we examined antioxidant enzymes activities, superoxide dismutase and glutathione peroxidase, to assess the effects of reactive oxygen species. Exhaustive exercise did not change superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels neither immediately (0 min) nor at 3, 6, 12, 24 and 48 h after the cessation of exercise in the brain. These results indicate that acute exhaustive exercise may not cause significant lipid peroxidation in the hippocampus, prefrontal cortex and striatum during the post-exercise period.

Developing brain is much more sensitive to all kind of stressors than the developed brain. Early maternal deprivation causes some behavioural and physiological effects on rats. After the birth, there is no endocrinological response to stressors between post-natal 4 and 14th days, which is called stress-hyporesponsive period (SHRP) in rats. This hypo-responsiveness is time- and stressor-specific, as some more severe stressors have been shown to induce a stress response. The present study examined the effects of maternal deprivation on oxidative stress in the hippocampus, prefrontal cortex (PFC) and striatum regions of the brain both during and after SHRP of the infant rats. The results showed that maternal deprivation in SHRP increased antioxidant enzyme activities and reduced lipid peroxidation in infant rat brain. However, by the termination of SHRP, maternal deprivation reduced enzyme activities and increased lipid peroxidation. The results indicated that infant brain might be protected in SHRP from maternal deprivation-induced oxidative stress.

It is known that positive effects of regular aerobic exercise on cognitive functions in humans and also animals; but how to the effects of aerobic exercise in adolescent period is unknown. The present study examined the effects of regular aerobic exercise on spatial memory using the Morris water maze, cell density and apoptosis of hippocampus in adolescent rats. Twenty-two days of age male rats were run on a treadmill for 30 min/session at a speed of 8m/min and 0 degrees slope, five times a week for 8 weeks. The present study showed that exercise induced significant cognitive improvement throughout brain maturation in rats. The number of hippocampal CA1 and CA3 neurons, and gyrus dentatus neurons were significantly increased in the exercised rats. There was no significant difference of CA2 neuron density between exercise and control groups. There was no significantly differences in any groups according to the results of apoptosis that account of TUNEL positive cells. The present results suggest that regular moderate aerobic treadmill exercise benefit in cognitive functions. This result may derive from treadmill exercise-induced increase cell density without altering of apoptosis in the hippocampus and dentate gyrus of adolescent rats.

Objectives: L-carnitine is a naturally compound widely distributed in the body. It has an antiradical effect and decreases lipid peroxidation. In acute or chronic streptozotocin (STZ)-induced diabetic rats, the pancreatic content of carnitine was found to be significantly lower than nondiabetic group. We investigated the effects of L-carnitine on the development of STZ-induced diabetes in rats, to determine if L-carnitine can prevent the onset of diabetes or reduce the severity of hyperglycemia and this prevention/reduction is associated with the reduction in oxidative stress., Setting and Design: The rats were divided into 3 groups: Control, STZ-treated (65 mg/kg intraperitoneally) and L-carnitine (500 mg/kg) and STZ-treated., Methods: Oxidative stress was assessed by measuring pancreatic thiobarbituric acid reactive substance (TBARS) formation levels using the method of Rehncrona et al, pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities using a Randox test combination (RANSOD and RANDOX)., Results: L-carnitine did not prevent the onset of diabetes at this dose. Development of diabetes was associated with an increase in pancreatic TBARS (0.028 +/- 0.008 and 0.046 +/- 0.017 nmol/mg Protein, respectively), and GPx activity (0.067 +/- 0.011 and 0.098 +/- 0.016 U/mg Protein, respectively)., Main Findings: L-carnitine prevented this increase induced by diabetes; TBARS (0.039 +/- 0.006 nmol/mg Protein) and GPx activity (0.053 +/- 0.011 U/mg Protein)., Conclusion: These results suggest that L-carnitine exerts anti-oxidative effect in experimental diabetes.

This study aimed to determine whether high-dose antioxidant supplementation had an impact on the acute exercise effects related to erythrocyte membrane mechanics. Experimental animals (n=32) were divided into four groups as control, exercised, supplemented, and supplemented + exercise. Four-week antioxidant supplementation (vitamin C, vitamin E, and zinc) was applied to experimental animals. Following acute exercise on a motor-driven rodent treadmill, erythrocyte aggregation and deformability, erythrocyte adhesion to endothelial cells, superoxide dismutase (SOD), and glutathione peroxidase activities of the erythrocytes were analyzed. In both supplemented and non-supplemented exercised groups, there was a significant decrease in SOD activities and erythrocyte aggregation, and an increase in adhesion to endothelial cell although there was no change on erythrocyte deformability. There were no differences in the responses to the exercise of supplemented and nonsupplemented rats. The data suggested that high-dose antioxidant supplementation did not alter the effects of acute exercise on erythrocyte membrane mechanics.

Although numerous studies have tested the effects of continuous exercise regimens on antioxidant defences, information on the effect of sprint exercise on the antioxidant defence system and lipid peroxidation levels of tissues is scant. The present study was designed to determine the effects of sprint exercise on the lipid peroxidation and antioxidant enzyme system in liver and skeletal muscle during the post-exercise recovery period in untrained mice. Mice performed 15 bouts of exercise, each comprising running on a treadmill for 30 s at 35 m.min(-1) and a 5 degrees slope, with a 10-s rest interval between bouts. They were then killed by cervical dislocation either immediately (0 h), 0.5 h, 3 h or 24 h after completion of the exercise. Their gastrocnemius muscle and liver tissues were quickly removed. It was found that blood lactate levels increased immediately after the exercise, but had returned to control levels by 0.5 h post-exercise. This exercise regimen had no effect on the activity of superoxide dismutase and glutathione peroxidase in these tissues. Levels of muscle thiobarbituric acid reactive substances (TBARS) had increased at 0.5 and 3 h post-exercise, and then returned to control levels by 24 h post-exercise. In conclusion, acute sprint exercise in mice resulted in an increase in TBARS levels in skeletal muscle; no change was observed in the liver. Antioxidant enzyme activities remained unaffected by acute sprint exercise in these tissues.

The administration of methamphetamine to experimental animals results in damage to dopaminergic neurons. The hypothesis that methamphetamine-induced neurotoxicity is mediated by reactive oxygen species was evaluated. It was found that acute administration of methamphetamine (5 and 15 mg kg(-1)) resulted in production of oxidative stress as demonstrated by decreased glutathione and increased oxidized glutathione levels in the rat striatum and prefrontal cortex. These changes in glutathione and oxidized glutathione levels were dose-dependent in striatum but not in prefrontal cortex. In conclusion, the results of present study provide further evidence in support of the notion that oxidative stress may play an important role in the methamphetamine-induced neurotoxicity.

The present study was designed to determine the effects of exercise on the antioxidant enzymatic system and lipid peroxidation in small intestine and kidney, during the post-exercise period in untrained mice. Two days after the last adaptation running exercise, animals were ran on the treadmill for 60 min at 18 m/min. 5 degrees slope. After the acute exercise the animals were killed by cervical dislocation, immediately (0 h), 3 hours (3 h) and 24 hours (24 h) after the exercise. Control animals were killed without running exercise. Their proximal small intestinal and renal tissues were quickly removed. Changes in the concentration of thiobarbituric acid reactive substance (TBARS), as an index of lipid peroxidation, in intestine and kidney were studied in mice after the running exercise and in unexercised control group. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were determined in these tissues. Tissue SOD, GPx activities and TBARS level were not increase by the exercise in kidney. Intestinal SOD activity decreased after exercise (0 h and 3 h respectively, p<0.05, p<0.01) and retumed to control levels. Intestinal GPx activity increased after exercise (0 h, p<0.05) and returned to control levels. There was no significant difference among groups in intestinal tissue TBARS levels. These findings could suggest that submaximal exercise may not cause oxidative stress in proximal small intestinal tissue and kidney.

To investigate the effect of blood perfusion difference on oxidant status, mice were trained by a 7-week running program. Two days after the last training session, mice were exercised for 60 minutes at the same training intensity. Changes in the concentration of thiobarbituric acid reactive substance (TBARS), as an index of lipid peroxidation, in intestine, kidney and muscle, were studied in trained mice immediately (0 h), 3 h and 24 h after the running exercise and in unexercised control group. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and xanthine oxidase (XO) were determined in these tissues. Tissue SOD activities were unaffected by the exercise. Muscle GPx activity increased after exercise (0 h and 3 h group, P < 0.01) and returned to control levels at 24 h, but there was not any significant difference in intestinal and renal tissues. Renal tissue XO activity could not be determined. There was not any significant difference among groups in intestinal tissue XO activity. The activity of XO was decreased only in skeletal muscle at 0 h (P < 0.05). TBARS levels of exercised groups were higher than control in muscle (P < 0.01). Intestinal TBARS levels decreased at 0 h (P < 0.05), than reached to control level. Renal TBARS levels of 0 h and 24 h group was higher than control (P < 0.01, P < 0.01 respectively). The results show that a long distance running exercise may cause lipid peroxidation damage in skeletal muscle and kidney.

The administration of methamphetamine to experimental animals results in damage to dopaminergic neurons. In the present study, we demonstrated that a single dose (15 mg/kg) of methamphetamine results in production of oxidative stress as demonstrated by increased thiobarbituric acid reactive substances levels in the rat striatum and prefrontal cortex. In conclusion, the results of present study provide further evidence in support of the notion that oxidative stress may play an important role in the methamphetamine-induced neurotoxicity.

Mild footshock stress results in an increase dopamine metabolism in the prefrontal cortex. Increases in either the intensity or duration of stress enhance dopamine metabolism in the nucleus accumbens and striatum, as well as in the prefrontal cortex. Dopamine is metabolized by monoamine oxidase with hydrogen peroxide as a product. In this study we have demonstrated that while very mild (0.2 mA) footshock stress did not change glutathione peroxidase activity in the rat prefrontal cortex and striatum, more intense (1.6 mA) footshock stress increased glutathione peroxidase activity at 0, 15, 30 and 60 min after the footshock in the prefrontal cortex and at 30 min after the footshock in the striatum. Stress did not change superoxide dismutase activity and thiobarbituric acid reactive substances levels. These results indicate that increased dopamine metabolism induced by footshock stress is probably responsible for the increase of glutathione peroxidase activity.

The purpose of the present study was to investigate the effects of aerobic and anaerobic training on serum lipid peroxidation levels and on antioxidant enzyme activities. Long distance runners for aerobic training group, and wrestlers for anaerobic training group were chosen. Non-sporting men were used as control group. When the aerobic power was compared; indirect VO2max of long-distance runners were found higher than wrestlers and control group (p<0.001, p<0.001). When lipid peroxidation levels were compared; levels of the thiobarbituric acid reactive substances (TBARS) of long distance runners were found to be lower than those in the control group (p<0.05), but similar to those found in wrestlers. Comparison of antioxidant enzyme activities in erythrocytes show that there were no significant difference among the groups in superoxide dismutase enzyme activities, but glutathione peroxidase (GPx) activity of long distance runners was higher than that measured in wrestlers (p<0.05). These results suggest that aerobic training increased in erythrocytes GPx activity with a subsequent decrease in plasma TBARS levels but anaerobic training had no effect on this process.

The administration of methamphetamine to experimental animals results in damage to nigrostriatal dopaminergic neurons. In the present study, we demonstrated that both the acute repeated and the chronic administration of methamphetamine causes an increase in thiobarbituric acid reactive substances, which are indicators of lipid peroxidation, and superoxide dismutase activity in the rat striatum. The results of present study strengthen the notion that reactive oxygen species may play an important role in the methamphetamine-induced neurotoxicity., (Copyright 1998 Elsevier Science B.V.)

Total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C) and HDL-C/TC levels are important in determining the risk of coronary heart disease. The serum lipids and lipoprotein levels of regularly training sportspersons and non-sporting controls were determined and compared with each other to investigate the effects of exercise and sex on these factors. HDL-C levels of male and female training groups were higher than those of corresponding non-sporting groups (respectively P < 0.01, P < 0.001). The sportswomen's HDL-C levels were higher (P < 0.05); and TC, TG, and LDL-C levels were lower. (P < 0.001) than those of sportsmen's levels. The non-sporting women's TC and TG levels were lower than those of non-sporting men's levels (P < 0.001). HDL-C/TC ratio of active females was higher than that of control females (P < 0.01). The corresponding difference in males was also significant. We conclude that physical activity and sex have effects on risk factors for cardiovascular disease.