Muscles produce oxidants, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), from a variety of intracellular sources. Oxidants are detectable in muscle at low levels durin...

https://www.physiology.org/doi/pdf/10.1152/japplphysiol.00953.2007

Muscle-derived ROS and thiol regulation in muscle fatigue.

Strenuous exercise induces oxidative stress and modification of intracellular proteins. Exercise training, however, upregulates endogenous antioxidant defenses and heat shock protein (HSP) expression. In diabetes, perturbations in the endogenous antioxidant and HSP protection have been reported. The aim of this study was to examine the effect of 8 wk of endurance training on HSP expression and oxidative stress markers in the skeletal muscle, heart, and liver of streptozotocin-induced diabetic (SID) and nondiabetic control rats. Induction of diabetes decreased HSP72 expression in heart, liver, and vastus lateralis muscles. SID increased heme oxygenase-1, an oxidative stress-inducible HSP, in liver, red gastrocnemius muscle, and vastus lateralis muscle and glucose-regulated protein 75 in liver. SID increased HSP90 levels in the heart, but levels decreased in the liver. Diabetes induced oxidative stress marker protein carbonyl levels and tissue inflammation. Although endurance training increased the expression of HSP72 in all of the tissues examined, this induction was less pronounced in diabetic rats than in nondiabetic controls. Furthermore, endurance training induced the activation and expression of transcriptional regulator heat shock factor-1 only in nondiabetic control animals. In summary, diabetes may increase susceptibility to oxidative damage and impair HSP protection, but endurance training may offset some of the adverse effects of diabetes by upregulating tissue HSP expression. Our results suggest that diabetes impairs HSP protection, possibly via transcriptionally mediated mechanisms.

Exercise training modulates heat shock protein response in diabetic rats.

Free radicals in cigarette smoke (CS) cause oxidative damage to proteins, DNA, and lipids, contributing to the pathobiology of atherosclerosis, heart disease, and cancer. In vitro studies have shown that antioxidants quench free radicals and ameliorate certain aspects of biomolecular damage caused by CS. It is hypothesized that a combination of antioxidants is more effective than a single antioxidant, due to their interactions. To investigate whether supplemental antioxidants reduce CS-related lipid peroxidation in vivo and whether they are more effective in combination, we conducted an intervention study in smokers. In a randomized double-blind placebo-controlled trial, we investigated whether vitamin C or an antioxidant mixture containing vitamin C, alpha-lipoic acid, and vitamin E decreases plasma F(2)-isoprostane levels, an index of oxidant stress, in smokers. Plasma of 126 smokers (mean age, 46 years; age range, 20-78 years) was analyzed for F(2)-isoprostanes at baseline and after intervention with antioxidants and placebo. In smokers with a body mass index (BMI) above the median, 2 months of daily supplementation with 500 mg of vitamin C decreased plasma F(2)-isoprostane levels by 28.8 pmol/liter when compared with the placebo group (P = 0.001); levels in the mixture group were 7.45 pmol/liter lower after treatment, but this difference was not statistically significant (P = 0.14). There was no treatment effect in smokers with a low BMI. BMI was significantly positively associated with plasma F(2)-isoprostane levels (trend P = 0.001). Antioxidants decrease smoking-related lipid peroxidation markers of oxidative stress in humans with high BMI. Our results do not indicate that an antioxidant combination is more effective than vitamin C alone. The intake of antioxidants may help prevent smoking-related diseases. Smoking cessation should still be considered the most effective way to prevent smoking-related diseases.

Antioxidant Supplementation Decreases Lipid Peroxidation Biomarker F2-isoprostanes in Plasma of Smokers

Physical exercise may be associated with a 10- to 20-fold increase in whole body oxygen uptake. Oxygen flux in the active peripheral skeletal muscle fibres may increase by as much as 100- to 200-fold during exercise. Studies during the past 2 decades suggest that during strenuous exercise, generation of reactive oxygen species (ROS) is elevated to a level that overwhelms tissue antioxidant defence systems. The result is oxidative stress. The magnitude of the stress depends on the ability of the tissues to detoxify ROS, that is, antioxidant defences. Antioxidants produced by the body act in concert with their exogenous, mainly dietary, counterparts to provide protection against the ravages of reactive oxygen as well as nitrogen species. Antioxidant supplementation is likely to provide beneficial effects against exercise-induced oxidative tissue damage. While universal recommendations specifying types and dosages of antioxidants are difficult to make, it would be prudent for competitive athletes routinely engaged in strenuous exercise to seek an estimate of individual requirement. A new dimension in oxidant biology has recently unfolded. Although excessive oxidants may cause damage to tissues, lower levels of oxidants in biological cells may act as messenger molecules enabling the function of numerous physiological processes. It is plausible that some exercise-induced beneficial effects are actually oxidant-mediated. Such developments call for an even more careful analysis of the overall significance of types and amounts of antioxidants in diet. While these complexities pose significant challenges, experts agree that if used prudently, oxidants and antioxidants may serve as potent therapeutic tools. Efforts to determine individual needs of athletes and a balanced diet rich in antioxidant supplements are highly recommended.

Antioxidants in Exercise Nutrition

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h x day(-1), 5 days a week for 8 weeks, reaching the speed of 2.1 km x h(-1) at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km x h(-1) at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.

Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat.

A RF magnetron sputter system was used to deposit lithium niobate (LiNbO 3 ) thin films on (1 1 1)-oriented Si substrates. An optimal sputtering condition with RF power of 100 W, Ar/O 2 ratio of 1 and substrate temperature of 575 °C was investigated. The smallest surface roughness of 6.0 nm for the deposited LiNbO 3 was measured using atomic force microscopy. The crystallinity was examined by low angle X-ray diffractometer. Using the SOPRA GES5 spectroscopic ellipsometer, the associated refractive index and extinction coefficient as a function of wavelength were measured. High optical performance with crystallinity structure of the deposited LiNbO 3 thin films was demonstrated.

Investigation of LiNbO3 thin films grown on Si substrate using magnetron sputter

An electromagnetic field sensor linking a LiNbO3 electrooptical modulator with a circular antenna was studied In this sensor, a Mach-Zehnder electrooptical modulator was used as one of the fundamental building blocks The frequency response was flat from 50 MHz to 3 GHz The minimum detectable electromagnetic field intensity is 07 mV/m at 50 MHz and 12 mV/m at 3 GHz, respectively © 2006 Wiley Periodicals,IncMicrowave Opt Technol Lett 48:1897–1899, 2006; Published online in Wiley InterScience (wwwintersciencewileycom) DOI 101002/mop21776

Electromagnetic field sensor using Mach-Zehnder waveguide modulator

Based on the bidirectional fast Fourier transform beam propagation method (FFT-BPM), a self-consistent Nd:Ti:LiNbO3 Fabry-Perot waveguide laser model has been developed. By using the bidirectional FFT-BPM and the attenuation effect of pumping and resultant lasers within the waveguide cavity, the interference effect and physical behaviors of the population inversion longitudinal and transversal spatial effects were observed. The resultant laser power is saturated if the waveguide is longer than a critical length, which is a function of the pumping power. Moreover, the resultant laser power density is a nonuniform function along the longitudinal dimension within the waveguide cavity.

Fu Tsai Hwang

Papers

Investigation of LiNbO3 thin films grown on Si substrate using magnetron sputter

Electromagnetic field sensor using Mach-Zehnder waveguide modulator

Analysis and modeling of Nd:Ti:LiNbO3 Fabry-Pérot channel waveguide lasers