Effects of cryotherapy on the regeneration process and muscular mechanical properties after lacerative injury model.

Cryotherapy is a therapeutic modality widely used for the treatment of muscle injuries to control pain and inflammatory processes. This study aimed to investigate the effects of cryotherapy on the inflammatory and oxidative stress parameters and mechanical properties of, and pain in, the skeletal muscles of rats with lacerative muscle injury. The rats were anesthetized with 4% isoflurane and subjected to gastrocnemius muscle laceration injury. After injury, all animals in the intervention groups received cryotherapy treatment for 20 minutes using plastic bags containing crushed ice. The protocol comprised three daily applications at 3-hour intervals on the day of injury, with reapplication 24 hours later. Seventy-two male Wistar rats were divided into three groups: sham, muscle injury (MI), and MI + cryotherapy (MI + cryo). Muscle mechanical properties were analyzed by mechanical tensile testing on day 7 after injury. The MI + cryo group showed reduced TNF-α, IFN-γ, and IL1ß levels; elevated IL4, IL6, and IL10 levels; reduced oxidant production and carbonyl levels; and elevated sulfhydryl contents. Animals that underwent tissue cooling showed superoxide dismutase activity and glutathione levels close to those of the animals in the sham group. The MI and MI + cryo groups showed reduced values of the evaluated mechanical properties and lower mechanical thresholds compared to those of the animals from the sham group. Our results demonstrated that the proposed cryotherapy protocol reduced the inflammatory process and controlled oxidative stress but did not reverse the changes in the mechanical properties of muscle tissues or provide analgesic effects within the time frame analyzed.

Effects of low-level laser therapy (GaAs) in an animal model of muscular damage induced by trauma.

It has been demonstrated that reactive oxygen species (ROS) formation and oxidative damage markers are increased after muscle damage. Recent studies have demonstrated that low-level laser therapy (LLLT) modulates many biochemical processes mainly those related to reduction of muscular injures, increment of mitochondrial respiration and ATP synthesis, as well as acceleration of the healing process. The objective of the present investigation was to verify the influence of LLLT in some parameters of muscular injury, oxidative damage, antioxidant activity, and synthesis of collagen after traumatic muscular injury. Adult male Wistar rats were divided randomly into three groups (n = 6), namely, sham (uninjured muscle), muscle injury without treatment, and muscle injury with LLLT (GaAs, 904 nm). Each treated point received 5 J/cm(2) or 0.5 J of energy density (12.5 s) and 2.5 J per treatment (five regions). LLLT was administered 2, 12, 24, 48, 72, 96, and 120 h after muscle trauma. The serum creatine kinase activity was used as an index of skeletal muscle injury. Superoxide anion, thiobarbituric acid reactive substance (TBARS) measurement, and superoxide dismutase (SOD) activity were used as indicators of oxidative stress. In order to assess the synthesis of collagen, levels of hydroxyproline were measured. Our results have shown that the model of traumatic injury induces a significant increase in serum creatine kinase activity, hydroxyproline content, superoxide anion production, TBARS level, and activity of SOD compared to control. LLLT accelerated the muscular healing by significantly decreasing superoxide anion production, TBARS levels, the activity of SOD, and hydroxyproline content. The data strongly indicate that increased ROS production and augmented collagen synthesis are elicited by traumatic muscular injury, effects that were significantly decreased by LLLT.

Physical exercise is effective in preventing cigarette smoke-induced pulmonary oxidative response in mice.

Reactive oxygen species (ROS) are important in the pathogenesis of pulmonary injury induced by cigarette smoke (CS) exposure, and physical exercise (Ex) is useful in combating impaired oxidative process. We verified the preventive effects of Ex on lung oxidative markers induced by smoking. In this study, 36 mice (C57BL-6, 30-35 g) were split into four groups: control, CS, Ex, and CS plus Ex. Ex groups were given prior physical training in water (2×30 min/d, 5 days/wk, 8 weeks). After training, the CS groups were subjected to passive exposure to four cigarettes, 3 × per day, for 60 consecutive days. After 24 hours from the last exposure, CS animals were sacrificed, and lung samples were collected for further analysis. Left lung sample was prepared for histological analysis, and right lung was used for biochemical analysis (superoxide, hydroxyproline, lipid peroxidation [thiobarbituric acid reactive species], protein carbonylation [carbonyl groups formation], superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx] activities). Group comparisons were evaluated by analysis of variance (ANOVA). Results were expressed as mean ± standard deviation, with P<0.05 considered significantly different. Preventive Ex impeded histological changes and increased the enzymatic defense system (SOD and GPx) by reducing oxidative damage in lipids and proteins. This preventive effect of prior physical Ex alleviates damage caused by CS exposure.

Therapeutic action of physical exercise on markers of oxidative stress induced by chronic kidney disease.

AIMS: To investigate the effects physical training exerts on markers of oxidative stress in rats with chronic kidney disease (CKD). MAIN METHODS: Twenty-four male Wistar rats were divided into four groups (n=6): sham, CKD, exercise-sham and exercise-CKD. Surgical reduction of the renal mass was performed (5/6 nephrectomized) and exercise was conducted on a treadmill (50 min/day up to 1 km/h for, 5 days/week for eight weeks). Forty-eight hours after the last exercise session, blood (1 mL) was collected from the abdominal aorta and animals were decapitated. The left kidney was surgically removed and stored at -70 °C for subsequent analysis. KEY FINDINGS: An increase was observed in creatinine and urea levels, superoxide production, antioxidant enzymes, and oxidative damage in the CKD group, as compared to sham animals (p<0.05). Physical training made superoxide production and oxidative damage decrease in the CKD group (p<0.05), increasing SOD and GPX activity, though it did not increase the antioxidant effects of CAT, and renal parameters. SIGNIFICANCE: Even without altering renal function in animals induced to CKD model, the results show that physical training is an important component in the treatment of CKD, because it exerted a positive influence on oxidative stress parameters, especially on the reduction in superoxide production and oxidative damage, as well as an improvement in the antioxidant defense system, like SOD and GPX.