Exercise Intensity and Recovery: Biomarkers of Injury, Inflammation, and Oxidative Stress.

Biomarkers of inflammation, muscle damage, and oxidative stress after high-intensity exercise have been described previously; however, further understanding of their role in the postexercise recovery period is necessary. Because these markers have been implicated in cell signaling, they may be specifically related to the training adaptations induced by high-intensity exercise. Thus, a clear model showing their responses to exercise may be useful in characterizing the relative recovery status of an athlete. The purpose of this study was twofold: (a) to investigate the time course of markers of muscle damage and inflammation in the blood from 3 to 72 hours after combined training exercises and (b) to investigate indicators of oxidative stress and damage associated with increased reactive oxygen species production during high-intensity exercise in elite athletes. Nineteen male athletes performed a combination of high-intensity aerobic and anaerobic training exercises. Samples were acquired immediately before and at 3, 6, 12, 24, 48, and 72 hours after exercise. The appearance and clearance of creatine kinase and lactate dehydrogenase in the blood occurred faster than previous studies have reported. The neutrophil/lymphocyte ratio summarizes the mobilization of 2 leukocyte subpopulations in a single marker and may be used to predict the end of the postexercise recovery period. Further analysis of the immune response using serum cytokines indicated that high-intensity exercise performed by highly trained athletes only generated inflammation that was localized to the skeletal muscle. Biomarkers are not a replacement for performance tests, but when used in conjunction, they may offer a better indication of metabolic recovery status. Therefore, the use of biomarkers can improve a coach's ability to assess the recovery period after an exercise session and to establish the intensity of subsequent training sessions.

The higher exercise intensity and the presence of allele I of ACE gene elicit a higher post-exercise blood pressure reduction and nitric oxide release in elderly women: an experimental study.

BACKGROUND: The absence of the I allele of the angiotensin converting enzyme (ACE) gene has been associated with higher levels of circulating ACE, lower nitric oxide (NO) release and hypertension. The purposes of this study were to analyze the post-exercise salivary nitrite (NO2-) and blood pressure (BP) responses to different exercise intensities in elderly women divided according to their ACE genotype. METHODS: Participants (n = 30; II/ID = 20 and DD = 10) underwent three experimental sessions: incremental test - IT (15 watts workload increase/3 min) until exhaustion; 20 min exercise 90% anaerobic threshold (90% AT); and 20 min control session without exercise. Volunteers had their BP and NO2- measured before and after experimental sessions. RESULTS: Despite both intensities showed protective effect on preventing the increase of BP during post-exercise recovery compared to control, post-exercise hypotension and increased NO2- release was observed only for carriers of the I allele (p < 0.05). CONCLUSION: Genotypes of the ACE gene may exert a role in post-exercise NO release and BP response.

Phaseolamin treatment prevents oxidative stress and collagen deposition in the hearts of streptozotocin-induced diabetic rats.

The development of cardiovascular complications in patients with diabetes is often associated with an imbalance between reactive oxygen species and antioxidant systems. This imbalance can contribute to high cardiac collagen content, which increases cross-linking and the stiffness of the myocardium. In this study, the protective effect of phaseolamin against damage under oxidative stress and collagen deposition in the cardiac tissue in association with diabetes was evaluated. Non-diabetic and diabetic animals were distributed into groups and treated for 20 days with commercial phaseolamin. The phaseolamin treatment increased total antioxidant activity but reduced the following in diabetic rats: (a) hyperglycaemic state, (b) catalase and superoxide dismutase activity and (c) tissue damage caused by lipid peroxidation. Additionally, the phaseolamin treatment attenuated the collagen levels compared to non-treated diabetic rats. Thus, the short-term anti-hyperglycaemic effect of the phaseolamin treatment may prevent the initial changes caused by oxidative stress and the deposition of collagen, as well as reduce the incidence of heart complications.