Exercise training is known to induce an increase in free radical production potentially leading to enhanced muscle injury. Vitamins C and E are well known antioxidants that may prevent muscle cell damage. The purpose of this study was to determine the effects of these supplemental antioxidant vitamins on markers of oxidative stress, muscle damage and performance of elite soccer players. Ten male young soccer players were divided into two groups. Supplementation group (n=5) received vitamins C and E supplementation daily during the pre-competitive season (S group), while the placebo group (PL group, n=5) received a pill containing maltodextrin. Both groups performed the same training load during the three-month pre-season training period. Erythrocyte antioxidant enzymes glutathione reductase, catalase and plasma carbonyl derivatives did not show any significant variation among the experimental groups. Similarly, fitness level markers did not differ among the experimental groups. However, S group demonstrated lower lipid peroxidation and muscle damage levels (p<0.05) compared to PL group at the final phase of pre-competitive season. In conclusion, our data demonstrated that vitamin C and E supplementation in soccer players may reduce lipid peroxidation and muscle damage during high intensity efforts, but did not enhance performance.
Purpose: This study aimed to investigate changes in muscle damage during the course of a 217-km mountain ultramarathon (MUM). In an integrative perspective, inflammatory response and renal function were also studied.Methods: Six male ultra-runners were tested four times: pre-race, at 84 km, at 177 km, and immediately after the race. Blood samples were analyzed for serum muscle enzymes, acute-phase protein, cortisol, and renal function biomarkers.Results: Serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) increased significantly throughout the race (P < 0.001, P < 0.001; P = 0.002, respectively), and effect size (ES) denoted a large magnitude of muscle damage. These enzymes increased from pre-race (132 ± 18, 371 ± 66, and 28 ± 3 U/L, respectively) to 84 km (30, 1.8, and 3.9-fold, respectively); further increased from 84 to 177 km (4.6, 2.9, and 6.1-fold, respectively), followed by a stable phase until the finish line. Regarding the inflammatory response, significant differences were found for C-reactive protein (CRP) (P < 0.001) and cortisol (P < 0.001). CRP increased from pre-race (0.9 ± 0.3 mg/L) to 177 km (243-fold), cortisol increased from pre-race (257 ± 30 mmol/L) to the 84 km (2.9-fold), and both remained augmented until the finish line. Significant changes were observed for creatinine (P = 0.03), urea (P = 0.001), and glomerular filtration rate (GFR) (P < 0.001), and ES confirmed a moderate magnitude of changes in renal function biomarkers. Creatinine and urea increased, and GFR decreased from pre-race (1.00 ± 0.03 mg/dL, 33 ± 6 mg/dL, and 89 ± 5 ml/min/1.73 m2, respectively) to 84 km (1.3, 3.5, and 0.7-fold, respectively), followed by a plateau phase until the finish line.Conclusion: This study shows evidence that muscle damage biomarkers presented early peak levels and they were followed by a plateau phase during the last segment of a 217-km MUM. The acute-phase response had a similar change of muscle damage. In addition, our data showed that our volunteers meet the risk criteria for acute kidney injury from 84 km until they finished the race, without demonstrating any clinical symptomatology.
The cause-effect relationship between lactic acid, acidosis, and muscle fatigue has been established in the literature. However, current experiments contradict this premise. Here, we describe an experiment developed by first-year university students planned to answer the following questions: 1) Which metabolic pathways of energy metabolism are responsible for meeting the high ATP demand during high-intensity intermittent exercise? 2) Which metabolic pathways are active during the pause, and how do they influence phosphocreatine synthesis? and 3) Is lactate production related to muscular fatigue? Along with these questions, students received a list of materials available for the experiment. In the classroom, they proposed two protocols of eight 30-m sprints at maximum speed, one protocol with pauses of 120 s and the other protocol with pauses of 20 s between sprints. Their performances were analyzed through the velocity registered by photocells. Blood lactate was analyzed before the first sprint and after the eighth sprint. Blood uric acid was analyzed before exercise and 15 and 60 min after exercises. When discussing the data, students concluded that phosphocreatine restoration is time dependent, and this fact influenced the steady level of performance in the protocol with pauses of 120 s compared with the performance decrease noted in the protocol with pauses of 20 s. As the blood lactate levels showed similar absolute increases after both exercises, the students concluded that lactate production is not related to the performance decrement. This activity allows students to integrate the understanding of muscular energy pathways and to reconsider a controversial concept with facts that challenge the universality of the hypothesis relating lactate production to muscular fatigue.
Ultramarathon races are fairly demanding and impose substantial physiological stress on healthy athletes. These competitions may thus be considerably more challenging for individuals with diabetes. This case study aims to describe glycemic control, muscle damage, inflammation, and renal function in 3 athletes with type 1 diabetes during a successful performance in a relay ultramarathon. The team completed the race in 29 hours and 28 minutes, earning third place. The total distance covered by each athlete was 68.7, 84.5, and 65.1 km. Most blood glucose levels showed that athletes were in a zone where it was safe to exercise (90-250 mg/dL or 5.0-13.9 mmol/L). Creatine kinase, lactate dehydrogenase, and aspartate aminotransferase serum levels increased 1.2- to 50.7-fold prerace to postrace, and were higher than the reference ranges for all the athletes postrace. Blood leukocytes, neutrophils, and serum C-reactive protein (CRP) increased 1.6- to 52-fold prerace to postrace and were higher than the reference ranges for 2 athletes after the race. Serum creatinine increased 1.2-fold prerace to postrace for all the athletes but did not meet the risk criteria for acute kidney injury. In conclusion, our main findings show evidence of satisfactory glycemic control in athletes with type 1 diabetes during a relay ultramarathon. Moreover, elevation of muscle damage and inflammatory biomarkers occurred without affecting renal function and challenging the maintenance of blood glucose among athletes. These findings are novel and provide an initial understanding of the physiological responses in athletes with type 1 diabetes during ultramarathon races.
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