Search

Exercise induced muscle damage. Anatomopathology and Physiopathology. Exhaustive and unusual physical exercise induces structural and ultra-structural alterations in skeletal muscular whose physiopathology is still unclear. These alterations are described in detail, giving special importance to irregularities of cross striated pattern, paleness with Schiff periodic acid, vacuolization, segmental necrosis, central nuclei, activation of satellite cells and fibroblasts, intra-cellular edema and to the muscular inflammatory reaction with phagocytes infiltration. Their onset times and hypothetical underlying mechanisms are also analyzed. In the origin of these anomalies are metabolic and mechanical factors whose contribution is conditioned by the type of exercise. Experimental data suggests that morphological characteristics of muscle damage induced by exercise are variable according to the metabolic or mechanical stress of exercise.

Oral creatine supplementation is increasingly practised by athletes to improve performance in various types of exercise. While many studies have investigated the effects on skeletal muscle, little is known about the effects of creatine ingestion on hepatic tissue. In this study, a group of mice received creatine supplementation for a period of six days and some hepatic parameters were compared with a control group. The creatine supplemented animals showed a pronounced gain in body weight probably due to water retention. Their hepatic protein content was increased by 23%, and liver phosphocreatine concentration showed a similar increase. Among the hepatic enzymes studied, GOT decreased and GPT showed a tendency to increase; both changes can be explained by metabolic alterations due to overload of the amino acid components of creatine. ATP concentrations and CK activity did not change after creatine feeding. The results speak in favour of a moderate hepatic protein overload with concomitant metabolic alterations after creatine supplementation.

The role of acclimatization and the effect of persistent severe hypoxia (7000 m) were analyzed in mice soleus muscle with respect to oxidative stress (glutathione redox status) and damage markers (TBARS and SH protein groups), NAG and SOD activities and HSP70 expression. Forty mice were divided into one normobaric-normoxic control group and four hypobaric-hypoxic experimental groups (n = 8). One experimental group (1 D) was acutely exposed to a simulated altitude of 7000 m in a hypobaric chamber for 1 day. Another experimental group (ACCL + 1 D) was exposed to a 3 days acclimatization period plus 1 day of hypoxia exposure at 7000 m. The third experimental group (ACCL + 8 D) was exposed to the same acclimatization protocol, remaining 8 subsequent days at 7000 m. The fourth experimental group (8 D) was chronically exposed without acclimatization. ACCL + 1 D showed a significant decrease (p < 0.05) in oxidative stress and damage compared to the 1 D group. Concerning chronic severe hypoxia, acclimatization was truly vital, since 8 D animals died after 5 days of exposure. Oxidative stress and damage markers in ACCL + 8 D tended to gradually increase throughout the 8 days of the hypoxic period. Total SOD activity did not change in 1 D compared to control; however, it increased significantly (p < 0.05) in ACCL + 1 D and ACCL + 8 D. HSP70 expression followed the observed oxidative stress and damage pattern, suggesting a protective role against hypoxia-induced oxidative stress. The present study supports the hypothesis that acclimatization attenuates oxidative stress and damage induced by acute hypoxia, although a trend to a gradually increased oxidative deleterious effect in skeletal muscle seems to occur during persistent severe hypoxia even after a previous acclimatization period.

Investigations on the mechanisms capable of influencing heart mitochondrial function constitute a central contribution to the understanding of cardiac bioenergetics. In contrast to the conventional idea that reactive oxygen species (ROS) mostly act as a trigger for oxidative damage of biological structures, in low physiological concentrations they can regulate a variety of important molecular mechanisms, including those related to mitochondrial respiratory function. Among others, moderate physical exercise seems to be an important agent to induce cellular and mitochondrial environmental redox modifications and it is possible that these alterations could mediate cardiac mitochondrial respiration patterns. This brief review summarizes some current knowledge on mitochondrial respiratory pathways and focuses on data provided by studies dealing with exercise and cardiac respiratory mechanisms. It is emphasized the need of further experimental studies that analyze the association between physical exercise, particularly endurance training, and several mechanisms hypothetically related to the improvement of mitochondrial function, such as the overexpression of some important chaperone machinery and the up-regulation of both cellular and mitochondrial antioxidants. The influence of chronic moderate exercise on the functionality of some inner membrane components and on mitochondrial calcium loading capacity remains to be established.

Context: Epidemiologic information on the incidence of youth soccer injuries in southern Europe is limited. Objective: To compare the incidence, type, location, and severity of injuries sustained by male subelite youth soccer players over the 2008–2009 season. Design: Descriptive epidemiology study. Setting: Twenty-eight Portuguese male youth soccer teams. Patients or Other Participants: A total of 674 youth male subelite soccer players in 4 age groups: 179 U-13 (age range, 11–12 years), 169 U-15 (age range, 13–14 years), 165 U-17 (age range, 15–16 years), and 161 U-19 (age range, 17–18 years). Main Outcome Measure(s): Injuries that led to participation time missed from training and match play prospectively reported by medical or coaching staff of the clubs. Results: In total, 199 injuries reported in 191 players accounted for 14.6 ± 13.0 days of absence from practice. The incidence was 1.2 injuries per 1000 hours of exposure to soccer (95% confidence interval [CI] = 0.8, 1.6), with a 4.2-fold higher incidence during match play (4.7 injuries per 1000 hours of exposure; 95% CI = 3.0, 6.5) than during training (0.9 injuries per 1000 hours of exposure; 95% CI = 0.6, 1.3) (F1,673 = 17.592, P < .001). The overall incidence of injury did not increase with age (F1,673 = 1.299, P = .30), and the incidence of injury during matches (F1,673 = 2.037, P = .14) and training (F1,673 = 0.927, P = .44) did not differ among age groups. Collisions accounted for 57% (n = 113) of all injuries, but participation time missed due to traumatic injury did not differ among age groups (F3,110 = 1.044, P = .38). Most injuries (86%, n = 172) involved the lower extremity. The thigh was the most affected region (30%, n = 60) in all age groups. Muscle strains were the most common injuries among the U-19 (34%, n = 26), U-17 (30%, n = 17), and U-15 (34%, n = 14) age groups, whereas contusions and tendon injuries were the most common injuries in U-13 players (both 32%, n = 8). The relative risk of injury slightly increased with the age of the competitors. Conclusions: The higher incidence of injury during matches than training highlights the need for education and prevention programs in youth soccer. These programs should focus on coach education aimed at improving skills, techniques, and fair play during competitions with the goal of reducing injuries.

Signs of overuse after intense muscular exertion are well described in adults, while little research has been conducted in children. The aim of the study was to investigate some indirect markers of muscle damage in 13 years old boys following two different protocols of one-leg stepping exercise to exhaustion. This stepping exercise was performed by two experimental groups with different contributions of concentric and eccentric contractions in a 1:1 vs 1:2 ratio of timing. Subjective soreness perception and maximum voluntary isometric force of the knee extensor muscles were measured immediately prior to and immediately following the exercise, and at 1, 3, 24, 48, 72, 96 hours post exercise. Metabolic markers of exercise stress were taken at similar time intervals and included plasma glutathione concentrations as a marker for oxidative stress, circulating leukocyte numbers, and plasma creatine kinase (CK) activity. All parameters studied demonstrated a higher level of muscular exertion, with more evident signs of overuse in the group with the more eccentric contribution. Complete recovery was achieved between 72 and 96 hours after exertion. However, in this group of boys, the CK activity did not show the typical adult-like increase. Therefore the wide use of CK as an indicator of intense muscle exertion was not supported in this group of children. It can be concluded that children, like adults, experience similar degrees of muscle disturbances following intense exercise and that they may recover more quickly from such exercise.