Injury type and incidence among elite level curlers during world championship competition.

Our objective was to investigate the incidence of musculoskeletal injuries sustained by elite level curling athletes during international competition. This study was conducted during the 2008 World Men's Curling Championships. All registered athletes and the tournament medical team were given report forms for documenting injuries that occurred during the tournament. Report form information included demographics, area injured, types of injuries sustained, and curling-specific aggravating conditions. During the competition five injuries were reported, resulting in an injury rate of .07 injuries per game. Only one reported injury resulted in missed competition (.014 injuries per game). All reported injuries involved increased pain during curling-specific activities. At the elite international competitive level, injury incidence in curling was found to be low. Future exploration over the course of a season may be beneficial to identify risk factors and to assist with formulating training strategies to decrease injury risk.

A prospective study of injury affecting competitive collegiate swimmers.

The purposes of this study were to determine the incidence and distribution of injuries affecting collegiate competitive swimmers and to test possible injury risk factors. A prospective cohort design was used to follow 34 swimmers (16 M, 18 F) from an NCAA Division I Midwest University over one academic year. Exposure-based injury rates were determined for both practice and competition. Risk of injury was assessed relative to gender, years swimming, and history of injury. Twenty of 34 swimmers sustained 31 injuries with overall injury rates of 5.55 injuries per 1000 athlete exposures and 3.04 injuries per 1000 hours exposure. Practice injury rates for female swimmers were higher than for women's practice injury rates in other NCAA sports. The most common injury locations were the shoulder, back, and knee. Risk factors that remained significant in the multivariate analysis were history of injury to the same anatomical location and history of injury at other anatomical sites.

Long-lived Ames dwarf mouse exhibits increased antioxidant defense in skeletal muscle.

Resting and exercised (both acute and chronic) hindlimb skeletal muscle from long-lived Ames dwarf and wild type mice at 3, 12, 18, and 24 months of age was tested for antioxidant enzyme activity and protein, non-enzymatic antioxidant ratios, mitochondrial hydrogen peroxide concentration, and plasma lactate levels. Differences were observed in GPX enzyme activity between mouse genotypes at all physical activity levels, with dwarf mice exhibiting depressed levels at younger ages (3 months: P = 0.09 [non-swim], P = 0.03 [acute swim], P = 0.04 [chronic swim]) and comparatively higher levels than wild type mice at older ages (18-24 months: P = 0.05 [acute swim], P = 0.07 [chronic swim]). Catalase enzyme activity and the GSH system rarely demonstrated significant differences between genotypes, regardless of age or activity. However, the chronic exercise group displayed a difference in GSH:GSSG ratios between mouse genotypes (P = 0.005). Plasma lactate concentrations were elevated in the wild type mice compared to the dwarf mice at all ages in all activity groups. These results suggest there are biological differences with regard to antioxidant defense that favor the Ames dwarf mouse in active and resting skeletal muscle when compared to wild type mice.

Effects of growth hormone and insulin-like growth factor-1 on hepatocyte antioxidative enzymes.

The physiological decline that occurs in aging is thought to result, in part, from accumulation of oxidative damage generated by reactive oxygen species during normal metabolic processes. Elevated levels of antioxidative enzymes in liver tissues are present in the Ames dwarf, a growth hormone (GH)-deficient mouse that lives more than 1 year longer than wild-type mice from the same line. In contrast, transgenic mice that overexpress GH exhibit depressed hepatic levels of catalase and have significantly shortened life spans. In this study, we evaluated the in vitro effects of GH and insulin-like growth factor 1 (IGF-1) on antioxidative enzymes in mouse hepatocytes. Hepatocytes were isolated from wild-type mice following perfusion of livers with a collagenase-based buffer. Dispersed cells were plated on Matrigel and treated with rat GH (0.1, 1.0, or 10 microg/ml) or IGF-1 (0.5, 5.0, or 50 nM) for 24 hr. Hepatocytes were recovered and protein was extracted for immunoblotting and enzyme activity assays of catalase (CAT), glutathione peroxidase (GPX), and manganese superoxide dismutase (MnSOD). A 41% and 27% decrease in catalase activity was detected in cells treated with GH, whereas IGF-1 reduced CAT activity levels to a greater extent than GH (P < 0.0001). The activity and protein levels of GPX were also significantly depressed in cells treated with GH, whereas activity alone was decreased in cells treated with IGF-1 (P < 0.04). GH significantly suppressed MnSOD levels by 40% and 66% in 1.0 and 0.1 microg/ml concentrations, respectively. Similarly, IGF-1 decreased MnSOD protein levels (5 nM; P < 0.05). These results suggest that GH and IGF-1 may decrease the ability of hepatocytes to counter oxidative stress. In addition, these experiments provide an explanation for the differing antioxidative defense capacity of GH-deficient versus GH-overexpressing mice, and they suggest that GH is directly involved in antioxidant regulation and the aging process.