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Background: Regular exercise has been recommended clinically for all individuals to protect against hypertension but the underlying mechanisms are not fully elucidated. We recently found a significant mitochondrial fragmentation in the vascular endothelium of hypertensive human subjects. In this study, we investigated whether exercise could restore endothelial mitochondrial dynamics and thus improve vascular function in hypertension.Methods: Vascular endothelial mitochondrial morphological alterations were examined in patients with hypertension and hypertensive animal models. Furthermore, swimming exercise-induced endothelial mitochondrial dynamics and vascular function changes were investigated in spontaneously hypertensive rats (SHRs).Results: Mitochondrial fragmentation with an elevated mitochondrial fission mediator Drp1 (dynamin-related protein-1) was observed in the mesenteric artery endothelium from hypertensive patients. A similar mitochondrial fragmentation with increased Drp1 expression were exhibited in the aortic endothelium of angiotensin II-induced hypertensive mice and SHRs. Interestingly, swimming exercise significantly reduced vascular Drp1 expression and alleviated endothelial mitochondrial fragmentation, thus improving blood pressure in SHRs. In cultured endothelial cells, angiotensin II exposure induced Drp1 upregulation, mitochondrial fragmentation and dysfunction, and reduced nitric oxide production, which was blunted by Drp1 genetic reduction or its inhibitor Mdivi-1. Mdivi-1 administration also ameliorated endothelial mitochondrial fragmentation, vascular dysfunction and blood pressure elevation in SHRs while swimming exercise plus Mdivi-1 treatment provided no additional benefits, suggesting that Drp1 inhibition may partially contribute to swimming exercise-conferred anti-hypertensive effects.Conclusions: These findings suggest that swimming exercise alleviates endothelial mitochondrial fragmentation via inhibiting Drp1, which may contribute to exercise-induced improvement of vascular function and blood pressure in hypertension. [ABSTRACT FROM AUTHOR]

Objective: Although a popular endeavor, boxing has fallen under increased scrutiny because of its association with traumatic brain injury. However, few studies have investigated the overall epidemiology of boxing injuries from representative samples, and no study has ever documented the incidence of injuries in female boxers. This study is a review of professional boxing data from the state of Nevada from September 2001 through March 2003. Materials and Methods: Medical and outcome data for all professional boxing matches occurring in Nevada between September 2001 and March 2003 (n = 524 matches) were analyzed on the basis of a pair-matched, case-control design. Cases were boxers who received an injury during the boxing matches. Boxers who were not injured served as control subjects. Both conditional and unconditional logistic regression models were used to assess risk factors for injury. Results; The overall incidence rate of injury was 17.1 per 100 boxer-matches, or 3.4 per 100 boxer-rounds. Facial laceration accounted for 51% of all injuries, followed by hand injury (17%), eye injury (14%). and nose injury (5%). Male boxers were significantly more likely than female boxers to receive injuries (3.6 versus 1.2 per 100 boxer-rounds. P = 0.01). Male boxing matches also ended in knockouts and technical knockouts more often than did female matches (P < 0.001). The risk of injury for those who lost the matches was nearly twice the risk for the winners. Those who lost by knockout had double the risk of injury compared with those who lost by other means. Neither age nor weight was significantly associated with the risk of injury. Conclusions: The injury rate in professional boxing matches is high, particularly among male boxers. Superficial facial lacerations are the most common injury reported. Male boxers have a higher rate of knockout and technical knockouts than female boxers. Further research is necessary to determine the outcomes of injury, particularly the long-term neurologic outcome differences between sexes. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to assess the impact of the 1997 Arkansas helmet law repeal on motorcycle registrations, crash and fatality risks, and alcohol involvement in motorcycle crashes. Methods: Annual motorcycle registration data for the years 1990 through 2001 were obtained from the Arkansas Department of Finance and Administration. These motorcycle registration data were complemented by the motorcycle crash data from the Arkansas State Police Highway Safety Office and motorcycle fatality data for the state of Arkansas from the Fatality Analysis Reporting System. The impact of the repeal on crash rates, helmet usage, and alcohol involvement was assessed through comparisons of data from before (1993 to 1996) and after (1998 to 2001) the repeal. Results: After the repeal, an increase in motorcycle registrations correlated with a marked rise in the total number of crashes and fatalities; however, fatalities per crash remained virtually the same. The proportion of motorcycle fatalities that were not wearing a helmet increased from 47.0% (47/100) before the repeal to 78.2% (104/133) after the repeal (P = 0.001). The overall percentage of fatal motorcycle crashes involving alcohol use remained unchanged after the repeal (37.6% [29/77] to 38.5% [40/104], P = 0.91), but the percentage of fatal crashes involving drinking nonhelmeted drivers increased from 14.2% (11/77) to 33.6% (35/104) (P = 0.003). Inebriated motorcyclists killed in crashes were overwhelmingly nonhelmeted (87.5%, 35/40) after the repeal, up from 37.9% (11/29) before the repeal (P < 0.001). Conclusions: These findings suggest that the repeal of the mandatory helmet law in Arkansas has had a significant adverse effect on road safety. [ABSTRACT FROM AUTHOR]