Cigarette smoking and exercise-related injuries among young men and women.

BACKGROUND: We evaluate whether a recent history of cigarette smoking is a risk factor for exercise-related injuries sustained during Army basic training, controlling for factors such as demographic, physical fitness, and health variables. METHODS: We conducted an observational cohort study in 1087 male and 915 female Army recruits undergoing 8-week basic military training. Data were collected from questionnaires, anthropometric measurements, physical fitness tests, company training logs, and medical records of all clinic visits. RESULTS: During the 8-week training period, 33% of men and 50% of women had at least one clinic visit for injury, including 14% of men and 25% of women who lost more than 5 days of training due to injury. Recruits who reported smoking at least one cigarette in the month prior to beginning basic training (which was conducted in a smoke-free environment) had significantly higher injury rates during training than those who did not report smoking (40% versus 29% for men, and 56% versus 46% for women). The relationship with smoking history was present most strongly for overuse injuries (32% versus 24% in men and 51% versus 40% in women). Multiple logistic regression analyses controlling for all other factors consistently showed adjusted odds ratios of about 1.5 for injury rate in those with a history of smoking compared to those without. CONCLUSIONS: The association of history of cigarette smoking with injury occurrence was consistent throughout the analyses, with very little confounding by other factors. The detrimental effects of smoking on injuries appears to persist at least several weeks after cessation of smoking.

Peptide alpha-amidation: differential regulation by disulfiram and its metabolite, diethyldithiocarbamate.

The rate limiting step in the alpha-amidation of bioactive peptides is catalyzed by peptidylglycine-alpha-hydroxylating mono-oxygenase (PHM; EC 1.14.17.3). Sustained treatment with disulfiram (Antabuse), the disulfide dimer of diethyldithiocarbamate (DDC), inhibits PHM in vivo, causing tissue levels of alpha-amidated peptides to decrease. As a compensatory response, PHM protein is modified in such a way that its activity is increased when assayed under optimal conditions in a test tube. Because disulfiram is rapidly reduced to DDC in vivo, this investigation sought to determine if metabolic transformation plays a role in the effects of disulfiram treatment on alpha-amidation. While disulfiram treatment reduced concentrations of alpha-amidated peptides in the pituitary neurointermediate lobe and brain, DDC treatment did not, even at comparatively high doses. Both treatments increased the activity of PHM extracted from the neurointermediate pituitary and assayed under optimal copper conditions in vitro. Only disulfiram treatment elicited an increase in PHM activity extracted from cardiac atrium. It is concluded that the activity of PHM is regulated in a tissue specific fashion and that not all of the actions of disulfiram require its metabolism to DDC.