title: The acute rise in plasma fibrinogen concentration with exercise is influenced by the G-453-A polymorphism of the beta-fibrinogen gene.
abstract: We have investigated the effects of chronic physical training and acute intensive exercise on plasma fibrinogen levels and the relationship of these responses to beta-fibrinogen G-453-A polymorphism genotype. One hundred fifty-six male British Army recruits were studied at the start of their 10-week basic training, which emphasizes physical fitness. Cohorts were restudied between 0.5 and 5 days after a major 2-day strenuous military exercise (ME) undertaken in their final week of training. Changes in fibrinogen concentration were adjusted for the effects of age, body mass index, and smoking history. Compared with baseline values, fibrinogen concentrations were significantly lower (11.9%, P=.04) at day 5 after ME, consistent with the beneficial effect of training. However, they were higher on days 1 through 3 after ME (suggesting an "acute-phase" response to strenuous exercise) and were maximal on days 1 and 2 (27.2%, P<.001 and 37.1%, P<.001 respectively). Fibrinogen genotype was available in 149 individuals. As expected from previous studies, men with one or more fibrinogen gene A-453 alleles had plasma fibrinogen concentration slightly but significantly higher at baseline (4.5%, P=.11). During the acute-phase response (days 2 and 3), however, the degree of rise was strongly related to the presence of the A allele, being 26.7+/-5.4% (mean+/-SE), 36.5+/-11.0%, and 89.2+/-30.7 for the GG, GA, and AA genotypes, respectively (P=.01). These results confirm that chronic exercise training lowers plasma fibrinogen levels, that intensive exercise generates an acute-phase rise in levels, and that this acute response is strongly influenced by the G/A polymorphism of the beta-fibrinogen gene.
authors.affiliation: Hatter Institute for Cardiovascular Studies, Department of Cardiology, University College London Medical School, UK.
authors.forename: H E
authors.initials: HE
authors.lastname: Montgomery
authors.forename: P
authors.initials: P
authors.lastname: Clarkson
authors.forename: O M
authors.initials: OM
authors.lastname: Nwose
authors.forename: D P
authors.initials: DP
authors.lastname: Mikailidis
authors.forename: I A
authors.initials: IA
authors.lastname: Jagroop
authors.forename: C
authors.initials: C
authors.lastname: Dollery
authors.forename: J
authors.initials: J
authors.lastname: Moult
authors.forename: F
authors.initials: F
authors.lastname: Benhizia
authors.forename: J
authors.initials: J
authors.lastname: Deanfield
authors.forename: M
authors.initials: M
authors.lastname: Jubb
authors.forename: M
authors.initials: M
authors.lastname: World
authors.forename: J R
authors.initials: JR
authors.lastname: McEwan
authors.forename: A
authors.initials: A
authors.lastname: Winder
authors.forename: S
authors.initials: S
authors.lastname: Humphries
mesh_terms: D000293:Adolescent; D000328:Adult; D015444:Exercise; D005340:Fibrinogen / Q000032:analysis / Q000235:genetics*; D005838:Genotype; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic
chemical_list: D005340:Fibrinogen