12
4.2.4 Novel Risk Factors
Several studies have considered the role of physical activity in altering haemostatic
dysfunction [ 69 ]. There is some evidence that a single bout of vigorous (but not
moderate) intensity exercise induces a prothrombic state characterised by platelet
hyper-aggregability, blood hyper-coagulability and hypo-fibrinolysis [ 70 ]. This
response to strenuous exercise appears to be more pronounced in individuals who
are normally sedentary [ 71 ] and may be one of the causes for the transient increase
in the risk of cardiac arrest during and after strenuous exercise [ 72 ]. These findings
support the notion that low- or moderate-intensity exercise is the most suitable start-
ing point for inactive individuals.
Epidemiological evidence suggests a positive relationship between regular exer-cise and blood haemostasis and inflammatory markers. Fibrinogen, an acute phase
reactant protein that plays an important role in blood clotting, is lower in those
participating in vigorous physical training even when age, smoking, alcohol intake
and body mass are taken into account [ 73 ]. Those who take part in regular low- to
moderate-intensity physical activity may also demonstrate lower platelet aggrega-
tion and adhesion [ 74 ]. In a 20-year follow-up to the British Regional Heart Study,
Wannamathee and colleagues [ 75 ] showed a reduction in coagulation (measured by
plasma fibrinogen, plasma and blood viscosity and coagulation factors VIII and IX),
inflammatory markers (CRP, white cell count), and increased fibrinolysis (measured
by fibrin D-dimer and tissue plasminogen activator antigen) in those who were
physically active. These changes were dependent upon current activity level with
those who took up at least light activity approaching those who were always active
and those who became inactive over the 20 year period demonstrating levels similar
to the inactive [ 75 ].
Such epidemiological observations are less well-substantiated by exercise inter-ventions. Wang and colleagues have shown that an eight-week programme of
moderate- intensity exercise decreases adhesive and aggregative properties of plate-
lets in healthy young men [ 76 ] and women [ 77 ] and have demonstrated that this
beneficial effect is reversed by a similar period of de-conditioning. These authors
have also demonstrated that regular exercise training may desensitise the exagger-
ated platelet reactivity response associated with strenuous exercise in sedentary
individuals [ 78 ]. Exercise interventions comparing blood fibrinolysis before and
after training have yielded equally inconsistent results [ 79 ].
Exercise interventions generally appear to demonstrate reductions in inflamma-tory markers if accompanied by weight loss, especially among women. For example,
in 152 female smokers, there were no changes in CRP or fibrinogen after a 12-week
exercise program that improved physical fitness, but was not accompanied by sig-
nificant weight loss [ 80 ]. In contrast, a two-year program designed to improve diet
and increase physical activity resulted in significant weight loss and reductions in
CRP and IL-6 among 120 obese women [ 81 ]. However, in another large RCT con-
taining 193 sedentary, mildly obese, dyslipidemic men and women, 6 months’ exer-
cise training did not alter levels of CRP despite improvements in fitness, visceral
adiposity and subcutaneous adiposity [ 82 ]. The equivocal nature of these findings
M. Hamer et al.