Atherosclerotic vascular diseases
Pathological changes to the arterial wall give rise
to atherosclerotic plaques, complex structures
which result from proliferation of the smooth
muscle cells and collagen, with deposition of
cholesterol-rich lipid. These probably begin as
fatty streaks which develop when lipid-laden
macrophages accumulate after the integrity of
the endothelium is breached and blood compo-
nents are exposed to collagen in the wall of the
artery. The clinical outcome depends on the
site(s) and extent of the lesion: in coronary arter-
ies, myocardial blood flow is reduced, leading
to chest pain on effort (angina) and a risk of
thrombotic occlusion (heart attack) and/or dis-
turbances in the electrical coordination of con-
traction; blood supply to the limbs is impaired
when the arteries supplying the legs are
narrowed, imposing severe limits on walking
capability; and stroke occurs when there is
thrombolytic occlusion of a cerebral artery or a
local haemorrhage from a vessel with atheroscle-
rotic damage. Links with nutrition are clear from,
for example, the association between levels of
saturated fat in the diet and the risk of CHD.
Coronary heart disease
Epidemiological studies have shown significant
associations between indices of both physical
activity (a behaviour) and physical fitness (a
set of characteristics arising from the regular
pursuance of this behaviour) and risk of the com-
monest manifestation of atherosclerosis, CHD—
a disease responsible for one in four male deaths
and one in five female deaths in the UK in 1994.
40 nutrition and exercise
We must be careful in our interpretation of asso-
ciations, however, because exercisers may be
constitutionally different from sedentary people
in ways which decrease the likelihood of their
developing the disease. Complementary scien-
tific evidence of plausible mechanisms has much
to contribute and the role of exercise in this will
be discussed later.
More than 50 population studies have com-
pared the risk of CHD in physically active men
with that of their sedentary counterparts. Careful
scrutiny of their findings shows that sedentary
men experience about twice the risk seen in
active men (see Whaley & Blair 1995). This rela-
tive risk is of the same order of magnitude as that
associated with hypertension (systolic blood
pressure>150 mmHg vs.<120 mmHg), smoking
(≥20 cigarettes · day–1vs. no smoking) and high
serum total cholesterol levels (>6.9 mmol · l–1vs.
£5.6 mmol · l–1). Estimates of the protective effect
of exercise are highest in those studies with the
soundest design and methodology and no study
has found a higherrisk in active men. The effect is
independent of hypertension, smoking and high
total cholesterol levels.
Early studies compared groups of men with
different levels of occupational work. For
example, postal workers who walked and cycled
delivering mail and dock workers with high
levels of habitual on-the-job energy expenditure
experienced less heart disease than colleagues in
less physically demanding jobs. Leisure time
physical activity has also been studied and an
inverse, graded relationship between leisure
time physical activity and CHD was found
among graduates (alumni) of Harvard and
Pennsylvania universities (Paffenbarger et al.Table 3.1Average daily energy intake (MJ) and future risk of coronary heart disease. Adapted from Wood (1987).
Cohort Heart disease victims SurvivorsEnglish banking and 11.11 12.00
London bus workers
Framingham, Massachusetts 9.91 10.97
Puerto Rico 9.30 10.02
Honolulu, Hawaii 8.99 9.70