Bone matrix is a mixture of tough fibres (made
of type I collagen), which resist pulling forces,
and solid particles (calcium phosphate as hy-
droxyapatite crystals), which resist compression.
Bone is by no means a permanent and immutable
tissue. There is a continuous turnover and
remodelling of the matrix with a concomitant
release and uptake of calcium: the cells involved
in bone breakdown are osteoclasts, while the
osteoblasts are involved in bone formation. The
regulators of calcium metabolism in bone tissue
are two hormones, parathyroid hormone (PTH)
and calcitonin. Excess PTH results in a rise in the
blood calcium with a corresponding fall in the
calcium content of the bones, and a loss of
calcium from the body by increased excretion in
the urine. PTH, and exposure to sunlight, also
stimulates the formation of the active form of
vitamin D, which governs the absorption of
calcium from the small intestine. The ability to
regulate the uptake of calcium is important, and
differences in bone mineral density can be
demonstrated in response to exercise, even
between groups with the same dietary calcium
intake. Calcitonin is released when plasma
calcium increases and stimulates bone forma-
tion. Calcium is excreted by the large intestine
and, to a lesser extent, by the kidney and by the
dermis.
In the overall function of skeletal muscle,
calcium plays two essential regulatory roles.
First, calcium is the link between excitation and
contraction. The concentration of free calcium in
the cytosol is low (about 10–8m) in resting muscle
(Martonosi & Beeler 1983), whereas its con-
centration in the extracellular fluid and in the
endoplasmic reticulum (ER) is high. Calcium is
involved in a series of events which converts the
electrical signal of the action potential arriving at
the synaptic terminal into a chemical signal that
travels across the synapse where it is converted
back into an electrical signal in the postsynaptic
cell. Release of calcium from the terminal cister-
nae of the sarcoplasmic reticulum in response to
membrane depolarization upon the arrival of an
action potential allows the actin and myosin fila-
ments to interact. The plasma membrane and the
ER membrane have mechanisms to regulate the
calcium concentration gradient during resting
conditions and to restore it after muscle and
nerve cell stimulation (Alberts et al. 1994). The
activation process involves the binding of
calcium to troponin C, one of the regulatory pro-
teins associated with the actin filaments, and the
change in shape of these proteins allows interac-
tion between actin and myosin to occur. Calcium
is then pumped back into the terminal cisternae
by an energy-dependent transporter in a process
that consumes adenosine triphosphate (ATP),
allowing relaxation of the muscle to occur. There
is good evidence that fatigue during high-
intensity exercise may involve a disruption of
the cell’s calcium-handling capability (Maughan
et al. 1997). A number of substances, including
caffeine, can alter the response of the muscle to a
single action potential, and the effects of some of
these compounds on exercise capacity may be
mediated by effects on calcium transport. These
processes are described in detail by Jones and
Round (1990).
A second key process requiring calcium is
the activation of numerous cellular enzymes
involved in energy production, and calcium is
important to both glycogenolysis and the gly-
colytic pathway in generating ATP (Tate et al.
1991; Clarkson & Haymes 1995). It seems sen-
sible that the same process that allows the muscle
to do work is involved in the regulation of ATP
provision. The activity of phosphorylase, the key
enzyme involved in glycogen breakdown, is
stimulated by increasing cytosolic calcium con-
centration (Maughan et al. 1997) and this is
important for the activation of the glycolytic
pathway at the onset of exercise.Calcium intake
An adequate calcium intake is needed to achieve
optimal peak bone mass in the first two or three
decades of life, to maintain bone mass through-
out the middle years of life, and to minimize
bone loss in the later years (Andersson 1996). A
daily calcium intake that is sufficient to meet the
requirement may be achieved through diet alone,