the secretion of these hormones in fasting. Other inputs at all
intensities of exercise include increased circulating epinephrine
and increased activity of the sympathetic neurons supplying the
pancreatic islets. Thus, the increased sympathetic nervous system
activity characteristic of exercise not only contributes directly
to fuel mobilization by acting on the liver and adipose tissue,
but contributes indirectly by inhibiting the secretion of insulin
and stimulating that of glucagon. This sympathetic output is
not triggered by changes in plasma glucose concentration but
is mediated by the central nervous system as part of the neural
response to exercise.
One component of the response to exercise is quite
different from the response to fasting: In exercise, glucose
uptake and utilization by the muscles are increased, whereas
during fasting they are markedly reduced. How is it that, dur-
ing exercise, the movement of glucose via facilitated diffu-
sion into muscle can remain high in the presence of reduced
plasma insulin and increased plasma concentrations of cortisol
and growth hormone, all of which decrease glucose uptake by
skeletal muscle? By an as-yet-unidentiﬁ ed mechanism, muscle
contraction causes migration of an intracellular store of glu-
cose transporters to the plasma membrane. Thus, exercising
muscles require more glucose than do muscles at rest, but less
insulin to induce glucose transport into muscle cells.
Exercise and the postabsorptive state are not the only situ-
ations characterized by the endocrine proﬁ le of decreased insu-
lin and increased glucagon, sympathetic activity, cortisol, and
growth hormone. This proﬁ le also occurs in response to a vari-
ety of nonspeciﬁ c stresses, both physical and emotional. The
adaptive value of these endocrine responses to stress is that the
resulting metabolic shifts prepare the body for exercise (“ﬁ
ﬂ ight”) in the face of real or threatened injury. In addition, the
amino acids liberated by the catabolism of body protein stores
because of decreased insulin and increased cortisol not only pro-
vide energy via gluconeogenesis but also constitute a potential
source of amino acids for tissue repair should injury occur.
Chronic, intense exercise can also be stressful for the
human body. In such cases, certain nonessential functions shut
down so that nutrients can be directed primarily to muscle.
One of these nonessential functions is reproduction. Thus,
adolescents engaged in rigorous daily training regimens, such
as gymnastics, may show delayed puberty. Similarly, women
who perform chronic, intense exercise may become temporarily
infertile, a condition known as
(the lack of regular menstrual cycles; Chapter 17). This condi-
tion is seen in a variety of occupations that combine weight
loss and strenuous exercise, such as may occur in professional
ballerinas. Whether exercise-induced infertility occurs in men
is uncertain, but most evidence suggests it does not.
It should be clear from this discussion that the maintenance
of plasma glucose and other nutrients within a homeostatic range
is vitally important for proper functioning of the tissues and
organs in the body. When the regulation of these substances is
abnormal, the consequences may be severe, as we see next.
Plasma concentrations of glucose, glucagon, and insulin during
prolonged (240 min) moderate exercise at a ﬁ xed intensity.
Adapted from Felig and Wahren.
meaning “syphon” or “running through,”
denotes the increased urinary volume excreted by people
suffering from this disease.
distinguishes this urine from the large quantities of nonsweet
(“insipid”) urine produced by persons suffering from
vasopressin deﬁ ciency. As described in Chapter 14, the latter
disorder is known as diabetes insipidus, and the unmodiﬁ ed
is often used as a synonym for
a disease that affects over 15 million people in the
United States and that is increasing at an alarming rate.
Diabetes can be due to a deﬁ ciency of insulin or to a
decreased responsiveness to insulin. Thus, diabetes is not
ADDITIONAL CLINICAL EXAMPLES
one but two diseases with different causes. Classiﬁ cation
of these diseases rests on how much insulin a person’s
pancreas is secreting. In
type 1 diabetes mellitus
formerly called insulin-dependent diabetes mellitus), insulin
is completely or almost completely absent from the islets of
Langerhans and the plasma. Therefore, therapy with insulin
is essential. In
type 2 diabetes mellitus
called non-insulin-dependent diabetes mellitus), insulin is
usually present in plasma at nearly normal or even above-
normal levels, but cellular sensitivity to insulin is lower than
). Therefore, therapy may involve
some combination of insulin or drugs that increase cellular
sensitivity to insulin.