For Those Who Smoke Young
New research is first report of
smoking-induced alteration of skeletal muscle glycogen synthesis
August 1, 2003 – (Bethesda, MD) – The dangers of cigarette
smoking are well known, and each day America’s young people are exposed to a
number of public and privately sponsored anti-tobacco campaigns. Despite
the best efforts of health educators, children and adolescents become
regular tobacco users each day.
Many take up the habit believing that if they stop at a relatively young
age there will be no long-term adverse consequence to their health.
Unfortunately, these same young people are unaware that cigarette use has
been linked to insulin resistance and insulin-dependent glucose
metabolism. Insulin resistance is known to be a major risk factor
in the development of adult-onset diabetes, a disease reaching
epidemic proportions. Scientists also suggest there may be a dose-response
relationship between smoking and the risk of diabetes.
Impaired insulin-stimulated muscle glycogen synthesis is an
early defect in the cause of diabetes and is present in
individuals at high risk of diabetes before the development of
impaired glucose tolerance
Why? Significant differences in glycogen
replenishment can be attributed to hormone insulin. Insulin is released by
the pancreas in response to carbohydrate consumption. The hormone’s many
functions include the transportation of glucose into liver and muscle
tissues and to stimulate the synthesis of carbohydrate into muscle glycogen,
which is how the muscle stores energy. Because insulin is essential in
replenishing muscle glycogen after exercise, researchers have focused on
enhancing insulin release during recovery. It is well known that increasing
the amount of carbohydrate consumed will increase insulin levels and result
in more muscle glycogen storage.
Postexercise muscle metabolism plays a major role in systemic
carbohydrate balance and may be influenced by smoking. Although
the association of cigarette smoking with insulin resistance and
impaired glucose tolerance has been established through previous
research, the question of whether this smoking affects the final
step in the physiological process -- impaired muscle glycogen
storage – has yet to be addressed.
A New Study
Accordingly, a new study was undertaken to determine whether the
insulin-dependent phase of postexercise muscle glycogen synthesis
is impaired in a fasting population of young healthy cigarette
smokers. The authors of “Smoking Impairs Muscle Recovery from
Exercise” are Thomas B. Price,
Suchitra Krishnan-Sarin, and Douglas L. Rothman, all from the
Yale University School of Medicine, New Haven, CT. Their research
appears in the July 2003 edition of the of the American Journal of
Physiology—Endocrinology and Metabolism. The journal is one of 14
published each month by the American Physiological Society (APS).
Methodology
To evaluate smoking-induced effects on carbohydrate
metabolism, the researchers studied muscle glycogen recovery from
exercise in a young healthy population of eight smokers and ten
non-control subjects. The study used spectroscopy to compare
muscle glycogen and glucose 6-phosphate (G-6-P) levels during
recovery in exercised gastrocnemius muscles of randomized cohorts
of healthy male smokers and a control group. The smokers consumed
at least 20 cigarettes/day; their age was 24 ± 2 years, and they
weighed 70 ± 4 kg. The control group of ten non-smokers was of similar age
and weight. Subjects performed single-leg toe raises to deplete
glycogen to approximately 20 mmol/l, and glycogen resynthesis was
measured during the first four hours of recovery. Plasma samples
were assayed for glucose and insulin at rest and during recovery.
Results
The findings revealed that gastrocnemius glycogen concentrations were
similar in smokers and controls. Exercise-induced glycogen
depletion data indicate that both groups depleted similar
amounts of glycogen over a similar period of time while
performing a similar amount of work. After exercise, there was steady
glycogen resynthesis for approximately one hour that was similar in both
groups. During the four hours of recovery, steady
glycogen synthesis continued at a reduced rate in the control
group; however, glycogen synthesis ceased in the smokers. During
this recovery period, the glycogen synthesis rate in the smoking
group was 74 percent lower than in the control group. Total
glycogen recovery over the four-hour measurement period was
significantly greater (1.9-fold) in controls than in smokers.
Baseline concentrations of G-6-P, Pi, PCr,
and the intracellular pH were similar in the two groups. Throughout
the four-hour postexercise measurement period, Pi and PCr
concentrations and intracellular pH were similar between the two
groups. During the first hour of recovery, G-6-P levels
were not significantly different between the two groups. However,
over the subsequent three hours of recovery, mean G-6-P
concentrations were significantly lower in the smoking group (52
percent lower) compared with the control group.
The plasma glucose concentrations were not significantly
different between groups and controls, nor were they different after
exercise. Baseline insulin levels were also similar between the
smokers and controls. Plasma insulin levels were not
significantly different between smokers and controls during the
first hour of recovery or during the insulin-dependent period
(four hours of recovery).
Conclusions
This study reports that insulin-dependent muscle glycogen synthesis is
impaired in a healthy population of young smokers, much
like that observed in prediabetic subjects. This is, to their
knowledge, the first report of smoking-induced alteration of
skeletal muscle glycogen synthesis.
An important systemic factor in postexercise muscle glycogen
recovery is the efficiency with which plasma glucose is delivered
to the exercised muscle. Although cigarette smoking has been
shown to inhibit nitric oxide (NO) bioactivity, thereby enhancing
vasoconstriction, insulin induces NO-mediated widening of the blood vessels.
The findings point to an association between insulin and NO in
the vasodilatory response and the impact of cigarette smoking on
vasodilation could have exerted an effect on the level of
postexercise perfusion of the observed gastrocnemius muscle.
An initial insulin-independent glycogen synthesis rate between the
subject and control groups was not significant. However, it is possible that
a reduction in flow could have contributed to the slower rate seen in the
smokers. It is also possible that early insulin-independent postexercise
muscle glycogen synthesis has both an insulin-independent component and an
insulin-dependent component. Data from this study can neither confirm nor
refute the contribution of impaired blood flow to the observed impairment of
postexercise insulin-dependent glycogen synthesis. However, it is clear that
the end result is reduced muscle glycogen in smokers after four hours of
fasting recovery from glycogen-depleting exercise.
- end -
Source: July 2003 edition of the American Journal of
Physiology—Endocrinology and Metabolism.
The American Physiological Society (APS) was founded in 1887 to foster
basic and applied science, much of it relating to human health. The
Bethesda, MD-based Society has more than 10,000 members and publishes 3,800
articles in its 14 peer-reviewed journals every year.
***
Editor’s Note: A copy of the research article is
available in pdf format to the press. Members of the press are invited to
obtain a pdf copy of the study and to interview members of the research
team. To do so, please contact Donna Krupa at 703.527.7357 (direct dial),
703.967.2751 (cell) or djkrupa1@aol.com.
