August 2003 � 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.
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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.
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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.
Source: July 2003 edition of the American Journal of Physiology--Endocrinology and Metabolism.
Source: American Physiological Society
