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October 2002, Volume 26, Number 10, Pages 1310-1316
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Association of physical activity with insulin sensitivity in children
K H Schmitz1, D R Jacobs Jr1, C-P Hong1, J Steinberger2, A Moran2 and A R Sinaiko2

1Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA

2Department of Pediatrics, School of Medicine, University of Minnesota, Minneapolis, Minnesota, USA

Correspondence to: K H Schmitz, 1300 S 2nd St, Suite 300, Division of Epidemiology, University of Minnesota, Minneapolis, MN 55454, USA. E-mail:


BACKGROUND: Physical activity (PA) has been shown to improve insulin resistance and other cardiovascular disease risk factors in normal and diabetic adults and in obese youth, but not in non-diabetic, normal-weight children.

METHODS: Data from 357 non-diabetic children (10-16 y) were used to examine cross-sectional associations with PA. Insulin sensitivity was assessed with a euglycemic hyperinsulinemic clamp and expressed as Mffm (glucose utilization/kg of fat-free mass/min).

RESULTS: Correlations were adjusted for age, sex, race and Tanner stage. PA was significantly correlated with fasting insulin and insulin sensitivity (r=-0.12, P=0.03 and r=0.13, P=0.001, respectively), more strongly in children with above-median systolic blood pressure (r=-0.17, P=0.03 and r=0.35, P=0.0001, respectively). Further adjustment for body mass index, body fat percentage, waist circumference or lipids did not alter these observations.

CONCLUSIONS: Physical activity is correlated with lower fasting insulin and greater insulin sensitivity in childhood. These results are consistent with the hypothesis that increasing physical activity among youth may reduce the incidence of type 2 diabetes in children and adolescents.

International Journal of Obesity (2002) 26, 1310-1316. doi:10.1038/sj.ijo.0802137


exercise; insulin resistance; child


Insulin resistance is strongly associated with the cardiovascular risk factors of obesity, hypertension, elevated triglycerides and low levels of high-density lipoprotein cholesterol in adults.1 In epidemiologic studies in adults, physical activity level is predictive of future risk for type 2 diabetes,2,3 and controlled trials show that exercise improves insulin sensitivity (the inverse of insulin resistance) in adults with impaired glucose tolerance.4,5 A recent observational study reported that physical activity is directly associated with insulin sensitivity in adults without impaired glucose tolerance.6 Physical activity has also been shown to be associated with the constellation of risk factors comprising the insulin resistance syndrome in children and adults1,7,8,9 and to improve cardiovascular disease risk factors related to insulin sensitivity in adults.10,11,12

Prior studies in children have used fasting insulin and glucose as surrogates for insulin sensitivity to measure the effect of physical activity on insulin resistance.9,13,14,15,16,17 The results of these studies are consistent with the hypothesis that the association of physical activity with insulin sensitivity in children is similar to what has been observed in adults. However, these associations have often focused on obese children and there have been no prior insulin clamp studies in normal-weight, non-diabetic children. Defining the relation of physical activity to insulin sensitivity in non-diabetic children may determine whether programs to increase physical activity in youth could prevent early appearance of insulin resistance. These associations have become increasingly relevant, given recent reports of increases in the prevalence of type 2 diabetes in children and adolescents.18

In the present report, cross-sectional data from 357 insulin clamp studies of non-diabetic children age 10-16 y were used to examine correlations of physical activity with insulin sensitivity and anthropometric and laboratory measurements associated with cardiovascular risk.



Blood pressure screening was conducted in 12 043 (93% of all eligible) 5th-8th grade students in the Minneapolis Public Schools (3819 black, 4216 white; 6035 male, 6008 female). Following this screening, a random selection of 2915 black and non-Hispanic white children, stratified as to race, sex and blood pressure (upper 25 percentiles and lower 75 percentiles of the systolic blood pressure distribution to enrich the potential number of at risk individuals in the study sample), were invited to participate in a euglycemic insulin clamp study. Of the children invited to participate, 537 attended information sessions and 401 children and their parents signed the consent form. The euglycemic insulin clamp study was successfully completed in 357 black and white children (25 refused the clinic visit, two were ineligible due to chronic illness, and 17 were unable to complete the clamp study). The present analyses also excluded one participant with an exaggerated prediction of body fat (88%) and one participant with missing Tanner stage data, for a final sample size of 355 children. Comparison of the ages, blood pressures, heights and weights of these 355 participants with the rest of the 2915 randomly chosen for invitation into the study revealed no differences. This study was approved by and adhered to all guidelines and regulations of the University of Minnesota Institutional Review Board for the protection of human subjects in research.


An initial clinic visit included anthropometric and blood pressure measurements and a physical examination by a pediatrician. The stage of sexual maturation, ie Tanner stage, was determined according to pubic hair development.19 Weight was measured using a balance beam scale and height was measured using a wall-mounted stadiometer. Triceps and subscapular skinfolds were measured in duplicate with Lange calipers (Cambridge Scientific Instruments, Salisbury, MD, USA), and the sum of the mean triceps and subscapular skinfolds was used to predict body fat percentage using a regression equation developed specifically for this age group by Slaughter et al.20,21 Waist circumference was measured to the nearest 0.5 cm. Seated blood pressure was measured twice after a 5 min rest using a random-zero sphygmomanometer, with 1 min between measurements. The average of the two measures was used for analyses of systolic and fifth-phase Korotkoff diastolic blood pressures.

Physical activity (leisure time, stair climbing and walking) was measured using the Paffenbarger physical activity survey22 and expressed in kilocalories expended per day. In adults, test-retest correlations have ranged from 0.34 to 0.73, similar to other physical activity surveys.23 Estimated kilocalorie expenditure from the Paffenbarger survey was found to be strongly correlated with several physiological variables associated with physical activity and fitness in adults, including maximal aerobic capacity (r=0.52) and body fat percentage (r=-0.32).23 Although the reliability and validity of the Paffenbarger survey has not been evaluated in 10-16-y-olds, several other commonly used physical activity surveys developed for adults have been administered to 5th-11th grade children24 and found to show reliability (test-retest r=0.77-0.89) and validity (r=0.44-0.53 compared with heart rate monitoring data). These reliability and validity coefficients are quite similar to values for adults for the same surveys.23 For some analyses, physical activity score was categorized into quartiles for the total sample.

The euglycemic insulin clamp studies were conducted in the University of Minnesota Clinical Research Center. Participants were admitted after a 10 h overnight fast. An intravenous catheter was inserted into an arm vein 1 h prior to the clamp studies, and a blood sample was obtained immediately for measurement of serum lipids. This catheter was used for infusion of potassium phosphate, insulin and glucose. A contralateral vein was cannulated for blood sampling, and the hand was placed in a heated box (65°C) to arterialize venous blood for measurement of glucose levels. Insulin was infused at a rate of 1 mU/kg/min for 3 h. A variable infusion of 20% glucose was adjusted, based on blood glucose levels measured every 5 min, to maintain euglycemia, ie blood glucose at 5.6 mmol/l. Insulin sensitivity was determined from the amount of glucose required to maintain euglycemia over the final 40 min of the euglycemic clamp study and was expressed as Mffm (ie glucose utilization/kg fat-free mass/min).

Blood samples for serum insulin levels were obtained at baseline (-10, -5, and 0 min before starting the insulin infusion). The insulin samples were collected on ice and centrifuged within 20 min. Insulin levels were determined using a radioimmunoassay kit (Equate RIA, Binax Corp., Portland, Maine, USA). The average of the three baseline measurements was used in the analyses. Blood samples for serum lipids were analyzed in the University of Minnesota laboratory using a Cobas FARA. Cholesterol concentrations were determined by a standard enzymatic-cholesterol oxidase-based method; HDL-C was determined after precipitation of non-HDL lipoproteins with magnesium/dextran precipitating reagent; triglycerides were determined using a standard glycerol blanked, enzymatic triglyceride method. LDL-C was calculated by the Friedewald equation.25

Statistical analysis

SAS (SAS Institute, Cary, NC, USA) was used to determine differences in characteristics across quartiles of physical activity using bivariate linear regression and chi-square tests. Correlations for physical activity with insulin sensitivity and other variables were computed, adjusting for one or more of age, ethnicity, sex and Tanner stage. No modification of results was noted by gender, so all findings are reported for boys and girls combined, adjusting for gender to account for differing levels (but not slopes) of physical activity and insulin sensitivity in boys vs girls. Because changes in insulin may underlie the effect of physical activity (PA) on blood pressure,26 we hypothesized that the associations of PA and insulin sensitivity might differ by blood pressure level. We therefore studied whether blood pressure modified the association of PA and insulin variables. Given the outcome of this interaction analysis, we carried out further descriptive analyses of other possible modifiers of the association of PA with the insulin variables. Each test for modification of the association of physical activity and insulin sensitivity by another variable was performed by including a main effect term and the product of PA and the potential modifier in a regression model predicting insulin sensitivity. Mean levels of insulin sensitivity within each quartile of physical activity were determined using multiple linear regression, stratified by systolic blood pressure groups and again by percentage body fat groups, and adjusted for age, ethnicity, sex and Tanner stage. Results of analyses with log-transformed physical activity scores were not substantively different from those presented.


A wide spectrum of energy expenditure from physical activity was reported by the children (Table 1). Participants in the higher physical activity quartiles were older than participants in the lower physical activity quartiles (test for linear trend, P=0.0001). Girls and Caucasian participants were disproportionately represented in the lower physical activity quartiles (chi2, P=0.001 and P=0.003, respectively). There were no notable differences in the distribution of physical activity between Tanner stages (chi2, P=0.59). Body weight and body mass index (BMI) did not differ significantly across physical activity quartiles. However, body fat percentage decreased and fat-free mass increased linearly across physical activity quartiles (test for trend, P=0.03 and P=0.002, respectively). Mffm increased and fasting insulin decreased between the second and highest physical activity quartile (test for linear trend, P=0.0001 and P=0.003, respectively). There were no differences according to physical activity quartile in the mean level of blood pressure or serum lipids.

Correlation analyses were conducted using the entire cohort, after adjustment for age, ethnicity, gender and Tanner stage. Physical activity was significantly inversely correlated with fasting insulin, and positively correlated with Mffm and fat-free mass, but was not significantly correlated with body fat percentage, BMI, waist circumference, blood pressure and serum lipids. The association of physical activity and Mffm differed according to systolic blood pressure (F=9.91, P=0.002). There was no modification of the association of physical activity and Mffm according to gender, Tanner stage, BMI, HDL-C, triglycerides or diastolic blood pressure (F-tests P-values 0.67, 0.14, 0.79, 0.12, 0.78 and 0.44, respectively). Although effect modification was suggested for percentage body fat (F=4.84, P=0.03), this finding was viewed as not statistically significant, because of the number of a posteriori tests. Figure 1 shows level of insulin sensitivity (Mffm) in children in each physical activity quartile for children above and below median systolic blood pressure.

Table 2 shows the correlations between physical activity and the risk factors for the entire cohort and for children in groups above and below median systolic blood pressure and percentage body fat. The correlations of physical activity with fasting insulin and Mffm were not significant in children with below median systolic blood pressure or below median percentage body fat. The correlations of physical activity with fasting insulin and Mffm were significant in children with above median systolic blood pressure or above median percentage body fat. In contrast, physical activity was correlated with fat-free mass only in children with below median systolic blood pressure and percentage body fat (F for interaction of PA and percentage body fat, predicting fat-free mass, 6.82, P=0.009; F for interaction of PA and systolic blood pressure, predicting fat-free mass, 0.2, P=0.7). There were no significant correlations between physical activity and any other cardiovascular disease risk factors observed. Additional adjustment for BMI, body fat percentage, HDL-C or triglycerides did not change the significant correlations of physical activity with Mffm or fasting insulin reported in Table 2.


In the present study significant correlations were observed between physical activity and both fasting insulin and insulin sensitivity (Mffm) in 10-16-y-old children. Moreover, these correlations were significantly stronger in the subset of children with higher systolic blood pressure.

The mechanisms by which exercise training effects insulin sensitivity are still under investigation.27 Exercise may reduce fasting insulin and improve insulin sensitivity through enhanced glucose transport into muscle cells and increased production of muscle glycogen to replace the glycogen used during exercise.28 Exercise may also exert a long-term effect on reduction of fasting insulin and improvement in insulin sensitivity through increased fat-free mass, which increases the volume of muscle tissue into which glucose can be transported.29

Previous intervention trials relating physical activity to insulin sensitivity in children have tended to focus on obese and/or diabetic youth and have used fasting insulin to estimate insulin activity. An improvement in the glucose and insulin response to a mixed meal was noted in seven obese 15-y-old boys after a 15 week endurance training program.14 A decrease in fasting insulin with no change in fasting glucose, suggesting an increase in insulin sensitivity, occurred after 4 months of endurance training in 79 obese 7-11-y-old children in a randomized controlled trial.9 An uncontrolled weight loss trial that included exercise training as part of the intervention in 50 obese adolescent children also reported improvements in fasting insulin and glucose tolerance.17

Larger observational studies in children and adolescents have used self-reported physical activity to assess the relationship between exercise and fasting insulin. Low physical activity scores were associated with elevated fasting insulin in a study of 1300 Japanese children aged 6-1313 and insulin sensitivity, as measured by the homeostasis model (an index of insulin resistance based on fasting levels of insulin and glucose), was significantly greater in 62 male high school students who performed highly aerobic exercise compared to 114 less active boys.15 The Cardiovascular Risk in Young Finns Study reported that 12, 15 and 18-y-olds with a consistently sedentary lifestyle over 6 y of follow-up had higher fasting serum insulin than those who remained physically active over the same period.16 Moreover, changes in physical activity were inversely associated with changes in serum insulin.16

Physical activity was positively associated with insulin sensitivity, as determined by insulin clamp studies, in non-diabetic adults.6 The present study represents the first to show the same association using insulin clamps in non-diabetic children. Although the pattern of the correlations for physical activity with fasting insulin and insulin sensitivity were similar, the correlation of physical activity with insulin sensitivity (Mffm) was stronger than for fasting insulin. This suggests that using fasting insulin as a measure of insulin sensitivity underestimates the magnitude of the potential for physical activity to improve insulin sensitivity.

A linear association between physical activity level and resting systolic or diastolic blood pressure was not observed in this cohort. This is consistent with previous studies that have shown a minimal effect of physical activity on blood pressure levels in normotensive adults10 and only a small effect (1-6 mmHg) of physical activity on resting blood pressure levels in children and adolescents with high normal blood pressure.7 However, we found that the positive association of physical activity with insulin sensitivity was stronger in children with above median systolic blood pressure and possibly above median percentage body fat. We considered it likely that the interaction with percentage body fat was an artifact of multiple comparisons. In contrast, the changes in insulin may underlie the effect of PA on blood pressure26 and the strongly significant interaction with blood pressure was hypothesized a priori. It has previously been demonstrated that both blood pressure and insulin resistance decrease in response to physical activity-induced weight loss in obese adolescents.17 Higher systolic blood pressure was closely associated with greater weight, percentage body fat and BMI in this study.30 This may suggest a threshold effect for the physical activity-insulin resistance relation that is based on blood pressure or body size or that the relation is more subtle and not recognized in smaller, thinner children. Despite the lack of correlation in the thinner children, there was a positive correlation of physical activity with fat-free mass in the group of children with below median systolic blood pressure or percentage body fat.

Physical activity was associated with fat-free mass, but not with percentage body fat, BMI, body mass or waist circumference. Results from previous studies have not been uniform regarding the association of physical activity and body size variables. NHANES III found that BMI and sum of trunk skinfolds were independent of physical activity.31 A more recent longitudinal observational study reported larger 1 y increases in BMI in association with lower self-reported physical activity levels in 9-14-y-old children,32 and other observational studies have reported an inverse association of body weight, percentage body fat or fat mass with physical activity in children.33,34 A new finding in the present study was the association of fat-free mass with physical activity only in children with below median systolic blood pressure or percentage body fat. Interpretation of this finding is challenging, because, in addition to higher relative and absolute fat mass, obese children also have higher fat-free mass than lean children.33,34 We speculate that in relatively lean children the effect of physical activity is concentrated on increasing fat-free mass development, rather than further reducing an already appropriate relative amount of body fat.

There was no association of physical activity with serum lipids in this cohort. Previous reports of associations between physical activity and blood lipids in children and adolescents have been inconsistent,8 paralleling the variable associations of physical activity and blood lipids reported in adults.12 It has been suggested that changes associated with aging and maturation during pubertal development could have an impact on these associations.35

In conclusion, this study has shown that physical activity is associated with lower fasting insulin and higher insulin sensitivity (Mffm) in normal healthy children. This finding, combined with the current national trend toward less time spent in physical activity among youth36 and increasing prevalence of type 2 diabetes in children and adolescents18 strongly suggests that educators, researchers and parents need to place a higher priority on increasing physical activity in children. In addition to the immediate health benefits during childhood, increased physical activity in youth is likely to contribute to establishment of healthy leisure habits over a lifetime37 and improved adult cardiovascular health.


This work was supported by NHLBI grant no. HL 52851 and NIH grant M01-RR-00400 (GCRC). Dr Schmitz was awarded the Jeremiah Stamler Research Award for New Investigators for this research at the American Heart Association Council on Epidemiology and Prevention annual meeting in March 2000.


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Figure 1 Relation of insulin sensitivity (Mffm) to quartiles of physical activity (PA) for children above and below the median systolic blood pressure (SBP). Test for linear trend: P=0.20 in low median SBP, P=0.0001 in high median SBP. (Dashed line) Low median SBP; (Solid line) high median SBP.


Table 1 Participant characteristics by physical activity quartiles (mean (s.d.) or percentage)

Table 2 Correlationsa between physical activity score and insulin sensitivity (Mffm) and other cardiovascular disease risk factors

Received 13 February 2002; revised 22 May 2002; accepted 27 May 2002
October 2002, Volume 26, Number 10, Pages 1310-1316
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