To investigate the effect of 2-month detraining on body composition and glucose tolerance for female collegiate dancers.
Longitudinal study of dancers who stopped their regular training for 2 months.
16 female collegiate dancers (age: 19.7±0.11 year, body mass index (BMI): 20.7±0.56 kg/m2).
BMI, waist-to-hip ratio (WHR), oral glucose tolerance test (OGTT), insulin response during OGTT, and blood lipids at baseline and after a 2-month detraining.
Glucose tolerance was not significantly affected by the detraining, but the fasted insulin and insulin levels during OGTT were significantly elevated. Fasted free fatty acid (FFA) and triglyceride levels were significantly elevated without change in cholesterol level. BMI was not significantly altered during this detraining period, but the waist circumference and WHR ratio were significantly elevated.
Only a 2-month cessation of regular training in female dancers significantly elevated basal and postprandial insulin levels and triglycerides, and were associated with increased basal FFA. This result appears to be partly related to the increased central fatness but not body mass, indicating that the early development of obesity due to reduced physical activity may not necessarily reflect on weight status. A warning is thus warranted for those young women who depend on weight measurement for body fat status monitoring.
The prevalence of obesity is being reflected in worldwide epidemics of metabolic syndrome and type 2 diabetes.1 Environmental changes that require less physical activities to maintain daily living have been considered as a major cause in the development of obesity, type 2 diabetes, and metabolic syndromes.1, 2, 3 It was suggested that increased adiposity would elicit a negative-feedback mechanism for preventing fuel overloading by reducing the whole-body insulin sensitivity.4, 5 This insulin-resistant state has been proposed as a common ground for development of type 2 diabetes, dyslipidemia, hypertension, coronary heart disease, stroke, and certain types of cancer.6, 7 The deteriorated metabolic condition is known to begin in early adulthood in a gender-specific manner, where women with similarly high body mass index (BMI) level are particularly in greater risk of developing diabetes compared with men.8 A few studies have been performed to document the impact of short-term detraining on body composition in highly trained female athletes.9 To investigate the lifestyle transition from physical activeness to inactiveness, collegiate female dancers are an excellent model since they are physically active but not as heavily trained as athletes. The present study was undertaken to determine the effects of a 2-month detraining period on the body composition of female collegiate dancers. The measures of development of metabolic syndromes, including blood glucose, insulin, and lipid levels, were determined as well. This information would improve the understanding on the interrelationships between body composition, carbohydrate metabolism, and blood lipid changes during the early stages of lifestyle transition of young active female subjects.
A total of 16 modern dancers (age 19.7±1.1 year) participating regular dancing classes in college voluntarily undertook a 2-month detraining study during summer. None of the subjects had a history of diabetes, hypertension, and other diagnosed metabolic disorders. Subjects' physical characteristics are listed in Table 1. Aims and methods were explained to all subjects, who then gave formal consent. Ethical approval for the study was obtained from the Human Subject Committee of Taipei Physical Education College (TPEC). All the subjects were female college students in modern dance major, who registered at various dancing classes for 7–8 h per week with a mean intensity of heart rate of 110±11 per min during classes We recorded the dancing intensity with a Polar Heart Monitor (Lake Success, NY, USA) during their regular dancing classes for a week. During the detraining period, these dancers did not participate in any type of dancing class or any other vigorous physical activity for 2 months. All subjects were asked to limit their vigorous physical activity under 30 min per week for 2 months. Their dietary intake during the detraining period was not significantly different from that during the semester, according to a 1-week dietary recall record.
Oral glucose tolerance test
An oral glucose tolerance test (OGTT) was performed 1 week before and at day 60 of the cessation training. The test procedure was according to the method described previously by Lee et al.10 Briefly, on the day of the OGTT, subjects reported to the researchers at 0830 after an overnight fast. A 75 g of glucose was delivered orally with 500 ml of pure water. Blood samples were collected from the fingertip at 0 (fasting value), 30, 50, and 80 min. A glucose analyzer (Lifescan, CA, USA) was utilized for glucose concentration determination.
Insulin and free fatty acid levels
Plasma sample was collected from 200 μl of fingertip blood and used for insulin and free fatty acid (FFA) determination. The insulin was determined on the ELISA analyzer (Tecan Genios, Salzburg, Austria) with the use of commercially available ELISA kits (Diagnostic Systems Laboratories Inc., Webster, TX, USA), according to the manufacturer's instructions. Plasma FFA concentrations were determined with a kit (Wako Pure Chemicals, Richmond, VA, USA) according to manufacturer's instructions.
Circumferences of the waist (umbilical level) and hip (maximum of buttocks) were measured to the centimeter, and the waist-to-hip ratio (WHR) was calculated to estimate the degree of central fat distribution. BMI was used as an indicator of being overweight (calculated as kilogram per square meter).
A paired t-test was used to compare the mean differences between the pre and the post values for all the subjects. A level of P<0.05 was set as significant on all tests, and all values are expressed as means±s.e.
Following the 2-month detraining, no significant change in weight and BMI was found in the subjects (Table 1). However, WHR was elevated at the end of the 2-month detraining (P<0.05). The waist circumference was increased by approximately 1.6 cm (P<0.05) without significant change in hip circumference.
Oral glucose tolerance test
There is no significant difference in the level of fasted glucose and OGTT glucose at all measured time points (Figure 1).
Fasted insulin level was significantly elevated after the 2-month detraining (Figure 2, P<0.05). Similarly, the insulin levels at 30, 50 and 80 min following oral glucose challenge were elevated after the 2-month detraining (P<0.05).
Free fatty acid
Fasted plasma FFA level was significantly elevated after the 2-month detraining (Figure 3, P<0.05). Following an oral glucose challenge, FFA was significantly depressed, where as no significant difference was found between the pre and the post values at 30, 50 and 80 min.
Plasma cholesterol and triglyceride
Fasted blood sample was used for the analysis. Triglyceride levels of the dancers were significantly elevated by the 2-month detraining (81±9.3 versus 115±16.6 mg/dl, P<0.05), whereas the cholesterol level was not significantly different before and after the detraining (143±5.1 versus 146±5.3 mg/dl, no significance) (Figure 4).
Previous studies in highly trained endurance athletes have shown that 7–10 days detraining would significantly reduce glucose tolerance.11 In contrast to this result, we found that 2-month detraining in these young female dancers did not significantly affect the whole-body glucose tolerance. However, the levels of fasted and postprandial insulin were substantially elevated. This result suggests that insulin sensitivity was reduced with a short-term cessation of physical activity, but this metabolic change may not reflect on glucose tolerance for those subjects who are not heavily trained but active. Hyperinsulinemia and insulin resistance have been recognized as an early sign of type 2 diabetes and several metabolic disorders in humans,6, 7 and this is generally associated with an increased body fatness.1 A warning is thus warranted for these young active women that an adverse metabolic drift could take place within a short period of time of lifestyle transition in physical activity.
The most important finding of this study was that, for a short-term lifestyle transition, reduced insulin sensitivity and increased abdominal fatness could occur without an observable increase in BMI. This is in contrast to the previous studies by Alméras et al.9 and Petibois et al.12 In both cases, they found that reduction in insulin sensitivity was associated with increased BMI. Discrepancy between their studies and the present one could be that their studies were performed on highly trained athletes with a much longer period of detraining. In clinical practice, body fat is most commonly estimated by BMI value using a formula that combines weight and height. The underlying assumption is that most variation in the weight of people of the same height is due to fat mass. The result of the current study clearly presents the limitation of using BMI as an obesity indicator for the early phase of lifestyle transition in previously active young female subjects.
Development of hyperinsulinemia by detraining could be caused by increased adiposity.10 It has been suggested that increased fat storage in adipocytes elevates several feedback signals that interfere with insulin action on fuel uptake and storage.4, 5, 13 FFA is one candidate of these feedback regulators that have been implicated in the development of insulin resistance associated with obesity.5, 14 It is consistently observed that experimental elevation of circulating FFA levels leads to insulin resistance in animals and humans.15, 16 In addition, it has also been found that FFA enhances pancreatic insulin secretion,17, 18 implicating its contribution to hyperinsulinemia. Another possibility that accounts for the reduced insulin sensitivity among those detrained female young dancers was the reduction in skeletal muscle GLUT4 protein expression. Skeletal muscle is the main tissue for postprandial glucose disposal,19 while GLUT4 protein is the main isoform of glucose transporter expressed in skeletal muscle. This protein has been found to be elevated by exercise20 and downregulated following short-term detraining.21
In this study, increased fat storage in the abdominal area was primarily promoted by decreased energy expenditure due to reduced physical activity in the dancers. This is based on the fact that the overall caloric intake and body mass were not changed after the detraining period. This is also evident in highly trained athletes that energy intake was reduced along with elevated body fat during a 2-year detraining.12 The result of the increased abdominal fatness without change in BMI is most likely due to the redistribution of postprandial nutrients among the energy-storage tissues. Skeletal muscle and adipose tissues are the two major energy-storage sites of the body. While muscular activity has no substantial effect on appetite or caloric intake,22 physical activity could be important for the regulation of body composition by repartition fuel toward the active site.23, 24 Previous studies have shown that greater physical activity can lead to greater storage of glycogen2 and triglycerides25 in the recruited skeletal muscle. Conversely, Simsolo et al.26 demonstrated that the decreased physical activity generates a condition favoring triglyceride partitioning to adipose tissue storage in contrast to skeletal muscle. Therefore, reduction in fuel uptake of skeletal muscle and increase in fat uptake of adipose tissue by detraining could account for the presently observed increase in waist circumference without showing an increase in body mass in these young female dancers.
Individuals with prolonged insulin resistance or hyperinsulinemia almost consistently manifest a serious abnormality in lipid metabolism6, 27 Previous studies have shown that 2-year detraining in highly trained endurance athletes elicits significant changes in both triglyceride and cholesterol levels.12 In keeping with these previous reports, the current study shows that triglyceride level can be elevated within only 2 months. It is also demonstrated in animal study28 that producing the hyperinsulinemic state with dietary fructose causes an increase in triglyceride concentration, and this increase appears to be caused not only by increased triglyceride production, but also by impaired triglyceride removal.
Current data demonstrate that switching lifestyle from active to sedentary for only 2 months would lead to hyperinsulinemia, without observable change in glucose tolerance. This unfavorable metabolic change is apparently associated with the development of high FFA level and central fatness. Furthermore, the most important implication of this study is that, during the early phases of lifestyle transition, increased abdominal fatness may not be reflected on body mass and BMI for young females.
Kopelman PG . Obesity as a medical problem. Nature 2000; 404: 635–643.
Ivy JL, Zderic TW, Fogt DL . Prevention and treatment of non-insulin-dependent diabetes mellitus. Exerc Sport Sci Rev 1999; 27: 1–35.
Ravussin E, Lillioja S, Knowler WC, Christin L, Freymond D, Abbott WG et al. Reduced rate of energy expenditure as a risk factor for body weight. N Engl J Med 1988; 318: 467–472.
Birnbaum MJ . Diabetes: dialogue between muscle and fat. Nature 2001; 409: 672–673.
Lewis GF, Carpentier A, Adeli K, Giacca A . Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes. Endocr Rev 2002; 23: 201–229.
Reaven GM . Role of insulin resistance in human disease. Diabetes 1988; 37: 1595–1607.
Facchini FS, Hua N, Abbasi F, Reaven GM . Insulin resistance as a predictor of age-related diseases. J Clin Endocrinol Metab 2001; 86: 3574–3578.
Willett WC, Dietz WH, Colditz GA . Guidelines for healthy weight. New Eng J Med 1999; 341: 427–434.
Alméras N, Lemieux S, Bouchard C, Tremblay A . Fat gain in female swimmers. Physiol Behav 1997; 61: 811–817.
Lee WC, Chen JJ, Hunt D, Hou CW, Lai YC, Lin FC et al. Effects of hiking at altitude on body composition and insulin sensitivity in recovery drug addicts. Prev Med 2004; 39: 681–688.
Arciero PJ, Smith DL, Calles-Escandon J . Effects of short-term inactivity on glucose tolerance, energy expenditure, and blood flow in trained subjects. J Appl Physiol 1998; 84: 1365–1373.
Petibois C, Cassaigne A, Gin H, Deleris G . Lipid profile disorders induced by long-term cessation of physical activity in previously highly endurance-trained subjects. J Clin Endocrinol Metab 2004; 89: 3377–3384.
Shulman GI . Cellular mechanisms of insulin resistance. J Clin Invest 2000; 106: 171–176.
Boden G, Chen X, Ruiz J, White JV, Rossetti L . Mechanism of fatty acid induced inhibition of glucose uptake. J Clin Invest 1994; 93: 2438–2446.
Chakley SM, Hettiarachchi M, Chisholm DJ, Kraegen EW . Five-hour fatty acid elevation increases muscle lipids and impairs glycogen synthesis in the rat. Metabolism 1998; 47: 1121–1126.
Dresner A, Laurent D, Marcucci M, Griffin ME, Dufour S, Cline GW et al. Effects of free fatty acids on glucose transport and IRS-1 associated phosphatidylinositol 3-kinase activity. J Clin Invest 1999; 103: 253–259.
Crespin SR, Greenough WB, Steinberg D . Stimulation of insulin secretion by long-chain free fatty acids. A direct pancreatic effect. J Clin Invest 1973; 52: 1979–1984.
Warnotte C, Gilon P, Nenquin M, Henquin JC . Mechanisms of the stimulation of insulin release by saturated fatty acids. A study of palmitate effects in mouse beta-cells. Diabetes 1994; 43: 703–711.
DeFronzo RA, Jacot E, Jequier E, Maeder E, Wahren J, Felber JP . The effect of insulin on the disposal of intravenous glucose. Results from indirect calorimetry and hepatic and femoral venous catheterization. Diabetes 1981; 30: 1000–1007.
Dohm GL . Regulation of skeletal muscle GLUT-4 expression by exercise. J Appl Physiol 2002; 93: 782–787.
McCoy M, Proietto J, Hargreves M . Effect of detraining on GLUT-4 protein in human skeletal muscle. J Appl Physiol 1994; 77: 1532–1536.
Blundell JE, King NA . Effects of exercise on appetite control: loose coupling between energy expenditure and energy intake. Int J Obes Relat Metab Disord Suppl 1998; 22: S22–S29.
Greiwe JS, Holloszy JO, Semenkovich CF . Exercise induces lipoprotein lipase and GLUT-4 protein in muscle independent of adrenergic-receptor signaling. J Appl Physiol 2000; 89: 176–181.
Ladu MJ, Kapsas H, Palmer WK . Regulation of lipoprotein lipase in muscle and adipose tissue during exercise. J Appl Physiol 1991; 71: 404–409.
Seip RL, Semenkovich CF . Skeletal muscle lipoprotein lipase: molecular regulation and physiological effects in relation to exercise. Exerc Sport Sci Rev 1998; 26: 191–218.
Simsolo RB, Ong JM, Kern PA . The regulation of adipose tissue and muscle lipoprotein lipase in runners by detraining. J Clin Invest 1993; 92: 2124–2130.
Schalch DS, Kipnis DM . Abnormalities in carbohydrate tolerance associated with elevated plasma nonesterified fatty acids. J Clin Invest 1965; 44: 2010–2020.
Kazumi T, Vranic M, Steiner G . Triglyceride kinetics: effects of dietary glucose, sucrose, or fructose alone or with hyperinsulinemia. Am J Physiol 1986; 250: E325–E330.
This study was partially supported by a research grant from the National Science Council, Republic of China, Grant Number NSC 93-2413-H-154-009.
About this article
Cite this article
Chen, SY., Chen, SM., Chang, WH. et al. Effect of 2-month detraining on body composition and insulin sensitivity in young female dancers. Int J Obes 30, 40–44 (2006). https://doi.org/10.1038/sj.ijo.0803073
- free fatty acid
- upper body fatness
Journal of Pediatric Endocrinology and Metabolism (2019)
Relation Between Serum Free Fatty Acids and Adiposity, Insulin Resistance, and Cardiovascular Risk Factors From Adolescence to Adulthood
Effects of intensified training and subsequent reduced training on glucose metabolism rate and peripheral insulin sensitivity in Standardbreds
American Journal of Veterinary Research (2012)
Peroxisome Proliferator-activated Receptor γ Coactivator 1α (PGC-1α) Promotes Skeletal Muscle Lipid Refueling in Vivo by Activating de Novo Lipogenesis and the Pentose Phosphate Pathway*
Journal of Biological Chemistry (2010)