The results of the present study demonstrate that this 12 wk controlled resistance exercise program increased strength, lean body mass and hepatic insulin sensitivity and slightly reduced glucose production in obese Hispanic adolescents. In contrast, the program had no effect on total body, visceral, hepatic and intramyocellular fat or peripheral insulin sensitivity.
Although increased muscle mass and hepatic insulin sensitivity are important results of the resistance exercise program, aerobic exercise seems to have more extensive effects. We demonstrated in a similar group of obese adolescents that the same volume of aerobic exercise significantly reduced total, visceral and hepatic fat content and increased both peripheral and hepatic insulin sensitivity (41
). These findings are in agreement with other studies in adults and children (12
). In contrast, the impact of resistance exercise is less clear (4
). While most studies reported increased strength and lean body mass (muscle mass) in response to resistance exercise (6
), only a few studies found effects on body fat (4
). Similarly, its influence on insulin sensitivity was inconsistent. Some studies reported improved insulin sensitivity (6
), while others found no metabolic effects of resistance exercise (4
). The methods used in the referenced studies (unlabeled FSIVGTT, unlabeled clamp, oral glucose tolerance test and HOMA-IR) provide a measure of whole body (i.e. peripheral + hepatic) insulin sensitivity. Using the stable label IVGTT and the Hepatic Insulin Sensitivity Index enabled us to determine peripheral and hepatic insulin sensitivity separately.
The increase in body weight resulting from the exercise program was almost completely explained by the increase in lean body mass. Theoretically, one would expect that increased lean body mass (muscle mass) i.e. increased insulin sensitive tissue mass would result in increased insulin sensitivity, primarily peripherally. The increase in lean body mass resulting from our program might have been insufficient to achieve this effect. Neither lean body mass at baseline and post-exercise nor exercise induced change in lean body mass correlated with peripheral or hepatic insulin sensitivity (data not shown). This is in agreement with the referenced studies, where changes in whole body insulin sensitivity (or lack thereof) were independent of changes in lean body mass (6
). In addition, muscular strength alone has been shown to be a positive predictor for insulin sensitivity (5
). It has been suggested that resistance training might increase insulin sensitivity as a result of qualitative changes within the muscle (6
). Brooks et al. (6
) and Holten et al. (15
) conducted muscle biopsies in adults with type 2 diabetes participating in a whole body (6
) or one leg resistance exercise program (15
). Brooks et al. (6
) demonstrated increased muscle quality (strength/unit of muscle mass) and increased areas of type I and type II fibers. The increase in type I fiber area correlated significantly with the decrease in insulin resistance. Holten et al. (15
) showed increased insulin activity and Glut 4 protein but no effect on markers of oxidative capacity in skeletal muscle. Since muscle biopsies cannot be performed in healthy children and adolescents for ethical reasons, we were not able to pursue potential cellular mechanisms. We did calculate peak torque/g leg muscle from the DXA and Biodex analyses as a surrogate measure of muscle quality. We found an increase in this value for the right leg and a value that approached significance (p=0.06) for the left. These values did not correlate with insulin sensitivity.
A failure to increase lipid oxidation during fasting might lead to intramyocellular fat deposition in obese individuals, subsequently contributing to patterns of insulin resistance (17
). Exercise could potentially improve fat oxidation, which might lead to reduced intramyocellular fat content. Indeed, Koopman et. al. (19
) demonstrated a decrease in intramyocellular fat directly after a resistance exercise session. However, 120 min after the exercise session the intramyocellular fat content had returned to pre-exercise levels indicating only a short term effect (19
). To our knowledge there are no published data on the effects of a resistance exercise program on intramyocellular fat content. We measured intramyocellular fat at baseline and post the exercise program using magnetic resonance spectroscopy but found no changes.
Resistance exercise significantly increased fasting hepatic insulin sensitivity. The mechanism for this effect is not clear. Hepatic fat content measured by magnetic resonance spectroscopy did not change in response to the program and did not correlate with hepatic insulin sensitivity. Thus, the improvements in hepatic insulin sensitivity could not be explained by any reduction in hepatic fat accumulation. This finding indicates that liver lipid content is not a reliable predictor of hepatic insulin resistance. Heled et al. (14
) reported that aerobic exercise training (treadmill) increased hepatic insulin sensitivity due to ameliorated insulin signaling response and inhibited PEPCK activity in the hepatocyte of diabetes prone fat sand rats. Since we could not perform liver biopsies in our healthy adolescents, hepatocellular mechanisms could not be investigated. While none of the more metabolically active fat deposits (visceral, hepatic and intramyocellular) changed in response to our resistance exercise program, we observed a small increase in subcutaneous abdominal fat. This finding might be of importance. It has been speculated that defective differentiation of subcutaneous fat might lead to defective fat storage in this compartment with subsequent overflow of fat into visceral, hepatic and intramyocellular fat deposits (9
). Increased subcutaneous abdominal fat without changes in visceral fat was also reported by Treuth et al. (39
) in response to a 5 month resistance exercise program in pre-pubertal girls.
Our study population consists of Hispanic adolescents, thus, the studies by Goran’s group (8
) in a similar population are of particular interest. In a first study, overweight adolescent Latino boys performed a resistance exercise program, 2 × 1 h/wk for 16 wks (32
). Insulin sensitivity increased by 45%. Lean body mass also increased and body fat% (but not fat mass) decreased. In a later study, overweight adolescent Latino boys and girls were subjected to the same resistance exercise program with an additional diet component aiming at reducing sugar and increasing fiber intake (8
). Surprisingly, in this study insulin sensitivity and body composition were completely unaffected. The investigators speculated that the diet intervention might have cancelled out the effect of the exercise. However, a post hoc analysis of the response to the diet intervention showed no difference between a control group, a diet alone group and the diet + strength training group (43
A weakness of our study might be that we did not include a non-exercising control group. However, it would be ethically questionable to subject healthy adolescents to comparatively invasive metabolic studies without any intervention. Muscle mass and strength increases until adulthood (3
). Since our participants were post pubertal and, thus, had passed their growth peak, it is unlikely that growth and maturation explain the increase in strength and muscle mass that was observed during the relatively short 12 wk exercise program. For the same reason, pubertal effects on insulin sensitivity are very unlikely.
Resistance exercise resulted in a small decrease (8%) in glucose production due to a decrease (12%) in glycogenolysis while gluconeogenesis remained unchanged. Most likely, the decrease in glucose production has limited clinical relevance in our normoglycemic adolescents with normal glucose tolerance. However, in diabetic adolescents, increased glucose production might result in hyperglycemia (10
). Thus, one might speculate that in these individuals, resistance exercise could be a tool to reduce glucose production and subsequently hyperglycemia. The association between decreased glycogenolysis and increased hepatic insulin sensitivity confirms that glycogenolysis is more sensitive to insulin than gluconeogenesis, as suggested by Gastaldelli et al. (11
Baseline leptin and hs-CRP concentrations were significantly higher compared to a previously studied group of lean adolescents of the same age (41
). The higher CRP concentrations indicate a low grade whole body inflammation in obese adolescents. Data regarding the effect of resistance exercise on adiponectin, leptin and hs-CRP concentrations are limited (6
). Brooks et al. (6
) found that adiponectin increased and CRP decreased in response to resistance exercise, while Klimcakova et. al. (18
) reported unchanged adiponectin and hs-CRP but decreased leptin concentration. We observed no exercise induced changes in these parameters.
In conclusion: Resistance exercise might be an attractive alternative to aerobic exercise for obese adolescents. Increased strength, lean body mass and hepatic insulin sensitivity are important findings. However, the more comprehensive effects of aerobic exercise involving metabolic parameters, body composition and body fat distribution might have a greater potential to prevent obesity related illnesses (41
). Thus, a program combining resistance and aerobic exercise might be a viable strategy to achieve the positive effects of both types of exercise.