It is a generally well-accepted notion that a positive imbalance between caloric intake and caloric expenditure contributes to the development of insulin resistance.20
Also, the aging process itself may place elderly individuals at an even greater risk for metabolic abnormalities.21
This has become an especially relevant issue in our current society with the rapid growth of an aging population and the corresponding increased burden on health-care resources.22
As such, elderly individuals need definitive physical activity recommendations that are based on the results of clinical studies in the geriatric population. Therefore, we chose to evaluate the efficacy of the minimal ACSM/CDC recommendations for physical activity on factors potentially responsible for the development of insulin resistance (i.e., excess regional adipose tissue and reduced levels of plasma adiponectin). The results of our supervised exercise training studies using matched caloric expenditure of 1000 kcal/week demonstrated that only HI facilitated a reduction in visceral fat. MI resulted in no change in visceral fat. Also, MI or HI (in the absence of weight loss) had no significant influence on abdominal subcutaneous fat, thigh fat, or plasma adiponectin.
Previous studies in middle-aged individuals with T2D have demonstrated significant reductions in visceral fat and subcutaneous fat as a result of high-intensity exercise training.23,24
In these studies, the training period of 8 weeks was 33% shorter, but the relative exercise intensity and mode of exercise training (i.e., cycle ergometer) were relatively consistent with that employed in the present investigation, except for the addition of interval type exercise within the training paradigm. More specifically, these authors used high-intensity, continuous cycle ergometer training at 75% of VO2peak
for 30 minutes on 2 days of the week, and an interval exercise training session consisting of five bouts at 85% VO2peak
for 2 minutes separated by intermittent bouts at 50% of VO2peak
for 3 minutes. Hence, using a modified interval training design in previously unfit individuals with T2D may have promoted use of fat as an energy source.25
In turn, this could have promoted a combined reduction in abdominal subcutaneous fat and visceral fat, even under conditions of relatively low caloric expenditure and no change in total body mass.
In addition to the previously mentioned studies incorporating the use of interval training, the studies by O'Leary et al. demonstrated an exercise training-induced reduction in visceral fat,9
abdominal subcutaneous fat, and total abdominal fat. In these studies, the volunteers exercised at ~70% of VO2max
, 5 days of week for 50–60 minutes and lost ~7 pounds over the course of the study. As such, these results have raised an interesting question as to whether weight loss may be required to initiate a reduction in the levels of visceral fat. In studies where the influence of exercise training (with and without weight loss) were compared, exercise training with weight loss (~8 pounds) resulted in a 26% reduction in visceral fat while exercise training without weight loss (complete caloric compensation for the energy expenditure of exercise training) still promoted a 17% reduction in visceral fat.26
Although the duration of the exercise training bouts were significantly longer (~40–60 minutes per session versus ~30 minutes in our study) in this study, the intensity of the exercise training was almost identical to the HI group in our present study. Therefore, we were able to demonstrate an exercise training-induced reduction in visceral fat (~20%) at the same relative exercise intensity, even with a 20–40% reduction in total exercise training duration.
Abdominal adiposity has been suggested as a more powerful predictor of insulin resistance than fitness, especially among older individuals.27
Although visceral fat decreased in HI, the lack of a change in abdominal subcutaneous fat in either exercise training group may be linked to a negligible or nonexistent change in adiponectin, due to the strong relationship between abdominal fat deposition and the dysregulation of adiponectin gene expression in adipose tissue.10
It is also interesting that an inverse relationship between adiponectin mRNA expression and tumor necrosis factor-α (TNF-α) has been demonstrated, potentially substantiating the importance of adiponectin as a suppressive mediator of proinflammatory cytokines.28
In short-term aerobic exercise training studies that incorporated a variety of exercise modalities, Bluher et al. demonstrated improvements in plasma adiponectin and Adipo R1/R2 mRNA expression without weight loss in persons with impaired glucose tolerance and T2D.13
In our studies, plasma adiponectin did increase in an absolute sense in MI and HI, and we recognize that the lack of a significant increase in adiponectin might be influenced by the relatively small sample size of our well-controlled, supervised study. However, other studies with either moderate- or high-intensity exercise training also did not find an improvement in plasma adiponectin.16,29
These authors were able to show that changes in visceral adipose tissue and TNF-α were indicative of efficacious changes in the degree of insulin resistance16
and support the contention that changes in the relationship between adiponectin and proinflammatory cytokines such as TNF-α represent their key contribution in the modulation of glucose metabolism.30
In conclusion, the results of studies support the efficacy of short-term, high-intensity aerobic exercise training for the reduction of visceral fat in elderly, overweight adults. The lack of a significant change in abdominal subcutaneous or thigh fat indicate that high-intensity exercise training exerts a preferential influence on the oxidation of visceral fat. Also, the lack of significant changes in plasma adiponectin suggests that moderate-or high-intensity exercise training in the absence of weight loss does not normalize metabolic dysfunction in a short-term intervention. However, the efficacy of long-term, high-intensity exercise training toward the amelioration of insulin resistance has not been well tested, and future studies are needed to identify potential changes in the expression of proinflammatory cytokines in abdominal adipose tissue and their relationship to changes in hepatic and peripheral insulin sensitivity.