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1 Pathobiology, Cleveland Clinic, Cleveland, Ohio, United States
2 Noll Physiological Research Center, Penn State University, University Park, Pennsylvania, United States
3 Gastroenterology/Hepatology, Cleveland Clinic, Cleveland, Ohio, United States; Pathobiology, Cleveland Clinic, Cleveland, Ohio, United States; Noll Physiological Research Center, Penn State University, University Park, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: kirwanj{at}ccf.org.
Older, obese, and sedentary individuals are at high risk of developing diabetes and cardiovascular disease. Exercise training improves metabolic anomalies associated with such diseases, but the effects of caloric restriction in addition to exercise in such a high risk group are not known. Changes in body composition and metabolism during a lifestyle intervention were investigated in twenty three older, obese men and women (aged 66±1years, BMI 33.2±1.4 kg.m-2) with impaired glucose tolerance. All volunteers undertook twelve weeks of aerobic exercise training (5 days per week for 60min@75% VO2max) with either normal caloric intake (eucaloric group, 1901±277 kcal.day-1) or a reduced-calorie diet (hypocaloric group, 1307±70kcal.day-1), as dictated by nutritional counseling. Body composition (decreased fat mass; maintained fat-free mass), aerobic fitness, leptinemia, insulin sensitivity, and intramyocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P<0.05). Improvements in body composition, leptin and basal fat oxidation were greater in the hypocaloric group. Following the intervention there was a correlation between the increase in basal fat oxidation and the decrease in IMCL (r=-0.53, P=0.04). In addition, basal fat oxidation was associated with circulating leptin after (r=0.65, P=0.0007), but not before the intervention (r=0.05, P=0.84). In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved, but that such a trend may rely on reducing caloric intake in addition to exercise training
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