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J Appl Physiol (October 25, 2002). doi:10.1152/japplphysiol.00746.2002
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Articles in PresS, published online ahead of print October 25, 2002
J Appl Physiol, 10.1152/jap.00746.2002
Submitted on August 13, 2002
Accepted on October 11, 2002

Impaired Substrate Oxidation in Healthy Elderly Men After Eccentric Exercise

Raj K Krishnan1, William J Evans2, and John P Kirwan3*

1 Noll Physiological Research Center and The General Clinical Research Center, The Pennsylvania State University, State College, PA, USA
2 Nutrition, Metabolism, and Exercise Division, University of Arkansas for Medial Sciences, Little Rock, AR, USA
3 Department of Reproductive Biology, Case Western Reserve School of Medicine at Metro Health Medical Center, Cleveland, OH, USA; Department of Nutrition, Case Western Reserve School of Medicine at Metro Health Medical Center, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: jpk10{at}po.cwru.edu.

Eccentric exercise results in muscle damage, transient insulin resistance and an increased insulin response to glucose among healthy young individuals. However, the bioenergetic response to eccentric exercise among healthy older individuals is unknown. Substrate metabolism was examined using hyperglycemic clamps (180 min, 10 mM) in 8 older (age, 66 ± 2 years; BMI, 25.5 ± 1.2 kg.m-2) and 9 younger (age, 23 ± 1 years; BMI, 23.6 ± 1.7 kg.m-2) sedentary men with normal oral glucose tolerance (OGTT), under control conditions and 48 h after eccentric exercise. Indirect calorimetry was performed at basal and 180 min of hyperglycemia to evaluate rates of carbohydrate and lipid oxidation (Cox and Lox, respectively). Eccentric exercise caused muscle soreness and increased plasma creatine kinase in both groups (P<0.02). Although a similar level of hyperglycemia was maintained in both groups, glucose infusion rates were lower (P<0.001) in older versus younger subjects, regardless of trial. Hyperglycemia stimulated an increase in Cox and a decrease in Lox during both trials in the younger group (P<0.03), but only under control conditions among older subjects (P<0.007). In order to evaluate the effects of eccentric exercise, oxidation rates during hyperglycemia were compared between control and exercise trials. Cox was unchanged after eccentric exercise in younger (4.00 ± 0.30 vs. 3.54 ± 0.44 mg.kgFFM-1.min-1; +13%, P=0.11; exercise vs. control), but suppressed by 20% among older men (3.37 ± 0.37 vs. 4.21 ± 0.23 mg.kgFFM-1.min-1; P<0.04). Moreover, Lox was diminished by 38% in younger subjects (0.47 ± 0.09 vs. 0.76 ± 0.10 mg.kgFFM-1.min-1; P<0.03), but augmented by 89% in the older group (0.68 ± 0.11 vs. 0.36 ± 0.08 mg.kgFFM-1.min-1; P<0.04). Respiratory exchange ratio (RER) increased in younger (0.93 ± 0.01 vs. 0.89 ± 0.02; P<0.03), and decreased in older subjects (0.89 ± 0.02 vs. 0.94 ± 0.01; P<0.03). In addition, hyperglycemia-stimulated Cox, Lox and RER responses to eccentric exercise were related to abdominal adiposity (r = -0.57, P<0.04, r = 0.66, P<0.02 and r = -0.60, P<0.02, respectively). Despite a normal OGTT and the absence of obesity per se, older men show aberrations in substrate metabolism after exercise-induced muscle damage. Thus, aging and modest increases in abdominal adiposity diminishes the metabolic response to hyperglycemia after a single bout of eccentric exercise.




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