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Cited by 14Muscle Physiology and DisordersMuscle metabolism and nutritionAdipose Tissue and Metabolism

Effect of Treadmill Training on Muscle Oxidative Capacity and Accretion in Young Male Obese and Nonobese Zucker Rats

Wardlaw, Gordon M., Kaplan, Murray L., Lanza-Jacoby, Susan·1986·The Journal of Nutrition
DOI 10.1093/jn/116.9.1841
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Abstract

This study was designed to determine if treadmill training of the male obese Zucker rat could reverse its deficit in muscle accretion, expose a possible latent defect in its muscle oxidative capacity or significantly alter its food intake and lipid deposition. At 12 wk of age muscle mass and myofibrillar protein concentration were significantly lower and body lipid and food intake were significantly higher in the sedentary obese than in the nonobese rat. Exercise, by both inducing hypophagia and increasing energy output, led to a lower body weight, body lipid, and muscle mass in the exercised than in the nonexercised rats. This response to exercise did not differ between both phenotypes, except for body lipid. In that case the reduction of body lipid was greater for the obese rats. Muscle mitochondrial enzyme activities and rates of mitochondrial respiration in the obese rats were not different or greater than those of their sedentary or pair-exercised nonobese counterparts. Taken together these data indicate that oxidative capacity per unit of muscle is not significantly lower in the obese rats than in nonobese rats in both sedentary and exercised states, but that total muscle oxidative capacity is lower on a whole-animal basis since total muscle mass is lower. Further, exercise reduces, but does not prevent the enhanced weight gain and lipid accretion that characterizes the obese rat.

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Crossref · 10.1093/jn/116.9.1841

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  • Although deficient muscle substrate oxidation capacity is observed during obesity, there is no alteration in mitochondrial activities of pivotal enzymes such as citrate synthase, succinate dehydrogenase, or β-hydroxyacetyl-CoA dehydrogenase.

    “However, and although deficient muscle substrate oxidation capacity is observed during obesity, there is no alteration in mitochondrial activities of pivotal enzymes such as citrate synthase, succinate dehydrogenase, or ␤-hydroxyacetyl-CoA dehydrogenase (19 -21).”

    From Expression of <i>Mfn2</i>, the Charcot-Marie-Tooth Neuropathy Type 2A Gene, in Human Skeletal Muscle (2005) · cites this paper as [19]

  • The mechanisms by which obesity leads to deficient muscle substrate oxidation remain unexplained and are concomitant with unaltered mitochondrial activities of pivotal enzymes such as pyruvate dehydrogenase, citrate synthase, succinate dehydrogenase, or beta-hydroxyacetyl-CoA dehydrogenase.

    “In particular, the mechanisms by which obesity leads to a deficient muscle substrate oxidation remain unexplained and are concomitant with unaltered mitochondrial activities of pivotal enzymes such as pyruvate dehydrogenase, citrate synthase, succinate dehydrogenase, or औ-hydroxyacetyl-CoA dehydrogenase (44-46”

    From Mitofusin-2 Determines Mitochondrial Network Architecture and Mitochondrial Metabolism (2003) · cites this paper as [44]

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Authors
Wardlaw, G. M., Kaplan, M. L., & Lanza-Jacoby, S.
Affiliations
Iowa State University (US)
Corresponding author
Kaplan, Murray L.
Venue
The Journal of Nutrition
Publisher
Elsevier BV
Published
1986-09
Volume
116
Issue
9
Pages
1841-1852
ISSN
0022-3166 (ISSN-L)
DOI
10.1093/jn/116.9.1841
OpenAlex
W1494740204
Cited by
14
References
27
Citations by year
2012: 2
FWCI
0.14
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Nutrition (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health (AM 28615)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
treadmill training, physical activity, obesity, Zucker rats, muscle oxidative capacity, mitochondrial respiration, mitochondrial enzyme activity, muscle mass, myofibrillar proteins, body lipids, dietary intake, hypophagia, weight gain, lipid accumulation, energy expenditure
MeSH terms
Animals, Body Weight, Physical Exertion, Food, Male, Mitochondria, Muscle, Muscles, Obesity, Oxygen Consumption, Physical Conditioning, Animal, Rats, Mutant Strains, Rats, Zucker, Lipid Metabolism, Rats

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