Muscle morphological and biochemical adaptations to training in obese Zucker rats
Abstract
The purposes of the present study were to characterize the histochemical and enzymatic profiles of various hindlimb skeletal muscles, as well as to determine maximal O2 consumption (VO2max) and respiratory exchange ratios (R) during steady-state exercise in the obese Zucker rat. The changes that occurred in these parameters in response to a 6-wk training program were then assessed. Obese rats were randomly assigned to a sedentary or training group. Lean littermates served as a second control. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 day/wk for 6 wk. During week 6, VO2max and R during a steady-state run (74% max) were determined. After 2 days of inactivity, hindlimb muscles were excised, stained for fiber type and capillaries, and assayed for hexokinase, citrate synthase, cytochrome oxidase, and beta-hydroxyacetyl-CoA dehydrogenase. The obese sedentary rats demonstrated greater oxidative enzyme activities per gram of muscle tissue than their lean littermates, greater R values during submaximal exercise of the same relative intensity, and greater absolute VO2max values. Training resulted in a 20-56% increase in oxidative enzymes, a 10% increase in VO2max, and an increase in capillary density in the soleus and plantaris. There was no alteration in R values during exercise at 74% VO2max or in fiber type composition in response to exercise training. Results suggest that the muscle of the obese Zucker rat manifests a greater oxidative capacity than the muscle of its lean littermates. The apparent inability of the obese rat to increase its use of fat during submaximal exercise of the same relative intensity in response to training remains to be elucidated.
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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 [20]
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 [45]
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Saengsirisuwan, V. (2003) · UA Campus Repository (The University of Arizona)
- Authors
- Torgan, C. E., Brozinick, J. T., Kastello, G. M., & Ivy, J. L.
- Affiliations
- The University of Texas at Austin (US)
- ORCID
- Brozinick, J. T.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 1989-11-01
- Volume
- 67
- Issue
- 5
- Pages
- 1807-1813
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2181248333
- Cited by
- 43
- References
- 0
- Citations by year
- 2023: 2 · 2019: 1 · 2017: 3 · 2015: 1 · 2012: 1
- FWCI
- 5.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- obesity, Zucker rats, exercise training, skeletal muscle, oxidative enzymes, citrate synthase, cytochrome c oxidase, hexokinase, beta-hydroxyacyl-CoA dehydrogenase, capillary density, muscle fiber composition, VO2max, respiratory exchange ratio, fat oxidation, treadmill running, hindlimb muscles
- MeSH terms
- Analysis of Variance, Animals, Capillaries, Citrate (si)-Synthase, Electron Transport Complex IV, Physical Exertion, Female, Hexokinase, Hindlimb, Muscles, Obesity, Oxygen Consumption, Partial Pressure, Random Allocation, Rats, Zucker, Respiration, 3-Hydroxyacyl CoA Dehydrogenases, Rats
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