# EXERCISE AND MUSCLE ATROPHY PREVENTION

> **NIH NIH R01** · UNIVERSITY OF ILLINOIS AT CHICAGO · 1989 · $117,034

## Abstract

Investigations in humans and animals over the last several years have
shown exercise is a potent inhibitor of skeletal muscle wasting
associated with diseases and experimental conditions resulting in
glucocorticoid excess The mechanism of exercise is conserving muscle
mass remains as yet unidentified. By examining hormone-responsive
proteins as models for understanding protein regulation, the long-term
objectives are to elucidate the molecular basis by which exercise
prevents muscle atrophy from this state. The specific aims are: (a) to
determine whether exercise inhibits the up-regulation of glutamine
synthetase enzyme induction and gene expression. (b) To evaluate whether
exercise reverses the down-regulation of myosin and specifically myosin
heavy chains. The parameters to be studied are myosin heavy chain
synthesis and MRNA content, native isomyosin characterization, and the
synthesis rates of each isoform. (c) Pathologic changes produced by
glucocorticoids, besides those in myofibrillar proteins, are also found
in the mitochondria. The use of CDNA probes for both a nuclear genome
and a mitochondrial genome for the multisubunit cytochrome c oxidase, a
mitochondrial marker enzyme, will allow us to identify whether there is
a coordinated transcriptional response by exercise in preventing the
mitochondrial alterations associated with muscle wasting, and will also
provide evidence as to whether there is a predilection for myofibrillar
or mitochondrial sparing in the prevention of atrophy by exercise. (d)
Myofibrillar protein degradation will also be measured to fully
comprehend the overall contributions of exercise in altering synthesis,
degradation, or both in protein sparing.


By comparing individual proteins, which are hormonally-regulated in
opposing directions, basic knowledge can be obtained into whether the
exercise-related interference of muscle atrophy is mediated
preferentially through up-regulated or down-regulated proteins or both.
By quantifying protein synthesis, enzyme induction, and gene expression,
we will be able to assess the roles of transcriptional or translational
control to these processes.

## Key facts

- **NIH application ID:** 3159558
- **Project number:** 1R01AR039496-01A1
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **SAM.gov UEI:** W8XEAJDKMXH3
- **Principal Investigator:** ROBERT C HICKSON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $117,034
- **Award type:** 1
- **Project period:** 1989-04-01 → 1992-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159558

## Citation

> US National Institutes of Health, RePORTER application 3159558, EXERCISE AND MUSCLE ATROPHY PREVENTION (1R01AR039496-01A1). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3159558. Licensed CC0.

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