FUNCTIONAL ORGANIZATION OF FACIAL MUSCLES

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Facial muscle are unique forms of mammalian skeletal muscle. The long- range goal of this research is to define the biological properties of facial muscles relative to other skeletal muscles. This project will focus on the response of facial muscles to certain biomechanical alterations and pharmacologic counter measures. Micro-gravity and other mechanical unloading conditions produce significant morphological changes in skeletal muscles in the hind-limbs and body wall, and also cause redistribution of blood and interstitial fluid toward the head. Certain beta-adrenoreceptor agonists promote lean skeletal muscle mass, and may mitigate the effects of unloading on skeletal muscles in the limbs. However, the effects of unloading conditions of facial and other cranial muscles, and the mechanisms by which beta-agonists act are not understood. The two working hypotheses of this project are: (1) Facial muscles will undergo hypertrophic changes while hind-limb muscles will undergo degenerative changes in responses to generalized unloading conditions; (2) Facial muscle will undergo more dramatic hypertrophic changes than limb muscles in response to beta-adrenergic agonist therapy that is designed to counteract the effects of generalized unloading. These hypothesis will be tested via two specific aims. Specific Aim (1): Compare certain structural and functional properties (muscle mass, fiber type composition, muscle protein metabolism, muscle energy metabolism, beta-adrenoreceptor expression, muscle-specific gene expression) of the vibrissae-operating facial muscle and selected hind-limb muscles (soleus, plantaris, extensor digitorum longus) in the adult rat under normal and hind-limb-suspension conditions. Specific Aim (2): Compare the muscle properties defined in Specific Aim (1) in adult rats treated with the beta-adrenergic agonist clenbuterol under normal and hind-limb-suspension-suspension conditions. Defining the responses of facial and hind-limb muscles to generalized unloading conditions (Specific Aim 1) will help clarify how muscle structure and function are differentially maintained, and how altered leading promotes muscle atrophy and/or hypertrophy in muscle-specific and/or region-specific patterns. Defining the responses of the muscle to beta-agonist therapy (Specific Aim 2) will help elucidate the mechanisms underlying beta-agonist effects, and will also aid in devising effective multi-component counter-measures (e.g., exercise, nutrition, drugs, hormones) to muscle atrophy and/or hypertrophy under common conditions (e.g., in astronauts in a "weightless" environment).