Healthy skeletal muscles are incredibly dynamic organs that are capable of adapting to a wide range of mechanical and metabolic stressors. For instance, repetitive loading leads to muscle growth, or hypertrophy, while disuse results in a loss of muscle size, or atrophy. Like most tissues in the body, skeletal muscle is also capable of repairing itself after damaging injury. Unfortunately, these processes of growth and repair often become short-circuited in old-age.
Aging itself is desireable - the only escape from aging is death. However, we all know that the effects of old age can be debilitating. There many contributors to age-related physiological dysfunction, including:
- altered communication between cells
- impaired cellular sensing of nutrients
- dysregulated protein synthesis and degradation
- mitochondrial dysfunction
- shortened telomeres
- unstable DNA
- cellular senescence
- loss of stem cells
- chronic inflammation
- epigenetic changes to gene expression
In my laboratory, our primary research interest is to understand the nature of age-related muscle dysfunction. This will be important in developing behavioral and pharmacological treatments for conditions where muscle mass is compromised. We are particularly interested in the loss of old muscle’s ability to maintain or increase its size and to repair itself after injury.
Secondarily, since we view insulin resistance (an underlying cause of type II diabetes) as a premature aging-condition (old and insulin-resistant muscles exhibit very similar dysfunctions), we are also interested in the regulation of muscle function in obesity and diabetes.
Provo, UT 84602