Muscle Biology Laboratory

“The Muscle Biology Laboratory aims to discover how skeletal muscle glucose metabolism is influenced by exercise, diet and aging. Our research targets insulin resistance, a primary cause of Type 2 diabetes, and aims to understand how individuals affected by insulin resistance can use exercise and diet to improve their health and well-being. The goal is to modify diet and exercise to be more effective and to develop alternative therapies for those physically unable to exercise.”
Dr. Greg Cartee, Director and Professor of Movement Science

Muscle Biology Laboratory


CCRB 1200
401 Washtenaw Ave.
Ann Arbor, MI 48109-2214
(734) 936-0281
(734) 936-1925



Mechanisms Responsible for Greater Insulin-Stimulated Glucose Transport after Exercise

The precise mechanisms that underlie this important benefit of exercise remain uncertain. We are currently performing experiments to fill this gap in knowledge. We are probing the processes that account for the sustained effect of exercise on phosphorylation of the key signaling protein called AS160 (also known as TBC1D4) and evaluating the role that AS160 plays in mediating exercise-induced improvement in insulin sensitivity. We recently performed experiments to evaluate exercise effects on muscle from both healthy rats (with normal insulin sensitivity) and obese and insulin-resistant rats. Both groups had greater AS160 phosphorylation and elevated insulin-stimulated glucose uptake. We are now trying to identify the mechanisms for the exercise effect on AS160 and determine if this effect on AS160 is required for increased insulin sensitivity after exercise. We are also performing experiments to determine exercise effects on glucose uptake by single muscle fibers of different fiber types.

Mechanisms Responsible for Greater Insulin-Stimulated Glucose Transport after Calorie Restriction

We have documented that animals (rats or mice) have increased insulin sensitivity for glucose transport in muscles from rats undergoing a moderate reduction in calorie intake (calorie restriction, CR). Our research has revealed that enhanced activation of a protein called Akt2 is the most robust effect of CR on the insulin signaling pathway that regulates glucose transport in skeletal muscle. We are performing experiments to elucidate precisely how CR acts on both Akt2 and glucose transport in whole muscle and single muscle fibers from young adult and older individuals.

Independent and Combined Effects of Exercise and Calorie Restriction in Old Age

Because the development of whole body insulin resistance is integral to many age-related diseases, identifying and understanding treatments that improve glucose homeostasis during old age has important health implications. Either calorie restriction [CR; consuming 65% of ad libitum food intake] or acute exercise can independently improve insulin sensitivity in old age, but their combined effects on muscle insulin signaling and glucose uptake have previously been unknown. Therefore, we are testing the independent and combined effects of CR and a single bout of exercise on insulin signaling and glucose uptake in insulin-stimulated skeletal muscles from older rats.

Regulation of Glucose Uptake by Single Muscle Fibers

Skeletal muscle is a heterogenous tissue composed of many fibers with different functional characteristics, and to fully understand skeletal muscle at the cellular level, it is essential to evaluate single muscle fibers.  We recently developed and validated a novel method to determine both glucose uptake and fiber type in a single rat skeletal muscle fiber, making it possible to compare glucose uptake by single fibers of different fiber types from the same muscle.  We aim to use this model to test for potential fiber type differences with exercise or dietary interventions that influence muscle insulin sensitivity.