Seminars

Georgia Tech Applied Physiology

Friday, March 29, 2013, 11:00 am - 12:00 pm

Location: College of Computing, Room 101

Integrating physiological, mathematical and 'musculo-robotic' tools to explore frog swimming and the design of vertebrate limbs

Chris Richards, PhD

Propulsion Physiology Lab Harvard University

Abstract

"A frog is a frog is a frog," wrote a famous poet. Comparative morphologists agreed, having observed stereotypical skeletal features making frogs unique among vertebrates. Meanwhile, motivated by separate interests, physiologists characterized intrinsic properties of frog muscle. Yet, despite our familiarity with frogs, the question of how they swim and jump as well as they do remains unanswered. How is this possible, given our rich knowledge of skeletal structure and muscle function? The unanswered question hints a broader issue: experimental biomechanics cannot directly test how muscle mechanics and skeletal morphology interact to determine locomotor performance. My research addresses this problem using aquatic frogs as a model. Integrating in vivo muscle techniques and hydrodynamic modeling, I found that aquatic frogs power swimming mainly from their ankle muscle (plantaris). In light of this, I developed a bio-robotic frog foot actuated by a living plantaris muscle in order to manipulate bio-robotic limb morphology, intrinsic muscle properties and motor control. My findings give new insight into how natural selection may adapt the morphological features of the skeleton to match the intrinsic properties of muscle (or vice versa). Specifically, I found that the contractile force and speed of the plantaris muscle are precisely 'tuned' to joint and webbed foot morphology such that frogs maximize muscle power produced as they swim. These findings may predict the limits of swimming speed across a broad range of size and timescales from aquatic insects to human rowing. Current and future work expands my 'musculo-robotics' tools to explore the musculoskeletal dynamics of walking, running and the evolution vertebrate limbs.

Georgia Tech Applied Physiology

Brown-bag seminar series

February 22, 2013 12:00 pm Room 1253, 555 14th St NW

Age-related changes in human skeletal muscle from the myosin molecule to the whole muscle

Mark S. Miller, Ph.D.

Department of Molecular Physiology and Biophysics University of Vermont

This seminar will focus on the effects of aging on human skeletal muscle and the use of a model system, Drosophila melanogaster (fruit fly), to help interpret the findings. Age-related skeletal muscle dysfunction and physical disability may be partially explained by alterations in the function of the myosin molecule. To test this possibility, skeletal muscle structure and function at the whole muscle, single fiber and molecular levels was measured in the knee extensors of young (21-35 years) and older (65-75 years) male and female volunteers matched for physical activity level. After adjusting for muscle size, older adults had similar isometric torque values compared to young, but had lower isokinetic power, primarily in females. At the molecular level, older adults, especially females, had slower myosin-actin cross-bridge kinetics (longer myosin attachment times and reduced rates of myosin force production), which may be explained by their reduced phosphorylation of the myosin regulatory light chain (RLC). The RLC phosphorylation decrease likely reduces cross-bridge formation by altering myosin’s orientation to actin, as found in Drosophila, an ideal system for examining muscle structure as measurements can be performed in living flies. Notably, cross-bridge kinetics in myosin heavy chain (MHC) IIA fibers correlated with whole muscle power output, indicating age-related changes at the molecular level decrease whole muscle dynamic performance in humans. A link between contractile and metabolic function was found as mitochondrial size was decreased in older adults, especially females, and was correlated to cross-bridge kinetics and whole muscle power output. These results are supported by Drosophila experiments that indicate mitochondria play a role in loss of flight ability with age. Collectively, our results show that age-related reductions in cross-bridge kinetics, most notable in females, represent a potential molecular mechanism underlying the development of physical disability with age. A possible future direction for this work is to evaluate rehabilitative interventions designed to increase cross-bridge kinetics, which may need to be sex-specific to address the unique cellular/molecular adaptations with age of males and females.