Megan Hoffman
University of Dallas
Irving, TX
Faculty Mentor: Dr. Robert Fitts

Flights aboard the Russian space station Mir and more recently the international space station have shown that weightlessness induces muscle atrophy (up to 25% loss of calf muscle mass within six months), fiber type shifting (slow to fast), and increased susceptibility to damage upon reloading (return to 1-G). Effective countermeasures for these problems need to be developed before NASA can embark on exploration of Mars (approximately a three year project) and points beyond. To facilitate the goal, a rat model of weightlessness has been developed where the hind limbs are unloaded (hindlimb-unloading, HU) by tail suspension. The rat’s forelimbs remain on the ground allowing the rat full access to food and water.

Previous experiments have shown that the soleus, a weight-bearing muscle in the rat’s calf, develops lesions, due to a loss of myofilaments, termed central core lesions (CCL), after 12 days of HU. The lesions are observed by cross-sectioning the soleus and staining the muscle sections for myosin ATPase activity, revealing the presence/absence of myosin. These lesions lead to a loss of force and power and may contribute to the increased susceptibility to re-loading damage. During space flight in humans and rats and during HU in rats, the foot is plantar flexed (extended) which places the soleus in a shortened position. Our working hypothesis is that the shortened length rather than the condition of unloading or decreased electrical activity causes the CCLs.

A previous study showed that returning the rats to weight-bearing conditions for ten minutes twice a day significantly reduced the occurrence of CCLs. In order to determine if the change in length rather than reloading reduced the CCLs, another study was done, this time using a foot splint to passively stretch the soleus muscle while the rat was HU, two times, ten minutes per day. In this case the soleus muscle was lengthened but not re-loaded. The study was successful in significantly reducing the amount of CCLs due to HU. In the current work we tested whether a shorter duration of splinting time (10 minutes, once per day) would be sufficient to reduce CCLs. CCLs were significantly reduced in the splinted soleus with only 3.3% of the fibers having lesions, whereas 27.5% of the fibers in the non-splinted soleus contained lesions. These results suggest that the shortened muscle length is triggering the selective loss of myofilaments producing CCLs. However, the possibility remains that the splinting process not only lengthens the muscle but also increases the electromyographic (EMG) activity via a stretch activated reflex. In order to test this possibility, an additional study was done to determine the EMG activity of the soleus before, during, and after the splinting process.

EMG electrodes were implanted into two rats to measure the activity of the left and right soleus during twelve days of HU. The rat’s left foot was splinted once a day for 10 minutes each and EMG recordings were taken for 15 minutes before, 10 minutes during, and 15 minutes after the splinting process. The results showed a significant increase in the duration of EMG activity in the left (splinted) soleus compared to the right (non-splinted) soleus. The near constant activity of the muscle during the splinting process reveals that the reduction in CCLs cannot be attributed only to a change in muscle length until further studies are done that eliminate any force production or EMG activity. The mechanism by which the splint works to reduce CCLs during HU is still unknown and can be attributed to either a change in length, EMG activity, force production, or any combination of the above.