Thursday, October 8, 2009

Grad Student in Australia to Discuss Exercise and Aging Tissue

Sure, exercise is good for the body. But what about the cells?

This is exactly what Kinesiology doctoral student, Andrew Ludlow, and his research team spent a year studying. He is currently in Australia to present their findings at the Keystone Symposia in Ashmore, Queensland.

The team's research revealed an accelerated shortening of the telomeres in Cast/ei J mice, indicating aging tissue, resulting from increased exercise.

Andy was kind enough to talk with the Healthy Turtle amidst packing for the big trip Down Under.

***
Healthy Turtle: So your research is about the telomere shortening in Cast/ei J mice. In my own advanced Wikipedia research, I found that means it has something to do with limiting cell division. Am I right?
Andy Ludlow:
Telomeres are considered a biomarker of aging and cell division. Telomeres shorten with each round of cell division, and it has been observed that as we age, our telomeres get shorter. Also, the Hayflick Limit theory states that when telomeres reach a critical length (i.e. too short) the cell can no longer divide, and thus over time as cells can no longer divide and replace damaged cells, tissue ages.

HT:
Even Wikipedia couldn't answer this question: What are Cast/ei J mice?
AL: Cast/EiJ mice are a wild-derived inbred mouse strain of laboratory mice. I choose to use this strain because they have shorter telomeres (i.e. more human like) than other typical laboratory mice.

HT: So in a nut shell, for the non-kines people out there like myself, what's the message of your presentation?
AL: The basic premise behind this research was to determine (observe) how chronic voluntary physical activity effected telomere biology. We know exercise is good for us and that remaining active may help us live longer or at least healthier, but we do not know what happens to the cells after a lifetime of chronic activity.

HT: How did you research this?
AL: We separated this mice into two groups, exercise and sedentary. We gave the exercise mice access to a running wheel, while the sedentary mice did not have access to a wheel. We were able to monitor the amount of exercise the mice performed by a computerized wheel monitoring system. After a year, we performed telomere length, telomerase enzyme active and multiple targets of gene expression that are known to be related to telomeres.

HT: How did SPH support your research?
AL:This research was funded by NIH and a graduate research initiative program grant (from the Kinesiology department) that I was awarded.

HT: Why is it important that we understand what happens to a bunch of mice under high levels of physical activity?
AL: Using mice as a model organism is beneficial to study telomeres because studying humans would take an entire lifetime to see the effects of chronic physical activity. We can also compare many different tissue types that we would not be able to get from a human subject. Also mice are voluntarily active and genetically identical which removes genetic variation from confounding our results.

***

Thanks Andy, and good luck in Australia!

1 comment:

  1. Interesting that the Nobel prize in Physiology/Medicine went to scientists studying telomeres and telemerases as well. Good job, Andy, but stay away from those great whites!!!

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