In today’s generation, especially in a college setting, the benefits of exercising is thrown around as a healthy method of stress management. This reminds me of Grandmas stuffing their kids with food because being "skinny" used to be seen as a sign of illness and weakness. Though forcing your grandchildren to eat an obscene about of food is an old concept, it got me thinking that every generation has a different epitome of health and thus, utilizes different methods in order to reach this standard. Though every generation may vary according to their epitome of a healthy life style, exercise is a universal method that even the smallest of species employ in order to increase their life expectancy.
Every animal can become victim to the detrimental effects of oxidative stress. In oxidative stress, free radicals are released from a malfunctioning mitochondria, which damage vital cellular proteins and DNA. In a normal functioning mitochondria, oxidative phosphorylation is responsible for the conversion or macronutrient energy to ATP (Lanza & Nair, 2009). Studies have linked oxidative stress to Parkinson’s Disease, Alzheimer’s Disease, Chronic Obstructive Pulmonary Disease, lung cancer, inflammation, and even death (Pastor et al., 2013). Furthermore, poor stress management can augment oxidative stress by changing the stress response signal pathway or the cellular and mitochondrial gene expression, and by increasing the number of oxidative stressors for the body to process (Dato, 2013). Healthy methods of stress management are obviously extremely important, and though some animals may not have conscious awareness of their own stress management tactics, they all employ different strategies in order to prolong a healthy life.
One strategy of stress management is exercise. The benefits of physical activity is extended to all species. Age and mitochondrial functioning are positively correlated (Lanza & Nair, 2009). Mitochondrial volume decreases with age because there is reduced gene transcription or mRNA instability with aging (Lanza & Nair, 2009). Thus, the mitochondrial DNA copy number decreases as well as the amount of supportive mitochondria in skeletal muscles (Lanza & Nair, 2009 ). Endurance exercise has been shown to reduce mitochondrial ROS production, protect against mitochondrial-mediated apoptosis, and increase the overall tissue capacity for oxidative metabolism (Lanza & Nair, 2009). Physical activity is correlated with longevity in humans, but this phenomenon can also be applied to the Caenorhabditis elegans
Caenorhabditis elegans Photo from http://genomics.nimr.mrc.ac.uk/online/worm-fl-db.html
The decrease in physical activity levels is a shared marker of aging that is shared among humans and the Caenorhabditis elegans worm. Different methods are implicated in different animals in order to manage stress and increase their longevity. In the C. Elegans, genes regulate their life expectancy (bec-1, Ce-atg7, AGE1 genes) by regulating mitochondrial autophagy (Lanza & Nair, 2009). Though there may be different cellular processes, anatomical differences, and behavioral adaptations across species, physical exercise is a stress management technique that can be seen across species.
Work Cited
Lanza, I. R., & Nair, K. S. (2009). Mitochondrial function as a determinant of life span. Integrative Physiology, 459(2), 277-289. Retrieved from http://link.springer.com/article/10.1007/s00424-009-0724-5/fulltext.html
Dato, S., Crocco, P., & D'Aquila, P. (2013). Exploring the role of genetic variability and lifestyle in oxidative stress response for healthy aging and longevity. International Journal of Molecular Sciences, 14(8), 16443-16472. doi: 10.3390/ijms140816443
Pastor, M., Nogal, A., & Molina-Pinelo, S. (2013). Identification of oxidative stress related proteins as biomarkers for lung cancer and chronic obstructive pulmonary disease in bronchoalveolar lavage. International Journal of Molecular Sciences, 14(2), 3440-3455.
You mentioned that C. elegans can increase their lifespan by regulating mitochondrial autophagy. I didn’t have a clue what “mitochondrial autophagy” actually was, so I looked it up! Autophagy, or “self-eating,” is a catabolic mechanism in which cells degrade superfluous or damaged cell material through the use of lysosomes, and is a mode of survival during starvation. More specifically, mitochondrial autophagy (mitophagy) is a way for cells to destroy dysfunctional mitochondria, eliminate ROSs, prevent cell death, and spur mitochondrial biogenesis.
ReplyDeleteWhile researching, I came across a study in which the authors found that there is a higher activation of autophagy in mouse skeletal muscle during endurance exercise in the fasted state. During endurance exercise, muscles become stressed and homeostasis is disturbed; in response to these physical stressors, remodeling and protein degradation occur, along with autophagy. New research has shown that activation of the lysosomal-autophagy pathway is critical for skeletal muscle adaptation after endurance exercise. In light of the importance of autophagy, Jamart et al. (2013) set out to find what physiological conditions optimize autophagy activation. Through examining autophagy related proteins and genes of exercised fasting and non-fasting mice, the authors found that autophagy and mitophagy in skeletal muscle was increased in fasting mice. These results suggest that fasting before exercise may increase the benefits of the activity, but of course this needs to be verified with further experiments.
Jamart C, Naslain D, Gilson H, Francaux M. 2013. Higher activation of autophagy in skeletal
muscle of mice during endurance exercise in the fasted state. Am J Physiol Endocrinol Metab [Internet]. [cited 2013 Nov 26]. 305: 964-974. DOI: http://10.1152/ajpendo.00270.2013 Available from: http://ajpendo.physiology.org/content/ajpendo/305/8/E964.full.pdf