Muscle Fatigue - Annotated Bibliography

Muscle Fatigue - Annotated Bibliography

Muscle fatigue has long challenged researchers in human physiology, because of the significant ramifications of this bodily function. This month (February), Columbia University Medical Center (Bellinger et. al., 2008) confirmed findings that a "leak allows calcium to continuously leak inside muscle cells and weakens the force produced by the muscle and also turns on a protein-digesting enzyme that damages the muscle fibers," (Kolata, 2008).

Annotated Bibliography

Bellinger, a.M., Reiken, S., Dura, M., Murphy, P.W., Deng, S., Landry, D.W., Nieman, D., Lehnart, S., Samaru, M., LaCampagne, a., & Marks, a.R. (2008). Remodeling of ryanodine complexes causes "leaky" channels: A molecular mechanism for decreased exercise capacity. Proceedings of the National Academy of Sciences 105 (6): 2198-2202. Retrieved February 23, 2008, at http://www.pnas.org/cgi/content/abstract/0711074105v1?etoc

The authors, led by physiologist Andrew Marks of Columbia University, report that leaky calcium channels can provoke muscle fatigue. During usual muscle function, a neuron causes the release of calcium within a muscle cell, which makes the muscle proteins contract. The protein calstabin shuts the calcium channels during the contraction until they are "told" to open. The team had observed that calstabin does not function well in mice with heart failure. The heart cells are left without the calcium necessary for contraction, causing heart exhaustion. Now, the team checked if the same thing happens in case of muscle fatigue.

Lab mice swam daily for two, ninety-minute sessions, for two weeks. The group of control mice swam fifteen minutes twice daily. Similar to failing heart muscle, the calcium channels of the mice with greater physical exercise had turned chronically leaky; they had to rest for days to recover. When the researchers analyzed the calcium-channel structure in muscle samples from twelve elite athletes before and after a series of intense cycling sessions, their calcium channels were undergoing changes parallel to the mice.

Bellinger, a.M., Mongillo, M., & Marks, a.R. (2008). Stressed out: the skeletal muscle

Ryanodine receptor as a target of stress. Journal of Clinical Investigations. 118(2):

In this report prior the researchers addressed overall present understanding of muscle fatigue. For decades, the mechanisms underlying muscle fatigue and weakness were the emphasis of numerous studies. The dominant theory was that lactic acidosis caused muscle fatigue. However, dysregulation of sarcoplasmic reticulum (SR) Ca2+ release has been associated with impaired muscle function induced by a variety of stressors, from dystrophy to heart failure to muscle fatigue. Here, the authors addressed the topic of the altered regulation of SR Ca2+ release during chronic stress and focused on the role the release channel known as the type 1 ryanodine receptor plays.

Kolata, G. (2008, February 12.). Finds may solve riddle of muscle fatigue in muscles.

New York Times. Research. Retrieved February 23, 2008 at http://www.nytimes.com/2008/02/12/health/research/12musc.html?ref=science