I am sitting at my desk, my legs are gently aching and I can feel - slowly but surely - that the muscles in my upper body are stiffening as well. As long as I stay absolutely still everything is alright, but as soon as I move my body protests heavily. My condition has a name: delayed onset muscle soreness or DOMS.
This highly common phenomenon usually presents itself 24-48 hours after an intense work-out of muscle groups that are not used to exercise. Though it has a slow onset, DOMS comes with a vengeance: it causes a weakness in the muscles that leaves you to wobble around, it drastically reduces the types of movements you are able to make, and the energy levels in you muscles are lower. What I find most shocking though is that it can last from 4 up to 7 days!
According to popular belief the pains are caused by lactic acid in the muscle, but no scientific proof has been given for this idea. The real cause has still not been unveiled. However, it is generally thought that the damage done to the muscle tissue causes inflammation of the muscle and the inflammation is what gives you pain.
Stretching your arms far away from your body to catch that impossible ball or trying a high kick are likely causes of DOMS. These actions require an extension of the muscle and in an untrained muscle may perhaps result in small tears in the muscle tissue. The weakest, most likely to be affected spots in your body are those places where muscles join tendons, but it is by no means limited to these places alone. In due course the soreness can, and often will, spread through the entire muscle.
What yields for every disease or disorder applies here too: not knowing the mechanisms behind DOMS does not make the search for cures and therapies easy. Many types of treatments have been tried and failed. Some non-steroidal pain killers such as ibuprofen may alleviate the soreness by damping down the inflammation. Massage techniques may, if applied at length, help too. Bathing in ice is – thank goodness – not a scientifically proven method to cure DOMS. There is one glimmer of hope though. An Australian research group at the university of Victoria in Melbourne found that when vibrations are applied to heavily exercised muscles, soreness does still occur, but to a lesser extent.
So, apart from using my vibrator to cause a buzz in my muscles, there is not much I can do. And even if there was, I wonder if I would. In a weird kind of way, I find this pain quite satisfying and addictive.
Thursday, 12 November 2009
Sunday, 8 November 2009
Brains powered by light
In the 1920s Felix the Cat had a brilliant idea and over his head a light bulb appeared; thus was created the signature of an epiphany. But recent advances in neuroscience leave you to wonder whether in the future a light bulb will be seen as the source of such inspiration rather than just the visual metaphor.
In the 1990s Peter Hegemann, a German biologist, discovered that green algae commonly found in ponds respond to light by wagging their tail, an interesting phenomenon given that they do not have eyes. When light photons hit the protein coils packed in the algae's cell membrane, a chemical reaction created a tiny gap, causing an ionic current to be produced and the algae's tail to wag. The protein that allowed this reaction is channelrhodopsin-2.
Some years later, American researchers started to wonder whether a similar mechanism could be used to control brain cells if certain neurons were made to behave somewhat like algae. By genetic engineering these scientists were able to do just this: not to make brain cells move but, using channelrhodopsin, to turn them on or off simply with light. The field of optogenetics was born.
What is so beautiful about this technique is that, by harnessing the cunning of viruses, it is possible to make the channelrhodopsin-encoding gene only be expressed in particular targeted neurons. And so far the results have been startling. Flies have been made to jump, mice made to walk in a certain direction, and both to remember events that never happened, all through the power of light. Optogenetics could therefore open the door to precise therapeutics in diseases such as Parkinson's disease and schizophrenia where presently only drugs or surgery can help, neural sledgehammers compared to the surgical scalpel enabled by light-controlled tools.
If its promise holds up, a bulb over someone’s head may someday be seen in a completely new light.
In the 1990s Peter Hegemann, a German biologist, discovered that green algae commonly found in ponds respond to light by wagging their tail, an interesting phenomenon given that they do not have eyes. When light photons hit the protein coils packed in the algae's cell membrane, a chemical reaction created a tiny gap, causing an ionic current to be produced and the algae's tail to wag. The protein that allowed this reaction is channelrhodopsin-2.
Some years later, American researchers started to wonder whether a similar mechanism could be used to control brain cells if certain neurons were made to behave somewhat like algae. By genetic engineering these scientists were able to do just this: not to make brain cells move but, using channelrhodopsin, to turn them on or off simply with light. The field of optogenetics was born.
What is so beautiful about this technique is that, by harnessing the cunning of viruses, it is possible to make the channelrhodopsin-encoding gene only be expressed in particular targeted neurons. And so far the results have been startling. Flies have been made to jump, mice made to walk in a certain direction, and both to remember events that never happened, all through the power of light. Optogenetics could therefore open the door to precise therapeutics in diseases such as Parkinson's disease and schizophrenia where presently only drugs or surgery can help, neural sledgehammers compared to the surgical scalpel enabled by light-controlled tools.
If its promise holds up, a bulb over someone’s head may someday be seen in a completely new light.
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