Icefish

In a perfect segue from the post below, if you do go swimming in Antarctic waters the picture to the left shows one of the strange creatures you might come across - the Antarctic Icefish (Chionodracus hamatus).

This fish lives in waters well below freezing and only just above the freezing point of salt water (about -2C). If you went swimming in water this cold wearing a Speedo then, as Lewis Pugh discovered, your cells would freeze and consequently suffer quite serious damage. If you stayed in more than a few minutes you would die.

So how does the ice-fish survive? The answer is that it has evolved an antifreeze glycoprotein in its blood. The glycoprotein molecules bind to ice crystals and prevent them from growing to a size where they would damage the fish’s body. Although this has been known since the 1960's work continues in this area, for example this paper, One-pot synthesis of cyclic antifreeze glycopeptides from earlier this year.

Of greater relevance to today's lecture is the strange clear, almost transparent, appearance of the fish. They are sometimes referred to as 'white blooded' because their blood contains no hemoglobin. Lots of antifreeze and no hemoglobin! So how do the fish survive? Well, remember that solubility of oxygen increases as temperature decreases. So the frigid waters of the Antarctic have considerably more oxygen in solution. Furthermore the blood plasma can hold more oxygen at low temperatures (for the same reason) and the animal's metabolic rate is lower. So the icefish can deliver sufficient oxygen to their cells in the plasma without requiring hemoglobin as a specific oxygen-carrying molecule. Cool.

It is not known whether there is any link between these two phenomena. It is not actually necessary for there to be a selective advantage to the loss of hemoglobin to explain its dissapearance (remember genetic drift?) but I can't help but wonder whether there is a link. For example if the presence of hemoglobin reduces the efficiency of the antifreeze.

If you want to read more then this 2006 paper will get you into the literature: When bad things happen to good fish: the loss of hemoglobin and myoglobin expression in Antarctic icefishes.

Anticipatory Thermogenesis

Yesterday Claudia mentioned that although control of the autonomic nervous system is generally considered to be involuntary we can, in addition, actually consciously influence many of these systems.

Posting a reference to Tim Noakes yesterday reminded me of his recent work with Lewis Gordon Pugh, a British 'Environmentalist, Explorer and Swimmer.'

Pugh is most famous for his cold water swims which he usually does to publicize global warming and the melting ice-caps. These swims are done without a wetsuit, in water as cold as zero degrees centigrade (because of the salt seawater freezes a couple of degrees below zero).

An article in New Scientist magazine a few months ago reveals some of the science behind Pugh's remarkable ability. Most interesting was the discovery by his trainer, the aforementioned Tim Noakes, that Pugh is able to consciously raise his body temperature.

As the swim gets closer, he psychs himself up by listening to music by the likes of Eminem and P. Diddy. In the minutes before entering the water, Pugh recalls these emotions and is able to raise his core temperature, without doing any physical exercise, to 38.4 °C. That's an extraordinary 1.4 °C above his normal body temperature. Such "anticipatory thermogenesis" has been observed before, but not to such a high degree.

You can read the actual paper in the appropriately named 'Journal of Thermal Biology': Body temperatures during three long-distance polar swims in water of 0–3 °C.

Pugh appears to have reached some of the limits of the human body:

In 2007 he swam 1 kilometre in the coldest water yet - a glacial -1.7 °C - at the geographic North Pole.

"When I went below 0 °C the cells in my fingers started to freeze. It took another four months before I could feel my hands again," he says. After reaching his goal of swimming both in the Arctic and in Antarctica, Pugh has for now hung up his towel.

Muscle pain - four recent(ish) papers and one new class

A good question today about why your heart never aches after exercise - after all, a good bout of exercise works your heart just as much, if not more, than any other muscle.

There's a simple answer, the heart doesn't have the same type of pain receptors as the muscles, but a fuller answer is much more interesting and shows some surprising gaps in our knowledge.

There are two types of muscle 'pain' associated with exercise. There is fatigue during exercise, and we don't really know what causes that, and there is pain after exercise (DOMS or Delayed Onset muscle Soreness), and we don't really know what causes that! The cause of fatigue is a pretty hot topic. One theory is that it is caused by a problem with the calcium flow inside muscle cells. One of the functions of calcium is to help control muscle contractions. Recent research published in PNAS found that after extended high-intensity exercise, small channels in the muscle cells begin to leak calcium, which leads to weakened muscle contractions. This leaked calcium also stimulates an enzyme that attacks muscle fibers and also leads to fatigue. It is really surprising to me that such a basic phenomenon is still fairly unknown.

DOMS is thought to be caused by a breakdown of muscle fibers and microscopic tears in muscle tissue that occurs as a result of exercise. This typically occurs 1 to 2 days after exercise, particularly if the exercise is new or extreme. There is also evidence that DOMS is more extreme if the muscle movement is eccentric - that is the muscle elongates whilst under tension (eg lowering a weight, starting out with your hand by your shoulder and gradually lowering the weight will produce an eccentric contraction of the biceps muscle).

It used to be thought that lactic acid was involved in both these phenomena but recent evidence suggests that lactic acid may have been unfairly blamed for years and that it may play a more useful role.

In both these cases actual pain is probably caused primarily by swelling which puts pressure on nerves and produces the sensation of muscle pain.

Although the heart does not have the same type of stretch receptor that registers this type of pain it does have some pain receptors. Strangely enough it has the same type of nerve receptors that register the burning sensation from the capsaicin in hot peppers. These are the receptors that are thought to cause the sensation of chest pain from a heart attack. The heart may be less vulnerable to DOMS since it does not undergo eccentric contraction.

All of this is somewhat complicated by the role of the brain. Obviously it is in your interest to stop exercising before damage occurs to your muscles, and, in particular, to your heart. Tim Noakes, a South African sports scientist, has renewed interest in a rather old theory, that Noakes calls the 'Central Governor Model', that the brain is the primary organ that dictates how fast, how long, and how hard humans can exercise.

As you can tell I find this whole intersection of physiology and exercise very interesting. So I have bitten the bullet and next quarter (ie Fall 2009) I will be teaching a CCS class on Endurance Physiology. This will be a seminar format class where we read and discuss papers very much like those listed above and look critically at the evidence for and against various theories and the implications these have for the way people train for what I have generally termed endurance events (swimming, cycling, and running or, for those crazy enough, all three). Loosely inspired by the fact that for the first time in over 25 years Santa Barbara will have a large Marathon event in the fall of 2009.

End the University as We Know It

Check out this Op-Ed, entitled 'End the University as We Know It' from the New York Times yesterday.

For many years, I have told students, “Do not do what I do; rather, take whatever I have to offer and do with it what I could never imagine doing and then come back and tell me about it.” My hope is that colleges and universities will be shaken out of their complacency and will open academia to a future we cannot conceive.

How many?

Dr Meg Lowman is the EEMB Seminar Speaker today (Monday 27th), 4:00 pm in the MSRB Auditorium in the MSI Building.

"Plant-insect interactions in tropical rain forest canopies - 10 million or 100 million species?"

Dr Lowman is Professor of Biology and Environmental Studies and Director of Environmental Initiatives, New College of Florida. Meg pioneered the science of forest canopy ecology, helping to develop the current techniques for canopy access and using them to study processes that maintain biodiversity in tropical forest canopies. Her most recent work focuses on environmental education and outreach, the role of science in environmental policy, and the development of research coordination networks (especially NEON).

Correlation Versus Causation

According to a study of the nearly 140,000 women who were enrolled in the Women’s Health Initiative, women who breast-fed their babies had a lower risk of developing heart disease and diabetes later in life than women who did not breast-feed their babies. The headline of the New York Times article about the research read “Breast-Feeding Benefits Mothers, Study Finds”. Is this a correct summary of the research?

The answer is “NO”! This is a classic case of the common misunderstanding about the relationship between correlation and causation. Yes, there is a clear correlation between breast-feeding and a lower risk of diabetes and heart disease later in life, according to the study. But that is not proof that the act of breast-feeding is what reduces the risk. What if women who breast-fed their children are just more health conscious overall throughout life? What if they exercise more often, or have healthier diets?

A more correct headline would be “Breast-Feeding May Benefit Mothers, Study Suggests”. Indeed, the article itself goes on to say that some experts are cautioning that an association (between breast-feeding and health benefits) does not prove a causal relationship, and that more research would be needed to determine the exact cause of the effect (lower risk).

More Llama

Hopefully some of you braved the hippies to see the Dalai Lama today. In other Llama related news BoingBoing had a great article today on how Llamas are involved in the war on terror - Llamas: Nature's Cute & Fluffy Crusaders Against Bioterrorism.

Llama blood may one day be able to help soldiers, scientists and city officials set up an early-warning system against the tiniest weapons of terror--biological agents like anthrax and smallpox. Authorities have long worried that, were these diseases to get loose, it would be difficult to know anything was wrong until innocent people started dying. Llama blood might provide a better detection method.

How? Antibodies, the tiny molecules that float around in the bloodstreams of people and almost all animals. Antibodies keep a sort of "memory" of all the diseases, allergens and other foreign invaders your body has come into contact with. If the same infiltrator shows up again, the antibodies can match it up with their stored records and immediately know how to fight it.
For a while now, scientists have used genetically altered antibodies to help ID and treat specific diseases. But these techniques always ran into a common problem: Antibodies were just too delicate to be of much use outside a lab or hospital setting. Enter the llama.

According to news stories about the research, llamas have extraordinarily tough and hardy antibodies, capable of sustaining exposure to temperatures as high as 200 degrees F. This discovery gave the researchers the idea to develop sensors, based on llama antibodies, that could be distributed to soldiers in a war, or around cities back home. Modified to be specifically on the lookout for likely-to-be-weaponized diseases, these sensors could pick up signs of a biochemical attack before victims started arriving at the hospital.