Author Archives: The Physiological Society

About The Physiological Society

The Physiological Society brings together over 3,500 scientists from over 60 countries. Since its foundation in 1876, its Members have made significant contributions to our knowledge of biological systems and the treatment of disease. We promote physiology and support those working in the field by organising world-class scientific meetings, offering grants for research, collaboration and international travel, and by publishing the latest developments in our leading scientific journals, The Journal of Physiology, Experimental Physiology and Physiological Reports.

The Ultra Cycle Diaries – Man vs Heat

A word of advice to budding ultra-cyclists: don’t climb steep hills in a heat wave! High temperatures came to define a large portion of my cycling race across Europe, especially the further eastwards I rode. On many days, the mercury pushed above the 40⁰C (104⁰F) mark and even reached 50⁰C (122⁰F) one day. The biological effects of physical exertion in high ambient temperatures are important to understand, especially if you plan on doing something like the Transcontinental Race.

Slowed down by Lucifer

Over exertion in the heat can increase core body temperature to an abnormal level and lead not only to a significant reduction in performance but more importantly to heat-related illnesses, such as heat stress, exhaustion and stroke. While these differ in severity, they share symptoms, including muscle weakness, dizziness, nausea and loss of appetite. I was acutely aware of the dangers of over-exerting myself in the heat, but because I was in a race, I did it anyway: competition is known to cause competitors to focus on the race so much they ignore sensory cues! That’s how I ended up climbing mountain roads that were not tree lined, in more than 40⁰C (104⁰F). Climbing up against the pull of gravity means the body has to work harder and consequently, generate more heat. You also go slower uphill, meaning there is limited moving air to evaporate sweat and cool the skin. The data I’ve collected show how temperature affected my performance.


Take a look at these two climbs (in grey), that I did quite early in the race, on consecutive days: Timmelsjoch in Austria followed by Monte Grappa in northern Italy. If we look closely we can see that on average, temperature (orange) was much higher when I climbed Monte Grappa than when I climbed Timmelsjoch. And whilst heart rate (red) is similar, power output (white) is much lower during the climb to the summit of Monte Grappa – I even stopped completely to cool down. A decrease in power output could be attributed to fatigue from the first climb, except that I did much better on another huge climb even later in the race… when the average temperature was much lower!

Your body in a heat wave

At ‘normal’ temperatures, 10-25⁰C (50-77⁰F), exercise feels comfortable; if temperature increases to over 35⁰C (95⁰F), the same intensity of exercise gets more difficult and cannot be maintained as long. Why? In both settings, exercise increases the amount of heat produced by our metabolism, but the way the body copes with it is affected by the temperature. In lower temperatures there is a large difference between the body temperature (high) and ambient temperature (low). Heat naturally travels down a thermal energy gradient towards the lower temperature environment so the body gets rid of the extra heat easily (using convection, conduction and radiation for those of you who did GCSE Physics). In addition, and to facilitate greater heat loss, sweating allows the surface of the skin to cool when sweat evaporates; this process relies on the energy state change: evaporation of liquid sweat into gas uses up heat, leaving the skin cooler. Now, when the ambient temperature is above the core temperature the human body, the usual processes of convection conduction and radiation happen very slowly, if at all. The body then relies a lot more on sweating; however, sweating too much causes dehydration and excessive loss of salt and minerals called electrolytes, with severe implications for performance and health (Cheuvront et al., 2010).

For example, in hot conditions blood vessels near the skin dilate, allowing blood to flow closer to the surface of the skin to cool it down – hence the red face. Heart rate increases to help fill these now larger blood vessels, yet because of sweating and dehydration, blood volume and blood pressure go down, making it even harder to fill the heart: the volume pumped per heart beat actually becomes smaller! This creates stress on the heart whilst it works hard to pump blood to all of the body’s tissues and organs. These constraints definitely place a limit to how much humans can safely exert themselves in the heat (Gonzalez-Alonso et al., 2008)!


Beating the heat

It is worth noting that a person’s ability to cope with high temperatures during physical exertion is not set and can be improved by training. For example, a two-week acclimation protocol of training at 40⁰C (104⁰F) ambient temperature can lead to increased sweating, retention of electrolytes by sweat glands and expanded plasma volume, all of which compensate, to a degree, for the problems highlighted above. But it’s important to note that you would need to drink more water, not less. It is a common misconception that acclimatising to heat means having to drink less water!

As for me, heat wasn’t the only thing that gave me trouble during the Transcontinental Race… tune in next week for a new episode.

Make sure you follow the blog and subscribe to our Youtube Channel to keep up with the Ultra Cycle Diaries. Check back every Wednesday for a new blog and video!


Cheuvront SN, Kenefick RW, Montain SJ & Sawka MN. (2010). Mechanisms of aerobic performance impairment with heat stress and dehydration. J Appl Physiol (1985) 109, 1989-1995.

Gonzalez-Alonso J, Crandall CG & Johnson JM. (2008). The cardiovascular challenge of exercising in the heat. J Physiol 586, 45-53.

Sir Roger Bannister and Exercise Physiology

Bannister_publicdomain_600pxBy Mark Burnley, University of Kent, UK.

On Saturday March 3, 2018, Sir Roger Bannister, the first person to run a mile in under 4 minutes, passed away. His run on the Iffley track in Oxford in May 1954 was one of the defining athletic feats of the 20th century. In reading Bannister’s autobiography, however, it is striking just how much one man managed to pack into life, and how relatively little of it was concerned with athletic performance. He was an amateur athlete whose career pathway was already chosen, and that career was clinical medicine.

Sir Roger Bannister was a neurologist first and an athlete second. This goes some way to describing how good he was at neurology! He published 81 papers on the part of our nervous system that controls involuntary actions like breathing (called the autonomic nervous system). He also wrote and edited several texts on disease in this system.

Bannister’s investigations of the physiology of the respiratory system during exercise took place during a research scholarship in the University Oxford’s Laboratory of Physiology in 1951. It may surprise you to know that this had nothing to do with his interest in athletics. Bannister was instead interested in respiratory control, and exercise was merely a means of testing stress placed on this system. This work was published in The Journal of Physiology in 1954.

In this study, he explored the effect of oxygen levels on the movement of air in and out of the lungs (called ventilation), and on physical performance. To do this he had participants, including himself, run at constant speeds and breathe room air, with 33%, 66%, and 100% oxygen. At the time, the reason for the reduction in ventilation and improvement in physical performance when breathing oxygen-enriched gases was not clear.


Roger Bannister in 2009. © Pruneau / Wikimedia Commons, via Wikimedia Commons

Each of Bannister’s four participants is identified by initials, which is of course not allowed now. We know of three for certain (Bannister and his supervisor, Dr Dan Cunningham, who co-authors the paper, as well as Norris McWhirter [N.D.McW]). The latter was able to run with relative ease breathing 66% oxygen, and only terminated the treadmill test because “he had a train to catch”!

Throughout the paper, Bannister seems to interpret his results as a clinician: the participant’s subjective experiences of the tests seem almost as important as the respiratory variables themselves. In light of the sometimes extreme volume of data modern laboratory technology can produce, we shouldn’t forget to ask participants in physiological research how it felt.

Physiological research requires interactions with people in other ways too. In his acknowledgements, Bannister thanks, among others, Prof. Claude Douglas for help and advice. Where would exercise physiology be without Douglas? Everybody stands on the shoulders of giants. Even other giants do.

Sir Roger Bannister was special because he was an ordinary man who produced an extraordinary life’s work: on the track, in the laboratory, as a patron and administrator in sport and sports medicine, and in his clinical practice. His humanity shone through in everything he did, and his The Journal of Physiology papers are no different. Thanks for everything, Sir Roger.

The Ultra Cycle Diaries – Setting off on the Transcontinental Race

At 21:59 pm on the 28 July 2017, I was sat on the saddle of my bike in the market square in Geerardsbergen, Belgium. One minute later I was racing my bike up a famous steep cobbled path called the Muur of Geraardsbergen hoping to complete challenge of a lifetime!

My name is Daniel Brayson, and most of the time I perform lab experiments at King’s College London, investigating the causes of a heart muscle disease called cardiomyopathy. By nature I am a restless individual and being confined to the lab environment, while a worthy cause, can lead me to become, well… restless! I like the notion of travel and adventure and have always considered myself an active individual. It was these traits which led me to take on the Transcontinental Race.

A self-supported race across Europe

The Transcontinental Race is the most notable of many emerging self-supported ultra-endurance cycle races. It traverses Europe from west to east, eating up 3500 – 4000 km depending on the route, which is never the same from one year to the next. It begins in Geraardsbergen in Flemish Belgium, finishing in previous years in Canakkale, Turkey and more recently at the UNESCO site of the ancient monasteries of Meteora, Greece.
The race is a series of checkpoints between which the route taken is the decision of the rider. As well as endurance fitness, this race tests mapping and planning skills: it is a survival race rather than a mere bike race, orienteering on two wheels if you will, which for many is part of the appeal.

Unlike stage racing with a daily start and finish time (i.e. the Tour de France), when the clock starts in the Transcontinental Race, it does not stop until you cross the finish line. It is at the discretion of the rider to decide when and where to stop, eat and sleep and is completely self-supported. One can use commercial outlets to buy supplies and even stay in hotels, as they are available to all other riders. However, the use of support teams, stopping at international friends’ houses en-route, or posting supplies to various points along your route, is strictly forbidden. All of these factors increase the logistical complexity of the race and it means that anything one may lack in physical fitness could well be compensated for with experience and know-how. Again, for many, this is part of the appeal.

A physical and psychological challenge


Riders are subjected to a unique set of demands and conditions during such races. Physically, increasing levels of fatigue may seem like an obvious hurdle to success, but experiencing this on the backdrop of having to think about your nutritional, rest and sleep requirements is also psychologically demanding. Environmental challenges such as extreme temperatures – hot days and cold nights – add to the demands, as does topography: climbing mountain roads is a challenge, but even more so above 2000 metres where oxygen starts to become sparse! Needless to say, that as a scientist I viewed these challenging demands as an exciting opportunity to try to observe and quantify the effect these have on the body in the field. So I did…

A physiological case study

Inspired by famous historical proponents of field and self-experimentation such as Griffith Pugh, who conducted field work into altitude physiology, discovering the secrets that put the first man on the summit of Everest, and Barry Marshall, who fed himself bacteria to prove the origins of stomach ulcers (and won a Nobel prize), I armed myself with a few lightweight gadgets before heading to the starting line of the 2017 Transcontinental Race.

The gadgets I had stowed away included a small device to measure sugar and fat from blood samples taken from pricking my finger, and a pulse oximeter, a device that clips onto the end of one’s finger to measure the percentage saturation of oxygen in the blood. On my smartphone, I had downloaded a cognitive test called the Stroop Test, to assess mental fatigue. I also had a bike computer that recorded metrics like heart rate, distance, elevation climbed and environmental temperature.

To find out if I was able to finish the race, tune in to the next episodes where I’ll take a more detailed look at the impact of ultra-endurance racing on my physiology!

Make sure you follow the blog and subscribe to our Youtube Channel to keep up with the Ultra Cycle Diaries. Check back every Wednesday for a new blog and video!

The shear effect of exercise

By Abigail Cook, University of Leeds, @abbycook94

Exercise is good for you. We see this statement daily in one form or another, whether it’s on social media, as advice from medical professionals or making headlines in the news. We know it’s good for our hearts, keeping our weight under control and is even beneficial for our mental health. A question I am often asked is: why is exercise so good for us? My research focuses on the effect of exercise on human arteries and the cells lining these arteries.

Helping blood vessels saves the heart

Cardiovascular disease (CVD) is one of the leading causes of death in the Western world and is responsible for 25% of all deaths in the UK (BHF, 2017). Only 60% of CVD cases, however, can be explained by traditional risk factors such as fat, high blood pressure, and diabetes (Mora et al., 2007). Of the rest, changes to blood vessels appears to play a major part.


Thus, targeting blood vessels appears to be an attractive way to reduce poor functioning of the blood vessels and CVD. As exercise directly impacts blood pressure, heart rate and the quantity of blood leaving the heart per beat, it provides a method of reaching this target without using drugs.

This is especially important given that physical inactivity is the fourth highest risk factor for mortality worldwide. Also physical fitness, when assessed by aerobic capacity (the maximum oxygen consumption in an exercise session), is the strongest predictor of death in populations with and without CVD.

The scene inside our blood vessels

For the appropriate amount of blood to be delivered to our organs and tissues, arteries need to widen appropriately. One of the key molecules that tells the arteries to widen is nitric oxide (NO). NO is produced by the inner lining of the blood vessel. Its release is controlled by the force, which I study in the lab, called shear stress, applied by blood to this lining.


Shear stress can be characterised in different ways, with each form resulting in different responses from the inner lining of the vessels. High levels of unidirectional shear stress occur in the straight sections of blood vessels. This is associated with the production of molecules that fight inflammation, which protect the cell from abnormal growth and proliferation, and even cell death. Low levels of bidirectional shear stress are most often found at curvatures and at branches of blood vessels. This type of shear stress generates molecules that are associated with inflammation.

The areas that are exposed to low levels bidirectional shear stress are at the greatest risk of developing atherosclerosis (a type of CVD), the disease where an artery becomes narrowed due to the build-up of plaques. Prolonged exposure to this type of shear stress can lead to dysfunction of the inner lining of blood vessels, which is an early indicator of CVD.

Exercise lends a helping hand

The ideal shear stress throughout the vasculature to minimise the likelihood of developing CVD such as atherosclerosis would be high levels of unidirectional shear stress. One way of increasing shear stress is by exercising.

Exercise increases heart rate, cardiac output, blood flow, and thus shear stress. Undertaking regular exercise has been shown to be protective against atherosclerosis and slow down the progression of CVD. It is unclear, however, what type of exercise training is most beneficial to the blood vessels. Continuous exercise may provide steady levels of shear stress, whereas interval exercise may allow shear stress to vary throughout exercise from a low to a high level.


My research uses ultrasound and MRI technology to understand the patterns and levels of shear stress applied to arteries during differing exercise protocols. The arteries of interest are both are susceptible to developing atherosclerosis (the aorta and the common femoral artery), and they can be monitored during an exercise protocol.

This is especially important in the common femoral artery as it is directly supplying blood to the working muscle during exercise. Then, I am examining what happens when these patterns and levels are replicated in cells grown in the laboratory, in order to see which type of exercise enhances cell function most effectively.

BHF. (2017). Cardiovascular Disease Statistics 2017. BHF.

Mora S, Cook N, Buring JE, Ridker PM & Lee IM. (2007). Physical activity and reduced risk of cardiovascular events: potential mediating mechanisms. Circulation 116, 2110-2118.

The female athlete: A balancing act between success and health

By Jessica Piasecki, Manchester Metropolitan University, UK, @JessCoulson90

A longer version of this article originally appeared in Physiology News.

There is a very fine line between training, competition, and recovery for the elite athletes (1). For female athletes, they have an extra balance to take into consideration: the menstrual cycle.

The monthly cycles

The menstrual cycle is a natural process and is essential to maintain bone health and fertility. It can start from the age of 12 and continues until the onset of menopause around the age of 49-52.

The cycle occurs over a period of 28 days. The first 14 days are known as the follicular phase. During this phase, around day 10, the hormones oestrogen, LH (luteinizing hormone) and FSH (follicular stimulating hormone) rise, reaching their peak around day 14.

LH reaches a level double than that of both oestrogen and FSH. After day 14 LH levels rapidly drop off while oestrogen and FSH fall off more slowly, over a 5 day period. The second 14 days are known as the luteal phase and there is a gradual increase in another hormone, progesterone, which reaches a peak around day 22 and returns to base levels at day 28.


Bone stability and structure

Of these three hormones, oestrogen is a key regulator of bone resorption, without oestrogen there would be an excess of bone being broken down over new bone being formed. Bone is in a state of constant turnover, with the help of two types of bone cells (osteoblasts and osteoclasts). Osteoblasts are involved in bone formation, while osteoclasts are involved in bone resorption.

Bone resorption occurs at a much higher rate than formation; bone resorption takes just 30 days whereas the bone remodelling cycle takes 4 months. Therefore, a slight imbalance can lead to a bone fracture very quickly (2).

More is not always better

Elite female athletes, particularly those involved in sports that usually adopt a leaner physique with low body fat, are at a greater risk of disordered eating. The reasons for this disordered eating could be external pressures from teams, coaches and sponsors, or the athletes themselves having the belief that the leaner and lighter they are, the quicker they will be. These pressures may also cause the athlete to push their body to further extremes.


Without the necessary energy intake, the menstrual cycle will most likely become irregular and eventually cease (which is known as amenorrhea). Amenorrhea causes the levels of oestrogen to become reduced, leaving a disproportionate ratio of osteoblasts and osteoclasts, and a higher rate of bone resorption.

This may ultimately lead to bone injuries, (the precursor to osteoporosis), or even osteoporosis at a very young age, making any further career achievements even more difficult.

These three symptoms (disordered eating, amenorrhea and osteoporosis) became more prevalent in the 1990s and were termed ‘The Female Athlete Triad’ in 1997 by the American College of Sports Medicine. It has been estimated that only 50% of trained physicians are knowledgeable about the female athlete triad (3). More recently the triad has been regrouped within a term known as RED-S (Relative energy deficient syndrome); deemed to result from continual disordered eating. Being in a state of energy deficiency for a long duration can disrupt many processes within the body, including the cardiovascular, digestive and hormonal . Redefining the RED-S also allows male athletes who present with similar issues to be included (4).

Current research has looked at the differing effects of the components of the triad on injuries, and bone and muscle health. At Manchester Metropolitan University, we have carried out our own research on some of the UK’s most renowned female endurance runners, investigating the effects of altered menstrual cycle on bone health. Athletes with amenorrhea presented with a greater endocortical circumference (the outer circumference of the inner cortical bone in the tibia (lower leg) and radius (forearm) than controls. Only the athletes with regular menstrual cycles (eumenorrheic) had a greater cortical area, in the tibia and radius, compared to controls. The athletes with amenorrhea had thinner bones (i.e. larger but not denser). We are working to better understand the issues, so accurate diagnosis will become more frequent.

What we really need is education at a young age, as most athletes become familiar with the triad only once they have been diagnosed with a bone injury. If athletes are made aware of the symptoms and issues around the triad before they occur, then nutrition and menstrual cycles can be more closely monitored as they progress through their athletic careers.

Read the full-length version of this article in our magazine, Physiology News.


  1. Barnett, A (2006). Using recovery modalities between training sessions in elite athletes does it help? Sports Med (36), 781-96
  2. Agerbaek, M. O., Eriksen, E. F., Kragstrup, J., Mosekilde, L. and Melsen, F. (1991) A reconstruction of the remodelling cycle in normal human cortical iliac bone. Bone Miner, 12 (2), pp. 101-12.
  3. Curry, E, Logan, C, Ackerman, K, McInnia K, Matzkin, E (2015) Female athlete triad awareness among multispecialty Physicians. Sports Med Open. 1:38.
  4. Tenforde, AS, Parziale, A, Popp, K, Ackerman, K. (2017) Low Bone mineral density in male athletes is associated with bone stress injuries at anatomic sites with greater trabecular composition. Am J Sports Med. DOI: 10.1177/0363546517730584

Tight squeeze: a new way to get larger drugs into the brain

by Michelle Pizzo & Robert Thorne, University of Wisconsin Madison, USA

The brain and spinal cord are a difficult body parts to fix. Only seven percent of drugs for diseases of the brain and spinal cord succeed, whereas fifteen percent of drugs for other parts of the body do (1). New research published in The Journal of Physiology may have found part of the solution: a method for getting bigger drugs into the brain.

The issue is, in part, that we still lack a detailed understanding of the complicated structure and physiology of the brain’s cells and fluids, including the communication between the cells and fluids (2). This limited knowledge has further compromised our understanding of the delivery and distribution of drugs in the central nervous system (brain and spinal cord, abbreviated as CNS), particularly for large-molecule drugs (bigger than about one nanometer) which are unable to cross the blood-brain barrier to reach the brain tissue.

A tight fit: getting big antibody drugs into tiny brain spaces

Among the best examples of promising large-molecule therapeutics are antibodies, the weapons of our immune system. They work by recognizing a part of a molecule (called an antigen). Indeed, five of the top ten drugs by revenue are antibodies (3).

Besides being great potential drugs, antibodies are very abundant in the fluid that bathes the brain and spinal cord (called cerebrospinal fluid, or CSF) (4). Antibodies in the CSF may play an important role in the brain’s immune system and contribute to central nervous system autoimmune disorders (like multiple sclerosis) that cause our immune system to attack our own body.

Because antibodies (and other large-molecule protein therapeutics) are 10 times the size of small-molecule drugs, it has long been thought that their distribution in the brain will in most cases be much more limited than small-molecule drugs (5).

However, a recent study published in The Journal of Physiology from the University of Wisconsin-Madison by Michelle Pizzo, Robert Thorne, and their colleagues (6) has uncovered an unappreciated key mechanism governing antibody transport within the CNS that may ultimately allow these big proteins to access much more of the brain from the CSF than previously thought.

This has important implications as there are numerous clinical trials that are ongoing in the United States for treatment of brain cancers with antibody drugs.

Go with the flow: using the fluids of the brain for antibody drug delivery

Injecting antibodies of two different sizes into the CSF of rodents, the researchers found two main mechanisms of transport—1) slower movement (called diffusion) in between the tightly packed brain cells, and 2) quicker transport along tubular spaces around blood vessels, (called perivascular spaces) (6).

As expected, they found that the slower movement of these large molecules by diffusion was quite limited, whereas the smaller antibodies penetrated further. Aspects of the quicker transport around the blood vessels appeared to be independent of size; both the smaller and larger antibodies could reach deep into the brain along the walls of blood vessels in a short amount of time.

This is great news for the CSF delivery of biotherapeutics, including protein drugs like antibodies. The quicker perivascular flow along these tubular pathways is thought to exist in humans, so such flows are likely translatable/scalable to the clinic. Slower, diffusive transport, on the other hand, does not scale across species. In other words, if effective drug diffusion is limited to a distance of one mm in the rat brain, it will also be limited to one mm in the much larger human brain. This distance may not be enough to treat most brain diseases.


A large, full-size antibody protein (green) infused into the fluid bathing the brain (cerebrospinal fluid) reaches deep into the brain along the spaces around blood vessels (red). Nuclei of all the brain/blood vessel cells are labeled in blue. (Photo credit: Michelle Pizzo)

They also found that the smaller antibody was able to get into more of these tubular perivascular spaces compared to the larger antibody, which meant a significantly poorer overall delivery was obtained for these full-sized antibodies. Two questions arose from this finding—1) what barrier is causing this size-dependent entry into the perivascular space, and 2) can the barrier be altered to improve delivery?

Let me in: identification of a new barrier between the CSF and brain and a strategy to open it

Pizzo and her colleagues found that a layer of cells wrapping around blood vessels on the surface of the brain, between the CSF and the perivascular spaces, is a likely candidate for the size-dependent barrier.

They suggested that pores or openings in these cells may contribute to a sieving effect, allowing smaller molecules into the perivascular space but making entry more difficult for larger molecules. A method that has previously been used to open cell barriers is to administer a hyperosmolar (which more or less means, concentrated) solution that makes these cells give up their water to dilute the surrounding solution. Thus the water exits the cells (by osmosis) and causes them to shrink, allowing gaps between cells and pores in the cells to open. Pizzo and colleagues then reasoned that if they were to administer this solution into the CSF, the larger antibodies would enter the perivascular spaces better.

This is essentially what they found; the larger antibody had significantly greater access (about 50%) to the perivascular spaces when it was delivered into the CSF with a hyperosmolar solution.

Numerous studies of protein drugs administered into the CSF are ongoing for brain cancer and childhood metabolic diseases that affect the brain (called neuropathic lysosomal storage disorders). Thus, an improved understanding of how these large molecules move through the brain is critical.

This new research has shed light on how these antibodies use different types of transport to move between the CSF and the brain in rodents, revealing that fast perivascular transport can reach deep into the brain and may offer the best hope for translation to humans.

Even more exciting is their new hypothesis for the cellular barrier that may regulate entry into these perivascular spaces. Manipulating this ‘barrier’ could lead to improved methods for delivery of drugs to the brain and spinal cord.


  1. Pangalos MN, Schechter LE, Hurko O (2007) Drug development for CNS disorders: strategies for balancing risk and reducing attrition. Nat Rev Drug Discov 6(7):521–32.
  2. Thorne RG (2014) Primer on Central Nervous System Structure/Function and the Vasculature, Ventricular System, and Fluids of the BRain. Drug Delivery to the Brain: Physiological Concepts, Methodologies, and Approaches, eds Hammarlund-Udenaes M, de Lange E, Thorne RG (Springer-Verlag, New York), pp 685–707.
  3. Lindsley CW (2015) 2014 global prescription medication statistics: strong growth and CNS well represented. ACS Chem Neurosci 6(4):505–506.
  4. Davson H, Segal MB (1996) Physiology of the CSF and blood-brain barriers (CRC Press).
  5. Wolak DJ, Thorne RG (2013) Diffusion of macromolecules in the brain: implications for drug delivery. Mol Pharm 10(5):1492–504.
  6. Pizzo M, et al. (2017) Intrathecal antibody distribution in the rat brain: surface diffusion, perivascular transport, and osmotic enhancement of delivery. J Physiol:Accepted manuscript.

Exercise, stress and Star Wars: Best of 2017 roundup

Happy New Year! In 2018, we look forward to more physiology fun, and to giving you an insight into the exciting new developments in the Science of Life!

Physio-what, you ask? Take a look at our animation below introducing physiology! Scroll down to find out more about a centuries-old shark patrolling the deep Arctic Ocean, how being active gives children’s hearts a head start for life, and why it’s time scientists took back control from exercise gurus, in our best of 2017 roundup!

1. Exercise scientists should fight the exercise gurus

Social media apps - With new Google logo

Exercise gurus build strong rapports with their audience to encourage commitment, but they will often simplify a large body of scientific evidence to back up their advice.

In this post, Gladys Onambele-Pearson and Kostas Tsintzas discuss the risks of letting exercise gurus disseminate exercise science to the public, and why it may be time for scientists to become the actual celebrities.

2. The Myth of a Sport Scientist


There is a mismatch between the perceptions and reality of what a sport scientist is and what skills this career entails: just because exercise scientists use models of sport performance, exercise bouts or physical activity sessions, doesn’t mean that there aren’t complex scientific skills, theories, analytics and techniques behind the work.

Read more from sport scientist Hannah Moir in this post.

3. Shark Diary, Episode I: On the trails of the Greenland shark


How do you keep lab chemicals cool when there’s no fridge in your room? Well, if you’re in chilly Denmark, you could just hang them outside your window.

Holly Shiels did just that in Copenhagen, on her way to Greenland to join a team of physiologists on a shark research mission. Their aim was to gather data on the physiology of the Greenland shark. Clarifying how these animals reach hundreds of years of age without developing diseases associated with human ageing, like cancer and heart disease, could lead to new therapies down the line, and understanding shark physiology is also important for their conservation.

Read more about the mission in this post, and check out watch below to see the researchers braving the icy waters of the North Atlantic and releasing a tagged Greenland shark.

4. Breath of the Sith: a case study on respiratory failure in a galaxy far, far away


Have you always wondered what actually is going on behind the mask? Darth Vader’s acute respiratory failure appears to be the consequence of a number of factors, including direct thermal injury to the airways, chemical damage to the lung parenchyma caused by inhalation of smoke and volcanic dust particles, carbon monoxide poisoning, as well as secondary effects to his severe third degree burns, which seems to cover ~100 % of his total body surface area.

Read on as Ronan Berg and Ronni Plovsing make a tongue-in-cheek diagnosis of the numerous respiratory ailments of everyone’s favourite Sith Lord.

5. Exercise now, thank yourself later


Exercise is good for the heart, but the benefits fade soon after we stop training… or so we thought. Studies so far have focused on adults, but research published last November in The Journal of Physiology reveals that exercise in early life could have lifelong benefits for heart health.

This is because young hearts are able to create new heart muscle cells in response to exercise, an ability that is mostly lost in adulthood. Glenn Wadley, Associate Professor at Deakin University and author of the study, explains the findings in this post, and makes the case for children to get active!

As if that wasn’t enough reason to exercise, being active is one of three tips that can help relieve the stress we feel for instance at the approach of exams. Watch our animation below to find out more about what stress does to our bodies, and start making good on those New Year resolutions!