Making sense of stress in the wild

By Kimberley Bennett, Abertay University

Imagine leaning forward over the edge of a precipice. Lurching back to safety, you picture the forest hundreds of metres below. Is your heart racing? Are your palms sweating? Our body’s stress response to an ever-changing environment enables us to survive and flourish.

Physiologists play a crucial role in developing our understanding of the mechanisms involved. To highlight the exciting work that they do, our 2017 theme is ‘Making Sense of Stress’. Follow the conversation on Twitter using #YearOfStress.

Launching the theme will be Dr Kimberley Bennett’s talk, ‘Making sense of stress in the wild’, at the Association for Science Education’s (ASE’s) Annual Conference on 6 January 2017. Read a teaser to her talk below!

Coping with stress is a major issue in modern society, but it’s easy to forget that wildlife experiences stress too. Without enough water, plants wilt and die and whole crops fail; without the right habitat, a small population of rare animals dwindles and dies out, causing extinction of the species; a whole coral reef bleaches when the water temperature gets too high, causing catastrophe for the ecosystem, and massively increasing flooding risk for people living by the coast. We really need to pay attention to stress in the wild because the consequences can herald disaster.

Stress is the biological response to a major challenge, whether it’s at the whole organism or cell level. A gazelle in the Serengeti chased by a lion experiences the same stress responses that we do – a surge of adrenaline and cortisol that cause increased heart rate and blood pressure and a release of glucose. These changes make sure there is enough fuel and oxygen to cope with increased demand at the tissue and cell levels. Sudden change or mismatch in the supply of oxygen and fuel leads to increased production of reactive molecules called ‘free radicals’ that can damage cells. If the temperature gets too hot too fast or if the acidity of the cell changes too much, proteins (the molecules that catalyse reactions, transport substances and provide structure) can fall apart or unravel. So cells have to increase their defence mechanisms too. Cellular defences include antioxidants that mop up the free radicals, and heat shock proteins, which refold damaged proteins and stop them forming a sticky mess inside the cell.

The old adage that what doesn’t kill you makes you stronger is often true: short term ‘good stress’ builds up these defences and makes organisms better able to deal with stress later on. However, sometimes defences can be overwhelmed or can’t be maintained for long periods. The organism then experiences the same sorts of problems as people under chronic stress: lower immunity, altered metabolism, anxiety and tissue damage (like ulcers). In wildlife, this can have major consequences for breeding success or even survival. By affecting whether organisms survive and thrive, stress dictates which individuals contribute to the next generation. Stress shapes population dynamics, lifestyle and adaptations, and is therefore a powerful agent of natural selection.


I work on seals, top marine predators that are used to stress as a normal part of their existence. Their individual and population level health is an indicator of ecosystem health. Seals are air breathing mammals that feed underwater, but need to come to the surface to breathe, and to come ashore to rest, breed and moult. Diving on a single breath hold means they need to conserve oxygen; to do this, blood flow is restricted mostly to the heart and brain, so that other tissues may experience free radical production while oxygen levels are low. On land, seals need to fast, often while they are doing energy-demanding activities i.e. shedding and replacing hair, producing milk, defending pups or territory, or undergoing rapid development. Injury and infection can occur from skirmishes or trampling. Seals may have to reduce their defences to deal with all these demands on their energy when food is not available. In addition to their ‘lifestyle stressors’, seals face stress from competition for access to fish, disturbance on haul out or displacement from foraging grounds as a result of human activity, and the accumulation of contaminants in their blubber.

We need to understand natural and man-made causes of stress in wild populations, distinguish good stress from bad stress, and understand how multiple stressors at the same time can create problems. That means we have to have effective tools to measure stress and its consequences in organisms that can’t tell us how they feel. But can we measure stress responses in wildlife? What do they mean in context? And can they help in managing stress in the wild?

I will address all these questions and more at the ASE’s Annual Conference on Friday 6 January 2017, as part of the annual Biology in the Real World (#BitRW) lecture series. Please drop by the Knight Building, LT 135, at the University of Reading, at 1.30pm to find out more!


Danger! High Voltage!

By Mark Dallas, University of Reading, @drmarkdallas

Standing between school students and their weekends was always going to be a tough gig, but it was #PhysiologyFriday and we were determined to put on a show. Together with Orla and Ioannis, PhD students from the University of Reading, I arrived at East Ham Town Hall and was greeted by over 200 excited students and their teachers.

Our mission was to deliver an engaging session around electricity and pass on an innovative human-human interface educational resource that the students had won as part of a Physiological Society competition, The Science of Life 2016. After a brief introduction to human electricity and how we can detect it, we took the students on a journey from the first electroencephalogram (EEG) to the potential of neuroprosthetics in treating paralysis. We then tackled a live demonstration of the kit and the students were intrigued to see the interface in action.


Surely, one human cannot control another’s arm using only their brain activity? The wonders of neuroscience said it should be possible, but we sensed some doubters in the audience. Using the human-human interface Ioannis was going to harness his brain power to move Orla’s arm against her wishes……

Thankfully the demonstration was up to scratch with the students requesting several encores, and even asking for the voltage to be turned up! Normally the complexities of electrophysiology remain in the lab due to expensive and static equipment, however this kit gave us the ability to be mobile and take the dark art of electrophysiology to young minds keen to explore neuroscience. It was well worth it. The students left school for the weekend with a sense of excitement and thirst to learn more. Orla, Ioannis and I left East Ham Town Hall feeling that we had sparked the interest of the next generation of physiologists.


Myth-busting: Do heart cells really have their own ‘pulse’?

By Andy James, University of Bristol

The comedian, Jake Yapp, has been presenting on BBC Radio 4’s website a series of short comic histories of science entitled, “Everything We’ve Ever Known About …” Informative and entertaining, these are invariably funny. A recent edition concerned the heart, neatly covering the development of our understanding of heart function through the millennia, from the ancient Egyptians to the present day – where Jake concludes by commenting that if you isolate a heart muscle cell it will have its own pulse. Actually, strictly speaking, a pulse is the increase in pressure within the arteries as a result of beating of the heart. ‘Rhythm’ is a better word.

It’s a commonly held misconception, even amongst specialists in cell biology, that all heart muscle cells have their own rhythm that synchronises when the cells couple together (meaning they join and allow electricity to flow between them). Beautiful as this idea is, it simply isn’t true. The heart’s rhythm originates as electrical activity in a specialised area of the heart known as the sinus node- the heart’s physiological pacemaker. The heart muscle cells of the sinus node generate rhythmic electrical activity so that, when isolated, they contract regularly.

In the intact heart, a conduction system ensures that the electrical activity is passed to the chambers to produce a well-coordinated contraction. Many of the cells of the conduction system would also beat when isolated. But the cells from the walls of the chambers that produce the pressure to – as the English anatomist, William Harvey, would have it – propel the blood, do not. Chamber cells only need to receive the signal, but not generate it themselves.

The persuasive and attractive idea that all heart muscle cells show their own rhythm may have arisen from attempts to maintain heart muscle cells for several days in a petri dish. Heart muscle cells from adult mammalian hearts do not generally multiply under these conditions and while it is possible to keep the cells alive for a short time, after a few days, the cells die. However, cells from embryonic, or even neonatal, hearts do multiply in culture. They often show rhythmic contractions and, yes, they synchronise once they form connections with their neighbours.

So do heart cells really have their own pulse? It depends! Cells from adult hearts are programmed to behave in a fixed way- as a pacemaker cell, a conducting cell or a contractile cell from a chamber wall. Cells from immature hearts, on the other hand, retain the ability to change their properties and tend to develop pacemaker-like function in the petri dish.

Measuring a moving target: Symposium on Hormone Sensing

By Julia Turan, Communications Manager, The Physiological Society

What do puberty, doping in athletics, and the meat industry have in common? The answer is hormones. Secreted into the blood by specialized organs and tissues, hormones communicate a bewildering array of signals to a myriad of target sites.

Two weeks ago, The Physiological Society brought together experts in physiology, endocrinology, chemistry, physics and engineering, to discuss how to produce a new generation of tools and methods for detecting hormones inside our bodies

“The biggest hurdle facing basic and clinical endocrinologists is how we can measure hormones inside the body,” said one of the symposium organizers, Timothy Wells, Senior Lecturer in Neuroscience at Cardiff University.

Addressed by UK and international experts in hormone-receptor interactions, light-based sensing and nanocarbon-based sensing, the Society’s symposium explored how these molecular interactions could be exploited to quantify the dynamic changes in circulating hormone levels.


Cutting edge work featured

One of the potential approaches was presented by Frank Vollmer and his colleagues from the Max Planck Institute for the Science of Light. He and his team are attempting to reach the ultimate limit of detection, by sensing single molecule interactions and the resultant changes in three-dimensional shape. Their new technique, which was published this week in Nature Photonics, may enable the detection of individual hormone molecules.

Thus, the day of talks highlighted just how far we’ve come since Ernest Starling coined the term hormone in 1905.

The event, titled “Novel approaches to Hormone Sensing, The Inaugural Bayliss-Starling Symposium,” was part of the society’s H3 symposia. The next symposium will be held on 15 November about one of the biggest discoveries in biotech, CRISPR. Visit our website for more info:

Prize Lecture Memoria – Edward Sharpey-Schafer

M0020242 Portrait of Sir E.A. Sharpey-Schafer

Sir Edward Albert Sharpey-Schafer (1850 –1935) was an English physiologist and Fellow of the Royal Society. Born Edward Schäfer, he studied under the physiologist William Sharpey and became the first Sharpey Scholar in 1873 at University College London (UCL). In 1874 he was appointed Assistant Professor of Practical Physiology at UCL where he went on to become Jodrell Professor. He was elected a Fellow of the Royal Society in 1878 at the age of just 28. Schäfer was appointed Chair of Physiology at the University of Edinburgh in 1899 where he would stay until his retirement. He was one of the nineteen founder members of the Physiological Society in 1876 and he also founded and edited [the Quarterly Journal of] Experimental Physiology from 1908 until 1933. Schäfer was knighted in 1913. He is renowned for his invention of the prone-pressure method or Schäfer method of artificial respiration. He was very active as a facilitator, mentor, coordinator, teacher and organiser through much of his career. He had started as a histologist and always emphasised the importance of structural knowledge. He was the co-discoverer (in 1894, with George Oliver) of adrenaline (as in the adrenal-derived, circulating hormone) and he coined the term ‘endocrine’ as the generic term for such secretions. He intuited (as did a few others, independently) that insulin must exist (i.e. a pancreatic hormone to account for diabetes mellitus) and coined the name (originally as ‘insuline’). (Banting and Best actually discovered what S-S and the others had predicted). Thus, he had a founding role in modern endocrinology. He also did important early work on the localisation of function (e.g. motor centres) to brain regions. After the death of his eldest son, John Sharpey Schafer, and in memory of his late professor William Sharpey, he changed his surname to Sharpey-Schafer in 1918. Sir Edward Albert Sharpey-Schafer died on 29 March 1935 aged 84. Funded by bequests from Sir Edward Sharpey-Schafer (1850–1935) and his daughter Miss GM Sharpey-Schafer and in memory of Sir Edward and his grandson Professor EP Sharpey-Schafer, The Physiological Society established the Sharpey-Schafer Prize Lecture. This is a triennial lecture given alternately by an established physiologist (preferably but not necessarily from abroad) and a young physiologist chosen by The Society.