Category Archives: Researcher Spotlight

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.

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!

The Myth of a Sport Scientist

Back in school, I was a sporty student taking part in a plethora of activities from netball and hockey, to kayaking, tennis and 1500m, but I was never keen on becoming a professional athlete. I was always nominated for the sport day events and typically took charge as captain. When looking at my A-level choices and what career to follow, I naturally pursued the sport route, aligning with topics such as physical education and biology.

Then, when it came to higher education, studying sport science was at the top of my list. Whilst visiting institutional open days, and speaking to friends, family and teachers, it became apparent that there was a mismatch between the perceptions of what a sport scientist is about and what skills it entails. Here I present some top common misconceptions of being a sport scientist.


Myth #1: You have to be an elite sportsperson

This is my pet hate and the main myth I try to debunk! It is not true that a sport scientist has to be good at sport; yes it can sometimes help to have an interest in physical activity, exercise or sport, but you don’t have be a Messi or Ronaldo. The whole benefit of studying sport science is that you can inspire anyone from the inactive to the elite. Studying sport science is more about being interested in the application of science to the interpretation and understanding of how the body responds to exercise. It involves expertise across a range of scientific disciplines including physiology, psychology, biomechanics, biochemistry, anatomy, and nutrition.


Myth # 2: You are either a physical education teacher or a coach

Another persistent myth about being interested in sport and studying sport science is that you run around a rugby pitch with a whistle. As much as I respect the talents and skills of PE teachers and coaches, and although many of our students may go into these careers, these are not the only skills and applications of a sport scientist. Sport scientists can be performance analysts. Or they may specialise in exercise physiology. They may even go into marketing, rehabilitation, PR, sport media, or education. The diversity and depth of transferable skills means that there are a variety of options and directions to take, whether you want to help improve the health and wellbeing of a population through exercise plans or the recovery of injured athletes. I always had an interest in teaching sport or science. It was during my PhD that I became aware of the opportunities and careers in academia. Then, becoming a lecturer became my focus, combining my love of the subject and passion for the research!

Finally, Myth #3: It’s not a ‘real’ science

This final myth really bothers me, and is most applicable to the research aspect of my job. It can be frustrating when we are not as respected in the field of science, where some say it’s not a ‘real’ science’. Many of us who are in the field of sport science are specialised in a discipline. For me, it was exercise physiology and biochemistry.


As an exercise physiologist, I am specifically interested in the relationship between the use of exercise as a stressor and how the body responds at a cellular level with specific use of biochemical and immunological analytical techniques. Just because we 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. My primary research focuses on how the immune system and metabolism help our skeletal muscles repair after physical activity, exercise, and training. My current research is about ultra-endurance running profiling of endurance performances, rehabilitation techniques for muscle damage and inflammation, and the use of exercise plans in management of diseases such as type 2 diabetes.

With the developments and interest in sport across the nation following events such as the 2012 and 2016 Olympics, and other events such as Wimbledon, the Football leagues and the Rugby World Cup, hopefully people are starting to realise how sport science can advance sport performance and health.

Dr Hannah Jayne Moir is a Senior Lecturer in Health & Exercise Prescription, at Kingston University, London. Her research is driven in the discipline of Sport & Exercise Sciences and she is co-chair and theme leader for the Sport, Exercise, Nutrition and Public Health Research Group.

This post is part of our Researcher Spotlight series. If you research, teach, do outreach, or do policy work in physiology, and would like to write on our blog, please get in touch with Julia at

Diet, exercise or drugs – how do we cure obesity?

by Simon Cork, Imperial College London, @simon_c_c

October 11th is officially “World Obesity Day”, a day observed internationally to promote practical solutions to end the obesity crisis. The term “obesity crisis” or “obesity epidemic” is often repeated by the media, but how big is the problem? Today, over 1.9 billion adults worldwide are overweight or obese. By 2025, this is projected to increase to 2.7 billion with an estimated annual cost of 1.2 trillion USD. Of particular concern is that 124 million children and adolescents worldwide are overweight or obese. In the UK, this equates to 1 in 10 children and adolescents and is projected to increase to 3.8 million by 2025. We know that obesity significantly raises the risk of developing 11 different types of cancer, stroke, type 2 diabetes, heart disease and non-alcoholic fatty liver disease, but worryingly, we now know that once someone becomes obese, physiological changes to the body’s metabolism make long-term weight loss challenging.

Our understanding of the physiology of food intake and metabolism and the pathophysiology of obesity has grown considerably over the past few decades. Obesity was seen, and often still is seen, as a social problem, rather than a medical issue: a lack of self-control and willpower. We now know that physiological changes occur in how our bodies respond to food intake. For example, hormones which are released from the gut following food intake and signal to the brain via the vagus nerve normally reduce food intake. However, in obesity, the secretion of these hormones is reduced, as is the sensitivity of the vagus nerve. The consequence of this is a reduced sensation of feeling full.


Imaging of the hypothalamus (a key region for keeping food intake at a balanced level) shows a reduction in activity following food intake in lean men, an effect which was absent in obesity. This effect may relate to a reduction in the body’s responses observed following food intake in obesity, such as balancing blood sugar and signalling that you are full. Furthermore, numerous studies have shown that obese individuals have a reduced availability of dopamine receptors, the structures on cells that respond to the pleasure chemical dopamine, in key brain regions associated with reward. Whether the reduction in dopamine receptor availability is a cause or consequence of obesity remains to be fully explored, but it is likely to be a combination of both of these factors. Individuals with a gene called the Taq1 A1, associated with a decreased availability of dopamine receptors, are more likely to become obese, suggesting that decreased responsiveness to high calorie foods leads to increased consumption in order to achieve the same level of reward. (Interestingly, this same gene is also associated with an increased risk of drug addiction). However, much like drug addiction, hyper-stimulation of the dopamine system (i.e. by consuming large quantities of dopamine-secreting, high calorie foods) can in turn lead to a reduction in dopamine receptor levels, thus creating a situation where more high calorie foods are required to stimulate the same level of reward.

It is therefore clear that obesity is not simply a manifestation of choice, but underpinned by complex changes in physiology which promote a surplus of food consumption, called positive energy balance. From an evolutionary standpoint, this makes sense, as maintaining a positive energy balance in times of abundant food would protect an individual in times of famine. However, evolution has failed to keep up with modern society, where 24-hour access to high calorie foods removes the threat of starvation. The good news is that we know that weight loss as small as 5% can yield significant improvements in health, and can often be managed without significant modification to lifestyle.



Presently, treatment options for obesity are limited. The first line treatment is still diet and exercise; but as the above examples of how our physiology changes show, maintaining long term weight loss through self-control alone is almost always impossible. However, the future does look bright, with new classes of drugs either recently licenced, or in production. Saxenda (a once-daily injectable drug which mimics the gut hormone GLP-1 made by Novo Nordisk) has recently been licenced for weight loss in patients with a BMI greater than 30. However, after 56 weeks treatment, average weight loss was a modest 8kg. Likewise Orlistat (which inhibits absorption of dietary fat, made by Roche) has been on the market for a number of years and shows average weight loss of around 10%. However, it is associated with unpleasant side effects, such as flatulence and oily stools. Presently, bariatric surgery is the only treatment that shows significant, long term weight loss (around 30%, depending on the surgical method used) and is also associated with long-term increases in gut hormone secretion and vagus nerve sensitivity.  Research is currently underway to assess whether the profile of gut hormones observed post-surgery can be mimicked pharmacologically. Studies have shown that administering select gut hormones in combination results in a reduction in body weight and food intake greater than the sum of either hormone when administered in isolation. This observed synergy between gut hormones will undoubtedly form the basis for future pharmacotherapies with improved efficacy, with various combinations currently in both clinical and pre-clinical trials.

For healthcare policy makers, the future obesity landscape does not make for happy reading. A combination of better therapies and improved public health messages are undoubtedly needed to stem the rising tide. However, both policy makers and society as a whole should be mindful that changes in ones physiology mean maintaining long-term weight loss through diet and exercise alone are unlikely to be the whole answer.

Watchers on the wall: Microglia and Alzheimer’s Disease

By Laura Thei, University of Reading, UK

The watch, worn by years of use, sits ticking on our table for the first time in two years. It has a simple ivory face and is the last memorabilia my partner has from Grandad Percy. Percy passed from us after a long personal battle with dementia, specifically Alzheimer’s disease. It is in his name that my partner and I will take to the beautiful winding pathways beside the Thames, to raise money for the Alzheimer’s Society.

We will be taking part in a 7 km Memory Walk, with thousands of others, some my colleagues from the University, each sponsored generously by friends and families, each who has had their life touched by this disease in some way. Last year nearly 80,000 people took part in 31 walks, raising a record £6.6 million. As a researcher in Alzheimer’s disease, I am acutely aware of every penny’s impact in helping to solve the riddle of dementia.


Alzheimer’s Society Memory Walk

Alzheimer’s disease is ridiculously complicated. Oh, the premise is simple enough: two proteins, amyloid beta and phosphorylated tau, become overproduced in the brain and start to clog up the cells like hair down a plug. This causes these cells to be deprived of nutrients, oxygen and other vital factors that keep them alive. This eventually causes regional loss in areas specific to memory and personality. It’s simple in theory, but the reality is that we still have much to learn.

Current, extensive research is starting to answer these questions and whilst there is a growing list of risk factors – genetic (APOE4, clusterin, presenilin 1 and 2) and environmental (age, exercise, blood pressure) – confirmation only occurs when a brain scan shows the loss of brain region volume in addition to the presence of amyloid beta and tau. This means that by the time someone knows they have the disease, it’s possible that it’s already been chugging away at their brains for some time.

So we need to push diagnoses earlier. To do that we need to look at the very early stages of the disease, down to a cellular level, to find out how we can prevent the build-up of amyloid and tau in the first place. This is what I, the group I’m in, and many other researchers nationally and globally are striving to do.


In a non-active state, microglia lie quietly surveying their local area of the brain. ©HBO

I am specifically focusing on the immune cells of the brain, microglia, and their contribution. Microglia are the most numerous cells in the brain. They act as the first line of defence, so their involvement and activation is often seen as an early sign of disease progression. Like all good defences, they tend to be alerted to damage before it becomes deadly. But, like the neurons (the basic building blocks of the brain), microglia are also susceptible to the disease. If they die, does that leave the brain more vulnerable to further insult? That is what I would like to know too!

In a non-active state, microglia lie quietly surveying their local area of the brain. When activated by a threat to the brain, they cluster around the targeted area, changing shape in the process. They then enter one of two states. The pro-inflammatory state releases molecules that attack the harmful pathogens directly, and the anti-inflammatory state releases ones that promote healing and protection of the area.


Microglia can change shape to either attack pathogens or protect the area. ©Nickelodeon

With Alzheimer’s, microglia are activated by the accumulation of amyloid, not damage. They absorb the amyloid beta, and in the process, trigger the pro-inflammatory response. This then increases the permeability of the brain’s blood supply, allowing immune cells into the brain to assist removal of the excess protein. However, in the brain of Alzheimer’s patients, the amyloid beta production outdoes the microglia’s ability to remove it. This creates a perpetual cycle of pro-inflammatory response, releasing molecules that can kill cells in the brain. It is unclear whether there is a threshold between beneficial or detrimental in the microglial response.


Microglial response to fight Alzheimer’s Disease can become detrimental. ©2011 Scott Maynard

Given the importance of microglia in neurodegenerative diseases, a new field of microglial therapeutics has recently emerged, ranging from pharmacologically manipulating existing microglia by switching their response status, to inhibiting microglial activation altogether. Continued research and clinical efforts in the future will help us to improve our understanding of microglial physiology and their roles in neurological diseases.

We’re making progress, but there’s still a long way to go, which is why every penny counts!

Researcher Spotlight: James Betts

PastedGraphic-1‘The timing of daily meals is important for our metabolism. It’s easy to change how frequently we eat.’

James Betts is a Reader (Associate Professor) in Nutrition, Metabolism and Statistics in the Department for Health at the University of Bath. He is interested in energy metabolism, and how components of energy balance interact to regulate human health and physiological function.


What is your research about?

I am interested in the effect of nutrition on human physiology. In particular, I have always been interested in energy metabolism and therefore the amount, type and timing of macronutrient ingestion. Recently my work has become most focused on the interactions between time and energy balance, for example considering the frequency or regularity of eating relative to other daily events such as exercise, sleep and other eating occasions.

How did you end up working in this field?

I remember already being fascinated by nutrition during my school days. I’ve also always played sports, so I was keen to study the scientific basis of exercise at University. Loughborough was a natural progression for me and it was there that I participated in countless experiments as an undergraduate. In my final year, I started conducting research, and haven’t looked back since. I studied the effects of taking vitamin C and E for six weeks on oxidative stress and muscle damage after exercise. (More recently, I submitted and published this work). That experience galvanised my passion for scientific research. During my PhD, supervised by Clyde Williams, I continued studying metabolism after exercise, but looked at carbohydrate and protein ingestion instead. I have maintained this interest in how exercise interacts with eating but now with greater focus on how the timing of nutrients affects metabolic regulation and health.

Why is your work important?

All studies of nutrition can be broadly categorised under the headings of how much (i.e. dose) of what (i.e. type) we eat when (i.e. timing). Mainstream media and primary research focus on the first two. However, the timing of daily meals is important for our metabolism. It’s easy to change how frequently we eat, and research is increasingly showing that we can optimise this to be healthier. Changing how frequently we eat might also help counter obesity and associated chronic diseases. These conditions are undoubtedly a great public health challenge in our generation and represent an incredible burden to many individuals, the economy and society.

What does your typical day, in and out of the lab/classroom involve?

I enjoy that my job is so varied and I get to meet many people by working on human metabolism. While well-controlled experiments are repetitive, I am always learning. My typical day starts taking adipose and muscle samples from our volunteers who fasted overnight. When not in the laboratory, I am either writing scientific papers and grant applications, or advising my students.


Researcher in the Spotlight June 2016

Lisa at Merton

Dr Lisa Heather PhD, is a Diabetes UK RD Lawrence Fellow in the Department of Physiology, Anatomy and Genetics, University of Oxford. Her research revolves around metabolism and energy generation in the heart.

Lisa will give The Physiological Society Bayliss-Starling Prize Lecture ‘Cardiac metabolism in disease: All fuels are equal, but some fuels are more equal than others’ at our main meeting P16 in Dublin, Sunday 31 July 9:00 am.



What is your research about?

I study energy metabolism in the heart. Metabolism explains how we extract energy from the fuels we eat: how we convert glucose and fatty acids into ATP via a series of chemical reactions within the cell. When this process goes wrong the cell can become starved of energy, and ATP dependent processes – such as contraction – will be impaired. Abnormal cardiac energy metabolism occurs in a large number of diseases, including diabetes and heart failure. Understanding why these metabolic abnormalities occur and whether changing metabolism is beneficial for cardiac function is my area of research.

How did you come to be working in this field and was this something you always wanted to do?

My undergraduate degree was in Medical Biochemistry at the University of Surrey, and I had an amazing lecturer, Dr Jack Salway, teaching metabolism. He made the subject exciting and relevant, and made me want to pursue it further to become a ‘die-hard metabolist’. I moved to Oxford in 2003 and joined the lab of Professor Kieran Clarke, studying the effects of disease on cardiac metabolism. Kieran was (and still is) an excellent mentor, providing support whenever I needed it, but equally allowing me freedom to explore my own directions and stand on my own two feet.

When I first started in the field of metabolism it wasn’t a particularly fashionable field – everyone was focused on genetics, and metabolism was viewed as a subject where all the questions had already been answered. Scientific fashions change, and in the last 10 years metabolism has had a huge renaissance, mainly driven by discoveries in the cancer field. It’s an exciting time to be working in this area, new collaborations are emerging between diverse fields that have realised metabolism is influencing or being influenced by their disease or cellular process. Suddenly, having a good understanding of the fundamentals of metabolism is a powerful tool.

I have never considered leaving the field of metabolism as it’s the area I love, and when I set up my own group in 2011 I decided it was the field of diabetes, the ultimate metabolic disease, that I wanted to specialise in.

Why is your work important?

Metabolism underpins all cellular processes. It provides ATP for all active processes to occur, it provides the building blocks and intermediates for diverse chemical reactions, and provides substrates for post-translational modifications. Changes in metabolism have been implicated in many diverse diseases of all organs in the body. As stated by Steven McKnight in Science in 2010 “One simple way of looking at things is to consider that 9 questions out of 10 could be solved without thinking about metabolism at all, but the 10th question is simply intractable…. if you are ignorant about the dynamics of metabolism”.

Do you think your work can make a difference?

I really hope so. Understanding how a disease develops and progresses is the first step to working out how to prevent or reverse it.

What does a typical day involve?

A typical day can involve any combination of lab work, discussing data with students, planning new studies, writing and rewriting papers, teaching undergrads, and meetings. Each day is different and that’s one of the things I really enjoy about being an academic.

What do you enjoy most in your job?

I love the ‘Aha!’ moments. When you have been busy trying to work out why something has changed or the mechanism involved, and suddenly everything fits together and makes sense. When you have discovered something, however small, that wasn’t known before. It reminds me of those “magic eye” pictures, when you stare at it long enough that the blurry 2D pattern finally turns into a beautiful 3D image. The “Aha” moments are the reward for all those times the experiments didn’t work.

 What do enjoy the least?

On a day to day basis, I really hate having to collect liquid nitrogen from our outside cylinder! It’s the worst job! I generally really love my job and feel grateful that I get to do this every day.

Tell us something about you that might surprise us…

I really really really like designer shoes. If only Manolo Blahnik could make mitochondria-inspired pumps!

What advice would you give to students/early career researchers?

Do what you love. Being a scientist is a tough career, so you have to love it to deal with the challenges, such as paper rejections and lack of job security. Have faith in your own abilities. Be nice to people and help people when you can, people are then more likely to come to your assistance when you need them. Smile :)!