Dr Bryan Taylor


I studied Physiology and Sports Science at the University of Glasgow (2000-2004) before completing a PhD (2004-2007) at Brunel University London with Dr Lee Romer. My PhD research helped to better understand the aetiology of exercise-induced respiratory muscle fatigue as well as how such fatigue is a major contributor to exercise limitation in healthy humans. Following my doctoral work, I remained at Brunel for a further two years and competed a British Paralympic Association funded project that quantified the respiratory system limitations to exercise tolerance in athletes with spinal cord injury, and examined the utility of inspiratory muscle training to improve exercise performance in this population.    

After being awarded a Fulbright Commission Distinguished Scholarship, I continued my postdoctoral training in the Division of Cardiovascular Diseases at Mayo Clinic, USA (2009-2014). Together with Professor Bruce Johnson, we investigated the mechanisms by which lung fluid volume is regulated in healthy humans at high-altitude and in stable heart failure patients. A key finding of our research was that stimulation of the β2-adrenergic receptors via nebulised albuterol reduced radiographic evidence of lung fluid in people with heart failure, suggesting that such stimulation could provide therapeutic aid to excessive lung fluid these patients. With further funding from the American Heart Association (Postdoctoral Fellowship), I went on to investigate the causes and consequences of pulmonary hypertension in heart failure patients. The key finding from this work was of a potential role for systemic hypoxaemia in the development of pre-capillary pulmonary hypertension in heart failure, which remains a highly novel concept and a potential avenue for therapeutic development.     

I then returned to the UK as a Lecturer in Exercise Physiology at the University of Exeter (2014) before joining the University of Leeds as a University Academic Fellow in Cardiovascular Exercise Medicine (2016).       



  • Biological Sciences Faculty Research Ethics Committee member
  • Physiological Society representative for the University of Leeds

Research interests

My research is focussed on the intricate interplay between the cardiovascular and respiratory systems, and how pathophysiological changes in cardiorespiratory function contribute to exercise intolerance, impaired quality of life, and mortality with ageing and in patients with heart failure. Of particular interest is the mechanistic causes and functional consequences of: pulmonary vascular dysfunction and pulmonary hypertension in these populations.


Ageing is associated with an increase in pulmonary vascular pressures. Like the systemic circulation, the pulmonary vasculature is affected by age-associated arterial remodelling leading to pulmonary vascular stiffening. In addition, the pulmonary artery is directly affected by an increase in left heart filling pressures secondary to age-related left-ventricle diastolic dysfunction. Increases in pulmonary vascular pressure are associated with breathlessness, impaired lung function, physical activity limitation, and reduced health-related quality-of-life, and can cause damage to the right-heart in older adults. Clinically-meaningful pulmonary hypertension occurs in up to 10% of the general population, and even a modest elevation in resting pulmonary arterial pressure (occurs in up to 35% of the general population) is associated with a significant increase in all-cause mortality in adults who are free from any cardiorespiratory and metabolic disease. As such, small increases in blood pressure in the pulmonary circulation represent an independent and novel cardiovascular risk factor, and an attractive target for therapeutic intervention in the healthy elderly. However, despite its clear importance and prognostic significance, the exact causes and characteristics of increased pulmonary vascular pressure and how such increases should be treated in older adults remain unclear.

Recently, we have shown that maintenance of aerobic fitness better preserves pulmonary vascular function (specifically pulmonary capillary function) with advancing age, as demonstrated by a greater pulmonary capillary blood volume and overall lung diffusing capacity at rest and during exercise in older highly fit adults (VO2peak > 150% predicted) relative to their less fit counterparts.     

Current research aims within my lab include:

  • To determine the influence of key lifestyle (e.g., physical activity, cardiorespiratory fitness), physiological (e.g., endothelial function), and innate (e.g., ‘risk’ variants in genes involved in the NO-cGMP pathway) factors on the development of pulmonary vascular dysfunction with ageing;
  • To examine the role of endothelin and endothelin-related gene polymorphisms in early pulmonary vascular ageing and pulmonary vascular dysfunction;
  • To investigate whether various forms of exercise training can be used to better preserve pulmonary vascular function and prevent pulmonary hypertension with ageing; 
  • To explore the use of nutraceuticals that target key pathways linked to vascular ageing and have anti-inflammatory properties or boost nitric oxide bioavailability to abate and/or reverse pulmonary vascular dysfunction with ageing.


Heart failure is a complex multi-organ system syndrome characterised by pathophysiological changes in cardiac, vascular, musculoskeletal, endocrine and pulmonary function. Pulmonary hypertension is a common and clinically important complication of heart failure; pulmonary hypertension affects up to 80% of patients and is a significant, independent predictor of all-cause mortality in heart failure.  

Exercise Therapy for People with Pulmonary Hypertension

People with pulmonary hypertension have substantially reduced exercise capacity. In the past, exercise therapy has been actively discouraged in people with pulmonary hypertension because of concerns that it may contribute to disease progression. Recent studies, however, have challenged this assumption, suggesting that exercise can be beneficial and safe in even the sickest pulmonary arterial hypertension (PAH) patients. Despite this, there remains a real lack of evidence regarding the potential effectiveness of exercise therapy in people with pulmonary hypertension secondary to heart failure. Through my research, I hope to determine the physiological/clinical efficacy (i.e. therapeutic benefit) and safety of exercise training in heart failure patients with pulmonary hypertension. In doing so, it is hoped that it will contribute to the paradigm shift that exercise therapy should be a fundamental management strategy in patients with any form of pulmonary hypertension.

Current research aims within my lab include:

  • To better understand the mechanisms by which pulmonary vascular dysfunction and pulmonary hypertension limit exercise capacity in heart failure patients;
  • To explore which type of exercise training (e.g., HIIT, eccentric, resistance) maximises multi-organ system benefit but minimises cardiovascular risk in heart failure patients with pulmonary hypertension;
  • To investigate the cost-effectiveness of exercise therapy in heart failure patients with pulmonary hypertension in an out-patient setting;
  • To examine whether adjunct therapies (e.g., inspiratory muscle training, sodium nitrate supplementation) further enhances the physiological benefit of exercise training in heart failure patients with pulmonary hypertension.

Hypoxia-mediated pathways and the development of combined pre- and post-capillary pulmonary hypertension

Two main subsets of pulmonary hypertension due to heart failure exist: 1) isolated post-capillary pulmonary hypertension (IpcPH); and 2) combined pre- and post-capillary pulmonary hypertension (CpcPH). CpcPH is characterised by abnormalities in pulmonary arterial structure and function, and is associated with an increased risk of death (~2-4 fold) compared with IpcPH. Our preliminary data (in collaboration with Professor Bruce Johnson at Mayo Clinic, USA) suggests that the pulmonary haemodynamic response to exercise is dysfunctional and greatly exaggerated in patients with CpcPH, a response that is directly related to impaired exercise capacity (lower VO2peak). In addition, I have shown greater impairments in pulmonary gas exchange and breathing efficiency during exercise in heart failure patients with CpcPH vs. IpcPH; these impairments were directly related to augmented pulmonary vascular pressures during exercise in CpcPH patients. Importantly, both dysfunctional pulmonary haemodynamic and pulmonary gas exchange responses to exercise are also highly prognostic in heart failure patients. Despite its prognostic significance, the mechanisms that underpin the pathophysiological development of CpcPH in heart failure remain elusive. In addition, there is currently no established treatment for any form of pulmonary hypertension due to heart failure.

In my laboratory, we are interested in the possible role of hypoxia-sensitive pathways in the development of CpcPH in heart failure. Previously, I have demonstrated an inverse relationship between the severity of pulmonary hypertension and arterial and mixed-venous oxygen levels ONLY in patients with CpcPH; that is, lower circulating oxygen levels (i.e. systemic hypoxaemia) are directly related to the severity of pulmonary vascular dysfunction in heart failure patients with CpcPH. I also found that plasma endothelin-1 concentration (a potent pulmonary vasoconstrictor) was related to both systemic oxygen levels and the severity of pulmonary hypertension in patients with CpcPH.  

Current research aims within my lab include:

  • To investigate the potential utility of endothelin-1 receptor antagonists to improve pulmonary vascular function, right heart mechanics, and exercise capacity in patients with CpcPH;
  • To examine the role of endothelin and endothelin-related gene polymorphisms in the development of CpcPH;
  • To explore whether short- and long-term supplemental oxygen (oxygen therapy) provides therapeutic benefit in patients with CpcPH;
  • To determine whether the use of nutraceuticals that have anti-inflammatory properties or boost nitric oxide bioavailability can abate and/or reverse pulmonary vascular dysfunction in patients with CpcPH;
  • To investigate the role of aberrant carotid body activity in the development of CpcPH. and whether blockade of carotid body afferents can reduce pulmonary arterial pressure and improve pulmonary vascular function in CpcPH.
<h4>Research projects</h4> <p>Any research projects I'm currently working on will be listed below. Our list of all <a href="https://biologicalsciences.leeds.ac.uk/dir/research-projects">research projects</a> allows you to view and search the full list of projects in the faculty.</p>


  • PhD (Brunel University London)
  • BSc (Hons) Physiology and Sports Science (University of Glasgow)

Professional memberships

  • American College of Sports Medicine
  • American Physiological Society
  • British Thoracic Society
  • European Respiratory Society
  • Physiological Society

Student education

Modules managed

SPSC1223 - Physiology of Exercise Testing and Performance

Modules taught

BMSC5301M - Advanced Research Topics

SPSC3061 - Research Project in Sport and Exercise Science II

SPSC3321 - Advanced Exercise Physiology

SPSC3326 - Exercise Prescription for Health and Disease

SPSC2205 – Environmental Exercise Physiology

FOBS1125 – Introduction to Physiology

Research groups and institutes

  • Sport and Exercise Sciences
<h4>Postgraduate research opportunities</h4> <p>We welcome enquiries from motivated and qualified applicants from all around the world who are interested in PhD study. Our <a href="https://phd.leeds.ac.uk">research opportunities</a> allow you to search for projects and scholarships.</p>