Dr Matthew Lancaster

BSc Physiology, Leeds; PhD 1998, Liverpool
Lecturer in Exercise Physiology
School of Biomedical Sciences

Background: BSc (Leeds), PhD (Liverpool), Postdoctoral research at Leeds. Lecturer in Exercise Physiology (2003?)

Contact: Garstang 7.52c, +44(0) 113 34 34285, email address for  

Research Interests

Cardiac adaptation, rhythms and arrhythmias

My group’s research is directed towards understanding how the heart adapts to changing stresses to ensure continued healthy function. Of particular interest are the stresses of exercise and ageing.

Failure of the heart to adapt leads to cardiac insufficiency whereas undesirable adaptations cause increased susceptibility to arrhythmias and sudden death. By studying cardiac function at the global, cellular and sub-cellular levels we hope to develop an understanding of how intrinsic cardiac responses are controlled and may be manipulated.

One key aspect of our research is directed at the initiation of heart beat. What makes the heart beat spontaneously? How does the pacemaker of the heart adapt? Why in old age does the normal heart's pacemaker begin to fail? By measuring cardiac electrical activity in people, animal models and cellular models we identify the key ionic currents and controlling processes that allow the heart to spontaneously beat and that modify this beating rate.  So far we have identified key changes in connections between cells and ionic currents that deteriorate with old age predisposing to problems.  Interestingly some of these changes may also occur with exercise leading to a lower heart rate but also potentially a predisposition to problems...

A further key issue we investigate is the multiple effects of ageing on cardiac performance. The aged heart is more susceptible to arrhythmias, shows reduced capacity for adaptation to common stresses such as exercise, and shows reduced tolerance to damaging insults such as a myocardial infarction. Research performed in conjunction with Dr Sandra Jones at the University of Hull as well as here in Leeds has created age-dependent profiles of cardiac function and adaptation allowing us to model cardiac ageing and identify key changes which eventually form the background for cardiac problems in the elderly.

Funding: Wellcome Trust & British Heart Foundation

Overseas collaborators: Haruo Honjo (Japan) and Scott Powers (USA)


Faculty Research and Innovation

Studentship information

Undergraduate project topics:

  • ECG changes in response to intense exercise
  • Cardiac risk factors in apparently healthy populations

Postgraduate studentship areas:

  • Cardiac adaptation to exercise
  • Ageing of the heart as a prelude to disorder

See also:

Modules managed

SPSC1220 - Foundations of Physiology
SPSC1221 - Cardio-respiratory Physiology and Exercise
SPSC1222 - Neuroscience for Exercise Science
SPSC2203 - Exercise Biochemistry
SPSC5314M - Personal Development and Employability for Sport and Exercise Scientists

Modules taught

SPSC1220 - Foundations of Physiology
SPSC1221 - Cardio-respiratory Physiology and Exercise
SPSC1222 - Neuroscience for Exercise Science
SPSC1225 - Physical Activity Across the Lifespan
SPSC2203 - Exercise Biochemistry
SPSC2302 - Exercise Physiology in Sport, Health and Disease
SPSC2302/BMSC2216 - Exercise Physiology
SPSC3061 - Research Project in Sport and Exercise Science II
SPSC3301 - Inter-disciplinary Issues in Sport and Exercise Science
SPSC3321 - Advanced Exercise Physiology
SPSC3326 - Exercise Prescription for Health and Disease
SPSC3389 - Research Project
SPSC5314M - Personal Development and Employability for Sport and Exercise Scientists

Academic roles

School Director of Taught Student Education - SPSC, January-August


Member of Faculty Taught Student Education Committee (Co-opted member)
Member of Undergraduate School Taught Student Education Committee (Exams Officer: Sport and Exercise Science, Sports Science and Physiology)

Centre membership: The Multidisciplinary Cardiovascular Research Centre (MCRC)

Group Leader Dr Matthew Lancaster  (Lecturer in Exercise Physiology)

Cardiac adaptation, rhythms and arrhythmias 

Ross SRPJ, Volz V, Lancaster MK, Divan A A generalizable framework for multi-scale auditing of digital learning provision in higher education Online Learning, 2017
View abstract

Walton RD, Jones SA, Rostron KA, Kayani AC, Close GL, McArdle A, Lancaster MK Interactions of Short-Term and Chronic Treadmill Training With Aging of the Left Ventricle of the Heart. J Gerontol A Biol Sci Med Sci 71 1005-1013, 2015
View abstract

Jones SA, Lancaster MK Progressive age-associated activation of JNK associates with conduction disruption in the aged atrium Mechanisms of Ageing and Development 146-148 72-80, 2015
View abstract


Hatch F, Lancaster MK, Jones SA Aging is a primary risk factor for cardiac arrhythmias: Disruption of intracellular Ca<sup>2+</sup>regulation as a key suspect Expert Review of Cardiovascular Therapy 9 1059-1067, 2011
View abstract

Jones SA, Lancaster MK Calcium-channel blockers and cardiac arrhythmias within the elderly population Future Cardiology 4 207-209, 2008

Jones SA, Yamamoto M, Tellez JO, Billeter R, Boyett MR, Honjo H, Lancaster MK Distinguishing Properties of Cells From the Myocardial Sleeves of the Pulmonary Veins A Comparison of Normal and Abnormal Pacemakers CIRC-ARRHYTHMIA ELEC 1 39-48, 2008

Boyett MR, Honjo H, Kodama I, Lancaster MK, Lei M, Musa H, Zhang H The sinoatrial node: CEll size does matter CIRC RES 101 E81-E82, 2007

Dobrzynski H, Li J, Tellez J, Greener ID, Nikolski VP, Wright SE, Parson SH, Jones SA, Lancaster MK, Yamamoto M, Honjo H, Takagishi Y, Kodama I, Efimov IR, Billeter R, Boyett MR Computer three-dimensional reconstruction of the sinoatrial node CIRCULATION 111 846-854, 2005

Jones SA, Lancaster MK, Boyett MR Ageing-related changes of connexins and conduction within the sinoatrial node J PHYSIOL-LONDON 560 429-437, 2004

Lei M, Jones SA, Liu J, Lancaster MK, Fung SSM, Dobrzynski H, Camelliti P, Maier SKG, Noble D, Boyett MR Requirement of neuronal- and cardiac-type sodium channels for murine sinoatrial node pacemaking J PHYSIOL-LONDON 559 835-848, 2004

Lancaster MK, Jones SA, Harrison SM, Boyett MR Intracellular Ca2+ and pacemaking within the rabbit sinoatrial node: heterogeneity of role and control J PHYSIOL-LONDON 556 481-494, 2004

Zhang H, Noble D, Cannell M, Orchard CH, Lancaster M, Jones SA, Boyett MR, Holden AV, Jafri MS, Sobie EA, Lederer WJ, Demir SS, Michailova A, Delprincipe F, Egger M, Niggli E, Smith GL, Loughrey CM, MacQuaide N, Dempster J, Trafford AW Dynamics of cardiac intracellular Ca2+ handling - From experiments to virtual cells INTERNATIONAL JOURNAL OF BIFURCATION AND CHAOS 13 3535-3560, 2003

Nikolski VP, Jones SA, Lancaster MK, Boyett MR, Efimov IR Cx43 and dual-pathway electrophysiology of the atrioventricular node and atrioventricular nodal reentry CIRC RES 92 469-475, 2003

Honjo H, Inada S, Lancaster MK, Yamamoto M, Niwa R, Jones SA, Shibata N, Mitsui K, Horiuchi T, Kamiya K, Kodama I, Boyett MR Sarcoplasmic reticulum Ca2+ release is not a dominating factor in sinoatrial node pacemaker activity CIRC RES 92 E41-E44, 2003

Boyett MR, Dobrzynski H, Lancaster MK, Jones SA, Honjo H, Kodama I Sophisticated architecture is required for the sinoatrial node to perform its normal pacemaker function J CARDIOVASC ELECTR 14 104-106, 2003

Musa H, Lei M, Honjo H, Jones SA, Dobrzynski H, Lancaster MK, Takagishi Y, Henderson Z, Kodama I, Boyett MR Heterogeneous expression of Ca2+ handling proteins in rabbit sinoatrial node J HISTOCHEM CYTOCHEM 50 311-324, 2002

Dobrzynski H, Lei M, Jones SA, Lancaster MK, Boyett MR The gradient model of the rabbit sinoatrial node. Korean Journal of Physiology and Pharmacology 6 173-181, 2002

Lei M, Lancaster MK, Jones SA, Boyett MR Role of fast sodium current iNa, in murine sino-atrial node pacemaking. Journal of Physiology 544 pp.39-, 2002

Jones SA, Lancaster MK, Boyett MR Changes associated with ageing in connexin43 protein expression within the sinoatrial node. Journal of Physiology 544 50-51, 2002

Boyett MR, Billeter-Clark R, Dobrzynski H, Honjo H, Inada S, Jones SA, Kodama I, Lancaster MK, Tellez J Heterogeneity and ageing of the sinoatrial node. Journal of Physiology 544 3-4, 2002

Lancaster MK, Jones SA, Boyett MR Differences in intracellular calcium release and removal within the sinoatrial node. Journal of Physiology 544 48-49, 2002

Jones SA, Lancaster MK, Boyett MR Age-associated disappearance of connexin43 within the sinoatrial node CIRCULATION 104 134-134, 2001

Lancaster MK, Jones SA, Harrison SM, Boyett MR Differences in the intracellular Ca2+ transient within the rabbit sinoatrial node J PHYSIOL-LONDON 533 30P-30P, 2001

Dibb KM, Leach R, Quinn CC, Lancaster MK, Findlay JBC, Boyett MR Glutamate residues in the H5 pore region of GIRK1-GIRK4 control Ba2+ block J PHYSIOL-LONDON 527 120P-121P, 2000

Leach RN, Lancaster MK, Boyett MR, Findlay JBC Direct binding of polyamines by Kir channel proteins J PHYSIOL-LONDON 527 118P-118P, 2000

Lancaster MK, Dibb KM, Leach R, Lee JK, Findlay JBC, Boyett MR Slow activation of the cardiac muscarinic K+ channel Kir3.1-Kir3.4 is due to polyamines unbinding from charged sites within the channel pore J PHYSIOL-LONDON 527 117P-117P, 2000

Lancaster MK, Bennett DL, Cook SJ, O'Neill SC Na/K pump alpha subunit expression in rabbit ventricle and regional variations of intracellular sodium regulation. Pflugers Arch 440 735-739, 2000
View abstract

Dibb KM, Leach R, Lancaster MK, Findlay JBC, Boyett MR Cs+ block of the cardiac muscarinic K+ channel, GIRK1/GIRK4, is not dependent on the aspartate residue at position 173. Pflugers Archiv: European Journal of Physiology 440 740-744, 2000

Lancaster MK, Dibb K, Quinn C, Leach R, Lee JK, Findlay JBC, Boyett MR Residues and mechanisms for slow activation and Ba2+ block of the cardiac muscarinic K+ channel, Kir3.1/Kir3.4 Journal of Biological Chemistry 275 35831-35839, 2000

Lancaster MK, Dibb KM, Leach R, Findlay JBC, Boyett MR Multiple residues are involved in the slow activation of the cardiac muscarinic K+ channel BIOPHYS J 78 345A-345A, 2000

Leach RN, Lancaster MK, Boyett MR, Findlay JBC Evidence for direct binding of polyamines to Kir3.1/Kir3.4 channel proteins BIOPHYS J 78 344A-344A, 2000

Dibb KM, Leach R, Lancaster MK, Findlay JBC, Boyett MR Block of the cardiac muscarinic K+ channel Kir3.1/Kir 3.4 by flufenamic acid BRIT J PHARMACOL 128 U21-U21, 1999

Lancaster MK, Bennett DL, Cook SJ, O'Neill SC Expression of Na+,K+-ATPase in rabbit left ventricle J PHYSIOL-LONDON 509P 138P-139P, 1998

Lancaster MK, Harrison SM Changes in contraction, cytosolic Ca2+ and pH during metabolic inhibition and upon restoration of mitochondrial respiration Experimental Physiology 83 349-360, 1998

Lancaster MK, Cook SJ The effects of levosimendan on [Ca2+]i in guinea-pig isolated ventricular myocytes. Eur J Pharmacol 339 97-100, 1997
View abstract

Lancaster MK, Cook SJ Does levosimendan increase calcium load in guinea-pig isolated ventricular myocytes? J PHYSIOL-LONDON 504P P94-P95, 1997

Cook SJ, Chamunorwa JP, Lancaster MK, O'Neill SC Regional differences in the regulation of intracellular sodium and in action potential configuration in rabbit left ventricle. Pflugers Arch 433 515-522, 1997
View abstract

Chamunorwa JP, Cook SJ, Lancaster MK, ONeill SC Rest effects in rabbit ventricular myocytes current clamped using the perforated patch technique BIOPHYS J 72 TH152-TH152, 1997

Díaz ME, Cook SJ, Chamunorwa JP, Trafford AW, Lancaster MK, O'Neill SC, Eisner DA Variability of spontaneous Ca2+ release between different rat ventricular myocytes is correlated with Na(+)-Ca2+ exchange and [Na+]i. Circ Res 78 857-862, 1996
View abstract