Research group of Integrative Clinical Physiology

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Our research program focuses are physical capacity and cardiovascular and skeletal muscle remodelling in healthy (young) individuals, in aging and in various diseases such as heart failure and intensive care unit (ICU) patients. Our main target tissue is skeletal muscle but other tissues/organ systems in our research programs are the myocardium and the vascular system.  Our approach is to be integrative and have a translational approach to create and use tools to answer specific scientific questions.

Our research program focuses are physical capacity, cardiovascular and skeletal muscle remodelling in healthy young individuals, in aging and in various diseases such as heart failure and intensive care unit (ICU) patients. Our main target tissue is skeletal muscle but other tissues/organ systems are included in our studies, such as the myocardium and the vascular system.  

The first component in our research program is to investigate mechanisms in healthy subjects, including signalling pathways involving capillary growth, mitochondrial biogenesis and protein synthesis in the skeletal muscle response to increased physical activity. At present, the focus in these projects includes analyses of satellite cells, circulating pluripotent cells and matrix degeneration in skeletal muscle remodelling.

Another important aspect of our research is to study the influence of gender on cardiovascular and skeletal muscle function,  by investigating these organ systems before and after sex reassignment. This will enable an evaluation regarding the effects of sex steroids on these systems in adult humans.  The second component is related to the changes in skeletal muscle structure and function involved, primarily or secondarily, in various diseases and states, such as heart failure, in ICU patients and in aging. In these conditions the importance of intrinsic skeletal muscle changes is well documented, and a common denominator is neuroendocrine stress. Beyond the processes described above, at present our aim is to investigate the importance of calcium disturbance in reduced skeletal muscle function and activation of atrophy processes. Our hypothesis is that neuroendocrine stress induces post-translational changes of intracellular calcium handling proteins in skeletal muscle, leading to a dysfunctional calcium handling. Elucidating the mechanisms behind such perturbations would provide an important future target in the protection of muscle loss in the diseases stated above.

The third and last component is to identify biomarkers for complex conditions such as sarcopenia and muscle wasting in critical illness. In these studies our aim is to identify genetic markers that are associated with early onset and risk of development of severe muscle loss and dysfunction in aging, critical illness and in the progress of heart failure disease. Secondly we want to identify genetic markers that distinguish responders from non-responders to physical activity. In these studies, the overall goal is to be able to better identify high-risk subjects and those that may benefit from more aggressive preventive strategies. 

Research group leader Thomas Gustafsson

Head of office

Thomas Gustafsson

Organizational unit: Division of clinical physiology

Group members

Seher AlamResearch assistant on study grant
Helene FischerSenior researcher
Thomas GustafssonSenior researcher
Eva JanssonProfessor, senior
Mats LiljaProject coordinator
Tommy LundbergSenior researcher
Eva MaretAssociated
Michael MelinClinical assistant
Barbara NormanSenior researcher
Karl OlssonGraduate Student
Eric RullmanSenior researcher
Amarjit SainiPostdoc
Carl Johan SundbergProfessor
Patrik SundbladAssociate professor
Anna WiikSenior researcher

Research techniques

  • Physiological testing (VO2, strength measurements, accelerometer)
  • Ultrasound (Cardiac and vascular system)
  • Blood and muscle sampling
  • Microdialysis and catheterisation
  • DNA (SNP, methylation) RNA (Real time, microarrays), miRNA, protein (Western and ELISA), protein localization (confocal and electron microscopy). 

External funding

Swedish Medical Research Council, Heart lung foundation, Wallenberg Foundation, ALF, Magn Bervall Foundation, KI foundation, Swedish National Centre for Research in Sports, Swedish Society for Medical Research, FP-07 Metapredict, Industrial cooperation 

Teaching assignments

Lecturing, laboratory teaching and examiner in the basic courses for nurse student, physical therapists students, biomedical science students, naprapathy student, medical students as well as in post graduate courses

Teaching areas: Physiology and pathophysiology in cardiopulmovascular, renal and gastrointestinal systems and in exercise an environmental physiology. Pathology in peripheral arterial diseases, myocardial ischemia and conductance disorders in the heart. Technology in ultrasonographic investigation of the cardiovascular system and use of this technique in the clinic. 

Selected publications

Bone marrow derived cells in adult skeletal muscle tissue in humans.
Strömberg A, Jansson M, Fischer H, Rullman E, Hägglund H, Gustafsson T
Skelet Muscle 2013 May;3(1):12

Modifications of skeletal muscle ryanodine receptor type 1 and exercise intolerance in heart failure.
Rullman E, Andersson D, Melin M, Reiken S, Mancini D, Marks A, et al
J. Heart Lung Transplant. 2013 Sep;32(9):925-9

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks.
Lessard S, Rivas D, Alves-Wagner A, Hirshman M, Gallagher I, Constantin-Teodosiu D, et al
Diabetes 2013 Aug;62(8):2717-27

Molecular networks of human muscle adaptation to exercise and age.
Phillips B, Williams J, Gustafsson T, Bouchard C, Rankinen T, Knudsen S, et al
PLoS Genet. 2013 Mar;9(3):e1003389

New records in aerobic power among octogenarian lifelong endurance athletes.
Trappe S, Hayes E, Galpin A, Kaminsky L, Jemiolo B, Fink W, et al
J. Appl. Physiol. 2013 Jan;114(1):3-10

AgeingCell BiologyMetabolismPhysical activity