The Biomedical Basis of Elite Performance 19-21 March 2012 London, UK
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The Biomedical Basis of Elite Performance 19-21 March 2012 London, UK Abstracts & Manuscripts Physiology 2012 2-5 July Edinburgh International Conference Centre United Kingdom Key dates Submit your abstracts by 31 March 2012 Apply for a travel grant by 31 May 2012 Prize lecturers Cori Bargmann - Rockefeller University, New York, USA Gareth Leng - University of Edinburgh, UK Diane Lipscombe - Brown University, Providence, USA Jere Mitchell - UT Southwestern Medical Center, Dallas, USA Peter Ratcliffe - University of Oxford, UK Holly Shiels - University of Manchester, UK www.physiology2012.org Contents Plenary Lecture abstracts 5 Symposium abstracts 9 Oral & Poster Communication abstracts 35 Abstract author index 144 Symposium speakers’ manuscripts 149 About the BPS With almost 3000 members, the British Pharmacological Society (BPS) is the primary learned society in the UK concerned with research into drugs and the way they work. 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YouTube Standard Tariff - Free Contact CLICK Become a member - Paul Tizard, Membership and Awards Officer www.bps.ac.uk/members Tel: +44 (0) 20 7239 0171 E-mail: [email protected] PL1 Contribution of respiratory and locomotor muscle afferents to the cardio-ventilatory responses to rhythmic exercise in humans - The Physiological Society’s 2012 Bayliss-Starling Prize Lecture J.A. Dempsey Population Health Sciences, University of Wisconsin-Madison, Madison, WI, USA When studied in isolation, stimulating muscle afferents clearly increases ventilation and sympathetic vasoconstriction – but their contribution remains uncertain when activated in a physiologic setting, i.e. in the presence of other powerful influences from central command and other reflex receptors. We and others have studied exercising canines and humans to determine that metaboreflexs from the diaphragm and expiratory muscles are activated in heavy exercise in health and during moderate exercise in disease states, thereby enhancing sympathetic vasoconstrictor outflow and affecting blood flow distribution between limb and respiratory muscles. These influ- ences on oxygen transport exacerbate the rate of exercise-induced locomotor muscle fatigue and reduce exercise performance. A unique vasoreactivity of the diaphragm vasculature contributes importantly to these selective responses. Blockade of opiate-sensitive spinal afferents from the legs all cycling intensities caused hypoventilation and reduced MAP and heart rate. Endurance exercise performance was also impaired primarily because of reduced O2 transport. On the other hand, loss of feedback via afferents from fatiguing limbs also meant less inhibition of central locomotor command, resulting in a “choice” to continue exercise (or augment power output), thereby precipitating excessive peripheral fatigue. The relative importance of muscle afferents is likely altered in the presence of CHF and COPD, with aging, in hypoxic environments and with training. Our understanding of exactly which stimuli / conditions during rhythmic exercise activates these metaboreceptors remains incomplete, as does our knowledge of additional influences arising from interactive effects between feedback and feedforward mechanisms. Supported by NHLBI. Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements. 5 PL2 The biological basis for exercise and health F.W. Booth, J.D. Brown, K.E. Parker, M.J. Will and M.D. Roberts University of Missouri, Missouri, MO, USA Epidemiology has associated physical inactivity with 35 detrimental conditions/diseases; they are: accelerated secondary aging, pre- mature death, low cardiorespiratory fitness, sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endo- thelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, preeclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases. Deteriorating function with physical inactivity underlies some of the above conditions. After 20 days, healthy young men in the classical Dallas bed rest study had 11% lower heart volumes, 26% lower maximal cardiac outputs, 29% lower maximal stroke volumes, and 28% lower maximal oxygen consumptions. Microgravity of 1-yr space flight produces hipbone loss that would take 10 years to occur on Earth, illustrating gravity’s role with physical inactivity. A 3rd example is reduced daily steps. Healthy young men who reduced their daily steps from 10,501 to 1,344 for a 2-wk period displayed a clustering of metabolic alterations that included an increased insulin response to an oral glucose tolerance test, increased plasma triglyceride response to an oral fat tolerance test, a 7% increase in visceral fat, and a 0.5-kg loss of lean leg mass. A cellular basis was decreased insulin-stimulated ratio of pAktthr308/total Akt in vastus lateralis muscle after step reduction. Two animal models utilized by us to delineate the molecular basis of inactivity will be described. In the first model, rats have been selec- tively bred now for 7 generations to separate and contrast the phenotypes of motivation to voluntarily run long distances (HVR) vs. the motivation to voluntarily run low distances (LVR). An average 6-fold distance in voluntary running now separates HVR and LVR selected lines. HVR had reduced voluntary running after injection of D1 dopamine receptor agonists and antagonists into the nucleus accumbens of the rat brain, while LVR had no responses (Physiol Behav 105:661, 2012). The second model locks wheels for voluntary running (WL) resulting in elimination of daily running. The mRNAs and proteins for the mechanosensor genes Ankrd2 and Csrp3 fell in young, grow- ing rats. Relative to WL5h controls, plantaris muscle Ankrd2 and Csrp3 mRNAs were lower at WL53h, WL173h, and SED; Ankrd2 protein tended to decrease at WL53h (p = 0.054) and Csrp3 protein was less in WL173h and SED rats (J Appl Physiol Epub Jan 26, 2012). Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements. 6 PL3 How science, medicine and engineering has changed how athletes train and perform S. Drawer and C. Cook UK Sport, London, UK Arguably sport science is in its infancy, with the first robust publications truly directed at the subject appearing many years after physi- ological and medical related treatises relevant to similar subject areas. While understanding in biomedical sciences has progressed almost exponentially since the advent of modern biology of the Watson and Crick era, the same can’t really be said for sport science at its application edge. Often sport science appears undertaken with little reference to more progressive and better work in fundamental fields of biomedical endeavor. This does not necessarily need to be the case. Much work of high caliber in biomedicine and engineering can be piggy-backed on to do innovative work at the applied end of sport science. While innovation is not always viewed as novel or pure in the academic sport science perspective it can both escalate and accelerate applied adoption of good fundamental concepts and indeed