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This Article Full Text Full Text (PDF) All Versions of this Article: 93/9/1065    most recent expphysiol.2008.042598v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Stones, R. Articles by White, E. PubMed PubMed Citation Articles by Stones, R. Articles by White, E. Related Collections Heart/Cardiac Muscle

¹ Institute of Membrane and Systems Biology, The University of Leeds, UK ² Departamento de Educação Física, Universidade Federal de Viçosa, MG, Brasil ³ Centre for Integrated Systems Biology and Medicine, University of Nottingham, UK

Regular exercise is beneficial to cardiovascular health. We tested whether mild voluntary exercise training modifies key myocardial parameters [ventricular mass, intracellular calcium ([Ca²⁺]_i) handling and the response to β-adrenoceptor (β-AR) stimulation] in a manner distinct from that reported for beneficial, intensive training and pathological hypertrophic stimuli. Female rats performed voluntary wheel-running exercise for 6–7 weeks. The mRNA expression of target proteins was measured in left ventricular tissue using real-time reverse transcriptase-polymerase chain reaction. Simultaneous measurement of cell shortening and [Ca²⁺]_i transients were made in single left ventricular myocytes and the inotropic response to β₁- and β₂-AR stimulation was measured. Voluntary exercise training resulted in cardiac hypertrophy, the heart weight to body weight ratio being significantly greater in trained compared with sedentary animals. However, voluntary exercise caused no significant alteration in the size or time course of myocyte shortening and [Ca²⁺]_i transients or in the mRNA levels of key proteins that regulate Ca²⁺ handling. The positive inotropic response to β₁-AR stimulation and the level of β₁-AR mRNA were unaltered by voluntary exercise but both mRNA levels and inotropic response to β₂-AR stimulation were significantly reduced in trained animals. The β₂-AR inotropic response was restored by exposure to pertussis toxin. We propose that in contrast to pathological stimuli and to beneficial, intense exercise training, modulation of Ca²⁺ handling is not a major adaptive mechanism in the response to mild voluntary exercise. In addition, and in a reversal of the situation seen in heart failure, voluntary exercise training maintains the β₁-AR response but reduces the β₂-AR response. Therefore, although voluntary exercise induces cardiac hypertrophy, there are distinct differences between its effects on key myocardial regulatory mechanisms and those of hypertrophic stimuli that eventually cause cardiac decompensation.

(Received 5 March 2008; accepted after revision 9 May 2008; first published online 16 May 2008)
Corresponding author R. Stones: Institute of Membrane and Systems Biology, The University of Leeds, Leeds LS2 9JT, UK. Email: r.stones{at}leeds.ac.uk