Voluntary exercise-induced changes in beta2-adrenoceptor signalling in rat ventricular myocytes

Area of Science:

• Cardiovascular Physiology
• Exercise Science
• Molecular Cardiology

Background:

• Regular exercise benefits cardiovascular health.
• Intense exercise training and pathological stimuli induce cardiac hypertrophy with distinct molecular adaptations.
• The effects of mild voluntary exercise on myocardial function remain less understood.

Purpose of the Study:

• To investigate how mild voluntary exercise training impacts key myocardial parameters.
• To compare these adaptations to those seen with intensive exercise and pathological hypertrophy.
• To examine changes in ventricular mass, intracellular calcium ([Ca2+]i) handling, and beta-adrenoceptor (beta-AR) stimulation responses.

Main Methods:

• Female rats underwent voluntary wheel-running for 6-7 weeks.
• Real-time reverse transcriptase-polymerase chain reaction measured mRNA expression in left ventricular tissue.
• Single left ventricular myocytes were used to measure cell shortening, [Ca2+]i transients, and inotropic responses to beta1- and beta2-AR stimulation.

Main Results:

• Voluntary exercise induced cardiac hypertrophy (increased heart weight to body weight ratio).
• No significant alterations were observed in myocyte shortening, [Ca2+]i transients, or key Ca2+ handling protein mRNA levels.
• Beta1-AR response and mRNA were unaltered, while beta2-AR mRNA levels and inotropic response were significantly reduced, with the latter restored by pertussis toxin.

Conclusions:

• Mild voluntary exercise induces cardiac hypertrophy but does not significantly alter intracellular calcium handling mechanisms.
• Unlike pathological hypertrophy, voluntary exercise distinctly modulates beta-adrenoceptor responses, reducing beta2-AR function while preserving beta1-AR function.
• These findings differentiate the adaptive responses to mild voluntary exercise from those of intense training and pathological cardiac stimuli.