Bone mechanical loading reduces heart rate and increases heart rate variability in mice

Area of Science:

• Physiology
• Cardiovascular Science
• Bone Biology

Background:

• Cardiovascular disease and osteoporosis are clinically linked.
• Bone responds to mechanical strain by altering structure and releasing signaling molecules.
• Bone also has endocrine functions affecting other tissues, including the heart.

Purpose of the Study:

• To investigate if mechanical loading of bone acutely alters cardiac function.
• To determine if neural and/or endocrine mechanisms mediate this bone-heart interaction.

Main Methods:

• In vivo mechanical loading of the tibia in anesthetized mice.
• Monitoring cardiac parameters using electrocardiogram (ECG).
• Utilizing pharmacological agents (lidocaine, propranolol, atropine) to probe neural pathways.

Main Results:

• Tibial loading caused an immediate, transient reduction in heart rate and increased heart rate variability.
• A minimum load of 3 N was required to elicit the cardiac response.
• The cardiac response to bone loading was blunted in aged mice (11-12 months).
• Lidocaine and propranolol (sympathetic antagonist) significantly diminished the heart rate response, while atropine (parasympathetic antagonist) did not.

Conclusions:

• Tibia bone loading acutely modulates cardiac function through a neuro-mechanical reflex.
• This bone-heart reflex involves a hindlimb afferent pathway and reduced efferent sympathetic tone.
• The bone-heart connection is age-dependent, weakening with aging.