What are the mechanisms of postprandial (after meal) increase in heart rate, also known as postprandial tachycardia?

From the Guidelines

The postprandial increase in heart rate is primarily driven by the interplay between the parasympathetic and sympathetic nervous systems, with vagally mediated atrial fibrillation occurring more commonly after meals 1. The mechanisms underlying this response are complex and multifaceted.

• The parasympathetic nervous system plays a key role in stimulating digestive processes, while the sympathetic nervous system increases cardiac output to maintain adequate blood pressure despite blood pooling in the digestive organs.
• The physical distension of the stomach and intestines activates stretch receptors, signaling the cardiovascular system to adjust accordingly.
• The digestion of food requires energy, increasing metabolic rate and oxygen demand, which necessitates increased cardiac output.
• Certain foods, particularly carbohydrates, can trigger insulin release, leading to vasodilation and a compensatory increase in heart rate.
• Additionally, some food components like caffeine, tyramine, or high sodium content can directly stimulate heart rate. It is essential to note that the postprandial cardiovascular response is typically more pronounced after large meals and in elderly individuals or those with autonomic dysfunction. The most recent and highest quality study on this topic is from 2011, which highlights the importance of considering the autonomic influences on atrial fibrillation, including the role of vagal and sympathetic activity 1. Overall, the postprandial increase in heart rate is a complex phenomenon that involves the coordinated effort of multiple physiological systems.

From the Research

Mechanisms of Postprandial Increase in Heart Rate

The postprandial increase in heart rate is a complex phenomenon that involves various physiological mechanisms. Some of the key factors that contribute to this increase include:

• Increased cardiac output (CO) in response to meal consumption, which is closely related to the increase in blood flow to the gastrointestinal organs 2
• Release of humoral agents, such as hormones from the duodenal-pancreatic region, which stimulate the heart to increase its postprandial performance 2
• Increases in stroke volume (SV) and heart rate (HR) in response to meal size, with larger meals resulting in greater increases in CO and HR 3
• Changes in total peripheral resistance, which is consistently and significantly reduced in the postprandial period, particularly after large meals 3
• Postprandial changes in left ventricular (LV) longitudinal systolic and diastolic functions, which are measured using tissue Doppler imaging and are correlated with increases in satiety, antral area, glucose, and insulin levels 4
• Increases in heart rate and decreases in blood pressure, which are observed in healthy elderly adults after meal consumption, particularly in the 31-90 min period after beginning eating 5

Key Findings

Some of the key findings related to the postprandial increase in heart rate include:

• The postprandial increase in CO is greater in patients with transplanted and denervated hearts than in normal controls, suggesting that the heart is induced to increase its postprandial performance through the action of a humoral agent 2
• The increase in CO after a large meal is considerably larger and lasts longer than the increase after a small meal 3
• Postprandial CO, HR, SV, and LV longitudinal systolic and diastolic functions increase concomitantly with increased satiety, antral area, glucose, and insulin levels 4
• The use of beta-blockers can influence mortality and the incidence of major cardiovascular events in patients with diabetes and coronary heart disease, particularly in those with a history of myocardial infarction or heart failure with reduced left ventricular ejection fraction 6