A normal heart does not beat with perfect regularity. Even at rest, the time between heartbeats varies by a few tens of milliseconds. This variation is called heart rate variability (HRV).
HRV reflects how the heart is influenced by the autonomic nervous system – the part of the nervous system that controls bodily functions without us having to think about them. High variability at rest is usually a sign that the body is well rested and that the calming branch of the nervous system is in charge. Low variability may mean that the body is tired, stressed, ill or not yet recovered from training.
Smartwatches and heart rate straps have made HRV something everyone can measure, through concepts such as «Body Battery» and «HRV status». On these pages I try to explain what lies behind the numbers, how they are measured, and why the type of sensor matters a great deal.
Where does the variation come from?
Heart rate is controlled by the autonomic nervous system:
- The parasympathetic system (the vagus nerve) brakes the heart. Its transmitter, acetylcholine, is inactivated only a few seconds after release, and the latency between a change in blood pressure and the vagal response is less than one second. This implies that vagal activity can influence the heart rate from beat to beat.
- The sympathetic system makes the heart run faster and contract harder, and redistributes blood flow by constricting or dilating blood vessels. Its transmitter, noradrenaline, is removed more slowly, and the full sympathetic response may not occur for as long as 20–30 seconds.
These differences in response delay form the basis for interpreting HRV. Changes in one branch are usually accompanied by opposite changes in the other.
A heart without any nervous control – for example a recently transplanted heart – beats at 110–120 beats per minute. At rest, vagal tone reduces the heart rate from this intrinsic value to 60–80 beats per minute.
The most obvious variation follows breathing. When you breathe in, the heart rate rises, and when you breathe out, it falls. Respiration causes rhythmic pressure fluctuations in the chest, which are followed by oscillations in blood pressure and vagal activity. There are also direct connections between the respiratory and cardiovascular centres, which lie close to each other in the brainstem. These spontaneous alterations in vagal activity are known as respiratory sinus arrhythmia, which is completely normal. It is most pronounced in the young and fit – the healthiest among us.
The control centre sits in the brainstem. It constantly receives signals from pressure sensors (baroreceptors) in the carotid arteries, the aorta and the heart. A rise in blood pressure stretches the arterial wall and triggers the baroreceptors, which increase their signalling to the cardiovascular centre. The centre responds by increasing vagal activity, slowing the heart. In this way the heart rate is adjusted beat by beat to keep blood flow stable.
Read more
- How HRV is measured – time domain, frequency domain, and why ECG beats optical sensors
- What affects HRV? – age, sleep, training, stress, medication and energy and readiness scores
- HRV and training – morning readings and DFA α1
- Pitfalls – ectopic beats, atrial fibrillation and noise
- My research – my doctoral thesis on autonomic control of the heart
References
- Sevre K, Rostrup M. Undersøkelser av hjertefrekvensvariabilitet og baroreflekssensitivitet [Heart rate variability and baroreflex sensitivity]. Tidsskr Nor Lægeforen 2001; 121: 3059–64.
- Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability: standards of measurement, physiological interpretation and clinical use. Circulation 1996; 93: 1043–65.
- Sevre K. Autonomic cardiovascular regulation in healthy subjects and patients with cardiovascular disease. Doctoral thesis. University of Oslo, 2001.