Heart Variability and Stress Explained: How to Measure It, Healthy Ranges, How to Increase It

Heart Rate Variability became an area of interest during the 70s, when it was deployed to monitor the health of newborn babies as well as to track recovery rates of athletes. Since this time, it has been shown to provide insights on the overall health status of the individual; it provides a quantified information that correlates well with many concerns, from general stress response, glycaemic status and inflammatory activity, to outcomes in depression, cardiovascular disease, IBS and beyond.

When we use HRV measurements

HRV measurements are used as a proxy for vagal tone. The vagus nerve has both afferent (body-to-brain) and efferent (brain-to-body) fibres. It uses this dual-direction communication to continuously monitor energy availability (itself a product of mitochondrial performance, insulin/thyroid signalling, etc) and the extent of energy-stealing processes (inflammation and stress). Then, based on the perceived level of resources, turns on signals from the brain to body. Increased vagal tone calms activity in defence-related systems (eg. immune system, HPA axis) and increases it in areas that relate to social engagement or homeostasis (eg. prefrontal cortex, digestive tract, etc). As such, it plays a central role in whether we are in ‘fight-or-flight’ or in ‘rest-and-digest’ mode, ie. stressed or relaxed, and HRV measurements allow us to quantify such tendencies in the individuals we work with.

It common summary of HRV is that it tells us how stressed we are. That being said, if we want to employ HRV measurements to assist in clinical decision-making, I have found it more useful to define HRV/vagal tone as an indicate of how much resources the individual has at their disposal for non-emergency tasks (in most scenarios, this is exactly the same thing, but I feel it better frames our considerations when structuring a treatment plan).

This is because practitioners will inevitably see a whole host of individuals who

1. show imbalances that call for major intervention, such as pronounced bacterial dysbiosis (undesirable balance of the microbial populations in the gut)
2. do not have the resources to benefit from the intervention

It can therefore be imperative to know who has the resources to benefit from the approaches that lab results indicate are necessary. If we do not have this information, we can easily pour energy and time into building a protocol that is intelligent in design and directly targets the issues revealed by testing… and see nothing but die-off symptoms, with no benefits to show in the aftermath. How  imperative is this information? Let’s go back to a survey I undertook in 2017. It’s not a scientific study, but it charts the progress observed in individuals based on HRV status (eight per group, apart from the final group, where there were only five). What did it show?

Note 1: there are some individuals who show paradoxically high HRV scores despite obvious stress-related pathology (who are discussed below). I rarely recommend any anti-microbial action for such individuals, and there they are not represented in these graphs.

Note 2: the graph above plots the responses of individuals to intestinal bacterial issues (eg. excessive Klebsiella, E Coli, Clostridium or insufficient lactobacillus, Bifidobacterium). I’ve observed repeatedly that low-HRV individuals have not shown the same problems when it comes to eradicating H Pylori and parasites – a potentially important point to share, although we will save discussion of this for another time.

In short, the reason we want to make us of HRV testing is that it can allow us to efficiently screen who is capable of responding to the intervention in question, and who may need more systemic support in pathways affecting energy/stress/inflammation ahead of taking the same steps. Put another way, it can save us and our clients a lot of time, disappointment and discomfort.

How Does HRV measure stress?

HRV measurements track the natural up-and-down variability in our heart rate, which is aligned to our breathing and mediated by vagal cardiac tone, which acts as the ‘brake’ on baseline stimulation of the heart rate. Whenever we breath in, sympathetic inputs into the heart are activated. When we breath out, the parasympathetic (vagal) inputs are activated. Measuring the strength of this braking effect provides us with a proxy of overall vagal tone and it is due to this relationship that we can gather insights as to the overall stress status.

The vagus nerve is the main nerve of the parasympathetic nervous system, the branch that is responsible for the ‘rest-and-digest’ response. It innervates almost every organ system in the body (in fact, its name originates from its ‘vagrant’ nature, and reflects its role as the wondering nerve); in doing so, it plays a permissive role for activity in many systems that use up energy but do not contribute to active defence. Think digestion, detoxification, cellular healing and other health-supportive activities. It plays a crucial role in giving mammals the metabolic flexibility needed to respond to threats, while also being able to switch into an undefended, socially-engaging mode (needed to yield the social support that has enhanced survival for millennia). In short, vagal tone is key in diverting energy investment away from unwanted stress responses and undesirable inflammatory activity, and instead towards health-promoting activity.

The emphatic role of the vagus nerve in supporting our well-being is well-demonstrated by research that shows how increased vagal tone enhances activation of the prefrontal cortex, an area of the brain that governs executive function, learning/planning, verbal clarity, mood and resilience to stress. The fundamental role it plays on energy distribution – that is to say, diverting resources from inflammation and the stress response towards those that support healthy metabolic activity – is further underscored when we see how it can predict risk of conditions as diverse as diabetes, depression, and dementia, as well as the ’medically unexplained’ issues (eg. chronic fatigue). What makes this field particularly exciting is that, as well tracking progression of such issues, HRV may have a role to play in improving outcomes; HRV-driven biofeedback has been shown to improve results in several studies, including those on depression, anxiety and overall emotional health.

The above should make clear why our profession is so keen to enhance vagal tone and why HRV measurements have been enthusiastically embraced by a growing number of practitioners.

However, there are caveats to the picture that we might otherwise form from the literature referenced above. As with most research, these papers outline the relationship between HRV measurements and overall vagal tone (and, thus, stress status of the individual) based on averages. As a result, it does not speak for the outliers, who make up only a tiny proportion of the population under study but are substantially more likely to seek out the support of naturopathic practitioners. To this end, it is important to recognize that, although healthy stress status reliably permits stronger vagal tone and explains why we see such strong correlations in the literature, there are two key points to consider:

• cardiac inputs from the vagal tone does not always reflect overall vagal tone
• The vagus nerve is activated whenever the autonomic nervous system wishes to ‘demobilize’ our defence systems, which can be part of a healthy response (no threat, no benefit in mobilizing, aims to free up resources for social engagement systems, ‘rest-and-digest’) or a particularly unhealthy response (overwhelming threat, no benefit in mobilizing, conserves resources to preserve life until threat has passed, ‘freeze’)
• Parasympathetic dominance does not equal ‘good’, it equals ‘demobilized’ (which is normally a good thing… more of this in a second).

These caveats are crucial when it comes to accurate interpretation of the measurements we obtain.

How to interpret measurements

Above, we touched on what HRV measurements are actually measuring (vagal modulation of heart rate) and how this is normally, but not always, a reliable reflection of vagal activity promoted by autonomic nervous system as part of the ‘rest-and-digest’ response.

As such, its normally a case that interpretation of HRV is simple: low numbers mean low variability in heart rate, which means low vagal influence, which reflects low vagal tone, which indicates low availability of resources (mobilized, aka stressed). High numbers mean high variability in heart rate, which means high vagal influence, which reflects high vagal tone, which indicates high availability of resources (demobilized, aka not stressed).

But not always. As mentioned above, the parasympathetic nervous system is deployed as a ‘brake’ on mobilizing our resources for defensive purposes. While this is crucial for diverting energy towards structures that promote homeostasis and social engagement, there is another circumstance where the autonomic nervous system shuts down our defences. This is not due to a lack of threat, a circumstance where defences are unnecessary, but the very opposite; when the threat is perceived as so overwhelming that defences are futile. This is the ‘freeze’ response and sees mammals ‘play dead’ until the threat passes. This too sees the parasympathetic system deployed to act as a brake on defences, and this includes a lowering of heart rate.

Crucially, this response to overwhelm results in a strong vagal input into the heart to achieve the desired effect. By repeatedly pushing the heart rate down, we see increased variability in the heart rate. This paradoxically produces the HRV figures we would otherwise expect in particularly healthy individuals.

Depending on the type of clientele that choose to get in touch, certain practitioners may only encounter these paradoxical HRV measures on very rare occasions. However, those that deal with more complex/chronic cases can expect to observe them much more frequently. For context, a 2006 study actually sub-grouped PTSD patients by their autonomic patterns and found that one third displayed this ‘freeze’ pattern (indexed by heart rate and HRV).

Identifying when high HRV scores reflect a healthy autonomic status and when it reflects the shut-down response is relatively easy, due to the patterns that we see on the frontline:

It is worth noting that, although the above chart neatly groups individuals into three categories, both clinical observations and the mechanistic literature (Porges et al, 2009) demonstrates that all systems are active at all times and that such classification relates to which system is dominant rather than to one of the parasympathetic/sympathetic branches being ‘on’ with the other ‘off’. I go into the patterns (and the implications that this has for both treatment decisions and tracking progress) in the Structuring a Treatment Plan module of the Academy course, but there are three major takeaways when working with individuals who are in a ‘freeze’ state:

• Should they engage in the Western medical system, they will be misunderstood, mislabelled and passed from one specialist to another (often slapped with labels like ‘functional autonomic disorder’)
• We should expect improved resources (eg. targeted mitochondrial support) to help take them out of the ‘freeze’ response, which means that they will reliably become ‘mobilized’ (sympathetic-dominant), with stress response and inflammatory activity increased accordingly (alongside the expected symptoms). This is not a ‘bad’ reaction but required updated support
• Transition between states is rarely a smooth/instant transition, and individuals will often do so in a ‘two steps forward, one step back pattern’ whereby support needs to be adapted/updated in line with these changing needs

What is a healthy range for HRV measurements?

The most common question when it comes to this subject! It can be difficult to make useful conclusions when looking at the literature, due to the changeable study population used by different researchers. However, a meta-study of 44 different publications found that the average HRV figures reported were 42 rMSSD.

Of course, the most enlightening information on this matter comes from observations on the front-line. To this end, the graph above (that charts success rates by HRV bands) tells an important story. It speaks both to the importance of available resources in influencing our responses to various interventions, but also on how HRV readings are predictive of success in these matters.

A rule of thumb for HRV measurements:

Less than 40 = fight and flight/maximally mobilized, all resources allocated to defence, no ability to divert resources away from the ‘emergency’

40 – 80 rMSSD = mobilized, substantial resource allocated to defence, varying flexibility to divert resources (although this will be limited and done so on a robbing-Peter-to-pay-Paul basis)

80 rMSSD and above = rest and digest/relaxed,

Why is this a rule of thumb rather than a universal law? Because there are caveats, which include the parasympathetic shutdown (‘freeze’) response described above, as well as additional factors that influence the readings we will see, such as sex and genetics. Those who are subject to the freeze response do not adhere to the sub-groupings laid out here (for reasons that I hope are obvious), although these rules will apply to them as much as anyone else once they shift into a sympathetic-dominant state (where they will normally join the ‘standard scale’ somewhere in the 20s).

What difference to genetics make? Enough to matter but not nearly as much as has been implied by the camps that assert that ‘you can’t compare your HRV scores to others’. The variance in view seems based on studies that report a large genetic component to the figures we observe; six studies have looked into this (here, here, here, here, here and here) and found that 11-57% of the reported differences were accounted for by genetics. This sounds big until we look a little deeper and realize that every single one of these studies excluded those with chronic disease or stress-related pathology. In other words, they all removed the major contributors to differences in HRV; remove the big factors, and you will substantially overstate the contribution of each factor that remains. Two of these studies reported rMSSD scores and, by taking maximal differences shown between groups (6.3-13.4) and the contribution allocated to genetics (11-57%), we can make a back-of-the-envelope calculation of the actual impact of genetics. This comes in at 0.7-7.7 rMSSD. Relevant, but not enough to invalidate comparisons between individuals.

Sex is also another factor for which a similar story applies.  A 2015 study found that younger females recorded HRV scores that were 2.5 rMSSD higher than their male counterparts, although there was no difference in the over-50 age groups.

How to measure HRV

The most common way to measure HRV is through the iconic Oura ring, which uses a tiny camera to measure the pulse rate. It comes in at around £250 (plus obligatory subscription, an annoying new feature that Oura brought in on their third generation ring), although it should still be easy enough to pick up a second generation model (no subscription). The change to the Oura offering comes at a time when competitor rings have recently hit the market, most notably the Circular ring. How this performs on the frontline is something I am yet to confirm (those who have tried it, please comment).

However, outside of the ring-based options, consumers remain subject to a range of options. These include the ECG belts (once the only way to get this data) and smart bands (Fitbit, Whoop and Apple are known to measure HRV). However, the cheapest way to get started with HRV monitoring is to make use of camera that most of us already own – the one on our smartphone – and pair it with a suitable app. There are several apps that do a good job here, although I’ve regularly recommended Camera Heart Rate Variability (£4.19 on Android, £7 on Apple) and been happy with the information and usability.