Effect of Water Ingestion on HRV: Implications for daily measures

One of the more challenging aspects of implementing HRV monitoring with athletes is ensuring that daily measures are performed reliably. Unreliable or inconsistent measurement procedures can lead to invalid data (false positives or false negatives) and therefore a misinterpretation of training and recovery status. With ultra-short HRV recordings (i.e., ~60 s) it is even more important that measures be strictly standardized to improve the quality of the data.

Waking measures are preferred to capture one’s HRV in a truly rested condition, before any external stimuli can confound the measure. A potential confounding variable that users should be aware of is the effect that water ingestion has on various physiological processes that stimulate autonomic activity and thus alter one’s HRV. This was brought to my attention several years ago by my colleague, Dr. James Heathers.

Immediate changes in HRV take place following water consumption that can last for up to 45 minutes or longer. For example, Routledge and colleagues1 tested the effects of 500 ml water ingestion on HRV in 10 healthy individuals between the ages of 24 and 34 years. On two separate occasions, the subjects reported to the lab in a randomized order for 500 ml water ingestion or 20 ml water ingestion (control). The experiments took place at 8 am before the subjects had anything to eat or drink and after bladder emptying. For a 30 minute period, subjects rested in a semi-supine position before water ingestion. HRV was determined from 5-min ECG windows immediately before and at 5, 20 and 35-min post water ingestion.

Resting HR on average was between 2 – 7 bpm lower than control throughout the post-consumption 45-min period. RMSSD increased between 8 -13 ms during this period compared to control which increased between 2 – 8.8 ms.


Out of curiosity I conducted a similar but much smaller experiment (n=1) to see how HRV responded to 500 ml water ingestion. The data is analyzed in 5-min segments before and after drinking in the seated position with a 1-min period excluded from analysis during which the water was ingested. The tachogram and results are posted below.

water tachogram

Tachogram including pre and post water ingestion

pre water consumption


Post water results


In Martin Buchheit’s, recent review paper, a 3% smallest worthwhile change for lnRMSSD is suggested. In this situation water consumption resulted in an increase in lnRMSSD nearly 2x the smallest worthwhile change.

results table water hrv

*Note that lnRMSSDx20 represents the modified HRV value provided by HRV app’s like ithlete. This has been highlighted for those who are only familiar with these values.

Why does water consumption increase HRV?

The autonomic responses to water ingestion appear to initially be due to the stimulation of osmoreceptors within the gut which causes vasoconstriction (a sympathetic response) and a slight increase in total peripheral resistance.2 Increased baroreceptor sensitivity and increased cardiac-vagal stimulation are thought to occur to counteract the pressor effect (increases in blood pressure) which is why we see a slowdown in resting HR and increase in HRV.2 Effects from the Renin-Angiotensin-Aldosterone system can also not be ruled out given their role in mediating body fluid levels that can effect cardiovascular responses. Water temperature may also have an effect as 250 ml of ice water appears to increase HRV to a greater extent than room-temperature water.3 This may be due to stimulation of thermal vagal receptors in the esophagus.3 Additionally, water ingestion following exercise has been shown to increase parasympathetic reactivation.4

Implications for Daily Monitoring

Tell your athletes to wait until after measuring their HRV to drink fluids and to do so consistently. Otherwise, values may be obscured with a false positive when they drink fluids before the measure.


  1. Routledge, H.C., Chowdhary, S., Coote, J. H., & Townend, J. N. (2002). Cardiac vagal response to water ingestion in normal human subjects. Clinical Science103, 157-162.
  2. Brown, C. M., Barberini, L., Dulloo, A. G., & Montani, J. P. (2005). Cardiovascular responses to water drinking: does osmolality play a role?.American Journal of Physiology-Regulatory, Integrative and Comparative Physiology289(6), R1687-R1692.
  3. Chiang, C. T., Chiu, T. W., Jong, Y. S., Chen, G. Y., & Kuo, C. D. (2010). The effect of ice water ingestion on autonomic modulation in healthy subjects.Clinical Autonomic Research20(6), 375-380.
  4. Oliveira, T. P., Ferreira, R. B., Mattos, R. A., Silva, J. P., & Lima, J. R. P. (2011). Influence of water intake on post-exercise heart rate variability recovery.Journal of Exercise Physiology Online.

Why Assess the ANS?

I just finished watching a presentation by Andy O’Brien entitled “Modern Concepts in Program Design – A Systematic Approach to Individualization”. Andy O’Brien works with elite athletes including NHL star Syndey Crosby. His presentation is 28 minutes long and is truly worth watching if you work with athletes. After listening to his talk, you’ll understand why he works with such high level athletes. I’d also like to add that this is yet another great free resource put out by John Berardi and his team at PN. I have no problem endorsing a company that continually puts out top notch information for free. The thoughts in this post are inspired from the ideas and concepts discussed by Andy O’Brien.

In his presentation, Coach O’Brien essentially views program design as problem solving. Naturally, the first step in designing a program is assessing the athlete. An assessment allows us to form a needs analysis and determine limiting factors that impede progression.

An example was provided of a weight loss client who wanted to lose X amount of fat in time for a wedding. After the trainer decided that diet was not the limiting factor, emphasis was placed on increasing calorie expenditure. What would appear to be a very effective program for improving body composition was prescribed (resistance training, aerobic and anaerobic conditioning, plus a thermogenic supplement). The results however were quite surprising. The client in fact gained fat after several weeks. The reason? Incorrect identification of the limiting factor.

It turns out that the client had a significant ANS imbalance of sympathetic predominance. Even before the exercise program, the nature of her work and lifestyle was highly stressful. Adding intense exercise 5 days/week only further increased this imbalance resulting in unfavorable hormonal responses and poor adaptation to the program.

O’Brien mentions a related study by Messina et al. (2012) entitled “Enhanced parasympathetic activity of sportive women is paradoxically associated to enhanced resting energy expenditure”. Unfortunately I do not have access to this text at the moment but here is an excerpt from the abstract; “These findings demonstrate that resting energy expenditure is higher in the athletes than in sedentary women, despite the augmented parasympathetic activity that is usually related to lower energy expenditure.”

This is one example of why it is important to assess the ANS. I think there are many folks who reject HRV as a useful metric in monitoring athletes or individuals. Perhaps this is because there is a misunderstanding of what the data is telling us or perhaps because interpretation of the data is difficult. Maybe it’s a compliance issue. Regardless, in my opinion, an objective measure of ANS status requires at the very least, periodic assessment for several reasons.

We measure strength, power, body comp, etc. yet ignore one major component of the body that largely acts as a moderator in training response and adaptation. HRV is likely the cheapest and most efficient non-invasive tool we can use to acquire ANS information.

To be clear, I’m not saying that HRV is first in the hierarchy of assessment (if one exists). I’m merely saying that the ANS plays a huge role in our health and performance and requires monitoring and assessing just as much as performance and body composition. How can we rule it out as a limiting factor if we don’t consider it at all?

If you’re not assessing (the ANS), you’re guessing

“If you’re not assessing, you’re guessing” is a phrase often used by strength and conditioning professionals to explain the importance of movement assessment prior to exercise prescription. Prescribing a program that doesn’t consider the athlete’s movement ability (or lack thereof) can end up causing problems.Essentially, you would be guessing that your exercise prescription is helpful when in fact it could be exacerbating a problem. I wholeheartedly agree with this. However this article has nothing to do with movement assessment. This was just my way of illustrating what my next point is.

I am going to apply the same logic we use for why we assess movement (to influence program design) with monitoring the function of the autonomic nervous system (ANS); if you’re not assessing the ANS, you’re guessing.

If you’re unfamiliar with what the ANS is and why it’s important I suggest you read this. In a nutshell the ANS governs “rest and digest” and “fight or flight” responses in the body. This is done without our conscious control. The two components of the ANS are the parasympathetic branch and sympathetic branch. Sympathetic activity is elevated in response to stress be it physical, or mental. Adrenaline is secreted and catabolic activity (the breakdown of structures) ensues. Parasympathetic activity is elevated in the absence of stress and functions to heal and repair the body.

We can monitor our ANS status non-invasively and inexpensively through heart rate variability (HRV). I explain how you can do this here.

HRV as an indicator of autonomic function can tell you a tremendous amount about your athlete’s responsiveness to training. I shared plenty of research in this post that lends support to HRV as an effective tool for; reflecting recovery status, showing better adaptation to training and even predicting performance. In a separate post I shared my thoughts on HRV as a predictor for injury.

Let me summarize what I shared in my initial research review post;

HRV reflects recovery status in elite Olympic weightlifters (Chen et al 2011), national level rowers (Iellamo et al 2004) and untrained athletes (Pichot et al 2002).

Cipryan et al (2007) showed that hockey players performed better when HRV was high while performance was rated lower when HRV was low.

Endurance athletes who improved vo2 max had consistently high HRV while athletes who did not improve vo2 max had low HRV (Hedelin et al 2001).

Endurance athletes who trained using HRV to determine their training loads had a significantly higher maximum running velocity compared to athletes in a pre planned training group (Kiviniemi et al 2007, Kiviniemi et al 2010).

Female athletes who used HRV to guide their training increased their fitness levels to the same level as females in a pre planned training group but the HRV group had fewer high intensity training days (Kiviniemi et al 2010).

(references for the above articles can be found in my original post here.

I’d now like to show some more research that lends support to the usefulness of HRV in monitoring athletes.

Mourot, L (2004) saw decreased HRV in overtrained aerobic athletes. Uusitalo et al (2000) also saw decreased HRV in overtrained female aerobic athletes.

Huovinen et al (2009) measured HRV and testosterone to cortisol (T-C) ratio in army recruits during their first week of basic training. The training was class room based (not physical) and therefore all stress can be considered mental. The authors found that HRV declined in several soldiers, though not all. This demonstrates that, what can be interpreted as stress is highly variable and dependent on the individual. The authors used the terms “high responders” and “low responders” to describe the differences among soldiers. Immediately I thought about the differences among athletes and how their bodies perceive stress. You can’t assume everyone is responding in kind to a training program. What is stressful for one athlete may not be as stressful to another.

All soldiers that showed decreases in HRV also showed lower T-C ratios. In contrast, soldiers with higher HRV had higher T-C ratio’s. Baseline T-C levels were not recorded so we shouldn’t draw any concrete conclusions however it appears that low HRV (increased sympathetic activity with parasympathetic withdrawl) is associated with a reduced T-C ratio.

Hellard et al. (2011) found that in national level swimmers, as HRV dropped (sympathetic predominance) there was an increased risk of illness. The drops in HRV that lead to illness were preceded by a sudden increase in parasympathetic activity the week prior to illness. The authors speculated that the preceding increase in HRV (parasympathetic/vagal activity) was a reflection of the body experiencing the first incubation period and that an increase in vagal activity was a protective response trying to modulate the magnitude of early immune responses to inflammatory stimuli. The subsequent increase in sympathetic activity and decrease in HRV occurs during the symptomatic phase of the illness.

In humans, increased sympathetic activity is generally associated with inflammatory responses while parasympathetic predominance actually inhibits inflammation. At this point in time I will not elaborate on this for the simple fact that I don’t fully understand it. However, we can speculate that if we’re seeing consistently low HRV scores in ourselves or our athletes there is probably an increase in inflammation occurring. Check out Thayer (2009) for more information regarding HRV and inflammation. Simon from iThlete sent me that paper and I’m still processing it.

When dealing with a team or if we train multiple athletes at the same time we need to be aware of how they are adapting and recovering from training. Work by Hautala et al (2001) shows that athletes will recover from exercise at different rates according to fitness levels (obviously). Basically, fit individuals recover faster and show less HRV fluctuation compared to less fit individuals. In a team setting, some individuals who are highly fit may not be getting a sufficient training stimulus while other athletes who are less fit can be overworked.

Kiviniemi et al (2010) found that females take longer to recover from aerobic training than males. This needs to be considered if you are training a mixed gender group.

Buchheit et al (2009) and Manzi et al (2009) both found HRV to be a predictor of aerobic performance.

I’m well aware that the development of athletes has been taking place without the use of HRV monitoring. There are many great coaches and trainers who have their own systems and methods of monitoring recovery in their athletes that work well.

HRV is a tool to use within your own systems. I have thoughts about how I would implement this in a team setting that I will share another time.

To truly autoregulate the training of ourselves or of athletes, we need as much information about present physiologic status as possible. Based on the research and my own personal experience with HRV, this technology takes much of the guesswork out of load/volume manipulation and training prescription. Training hard when HRV is low can be counterproductive and delay recovery. Training hard when HRV is chronically low can lead to illness, injury, overtraining syndrome and suppressed testosterone. Alternatively, increasing load/volume on days when HRV is high can lead to more favourable adaptation. HRV can tell us how stressful the training was for our athletes based on how long it takes HRV to reach baseline in subsequent days. HRV can indicate how much stress your athlete is experiencing outside of training. There are several indications one can take from a simple HRV measurement. Further research will reveal more correlation between HRV and sports performance.

I believe that to train an athlete optimally, we need to be assessing the state of the autonomic nervous system… otherwise we’re guessing.


Buchheit, M. et al (2009) Monitoring endurance running performance using cardiac parasympathetic function. European Journal of Applied Physiology, DOI 10.1007/s00421-009-1317-x

Hellard, P., et al. (2011) Modeling the Association between HR Variability and Illness in Elite Swimmers. Medicine & Science in Sports & Exercise, 43(6): 1063-1070

Huovinen, J. et al. (2009) Relationship between heart rate variability and the serum testosterone-to-cortisol ratio during military service. European Journal of Sports Science, 9(5): 277-284

Kiviniemi, A.M., Hautala A.J., Kinnunen, H., Nissila, J., Virtanen, P., Karjalainen, J., & Tulppo, M.P. (2010) Daily exercise prescription on the basis of HR variability among men and women. Medicine & Science in Sport & Exercise, 42(7): 1355-1363.

Manzi, V. et al (2009) Dose-response relationship of autonomic nervous system responses to individualized training impulse in marathon runners. American Journal of Physiology, 296(6): 1733-40

Mourot, L. et al (2004) Decrease in heart rate variability with overtraining: assessment by the Poincare plot analysis. Clinical Physiology & Functional Imaging, 24(1):10-8.

Thayer, J. (2009) Vagal tone and the inflammatory reflex. Cleveland Clinic Journal of Medicine, 76(2): 523-526

Uusitalo, A.L.T., et al (2000) Heart rate and blood pressure variability during heavy training and overtraining in the female athlete. International Journal of Sports Medicine, 21(1): 45-53