Archive for July, 2010

Heart Rate Variability (HRV) during exercise

July 18, 2010

The evidence discussed in my recent posts indicates that for moderately fit individuals there is only a narrow gap between the training load required to produce useful improvement in performance and that which results in the over-reaching that leads to reduced  benefits of training.  Hence to obtain optimum benefit from training, it is necessary to  have a reliable way of estimating recovery from previous training sessions.  Furthermore, the evidence, especially the evidence for the recent studies by Kiviniemi and colleagues [1, 2] indicates that adjusting training according to heart rate variability HRV) measured in the resting state each morning might lead to more efficient training.  As discussed in my post on 13th July, I think this evidence is promising but not compelling.

Heart rate during exercise

Many athletes use heart rate during exercise itself as a guide to progress with their training.  Assessment of fitness such as that proposed by Hadd, which employs the relationship between pace and heart rate, assessed over a range of different heart rates, are based on the assumption that a lower heart rate at a given pace is an indication of increased fitness.  On the other hand, when fatigue begins to build up during moderately heavy training, heart rate at a given pace tend to rise indicating the first phase of over-reaching.  In contrast, during very heavy training, a decreased heart rate at a given pace can actually indicate parasympathetic over-reaching.   Provided the measurements are interpreted in context, gradual changes in heart rate at a given pace over a period of many weeks can be a useful guide to changing level of fitness, while short term changes can provide an indication of over-training.

HRV during exercise

These observations raise the possibility that HRV during exercise might be a useful guide to the degree of exhaustion during a training session.  However, there is surprisingly little published information regarding the interpretation of HRV during exercise.  Why should this be so?  The main problem is that whereas HRV at rest is very strongly influenced by the autonomic nervous system, it is not clear what are the main factors influencing HRV during vigorous exercise.

Figure 1 shows a trace which I recorded last year using my Polar RS800cx in R-R mode, during a graded exercise session on the elliptical cross trainer in July.  (Note the figure shows beat-by-beat values of heart rate, which is the reciprocal of R-R interval).  After two minutes of standing still, I exercised at a cadence of 80 cycles per minute and adjusted the resistance such that the power output increased from 30 watts in 7 approximately equal steps, each lasting 4 minutes, up to 230 watts.  After completing 4 minutes at  230 watts, I maintained an output of 30 watts for a further 4 minutes and then stood still for another 4 minutes.

Fig 1. R-R record during progressive increase in Elliptical power output. (18July 2009)

There are a number of idiosyncratic features of the trace which I will ignore for the present discussion.  These include sharp spikes which might be premature atrial beats (or artifact due to disrupted electrode contact).  The dip in heart rate to a value below 80 bpm lasting for around 20 seconds at 5 minutes is a typical feature which I observe in many of my recordings while in the lower part of the aerobic zone, and at present remains a mystery to me.  I have seen this feature in the recordings of other athletes but have not found any descriptions of these dips in published research reports.  However, for present purposes, let us ignore both the spikes and the dips.

The main features of note are:

1)  a large amount of high frequency fluctuation (indicated by the thickness of the fuzzy line) when standing still, in the first two minutes;

2) the amount of high frequency fluctuation reduces subsantially (the line becomes less fuzzy) as HR increases into the range from 80 to 120 bpm, if we ignore the aberrant spikes and dips.  By HR 120 bpm, at around 12 minutes, there is relativley little high frequency variability, though of course HR is continuig to rise slowy under the influence  of the sympathetic nervous system.

3) the high frequency variability then builds up again as HR approaches 140 (my ventilatory threshold, where breathing rate rapidly increases from 40 breaths per minute to 80 breaths per minute), as indicated by the increased fuzziness at around 24 minutes;

4) and finally the variability diminishes slightly as HR approaches its maximum, at around 28 minutes.  (My true maximum HR is probably around160 bpm though I have not actually pushed myself to the maximum in recent years) .

Figure 2a shows the Poincare plot of each interval between consecutive beats against the interval between the preceding pair of consecutive beats, over a 60 second interval around 24 minutes (power output, 200watts).  If a series of beats were equally spaced, the point representing each pair of consecutive beats in the Poincare plot would lie on a straight line inclined at 45 degrees.  The degree of scatter away from the 45 degree line indicates beat by beat fluctuations in HR.  The amount of scatter can be quantified by calculating the quantity, SD1, the standard deviation of the scatter away from the 45 degree line.  In this plot, sd1 is 4.4 ms which is typical of values I observe at the upper end of the aerobic zone.  Figure 2b shows the natural log of SD1 calculated for 60 second epochs at the end of each of the 4 minute steps, when HR is relatively stable.

2a. Poincare plot at 200watts. 2b. Plot of log (SD1) against heart rate (18 Jul 2009). Red arrow denotes HR at 200watts

It should be noted that estimating HRV during a period when HR is varying due to increasing work load presents problems.  Various  measures other than SD1, such as a scaling factor designated alpha computed on the basis of the theory of nonlinear systems (i.e. chaos theory), have been proposed, but the interpretation of such measurements is fraught with difficulty.  This is illustrated by poor consistency between measurement of alpha in the same person in  sessions a week apart [3].  Hence I think it is best to employ SD1 despite the limitations of this measurement.   The reason that it is conventional to plot the log of SD1 is that during the early phase of increasing exercise intensity, parasympathetic influence falls away exponentially.  An exponential decay would be expected to produce a straight line when plotted on a logarithmic scale.

Figure 2b confirms that high frequency HRV (as quantified by the log of SD1) falls rapidly from standing to low intensity exercise; continues to diminish gradually in the lower aerobic zone and then increases around the anaerobic threshold before decreasing again as HR approaches maximum.  This is fairly typical of what is seen in other athletes, though I exhibit a more abrupt initial withdrawal than I observe in others.

What determines HRV during exercise?

It is widely accepted that the initial fall off in high frequency HRV (as HR increases from its resting value) is due to withdrawal of parasympathetic influence.  Once in the aerobic zone, parasympathetic input is minimal and further increase in heart rate is driven by increased sympathetic activity [4].   However, high frequency variation at around respiratory frequency is not entirely abolished even in the mid-aerobic zone, suggesting that some other factor is contributing.  It is quite likely that intrinsic variability in the function of the sinoatrial node (the collection of  specialized muscle cells in the right atrial wall which fire spontaneously and normally act as pace-maker) plays a substantial role.  In a transplanted heart, which does not receive any input for the parasympathetic or sympathetic nervous system, heart rate variability during exercise is similar to that in a heart with intact input from the nervous system.  Casadei and colleagues from Oxford carried out a study in which they used the pharmaceutical agent, atropine, to block parasympathetic nervous activity, and observed that about a third of the variability of heart rate in the lower aerobic zone, can be accounted for by non-neural mechanisms [5].   Perini and colleagues [6] have argued that the most plausible alternative mechanism is mechanical.  For example, respiration would be expected to produce rhythmic stretching of tissues that might change the excitability of the pace-maker leading to variability at the respiratory frequency.  Furthermore, mechanical effects are a plausible explanation for the prominent increase in the magnitude of high frequency fluctuation around the anaerobic threshold, at which point respiratory effort increases markedly.

However, I remain a little skeptical that mechanical effects account fully for the high frequency variation in the upper aerobic and anaerobic zones.  In particular, excessive high frequency fluctuation during vigorous exercise appears to be a significant predictor of poor long term health.  For example, in a large study of 1335 subjects, mainly males, Dewey and colleagues from Stanford University [7] demonstrated that increasing magnitude of high frequency fluctuation during vigorous exercise (and also during the recovery phase) was a significant predictor of mortality  in general, and especially of cardiac mortality, in the following five years.   This suggests that HRV during vigorous exercise might reflect some physiological process that is indicative of impaired cardiac well being, probably something more subtle than the simple mechanical effects of respiration.  Might that putative physiological marker of impaired cardiac well-being be sensitive to the state of recovery during training?

HRV during exercise when fatigued

Observations of my own HRV during exercise confirm this hypothesis.  Last summer, my preparation for the Robin Hood half marathon had been seriously disrupted by quite severe bout of illness in June.  I had missed about 4 weeks of training, and attempted to build up training volume in July, in preparation for the  race in early September.  As described in my blog posting on 31st August 2009, I developed quite marked fatigue during August.  In an attempt to determine if the fatigue was affecting my heart, I had repeated the graded increase in exercise on the elliptical cross trainer at the end of August, following an identical schedule with 4 minutes at a series of seven steps spanning a range of power output from 30 to 230 watts, to that employed on 18th July. The R-R trace for 31st August is shown in figure 3, while fig 3a is an expanded view comparing the variability in the period 23-25 minutes  on 31st Aug with that on 18th July.  Figure 4a depicts the Poincare plot based on R-R intervals at 23-24 minutes on 31st August and Figure 4b shows the natural log of SD1 calculated for 60 second epochs at the end of each of the 4 minute steps.

R-R trace during progressive increase in Elliptical power output (31 August 2009; fatigued)

fig 3a: Expanded view of HR variability in the period 23 to 25 minutes, before (18 July) and during fatigue (31 August)

4a. Poincare plot at 200watts. 4b Plot of log (SD1) against heart rate (31 August 2009, red arrow denotes HR at 200watts)

The most prominent feature is that on 31st August, there was a much more dramatic increase in high frequency HRV as I approached the anaerobic threshold (shown by the marked fuzziness of the line around 24 minutes).  Furthermore, despite a subsequent increase in power output from 200 to 230 watts,  heart rate scarcely rose in the following 4 minutes.  In contrast to the similar test on 18th July, when HR rose to 157 bpm at a power output of 230 watts, on 31st August the peak heart rate was 145 bpm.  Subjectively, I experienced tremendous fatigue and found it very difficult to complete the 4 minutes at 230 watts.  Thus, on this occasion overwhelming feelings of fatigue limited my power output and were associated with excessive high frequency HRV.

The greater amount of high frequency variability is also clear from the wide scatter of points away from the 45 degree line in the Poincare plot and the relatively large peak in the value of log (SD1) at a heart rate of 145 bpm, visible in the plot of log (SD1) against HR.   (Compare fig 4a and 4b with fig 2a and 2b).

Although I have not subsequently experienced such overwhelming fatigue, there have been a number of occasions in which I have observed excessive high frequency HRV in association with moderate fatigue, sometimes when exercising in the lower aerobic zone and sometimes near anaerobic threshold.  For example, a few weeks ago I became increasingly tired during a hectic week at work.  On the Friday evening (18th June) I set out to do an easy 7.2Km run in the lower aerobic zone.  I felt tired and lethargic throughout.  The R-R trace (figure 5)  for a 15 minute segment in the middle of the run, when my pace was stable at 5:56 min/Km, shows marked high frequency fluctuation in heart rate.  Average heart rate was 124 bpm and SD1 was 9.0 ms.  For comparison figure 6 shows a similar 15 minute segment in the mid-stage of a 7.2Km low aerobic run on the same path in January.   Pace was somewhat faster at 5:39 min/Km, average heart rate was a little lower at 122 bpm, and high frequency variability was much less (SD1= 3.8ms).

Fig 5. R-R record in the mid-section of a 7.2Km low aerobic run when exhausted (18 Jun 2010)

Fig 6. R-R record during the mid-section of a low aerobic run (3 Jan 2010)

The following week I developed signs of an upper respiratory tract infection.  The R-R trace during an interval session on the elliptical machine is shown in Figure  7.  High amplitude fluctuation in heart rate can be seen in the second, third and fourth effort epochs.  During the crest of the second effort epoch, SD1 = 12.8ms

For comparison the R-R trace during a virtually identical elliptical interval session performed a week later when the respiratory tract infection had resolved, is shown in figure 8.  The magnitude of HRV is much less, and SD1 at  a comparable period in the 2nd effort epoch is 2.5 ms.

Fig 7. R-R record during an interval session while suffering a mild viral infection (24 Jun 2010)

Fig 8. R-R record duirng an interval session after recovery from the viral infection (9 Jul 2010). (Vertical arrows denote dips in HR possibly due to sympathetic withdrawal)

Although not all of the data provides quite such clear-cut information as the illustrations I have presented here, on many occasions on which I have felt fatigued or sluggish, there as been excessive high frequency HRV.  This feature is observed in various different types of session including steady running in the lower aerobic zone, tempo sessions, interval sessions and progressive increases in exercise intensity from the low aerobic to the anaerobic zone.  In contrast to resting HRV, where increased high frequency HRV is generally an indication of good recovery (except during advanced stages of over-reaching)  increased high frequency HRV during vigorous exercise generally appears to be an indicator of greater stress.

I do not know what physiological process is responsible for this. Perhaps some central governor generates ‘protective’ parasympathetic activity even at exercise intensities at which parasympathetic influence would normally be minimal.  Alternatively, in view of the fact that I suffer from asthma, it is possible that these episodes of fatigue are associated with subliminal constriction of my airways that results in more labored breathing and hence greater mechanical forces on my heart.  However, I have observed this phenomenon on many occasions when I am not aware of any breathing difficulty.  I would be very interested to hear if anyone else has observed similar increases in high frequency variability during exercise when under stress.

The dips: could they be due to transient sympathetic withdrawal?

[Note added 29 Nov 2010: the dips are almost certainly due to a transient surge of parasympathetic actviity associated with relaxation of smooth muslce at the the oesophageal-gastric junction – as  discussed with Steve in the comment section below]

Although I have not hitherto focused on the dips in HR that I frequently observe when exercising in the lower aerobic zone, or as my heart rate drops during the recovery from intense exercise, I have marked these by black arrows in figure 8.  Similar dips are also visible in figs 1,5,6 & 7 .   I have no reason to connect these to the increases in HRV associated with fatigue.  In fact the duration of these dips is typically 10-20 seconds.  If they are due to influence of the autonomic nervous system, they might possibly reflect sympathetic withdrawal, which would be expected to act on this time scale   They do not appear to be a marker for fatigue, but nonetheless I wonder whether they too might reflect a protective effect generated by a putative central governor.  I  have observed these dips in the traces of other athletes, but would also be very pleased to hear from others who have observed similar dips.  Because of the relatively long time scale, such dips would in fact be seen more readily in a record of HR averaged over 5 second intervals.

Is ‘real time’ assessment of HRV during exercise practical?

If indeed the excess HRV during exercise is a reliable marker for undue stress, would this be of any practical use?   The R-R trace is not generally available for inspection until after the completion of the session. However, in principle it should be possible to produce a continuous read-out of HRV averaged over a preceding period of about 20 seconds.  In fact the Polar RS800cx produces a measure called RLX.  Although it is difficult to obtain a precise account of the computation on which RLX is based, it appears to be very closely related to a continuous estimate of SD1.  Furthermore, according to the Polar manual, it should be possible to present the continuously updated value of RLX in the display of the wrist unit.  I have been unable to do this, and think that it is yet another manifestation of the fact that my particular RS800cx is infested with gremlins.  However as far as I can tell from retrospective examination of RLX values, the Polar computation of RLX is based on computation over too short an interval to provide reliable values.  I suspect that if I can convince myself that it would be worthwhile having access to a continuous read-out of high frequency HRV while exercising, it would probably be necessary to develop some more sophisticated way of performing the computation.

References

[1] Antti Kiviniemi, Arto Hautala, Hannu Kinnunen & Mikko Tulppo (2007) Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol. 101(6):743-751.

[2] Kiviniemi AM, Hautala AJ, Kinnunen H, Nissilä J, Virtanen P, Karjalainen J, Tulppo MP . (2010) Daily exercise prescription based on Heart Rate Variability among men and women. Med Sci Sports Exerc. 42(7):1355-63

[3] Tan CO, Cohen MA, Eckberg DL, Taylor JA (2009) Fractal properties of human heart period variability:physiological and methodological implications J Physiol 587.15 pp 3929–3941

[4] Rowell LB, O’Leary DS (1990) Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes J. Appl. Physiol. 69(2): 407-418

[5} Casadei B, Moon, J, Johnston J, Caizza S, Sleight P (1996)  Is respiratory sinus arrhythmia a good index of cardiac vagal tone in exercise? J.Appl. Physiol. 81(2): 556-564,

[6] Perini R, Veicsteinas A (2003) Heart rate variability and autonomic activity at rest and during exercise in various physiological conditions. Eur J Appl Physiol  90: 317–325

[7] Dewey FE  Freeman JV, Engel G, Oviedo R, Abrol N, Ahmed N, Myers J, Floelicher VF (2007) Novel predictor of prognosis from exercise stress testing: heart rate variability response to the exercise treadmill test. Am Heart J, 153(2) 281-8.

More thoughts about HRV-guided training

July 13, 2010

After yesterdays’ post on HRV guided-training, in which I discussed the two studies by Kiviniemi and colleagues [1,2], I realized that what I had written might give the impression that I undervalue the findings of those studies.  Although I do not consider that those studies provide convincing evidence about the practical value of HRV-guided training, I do consider that they provide some very thought-provoking findings.  To me the crucial point in both studies is that they demonstrate that for recreational athletes, doing more than three intense sessions per week is likely to result in over-reaching. 

In the first study, the participants were club runners.  In the second study they were moderately active individuals doing about 2 exercise sessions per week.   In both studies, the intense sessions included 30 minutes of tempo running at 85% of HRmax.  In both studies, scheduled intense sessions were replaced by low intensity sessions or rest if there was a moderate decrease in HRV measured in the morning.  In both studies, the control group following the fixed training schedule did at least one more intense session per week than the HRV-guided group, implying that a decrease in HRV exceeding the threshold dictating abandonment of an intense session occurred at least once per week.   Furthermore, abandoning at least one high intensity session per week was associated with significantly greater improvement in performance by the end of the study

In the first study, the control group performed four high intensity sessions per week while in the second study the control group performed an average of 3.3 high intensity sessions per week  These studies provide clear scientific confirmation of a fact that many athletes and coaches have discovered through experience: doing more than three high intensity sessions per week  is counterproductive.  In the case of frequent intense sessions, more pain does not usually produce more gain.

The narrow gap between Scylla and Charybdis

A further conclusion that can be drawn from these studies is that even for recreational runners there is a fairly narrow gap between the training load that is required for worthwhile improvement in performance, and the training load that results in over-reaching.  Because most recreational athletes do not have an experienced coach to steer them between Scylla and Charybdis (the mythical sea monsters on opposing rocky shores, threatening to wreck hopes from either side) each individual needs to work out a satisfactory way of judging for themselves how intensely to train. 

What do we hear when we listen to the body.

One approach is simply to ‘listen to the body’; reduce intensity whenever the body complains; and rest whenever the level of fatigue becomes excessive.  The problem with this approach is that it is very difficult to decide what level of fatigue indicates significant over-reaching.  It is not uncommon to experience sluggishness during the early part of a training session and then fell lively later in the session.  If we rest whenever we feel moderate fatigue we are unlikely to achieve our full potential. 

Another approach is to include an easy week in the schedule every fourth or fifth week.  In general, this can be a fairly successful strategy, and is included in many recommended training schedules. However, there is little evidence to guide an individual regarding to the adjustment in load that is best for him or her.  Optimizing training for the individual requires knowledge abut the individual’s own response to training.  

The message from the heart

My own experience, particularly in the period following my episode of illness last summer, is that measurements of heart rate and heart rate variability do provide a useful guide in deciding whether feelings of fatigue indicate significant over-reaching.  However, I am still undecided as to which measurements are most informative.   Last August, I found that the decrease in the magnitude of the heart rate rise during an orthostatic test was the most reliable guide (as discussed in yesterday’s post).  However, at that time I was suffering from parasympathetic over-reaching. 

The studies by Kiviniemi and colleagues suggest that even the early phases of sympathetic overreaching are associated with diminished benefit from training.  Therefore, I am still eager to explore the possibility that HRV might be a practical guide to adjusting training intensity.  While I do not think the studies by Kiviniemi provide convincing evidence, I think the evidence that they do provide is encouraging.

References

[1] Antti Kiviniemi, Arto Hautala, hannu Kinnunen & Mikko Tulppo (2007) Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol. 101(6):743-751.

[2] Kiviniemi AM, Hautala AJ, Kinnunen H, Nissilä J, Virtanen P, Karjalainen J, Tulppo MP . (2010) Daily exercise prescription based on Heart Rate Variability among men and women. Med Sci Sports Exerc. 42(7):1355-63

Training guided by heart rate variability

July 12, 2010

In recent weeks I have focused on the role of my Polar RS800cx in alerting me to the possibility of atrial fibrillation.   While this has been an interesting and perhaps important diversion, my primary purpose in obtaining a Heart Rate Monitor with the capacity to measure heart rate variability (HRV) had been to explore its utility for monitoring my training, and in particular, for the identification of over-reaching and overtraining.   In this post, I will return to my original purpose, and address the question whether or not it has proven useful.  But first of all, it is worth reviewing the published literature on the subject.

HRV at rest

The most consistent body of evidence comes for studies that employ measurement of HRV at rest.  Several different processes contribute to fluctuations in heart rate. One of the most important is the fluctuations known as respiratory sinus arrhythmia (RSA).  Heart rate accelerates as you breath in and decelerates as you breath out. This fluctuation is a one of the main contributors to high frequency fluctuations in HR (frequency range 0.15 – 0.4 Hz).  At rest, RSA is governed by the parasympathetic division of the autonomic nervous system.  It serves to ensure that the flow of blood via the pulmonary artery from heart to the lungs in maximal when the lungs are full of air.  You can easily appreciate this variation in heart rate by manual palpation of the pulse at your wrist as you breathe in and out slowly.   The magnitude of this fluctuation provides a good measure of the activity of the parasympathetic nervous system, which has the overall role of regulating bodily processes concerned with rest and recovery.  Hence, the magnitude of RSA at rest is a fairly good indicator of how well recovered you are from a heavy training session.   

In general, heavy training causes a short term reduction in high frequency HRV but as recovery proceeds there tends to be a compensatory rebound reflecting increased fitness.   If HRV is still reduced the morning after an intense training session, yet another intense session is likely to produce yet further reduction the following morning, but eventually there is a somewhat paradoxical switch from parasympathetic under-activity to parasympathetic over-activity – perhaps the body’s self-defense strategy in the face of persistent stress   By this stage, parasympathetic over-reaching is on the way to becoming the seriously debilitating condition know as parasympathetic over-training, characterized by persistent fatigue, low mood and reduced performance.

In principle, monitoring high frequency HRV each morning can be used to determine whether or not you are sufficiently well recovered to undertake another heavy training session.  The practicality of this was first demonstrated in a study by Kiviniemi and colleagues from Oulu in Finland [1].  They used morning measurements of high frequency HRV to adjust the training of a group of male recreational athletes over a period of 4 weeks.  They compared increases in fitness, assessed by measurement of VO2max and also maximal running speed during a graded maximal exercise test on a treadmill, in 9 young men who trained according to HRV guidance, with the increases in fitness in a matched group of men who undertook a fixed training schedule comprising 4 high intensity sessions, 2 low intensity session and one rest day per week.  

In the HRV guided group, HRV was measured using a Polar s110 monitor, during 3 minutes of sitting followed by 5 minutes of standing at home each morning.  Because parasympathetic effects in fit athletes can be saturated when sitting, HRV during the 5 minutes of standing was employed to guide training. The calculation was done automatically using Polar software, and included a quite elaborate procedure for removal of artifact.  The full details of the schedule for adjusting training according to HRV were complex, but the crucial issue was that it high frequency HRV measurement was below a threshold level set at one standard deviation below the mean of the measurements in the  preceding 10 days, low intensity training or rest was selected for that day.    

To check on the reliability of the calculation of HRV, the data was subsequently examined in the laboratory using a more sophisticated procedure based on an 18th order autoregressive spectral model.  One the 10 subjects was dropped from the study because the laboratory check did not agree with the automatic computation performed at home.  In view of the frequency of artifacts in HRM data, this is perhaps not entirely surprising, though in my own experience, artifacts during resting or standing recordings are extremely rare if the belt has been properly moistened.  Maybe there was some other malfunction, or perhaps the subject had an abnormality of heart rhythm.  Whatever, the explanation, the fact that 1 in 10 subjects was dropped is an indication that automated measurement of HRV is not entirely free of technical hitches.

The outcome of the study was that the HRV guided group showed increase in both VO2max and also in maximum running speed in the treadmill test (from 15.5 to 16.4 Km/Hr).  The comparison group who followed the standard training protocol also showed improvement, with maximum running speed in the test increasing from 15.1 to 15.7 Km/Hr.  The increase in maximum running speed was significantly greater in the HRV guided group.  The difference between groups in in increase in VO2 max was not statistically significant.

Thus, this study provides encouraging evidence of benefits of HRV guided training. However, before recommending that serious athletes should invest in a HRM with the capability of measuring HRV, several points should be noted.  Most important was the fact that the standard training protocol included  4 intense sessions per week, in two back-to back  pairs of sessions.  Many coaches and athletes would regard back-to-back intense sessions as creating too great a risk of over-training.  The intense session involved warm-up followed by  30 minute tempo run at 85% HRmax, which I would regard as only moderately high intensity.  Nonetheless, the fact that in the HRV guide group the average number intense sessions was only three per week indicate that that appreciable  over-reaching occurred at least once per week on average, confirming what many sensible coaches and athletes know: back-to-back intense sessions are risky.   This would be  expected to impede the development of the benefits of training.  Furthermore, it is probable that at least some of the standard group were in a state of over-reaching which might have impaired performance on the test day.  In the example provided in the manuscript, illustrating the training of one of the  individuals  in the standard training group, the individual did show evidence of impaired HRV on the test day.   Finally, in view of the non-trivial the cost of a HRM capable of measuring HRV, it would be interesting to know if a resting pulse measurement, or maybe a measure of the orthostatic rise in pulse on standing from sitting, would have provide adequate information to guide training.

A replication

More recently Kiviniemi and colleagues have reported a similar study [2] in a group of 21 men and 22 women, with only a moderate level of preceding activity.  In this study, HRV was assessed similarly, during 3 minutes of standing.  The measurement employed was SD1 – the spread across the 45 degree line in the Poincare plot (as illustrated in my post of 17th July 2009).  SD1 is a little easier to compute than high frequency power, but is closely related to high frequency power.  The training program was for eight weeks. The standard protocol specified at least 3 high intensity sessions per week (the average number achieved was 3.3 /week) .  In the males, the outcome was very similar to the earlier study: improvement in maximum output during testing on a cycle ergometer was significantly greater in the HRV guided group than the standard training group, though the increase in VO2 max did not differ significantly between groups.  In the women, there was no significant  difference between groups in the improvement in fitness, but the HRV guided group did fewer intense sessions.  Again, it is clear that the HRV guided protocol detected over-reaching at least once per week, confirming that back-to-back intense sessions is undesirable.

 In conclusion, the two studies by Kiviniemi and colleagues confirm that HRV guided training produces greater improvement in fitness than standard training that includes excessively frequent  high intensity sessions.  The question of whether similar improvement in training could be achieved more cheaply by manual recording of morning heart rate, or by more sensible coaching, remains unanswered.

My own experience

Last summer, I was quite ill for several weeks, and as I recovered I faced the need to get fit enough to race a half-marathon in about 7 weeks time.  I cautiously increased training intensity to include two moderately intense sessions per week (eg 5K at 80-85% HRmax) and a longish run.  However I had not allowed for the degree to which I had been debilitated by my illness, and after about four weeks I began to feel quite marked fatigue.  Measurement of HRV suggested that I was suffering from over-reaching.  However simple measurement of the orthostatic rise in HR provided even clearer evidence that I was suffering from quite serious parasympathetic over-reaching.  I usually have an increase in HR of about 8-10 BPM on standing from resting, but this orthostatic increase was abolished entirely as the fatigue developed, as shown in the figure. 

Orthostatic increase in heart rate showing nadir on 18th August. red arrows indicate long-run days; blue arrows indicate rest days

I was able to implement adjustments to my training schedule that resulted in relief of the fatigue after about 2 weeks.  In fact I was not completely recovered, as I will reveal in my next post, but my aerobic fitness was enough to run the half-marathon.  Unfortunately due to inadequate number of long runs my leg muscles were not well conditioned and  I tore one of my hip adductors after about 10 Km.  I limped painfully with a stride that was very short and with virtually no airborne time, for the final 11 km.   Despite this mishap, my experience is that monitoring for signs of over-reaching is indeed worthwhile, though my experience does not answer the question of whether or not it is worth investing in a HRM capable of measuring HRV.

But what about measurement of HRV while running?  That is a far more complex question, which I will address in my next post*.

*Added note: discussion of HRV whle running deferred until the post after next

 

References

[1] Antti Kiviniemi, Arto Hautala, hannu Kinnunen & Mikko Tulppo (2007) Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol. 101(6):743-751.

[2] Kiviniemi AM, Hautala AJ, Kinnunen H, Nissilä J, Virtanen P, Karjalainen J, Tulppo MP . (2010) Daily exercise prescription based on Heart Rate Variability among men and women. Med Sci Sports Exerc. 42(7):1355-63

Rollercoaster

July 4, 2010

George Newton, the man who contributed  much of the material regarding the interpreting heart rate recording during atrial fibrillation (AF) on the afibbers website [1], had left an interesting comment on my previous post on 27th June questioning whether my Polar RS800cx was a boon or curse.  As illustrated in my post on 28th February, some of my chaotic recordings had raised the spectre of AF, but due to various inconsistencies in the data, I was left in a quandary.  George’s initial conclusion was ‘Your data clearly looks like afib’. 

AF is widely regarded as enigmatic and unpredictable, but in his own experience, George had found that systematic monitoring  using various different methods ranging for simple manual recording of the pulse to recording the full ECG, can provide a large measure of control over the condition  He has virtually eliminated his own AF by adjusting intake of electrolytes and other supplements according to the frequency of premature contractions, which at least in his case, are a fairly reliable indicator of imminent AF.  

Although he has acquired experience of many different recording devices, he largely uses a Polar S810 (similar to my RS800cx) to record the rhythm abnormalities.  By comparison with full ECG recordings, he has established the R-R tachogram signatures of the various relevant abnormalities, including premature atrial contractions (PACs), premature ventricular contractions (PVCs) and AF itself. He has also assembled a body of useful information about the artifacts that can arise from poor electrode contact or movement

I myself have had several reasons for continuing to doubt whether or not I truly had AF. The most important piece of evidence had emerged during a recent relaxed run in delightful countryside in Leicestershire with my friend Marie (who had run in the London marathon with her husband a few weeks after she had been diagnosed with cancer, and has subsequently recovered well from surgery).  During our run through the Leicestershire country-side I was feeling quite relaxed, but when I glanced at my Polar monitor I noted that it was displaying a heart rate around 125 whereas I would have expected a rate of around 110 at that pace.  I immediately stopped to palpate my pulse.  It was regular apart from the decreasing  rate expected on cessation of running.  There was certainly so evidence of AF, so we continued on our way. 

When I got home I was dismayed when I examined the beat-by-beat record of my hear rate (the R-R tachogram).  It indicated a horrible chaotic rhythm throughout much of the run – though frustratingly, it had failed to record the data for about half of the duration of the run,  including the time when I had stopped to examine my pulse manually.  The only absolutely certain conclusion was that my Polar RS800Cx was not storing data properly.  It was impossible to determine if my heart was also malfunctioning.  Nonetheless, the normal manual assessment during a run in which the recorded segments of the tachogram showed a chaotic rhythm raised serious doubts in my mind about the reliability of the evidence for AF.

I had also been puzzled by two other features of my chaotic tachograms.  In the recording I had posted in February, careful inspection reveals that interspersed with the chaos are many brief periods (typically 5-15 seconds in duration) of what appears to be fairly normal sinus rhythm (figure 1).  In fact the heart rate is a little higher than expected for the pace.  Within the periods of apparently normal sinus rhythm, the average rate was 122 bpm compared with an expected rate around 115, but in the icy conditions on that December day, I would not have been surprised if my average heart rate was a little higher than usual as I struggled to remain upright.  However, the heart rate variability is also somewhat greater than usual. At this pace, I would normally expect a value of RMSSD (root mean square of successive R-R intervals, a measure of high frequency variability) of around 5 ms, but RMMSD is in the range 10-20 ms during the periods of apparent sinus rhythm.  I would usually compute RMSSD over a longer period than 10 sec, so this value should be interpreted with caution.  Nonetheless, it suggests excessive parasympathetic activity.    Thus my provisional (and very speculative) interpretation of the rhythm during this period is of a series of premature atrial contractions occurring against a background of sinus rhythm with excessive parasympathetic activity. 

R-R tachogram showing apparent premature atrial contractions interspersed within sinus rhythm

Secondly, on several of the occasions when I had recorded apparent AF, the average pulse was as low, or lower, than that expected for the pace.  It is hard to imagine that a chaotic rhythm could pump enough blood to allow me to continue to run comfortably without any increase in overall rate to compensate for the inefficient ventricular filling.

With these uncertainties in mind I sent two of my tachograms to George – the one showing interspersed periods of apparently near normal sinus rhythm, and one showing a net decrease in rate.  He was kind enough to search through his own records and produced a similar record which included periods of normal sinus rhythm interspersed within chaos.  On account of the fact that his AF episodes are symptomatic, he was quite confident that this was not AF.  He was also able to reassure me that overall rate would certainly increase rather than decease during true AF.  Meanwhile Henry Szwinto, who had commented on my post of 5th June, had also sent me some traces of his experiences with AF while racing – confirming the dramatic increase in HR during AF.  As an aside, Henry achieved 2:41:11 in the London marathon this year and was 3rd placed in the 50 year old veteran group.

So in this roller-coaster experience in which the evidence has swung to and fro, the pendulum is now swinging away from a diagnosis of AF, though I think that the evidence does suggest that I am prone to premature atrial contractions.   There are still a few puzzles.  Why did the early evidence indicate a strong association with use of the salbutamol inhaler which I use to control my asthma?  As the evidence of chaotic rhythms has continued to accumulate, it has become clear that salbutamol was only associated with chaotic rhythm in winter. On some occasions when I had used salbutamol, I had noted in my log that the paths were icy, as in the run depicted in figure 1.  Perhaps freezing temperatures increase the risk of both wheeziness and poor electrode contact; or perhaps salbutamol increases the risk of premature atrial contractions.   

At this stage I am fairly optimistic that I do not have AF.  I am still on the waiting list for a 3 weeks continuous ECG recording and I will await the outcome of that before attempting to reach a definitive conclusion.  If the picture is still ambiguous after that, I will happily accept that some uncertainties in life are inevitable, and it would be foolish to limit ones activities for fear of vague uncertainty.  The simple fact that elderly men have a substantial risk of AF already places me in a high risk group, and ambiguous evidence from a heart rate monitor scarcely adds to the level of risk.

With regard to the question of whether or not my HRM is a boon or a curse, I am fairly sure the answer is that  a trustworthy HRM with the capability of recording R-R tachograms is a boon – although my unreliable RS800cx has been something of a nuisance.  I did not send it back to Polar last week because I was eager to acquire as much information about both the behavior of the monitor itself and the behavior of my heart before relinquishing it, but I will send it back this week.

The important issue that this episode of chaos has brought home to me is the fact that for an elderly runner, the risk of AF is appreciable, and the consequences potentially serious.   Furthermore, the experiences of George Newton, and others who have learned how to monitor their heart rhythm in an intelligent manner, is that paroxysmal AF is not necessarily an enigmatic mystery, but might be amenable to control. 

And finally, while the association between endurance training and increased risk of AF remains a subject of debate, it seems to me very plausible that the sustained autonomic imbalance associated with over-training is likely to play a large role in determining whether AF becomes an intractable problem or resolves relatively harmlessly.  I will return to a more detailed discussion of this issue in further posts, but meanwhile, I am more impressed than ever by the importance of avoiding over-training.  So far, the evidence suggests that systematic monitoring of autonomic function by recording both HR and HRV is a useful way to minimize the risk.

So the answer to the question posed in my last post is that my particular Polar RS800cx was indeed something of a nuisance, but despite this, it taught me a lot, and I have little doubt that a reliable HRM with R-R recording capability is a worthwhile investment for any ‘serious’ elderly athlete*.  

* For monitoring autonomic funtion via measurement of HRV to minimise risk of over-training; not for diagnosing AF, which requires  a clinical-quality ECG recording interpreted by a qualified person.

 References

[1] http://www.afibbers.org/conference/session52.pdf