Discussion: Training your heart rate

Why does training alter your minimum heart rate (resting) but not your maximum?

It has to deal with the differences in the two types of nervous systems that drive the heart rate up and down... further explanation requires a specialist.

A question I have pondered previously too!
It makes sense that bigger, fitter heart copes better, and doesnt need to work as hard.
However, if I use an analogy: Part of the the reason F1 car can go so much faster includes the fact that it can cope with higher RPM's than a normal car. Why therefore doesn't training allow you to INCREASE your max HR?

Something to do with the max rate (speed) of reload for muscle twitch maybe?

As far as I understand, the muscle can twitch faster but faster input to it is unavailable from the nerves that drive the HR up. To my again not very complete knowledge, the max HR has to deal with the topology of the cardiac plexus, specific to the individual and not readily trainable.

Minimum (resting heart rate) is determined by how much oxygen you need at rest. As you endurance train, your stroke volume (amount of blood pumped with each beat) increases, so you need a lower number of beats per minute to pump the same amount of blood, hence resting heart rate will fall (assuming you don't become anemic in the meantime).
The body's capacity to use oxygen is limited in areas other than the heart, so a faster max heart rate, pumping more blood wouldn't increase available oxygen to working muscles anyway.. as for the physiology of why it can't beat faster, I can't remember that bit.

I think the first statement was not quite correct! You need to redefine it.

After 30 years of running I know that training does affect my heart rate. When I'm unfit my max heart rate (let us say at an interval session) is much HIGHER than when I'm fit. The fitter I become the lower my max heart rate goes. The same is also true for my resting heart rate. Training lowers my heart rate across the board in general.

But it alters both my maximum and my minimum heart rate :)

There may be a sizeable difference between the heart rate you attain in an interval session and your actual, physical maximum rate.

ok, then how do you figure out your actual **real** max?

The general rule is 220 minus your age. So at my ripe old age my max would be somewhere about 180. During interval sessions I often get it up over 190 (when I'm unfit) and over 180 (when I'm fit). So that general rule doesn't apply.

Sport tests can also be used to calculate max heart rate. My last test (and I was fit) said my max heart rate was 186 (about 7 years ago). I did a max of 192 the very next week on the track, so clearly that rule doesn't apply.

The only rule that works for me is training. I know when I've pushed a hard session and that I've been to my max. that I can reach. And I also know that when I'm fitter, I go faster, I push harder and I'm still lowering my Heart Rate.

When I'm unfit my max heart rate (let us say at an interval session) is much HIGHER than when I'm fit.

For whatever it's worth, my max HR is utterly independnt of the level of fitness, resting HR also didn't budge after taking a year off, and until I took that year off, the decrease of max HR with age didn't happen with me, either.

220-age is a very broad generalisation to give you a ball-park to work in. There are a bunch of field tests that will get you close to your max HR. You'd probably get a slightly different number from each, depending on conditions, how fatigued you were when you did it, motivation levels etc

T/D I'm surprised your resting HR didn't change. Mine certainly floats higher when I have an extended break (but still not up to what most of the population would consider 'normal')

I've read that some people max drops when they are fit (nad some of the reasons why) but it seems to be something that varies a lot from inidividual to individual, much as the actual max HR value is different from person to person.

Topology(?) of cardiac plexus ... max rate (speed) of reload for muscle twitch?

A constraint on any credible explanation is that, unlike other useful but untrainable things (e.g. leg length), HRMax decreases with age. 220-age works pretty well for me, over enough years to believe the decline.

@Old_Fox: I heard a claim that it was physically possible to exceed "HRM", but at that point the heart wasn't filling completely so you were actually pumping less blood. So a well-trained body with effective feedback working won't let you do such a pointless thing, but if less-well trained, you might.

I've experience a HR of about 250 bpm, but I have a few heart conditions. As Graeme said, when this happens the chambers of the heart aren't actually filling properly each time, so cardiac output doesn't continue to increase.

My maxHR is actually 200 bpm, tested 2 weeks ago.

@ Nixon - high! Wow, having said that a few kids that I train in the age cat between 17 and 23 have (tested) heart rate maxs well over 200 (one had 218), so the 200 bpm is not that unusual (if you are young) I guess.

On the other hand my dad has the exact other problem. He will be 78 this year and is still actively running half marathons in about 2 hours. They put a pace-maker in about 6 months ago because his heart rate was too slow when he was resting and apparently this causes the heart to "forget" to beat. I've never asked him what his max is though, to be honest!

I estimate my max HR to be somewhere around 165-170 bpm. Don´t know if that is normal/high/low or not for my age (60+).

I haven´t had it tested - at least not in the past 40 years or so, but he 220 minus age formula is reasonably close and the rest of my estimation is based on actual HR at hard effort.

Resting HR, again not closely followed, around 58 bpm.

I'd been hoping a biologist would chime in on this, but it doesn't seem to have happened! So here goes a physicist's interpretation. If you look at an EKG (electrocardiogram) which is a picture of the time evolution of the electrical signals which drive the heart beat, you will see a little cluster of peaks (named creatively P, Q, R, S, and T) spaced over a time interval of about 300msec, followed by a long straight line, then another PQRST cluster looking just like the last one. Under exercise with faster heart rate, the length of the PQRST sequence doesn't change, the time between consecutive sequences just gets smaller and smaller, eventually approaching zero at maximum heart rate. The reason for the duration of around 300msec for the contraction and expansion in appropriate sequence of the various chambers in the heart is related to the propagation time of nerve impulses over the size of the heart, and the length of time for the muscle to respond the the nerve impulse and contract (also limited a bit by the time it takes the blood to get squeezed out of a chamber or refill). It is pretty much governed by the size of the heart, which doesn't differ a lot from individual to individual, though generally a little smaller in women, and of course considerably smaller in children. The amount of oxygen transported by the blood circulation is just proportional to the volume displaced in one beat of the heart times the number of beats per second. Training can change the volume of the heart, hence the amount of blood transferred in a single beat, but the volume of the heart varies as the cube of the linear dimensions, so the linear dimensions which change that electrical pulse propagation time change very little with training. So by having a heart that displaces a large volume with each contraction, you can have a very low resting heart rate because you only need a small number of beats per minute. On the other hand, your maximum heart rate is limited to (typically) a little over 200 beats per minute because it would really mess things up if another heartbeat started before the previous one was completed. The nervous system is essentially hard-wired to avoid starting up a new contraction before the previous one is completed (i.e. limiting to one heart beat every 300msec). When this mechanism breaks down you can get very rapid heart beat (fibrillation) with essentially no blood being pumped around. Some versions of this essentially seem to cure themselves after a few minutes, others result in a "heart attack" and death if somebody doesn't come along to provide CPR or help from an electric defibrillator. So the net effect is that if training leads to a heart with bigger volume, at rest it can move the same amount of blood with fewer heart beats, but the same larger volume actually reduces (but only very slightly) the maximum heart rate which is limited by the requirement that one heart beat not interfere with the next.

Great thorough explanation! I for one thank you for sharing your knowledge, as well as the length of time it must have taken to do all that typing!

Just done some googling and various people (Londeree and Moeschberger 1982) have tried to come up with a more precise HRM prediction formula. Apparently the 220 - age was only an observation, rather than a formula following research. One reseacher found athletes over 50 had HRM 3-5 beats more than expected based on age alone and younger athletes a few beats less lower than expected. Put the two together and maybe older athletes HRM slows less than none athletes. If that were the case then training would at least slow down the aging effects. I recall Steve Bird of Saxons (now in Australia) was researching HRM and aging effects with orienteers in the mid-90s.

@eldersmith. Nice... I have this suspicion its not a question that a biologist would ask - so obviously a physicist would know more than a biologist.

propagation time of nerve impulses over the size of the heart,
So you're saying that the nerve impulses propagate slower with age? That this can't be trained. And so 0.5% less oxygen shifted per year would seem to account for most of the slowing down with age up to about 45, when presumably muscle turns to mush too :(

Eldersmith is bang on with everything he says.

I'm not sure about the interpretation of age resulting in a slowing of nerve impulses though. This coming from someone who works on aging in the nervous system. I'm a central kind of girl, not a peripheral, but it's synapse integrity that goes in the brain resulting in slower or badly timed transmission rather than the speed of conduction along the nerve itself. Not sure about neuromuscular junctions though. Conductance slowing generally happens when the myelin lining (insulating) nerves disintegrates, such as in motor neurone disease...not sure about other possible causes.

In summary - despite this almost being my field, I really know nothing about it.

I think eldersmith's point was that the ~300msec PQRST complex is constant across gamut of young and old as well and untrained and trained. The decrease of max HR seen in aging is thus due to some other factor.

An interesting side point is that blood volume in trained endurance athletes seems to be increased 35-40% (abstract) which means that the heart has more to circulate.

@Becks. Nice to hear expert confirmation of what I found on google!
But what I don't understand is how loss of brain efficiency affects heart rate, which AFAIK isn't controlled by the brain?

I'm not sure that it would Graeme, that's why I'm not sure where the slowing is coming from. Certainly you need central input to get to max. Resting rate is pretty much intrinsic to the heart, although interesting slightly slowed by the brain. That's the one fun bit of CV physiology I remember, that if you cut the vagus nerve, (the one responsible for "rest and digest" instead of "fight or flight"), the resting heart rate will actually increase by 10-15 bpm.

I'm going to have to continue thinking about this aging vs max thing though.

A fascinating stream! By way of summary / encapsulation, a few additional insights from an erstwhile physiologist / pharmacologist :-)
1. MHR is genetically programmed via the intrinsic firing rate of the sino-atrial node (HRint).
2. HRint has a normal range of 100-115 bpm and cannot be influenced by extrinsic factors ie it is not trainable, but is influenced by intrinsic (physiological) factors.
3. HRint under “ normal” resting conditions is under predominant vagal tone influence resulting in a firing rate of 60-80 (NB AV node and Bundle of His have slower intrinsic firing rates of 40-60 and the last in the line of cardiac conduction, purkinje fibres @20-40; which if all else fails becomes the ventricular firing rate and is borderline life -supporting)
4. As noted previously, the unique hard-wiring prevents electro-mechanical dissociation under non-pathological conditions; hence protective and by physiologic necessity, limits the top end response
5. Deceased MHR with age is predominantly driven by reduction in HRint coupled with, but to a lesser extent, reduced chronotropic beta-adrenergic responsiveness (eg response to isoproterenol)
6. The governing principle for adaptation to exercise is summarized by the equation:
VO2 ~ CO (Q) = SV x HR ~ MAP/TPR, where CO = cardiac output (flow), SV = stroke volume or amount of output per contraction, MAP = mean arterial pressure and, TPR = total peripheral resistance (factors that display adaptation to training). So, greater central and peripheral organ efficiency reduces demand at rest and hence RHR decline with fitness.
7. Dynamic range for HR > SV (ie 3x vs. 1.7x), such that HR increases preferentially in exercise and pulse band width increases downward (ie RHR decrease) with training.

addendum by a sports physiologist:
your body adapts itself to training as to better cope with the demand. As others have correctly mentioned before there is a point at a high HR where increasing the HR would not pump more blood through the system but rather less, as filling time will be too short.So, you would not want to increase maxHR. There apparently are athletes that have a maxHR a few beats above the most efficient HR, but normally maxHR is just about the limit of efficient pumping. Most of the competitions are (at least in orienteering) also not run at maxHR, so maxHR is not really relevant, but rather the power output at a lower HR.

As to the decline of maxHR in ageing I'm not sure. What I know is that you can delay the decline by regularly working your heart at maxHR. However, I personally, would not recommend this to ageing people, as high heartrates can provoke symptoms of (un)known heart diseases.

As the heart is also a muscle, the decline of maxHR might come from general muscle deterioration (having to do with a different metabolism and hormone levels) ?

Rosstopher is completely right that my earlier post was not intended to look at the decline in max heart rate with age. It would be purely speculation (too lazy to go look things up on the internet!), but to address the decline in max heart rate with age I imagine we should be thinking about what makes the heart go faster when we try to exert more. I would guess that there is something that senses either CO2 levels or O2 levels in the blood, and tries to adjust the heart rate accordingly (since I vaguely remember hearing at some point that respiration is controlled by CO2 levels rather than oxygen, my betting would be on the CO2 level being what is important). If the muscles are burning too much energy, the heart rate will ramp up until it gets the CO2 back to an acceptable level, or until it can't go any faster. If the muscles have declined in mass, or ability to transport fuel or oxygen from the bloodstream into the cells, or CO2 and other metabolites back out of the cell into the nearest vein, then perhaps the heart never needs to go as fast as it in principle could in order to keep the CO2 level down. This would be why if a person keeps training consistently through life there might be very slight decline in max heart rate with age (a phenomenon that seems to be quite typical of readers of this list), while a more average member of the populace whose exercise largely stops upon graduation from school might well just not be able to produce enough CO2 per second to force the heart to crank up to top speed.

Up until the last five years or so when some health issues have reduced most of my training efforts, I think the previous 40+ years had seen a reduction of my own max heart rate by at most 15bpm since I was 20 and the standard formula still worked OK, and probably by rather less, since I'm just going on the basis of highest numbers seen on half-hour or so bike time trials, not from an effort to see what my maximum heart rate might be. So I personally have always been a bit skeptical of that famous linear formula slowing 1bpm per year!

Not to belabor the aging component of this thread (cos reality hurts) however worth positing a couple of thoughts / questions:
Clearly overall endurance performance decline with age is the product of central chronotropic AND inotropic AND peripheral response / utilization components (my earlier point above was merely to illustrate what is known about HRint and age). I suspect somebody has derived a regression equation for a physiologic mutli-compartment model to describe the relative impact of these components. Anyone seen such?
In the end of course this is moot; we OFs just use age-grading to demonstrate that as older athletes we perform as well, if not better than during peak years :-)
Now, some naive speculation on my part- perhaps the ontogenic relationship of specialized cardiac conduction tissue to myocytes, offers some intrinsic coupling protection eg chronotropic response and inotropic responses decay in a similar (maybe parallel) manner over time?
Re MHR per se, clearly a number of extrinsic and intrinsic factors come into play that affect the precision of estimation at any point in time - just as intersubject variability influences which MHR equation best suits an individual, so must intra-subject variability influence time point estimates and hence the reliability of the MHR-age decay constant (to Eric's point)- anyone know these CV numbers off hand?
Now where did I put my glasses?