If the pump don’t pump - - - - - you don’t go 
                                 Said by an ice hockey coach in my distant past

 

There is much discussion about training ones heart to pump more (safely).  We will start with some simple take-aways and as always keep your medical professional involved.

Here is a term to understand:  Cardiac Remodeling.  “People engaged in chronic exercise programs have improved cardiovascular function. This is observed not only in healthy subjects but mainly in those with any type of cardiovascular risk factor or disease. Even in people over 70 years old, exercise training can lower systolic, diastolic, and median blood pressure”….

…“From the cardiovascular point of view, increases the left ventricular (LV) ejection fraction, decreases end-diastolic pressure, improves vascular function, and increases cardiac angiogenesis and cardiac muscle mass. Among these adaptations, our focus in this review will primarily be on the increase in cardiac muscle mass termed herein as exercise training-induced cardiac hypertrophy” (Fernandes, et al., 2015).

Note:  “Lance Armstrong's heart rate (HR) rested at about 32 beats per minute (BPM), while Bolt's HR rested at around 33 BPM. Similarly, swimming legend Michael Phelps kept a resting HR of about 38 BPM throughout his professional career” (REAN, 2023).

From an engineer’s perspective the heart can be defined as a positive displacement diaphragm pump (Pumps.org, 2024).  As a diaphragm pump, this device used to move blood around, has two options or ways of making sure the right amount of blood is available for the given routine experienced by the body.  The first is, if the size of the pump remains the same, the blood demand is satiated by heart rate or beats per minute.  The faster your heart beats the more volume is realized.  Another way of thinking about this is rpm in your car.  The higher the rpm the faster you go.  The faster you go the more wear and tear you have on the pump.  This leads to the second option.

The second option is to obtain a bigger pump in terms of volume displaced per beat per minute.  Here, your rpm is lower and as such the wear and tear is less, but the volume demand is met.  Well, you cannot just switch out your heart for a bigger one, so what is the athlete left to do? 

Side bar:  In the world of horse racing, “at autopsy, the heart of the highly successful American racehorse Secretariat, was estimated to be ~10 kg (22 lbs). In comparison to normal horses, whose hearts weigh ~3.9 kg (8.8 lbs), hearts of these sizes would be capable of generating extremely large cardiac outputs. Examining the link between heart size and aerobic capacity in horses, Young and colleagues have shown strong positive relationships between various measures of heart size and 𝑉˙O2max, a key determinant of endurance performance” (Shave, et al., 2017).

Here is how the body “does” the second option and it’s termed Cardiac Remodeling as outlined above.  Remodeling means that the body makes the heart bigger along with the associated arteries and veins.  Why does it do that?  Simple, it reduces the wear and tear on the system.  The body is an amazing machine.

Example:  Uriah.  His hip flexor and hip extensor strength has not appreciably changed since high school nor has his stride length.  Here is what is really kewl, his heart rate is way less for the same speed in high school.  What changed?  His heart pumping system has become remodeled.  More about how he trained to attain this further on.

The next topic is what is an athletes maximum heart rate?  To cover this in more detail we first have to address a concept called the Central Governor Theory.  Noakes (2001) best explains the Theory this way:

“The central governor theory proposes that afferent sensory information from the heart, but also perhaps from the brain and respiratory muscles, informs the brain of any threat that hypoxia or ischaemia may develop in those organs. In response, the central governor acts via the motor cortex to reduce the efferent neural activation of the exercising muscles, thereby reducing the mass of muscle that can be recruited and, hence, reducing the exercise intensity that can be sustained. The existence of peripheral governors in skeletal muscle and heart is proved by the rapidly deleterious effects of ischaemia on contractile function of both the heart and skeletal muscles and the existence of the condition of myocardial hibernation” (Noakes, et al., 2001). (Afferent means carrying sensory information towards an organ, and efferent means carrying out away from an organ).

The following picture from Noakes (2001), shows the Central Governor Theory and how the interactions take place.

(Noakes et al., 2001)

Now, how do we determine maximum HR?  Well, there are three different ways to calculate it.  Starting first with “The age-predicted HRmax equation (i.e., 220 - age) is commonly used as a basis for prescribing exercise programs, as a criterion for achieving maximal exertion and as a clinical guide during diagnostic exercise testing” (Tanaka, et al., 2001).  Tanaka and associates went on to refine this value calculation with the following result(s):

“1) A regression equation to predict HRmax, is 208 – (0.7 x age) = HRmax in healthy adults.

2) HRmax is predicted, essentially, by age alone and is independent of gender and habitual physical activity status. Our findings suggest that the currently used equation underestimates HRmax in older adults. This would have the effect of underestimating the true level of physical stress imposed during exercise testing and the appropriate intensity of prescribed exercise programs” (Tanaka, et al., 2001).

So, let’s use the engineer “Geek-jock” author who is 71 yrs old.  220-age of 71 = 149 BPM maximum (theoretical).  Now let’s use the Tanaka regression analysis based on sound science;  208 – (.7 x 71) or  208 – (49.7) = 158.3 BPM.  The Geek does 168 BPM for 20 minutes and peaks at 175 BPM.

Now, let’s look at Uria.  He is 23 years old.  208 – (.7 x 23) or 208 – (16.1) = 191.9 BPM vs the age predicted equation of 220-23 = 197 BPM.  At present Uriah can run at 190 BPM for three miles XC and peaked at 206.  Now there is Caroline who is 26.  208 – (7. X 26) = 208 – (18.2) = 189.8 BPM vs age predicted equation of 220 – 26 = 194 BPM.  She cruised her cross country 6k at 175 BPM with her peak at 203 BPM. 

The third way is based on the work of Nes (2013) which then further refined the regression analysis and resolved the equation to be 211 – 0.64 x age = HRmax (Nes, et al., 2013).  So, this works out to:

Geek engineer:  211 – (.64 x 71) = 166 bpm

Uriah:  211 – (.64 x 23) = 196 bpm

Caroline:  211 – (.64 x 26) = 194 bpm

To summarize in BPM:

	Old way	Tanaka	Nes
Geek	149	158	166
Uriah	197	192	196
Carolin	194	190	194

In conclusion, just being at or higher than the Old way is quite an accomplishment, and you will see results.  Now for fun, in a parallel sports universe, “if you look at ice hockey players playing at the U18 world championships, their maximum bpm range was from 177 to 224 for forwards and 173 to 213 for defensemen.  The average range in bpm for the forwards was 148 to 176 and for the defensemen was 147 to 169.  Time played for the forwards ranged from 49 to 94 minutes and for the defensemen the time played ranged from 53 to 96 minutes.  The players ranged in age from 15 to 18 yrs old” (Stanula, et al., 2014).

In the universe of swimmers, how do swimmers compare to runners regarding heart rate?  Olstad (2019) pointed out, “Maximal heart rate was 6.7 ± 5.3 bpm lower for swimming compared to running (199.9 ± 8.9 bpm for running; p = 0.015)” (Olstad, et al., 2019). Additionally, “Two studies investigated the difference in max HR between swimming (mix of strokes) and running with the same population of elite swimmers through VO2max testing. They found max HR to be 15 beats-per-minute (bpm) lower during swimming (boys 184 ± 11; girls 186 ± 10 bpm) compared to running (boys 199 ± 10; girls 201 ± 7 bpm)” (Olstad, et al., 2019).

All of the above leads into the concept of heart rate training zones.  Science Technology reviews three different approaches or models.  Namely, the Three Zone, the Five Zone, and the Seven Zone (Science, 2024).  The high end of each zone is basically 95% to 100% of heart rate max. 

This now morphs into the work of Passelergue (2006).  “This study indicates that (1.) training at 100% max Heart Rate (HR100) and 100% max Running Speed (RS100) is more appropriate to improve high-intensity metabolic capacities (increased cortisol and lactate) while RS100 is too difficult to be maintained for 40 minutes for subjects at that level at least, (2) training at HR90%, however, is better to improve endurance and capacity to do a large amount of work considering cortisol and lactate homeostasis, and (3) training at a constant HR using a HR monitor is a good method to control the intensity of the training with subjects not used to pacing themselves with the split-time approach” (Passelergue, et al., 2006). 

Ok, I get it, heart rate matters and for many athletes they can train and perform at 100%+ of theoretical maximum regardless of the method of calculation.  Yes, I now know I need to train with a heart rate monitor.  Ok, how do I train?  In other words, the studies and science are fine but how to I “do it” and “do it” safely?

The following is a blend of anecdotal information, basic science, and basic personal observation of not only the Geek but the athletes the Geek has and does work with.  First let’s start with Paavo Nurmi’s trainer.  In a private conversation with the Geek’s Grandfather (also a Finn) he explained to Grandfather how Paavo Nurmi trained.  Grandfather was interested as he coached boxing and endurance is a big deal with boxers.  Grandfather was told that Paavo would routinely go for a long run for about an hour and when he came back, every time he came back, he sprinted from the last telephone pole to the house.  Every couple of runs he would go back another telephone pole (50 to 80 meters in spacing).  Eventually, he would sprint for many kilometers, but this took time to do, and it was tough to maintain.  Rest was important as well as sauna.  Today you would call that progressive load.

          Side Bar:  Grandfather coached Golden Gloves boxing for over 50 years with many state champions.  What was key was that his practices were only about an hour long and they only practiced Monday, Wednesday, and Friday as Tuesday and Thursday were rest days and so was the weekend.

In taking the work of Noakes into consideration on the Central Governor Theory, Paavo was overcoming the fear of high heart rates and high lactate levels and low glucose levels.  In the case of ice hockey players, the telephone poles are the length of the rink (about 200 feet) and the down and back drill now known as suicides is done.  Interesting that an ice hockey practice is about an hour long.  At that point your lactate is going up and your glucose is seriously depleted.  At the start of the season, they do this drill for about three down and backs or “6” telephone poles at nominally 20 miles per hour, with full gear, or the cover the length of the rink in just under seven seconds.  At this point in the season, at the end of this practice, the players are rubber legged, some are groggy, some vomit, and some faint, and some quit.  By the end of the season, they can do this drill at ever increasing speeds and increasing number of lengths of the ice. 

Fine, but I am a runner, what do I do?  Start with a chest strap heart rate monitor and a logbook.  This is what Uriah did as did other elite athletes I presently work with and have worked with, namely, Eric, Jeremy, Joe, EJAT, Ken, Ben, Aaron, Anthony, Carl, Ed, Ekaterina, Sasha, Ruslan, Ryan, Anastasia, the Geek and others.  After figuring out your HRmax, work out for about 50 minutes in the following progression.  15 minutes at 65% of max, followed by 15 minutes at 75%, followed by 15 minutes at 85%, followed by 5 minutes at 90% and finally 5 seconds at 100%.  Since there is much fear associated with this per Noakes, your brain will only do this 100% stuff for about 5 seconds initially and then starts shutting off your muscle groups you are using.  I like to say the front part of the brain needs to reassure the back part of the brain that damage will not be done and there is plenty of food available to replenish the glucose and lactate burned up. 

In hockey your quads are starting to burn and by the third down and back you are in real pain.  Now, you wait 48 hours and repeat, but this time your brain will allow you to go 5 seconds longer.  Yes, it’s still painful.  Now, this goes on for about 6 weeks and you have obtained about 105 seconds at max HR.  Then almost like magic the pain goes away and you can do 10 to 15 seconds per session.  The Geek engineer’s rule is one minute per month gained. 

Ok, now what is the nuts and bolts of this?  First make sure your Heart Rate Monitor (HRM) is functioning.  Suggest using a chest strap type and a dedicated wrist watch.  An example without endorsement is found here: 

Strap:  https://www.polar.com/us-en/sensors/h10-heart-rate-sensor

Watch:  https://www.polar.com/us-en/unite

One HR training option would be for the first 15 minutes do the hurdle drills without weights at a HR of 65%.  For the next 15 minutes run bleachers at 75% and maybe mix in some jump rope.  For the next 15 minutes at 85% get on an exercise bike.  For the last 15 minutes push to 100%, just for safety sake, I would use an exercise bike.  Alternatively, you can do the whole workout on an exercise bike, like EJAT did.  He was really committed and after six weeks he did the bike every day for two hours.  The second hour was eventually at maxHR for the whole hour (at 6’3” and 215 lbs., from what I was told, he shook the whole house while peddling).  Riding a bike recruits the same muscles as used in ice hockey.

Tip:  take one day off a week.  Three days of hurdles with weights and three days of cardio.  Keep it simple and don’t hard train for over an hour - - -it’s still all about recovery.

Since this Geek Engineer’s subspecialty is instrumentation and controls, my focus is measurement. You cannot hit what you cannot see.  For sure, you measure three things.  The first is max HR and how low you held it there.  The second is your waking heart rate.  The more the heart gets remodeled the lower the waking HR is as the pump is now larger.  A third way is to look at your average HR for a mile when you start this training and then 6 weeks later run the same mile at the same pace and see what your heart rate is.  Your HR should be lower as the pump is larger as thus needs less rpm to push the same amount of blood.

Opinion:  One requires sufficient HRmax equal to twice the length of your race starting with the 400 and ending up at the 5k.  So as an example, if your 800 time is two minutes you need four minutes.  If your 5k is 14 minutes you need 28.  Alternatively, do not spike your HR at a level you have never trained at. 

This now brings us to the “dreaded” Lactic Acid aka Lactate.  The following research finally brings to scientific light just what is going on.  Have no fear, the Geek will summarize. 

“The purported role of lactate in physiology and medicine is a century old, but understanding of the role has changed dramatically in the last three decades. No longer thought of as a dead-end metabolite, a fatigue agent, and metabolic poison, in contemporary physiology, lactate is seen as a major metabolic intermediate that has wide-ranging impacts in energy substrate distribution and utilization, gluconeogenesis, and cell signaling. While extensive data have been presented to support the lactate shuttle hypothesis in humans in vivo, little had been written to describe the role of lactate in cardiac metabolism or the role of the heart in terms of overall, whole body–energy substrate balance. Beyond the important role of lactate in supporting cardiac functioning, examination of the role of lactate in cardiac metabolism is illustrative overall regulation of energy substrate partitioning in other body tissues and organs” (Brooks, 2021).

Comment:  Some have argued that the heart runs best on lactate. 

“In terms of fuel energy substrate use, the heart is sometimes referred to as “omnivorous,” meaning it can simultaneously oxidize a variety of energy substrates including glucose, lactate, fatty acids, and ketones. The heart is also regarded as a “pay as you go” energy consumer because it relies heavily on exogenous as opposed to endogenous energy sources. As previously shown for skeletal muscle and whole-body metabolism, changes in cardiac work determine the rates and relative uses of energy substrates, with lesser work emphasizing lipid oxidation and greater work emphasizing carbohydrate (i.e., glucose and lactate) energy sources. The cardiac glycogen pool probably turns over, just as in skeletal muscle, but degradation in excess of synthesis is not as exaggerated as in working skeletal muscle. Hence, glycogen is not known to be a major energy source for the healthy heart. And strictly speaking in terms of the mobilization of endogenous energy sources, it is apparent that mobilization of intramuscular triglyceride can result in mobilization of fatty acids within the heart even though it is a net consumer of fatty acids from the systemic circulation” (Brooks, 2021)

Here is the kicker, “studies indicate that the heart depends heavily on exogenous lactate as a fuel when cardiac work is elevated. In contrast to the liver and kidneys, the heart is not a gluconeogenic organ. (Gluconeogenesis supplies the need for plasma glucose between meals, and it is typically done by the liver and the kidneys).  And while the heart continuously receives neuro-endocrine signaling from the vagus and cardiac nerves as well as arterial blood, the heart also releases atrial natriuretic peptide (ANP), a unique endocrine signaling function of the heart induced by mechanical atrial stretching when blood volume is elevated. ANP secretion is not known to involve lactate signaling” (Brooks, 2021).

The following is training food for thought, “given the known relationships among exercise intensity, circulating lactate level, and lactate uptake and oxidation determined across working muscle beds and at the whole-body level, a reasonable short-term prediction is that during hard exercise when arterial blood lactate concentration rises, myocardial lactate uptake and oxidation would rise also” (Brooks, 2021).

Nugget of knowledge:  when you work out at a HR of 60 to 65% you burn fat (Carey, 2009).  As soon as you increase HR that process is shut down and then glucose and lactate is used.

To summarize this very complex subject of Lactate, your body runs fine on Lactate and in fact your heart loves lactate.  When you exercise over an hour and a half, at that point you are now going into what the brain perceives as lactate debt.  Here you have burned off your glucose and are running completely on lactate.  Well, the brain wants to have some energy reserves in case of an emergency.  So, if you have not told your brain, in this day and age, food is everywhere your brain starts shutting off your muscle groups in the same fashion as when one spikes their HR.

A good example is the famous hitting the wall in a marathon.  I would bet that you either induced a HR spike,  the core temp became too high, or you did not train your lactate levels and thus the brain starts shutting off muscle groups. 

Tip:  Progress not perfection

Rock On!

The Geek

 

References

Brooks, G. A. (2021). Role of the Heart in Lactate Shuttling. Frontiers in Nutrition, 8, 663560. https://doi.org/10.3389/fnut.2021.663560

Carey, D. G. (2009). Quantifying differences in the "fat burning" zone and the aerobic zone: implications for training. Journal of Strength and Conditioning Research, 23(7), 2090–2095. https://doi.org/10.1519/JSC.0b013e3181bac5c5

Fernandes, T., Baraúna, V. G., Negrão, C. E., Phillips, M. I., & Oliveira, E. M. (2015). Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs. American Journal of Physiology. Heart and Circulatory Physiology, 309(4), H543–H552. https://doi.org/10.1152/ajpheart.00899.201

Nes, B. M., Janszky, I., Wisløff, U., Støylen, A., & Karlsen, T. (2013). Age-predicted maximal heart rate in healthy subjects: The HUNT fitness study. Scandinavian Journal of Medicine & Science in Sports, 23(6), 697–704. https://doi.org/10.1111/j.1600-0838.2012.01445.x

Noakes, Timothy D., Peltonen, Juha E., Heikki K., Rusko, J. (2001). Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia, Exp Biol (2001), 204 (18): 3225–3234. https://doi.org/10.1242/jeb.204.18.3225

Olstad, BH., Bjørlykke, V., Olstad, DS. (2019). Maximal Heart Rate for Swimmers. Sports. 7(11):235. https://doi.org/10.3390/sports7110235

Passelergue, P. A., Cormery, B., Lac, G., & Léger, L. A. (2006). Utility of the Conconi's heart rate deflection to monitor the intensity of aerobic training. Journal of Strength and Conditioning Research, 20(1), 88–94. https://doi.org/10.1519/R-15174.1

Pumps.org. (2024).  https://www.pumps.org/a-world-without-pumps-medicine/.  Hydraulic Institute, 300 Interpace Pkwy, Parsippany, NJ, 07054

REAN Foundation, October 9, 2023 9:19 am, Blog, https://www.reanfoundation.org/low-resting-heart-rate-and-lifespan/#:~:text=Studies%20on%20Athletes%20and%20Low%20Resting%20Heart%20Rate&text=It%20could%20also%20hint%20at,BPM%20throughout%20his%20professional%20career.

Science Training, Copyright © 2019–2024. Understanding Training Zones, the easy way.  https://www.sciencetraining.io/understanding-training-zones-the-easy-way/#:~:text=The%203%20zone%20model&text=Endurance%20%E2%80%93%20Zone%201%3A%20Intensity%20%3C,or%2082%2D100%25%20of%20HRmax

Shave, R., Howatson, G., Dickson, D., & Young, L. (2017). Exercise-Induced Cardiac Remodeling: Lessons from Humans, Horses, and Dogs. Veterinary Sciences, 4(1), 9. https://doi.org/10.3390/vetsci4010009

Stanula, A., Roczniok, R. (2014). Game intensity analysis of elite adolescent ice hockey players. Journal of Human Kinetics, 44, 211–221. https://doi.org/10.2478/hukin-2014-0126

Tanaka, H., Monahan, K. D., Seals, D. R. (2001). Age-predicted maximal heart rate revisited. Journal of the American College of Cardiology, 37(1), 153–156. https://doi.org/10.1016/s0735-1097(00)01054-8