Anti-Glycolytic Musings Part 1

Up front, there isn’t any direct science on kettlebells with this sort of protocol so hopefully, we can see some more research in the future to elucidate best practice. This blog should point you in the right direction for some useful research around this area and help you think critically about some of the claims associated with this protocol, which are not necessarily put forward by the author’s.

Anti-Glycolytic Musings Part 1 

Over the years I’ve had many questions about a variety of different training protocols. 

A cornerstone of many good programs is the ability to manage load and stress appropriately. One program that has been associated with kettlebell training is the anti-glycolytic training protocol, which proposes to reduce training stress by avoiding or reducing the negative byproducts of the glycolytic energy system, hence the name ‘anti-glycolytic’. In this blog, I will briefly cover the concept of training to knock out the glycolytic system, but as opposed to critiquing this protocol directly, I thought I would cover the benefits of training utilizing the glycolytic system given that there have been many negative associations directed towards it.

Glycolytic system introduction 

Briefly, we have three main types of energy systems. These are typically referred to as the alactic or creatine system, glycolytic and oxidative. The energy systems work hand in hand more like a volume switch, than an on-and-off light switch. For example, the breakdown of the high-energy molecules in the muscle will be detected (ATP to ADT) and trigger a response. Simply, phosphates think the creatine system, will kick in, but the glycolytic will also switch on, but isn’t quite as rapid, the aerobic system will also respond but takes much longer to build its energy supply up. 

Our focus today is the glycolytic system. The glycolytic pathways can use either glucose or glycogen. Both are a type of sugar, however, glycogen is typically locked within the muscle and can be metabolised slightly faster than glucose (commonly reserved for very high-intensity efforts). We sometimes use the terms Fast and Slow glycolysis, fast is sometimes called anaerobic glycolysis, in contrast, slow is sometimes called aerobic glycolysis. 

Note:

Lysis means breakdown so: Glycolysis is a term used when glucose is broken down into pyruvate, and Glycogenolysis is used when glycogen is broken down. 

When oxygen needs are being met, pyruvate gets turned into the dreaded lactic acid, which is quickly buffered to lactate. Lactate isn’t a problem, in fact, it is quite good. Lactate has been associated with other metabolic by-products that can cause fatigue such as hydrogen ions. 

What happens if you turn the volume down on the glycolytic system?

I don’t think the goal of the anti-glycolytic training is to completely remove this system altogether, but again rather to minimize it for general preparation. If we were to do that it would be quite detrimental to performance.

There is a very efficient way to reduce the glycolytic system’s ability to function. The glycolytic system requires carbohydrates, so low carbohydrate diets and their performance ramifications offer a potential insight into a marked reduction in this system’s power. It’s worth pointing out that the body can still make carbohydrates (gluconeogenesis) from other substrates (protein, fats etc), but the system power will be reduced. Low-intensity efforts can be maintained on low carbohydrate diets, however, high-intensity efforts suffer, particularly for longer efforts over 15 seconds. Kettlebell sport would be considered a high intensity effort. I’ve been lucky enough to test half a dozen people using a metabolic cart at the uni lab, and they have all recorded a respiratory exchange ratio (RER) of ⁓1 for 8-10 minute sets, which indicates they are predominantly using carbohydrates during the set. 

Long-term use of low carbohydrate diets can result in peripheral changes, which may be detrimental to kettlebell sport performance. Low carbohydrate diets reduce enzymes related to carbohydrates like pyruvate dehydrogenase (PDK), this in turn reduces metabolic flexibility. Reducing metabolic flexibility means that we can use our phosphogen (creatine) or aerobic (fat-mainly) systems. The 1st energy system doesn’t require oxygen and it responds very rapidly, in contrast, the aerobic system particularly when it uses fat as a substrate is much slower. 

Burning fat as energy is one of the many ways to switch on signalling to produce more mitochondria,  which are regularly referred to as the ‘powerhouse of the cell’. In theory. This should be good for performance, however, if you knock out your higher gears (no glycolysis) general exercise efficiency and your ability to sprint will also be reduced. Greater oxygen cost for the same workload has been found with this kind of approach. Training with low carbohydrate availability may have some benefits but when competing you want to have all your body’s available metabolic pathways available and ready to go.  In a previous blog (link), I covered nutrition periodization which attempts to get the best of both worlds.

Intensity and duration

Several different protocols target each of these energy systems, however, it’s very hard to completely isolate one. Commonly and simplified method to target the creatine system you would do efforts of 3-15s, the glycolytic system would typically involve efforts of approximately 30 seconds, and the aerobic system would be targeted if it’s over a minute.

With the above in mind, it makes sense that you target very short intervals and active recovery with much lower intensity to work the creatine system and the aerobic system. Typically there is a shift to more aerobic metabolism, even with short efforts making volume very important. For example, 4 seconds of max-effort cycling for 30 reps with 15, 30 and 45 s recovery between sprints resulted in a blood lactate mean level of 7.4, 5.6, 4.7 with a standard deviation of  0.6 or 0.7 for the groups. This indicates a significant activation of the glycolytic system for all groups. The perceived exertion never reached ‘very hard’ and the peak oxygen cost (VO2peak) was 72, 56, and 49% for the 15, 30, and 45 s rest intervals, respectively.  

It’s important to point out that cycling isn’t the same as doing kettlebell swings as cycling is on a much higher cadence, so this is where some more research would be fantastic. For context, The closest bit of kettlebell research I could find had found similar to a blood lactate level recorded during 12 swings in 15 seconds with 15 seconds recovery, with a 16 kg kettlebell, performed for 10 rounds in trained females. To build on this context, at the end of a VO2 max test strongman had a lactate level of 12 (this is pretty normal), but when they pull or push a car for 400m their blood lactate was 16 or 15, respectively. They had similar peak heart rate, however, their peak VO2 only reached 73% and 64% of their VO2 max test values. The higher blood lactate levels indicate that the anaerobic energy system had greater requirements placed upon it. So the above kettlebell protocol would not be anywhere near as anaerobic as max efforts lead pushes or drags,  however, it still had a significant use of the anaerobic energy system.

Current protocols in the scientific literature would suggest high-intensity interval training (think 2km time trial pace), not sprint interval training (max effort) with short interval length(15-60s), with the same recovery,  might be the best approach for improving the central and peripheral aerobic system without accumulating too much lactate. This protocol has not been proposed to not activate the glycolytic system, but rather not overload it to cause it to adapt. 

Kettlebell training seems to have a higher heart rate for the given oxygen cost when compared to running or rowing. This may indicate that it recruits the anaerobic energy systems slightly more (not to the same magnitude as the strongman training), however, more research is needed. 

Types of training

There are a few different ways to group endurance training, commonly we have interval training and continuous training. Interval training can be broken down into sprint interval training (SIT),  or high-intensity interval training (HIIT),  whereas continuous training can be broken down into threshold or low-intensity steady-state (LISS). These are all useful tools they just have to be implemented at the right time, it has been suggested that HIIT and SIT  can negatively affect the mitochondria and the heart.

Given that mitochondria play such a vital role in health and performance we want to optimize their function. Interestingly interval training and continuous training seem to have different molecular signalling pathways for mitochondrial biogenesis or producing more of the cells’ energy plants. Also, they can be prescribed for different adaptations. It’s been suggested that SIT results in improved mitochondrial respiration, but does not increase the number because it also activates mitophagy (recycling of the mitochondria), so old ones are removed and you have stronger newer mitochondria, continuous training builds up the total amount, but does not improve performance as much, and HIIT seems to be the best of both worlds Increasing both the amount and quality. All types of training can play an important role in a training program and can be part of promoting improved mitochondrial performance when programmed appropriately.

Typically we break down training adaptations into central and peripheral. We have just looked at some of the peripheral adaptations talking about the mitochondria because that’s most commonly talked about negatively in the context of glycolytic training. It has also been asserted that high-intensity training can be bad for the central adaptations (Cardiovascular system), however, it’s worth pointing out that in most contexts higher intensity training has a cardio-protective effect. Below are quotes from studies, that suggest HIIT training is just as protective effect cardiovascular system. Both studies used 4×4 minutes sets at roughly 90% of max heart rate, this would massively recruit the glycolytic system. 

Going into depth as to the protective effects of high-intensity training is outside of the scope of this blog but here are an informative infographic and quote with links to the papers that you can look at for more detail on this topic around cardiovascular health. As always context is important and things will depend on the individual so seek medical advice if you have any questions or concerns. 

See the above infographic from: Effect of exercise training for five years on all cause mortality in older adults—the Generation 100 study: randomised controlled trial

‘HIIT is more effective at improving brachial artery vascular function than MICT, perhaps due to its tendency to positively influence CRF, traditional CVD risk factors, oxidative stress, inflammation, and insulin sensitivity.’

Quote from: The Impact of High-Intensity Interval Training Versus Moderate-Intensity Continuous Training on Vascular Function: a Systematic Review and Meta-Analysis

Summary 

In this blog, I hope I’ve given you an insight into why the glycolytic system is important and put aside some negative connotations. Also, I hope to explore some of the ideas around anti-glycolytic training, to my knowledge there is no kettlebell-related research in this area.  Hopefully, we get some more in the future, if you found this interesting I made a look to expand and do a part 2.

Extra reading/viewing:

Physiological responses to maximal 4 s sprint interval cycling using inertial loading: the influence of inter‑sprint recovery duration

https://pubmed.ncbi.nlm.nih.gov/33974126

Effects of High-Intensity Interval vs. Moderate-Intensity Continuous Training on Cardiac Rehabilitation in Patients With Cardiovascular Disease: A Systematic Review and Meta-Analysis

https://www.frontiersin.org/articles/10.3389/fcvm.2022.845225/full

Effect of exercise training for five years on all cause mortality in older adults—the Generation 100 study: randomised controlled trial

https://www.bmj.com/content/371/bmj.m3485.short

The Impact of High-Intensity Interval Training Versus Moderate-Intensity Continuous Training on Vascular Function: a Systematic Review and Meta-Analysis

https://link.springer.com/article/10.1007/s40279-015-0321-z

Training for intense exercise performance: high-intensity or high-volume training?

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1600-0838.2010.01184.x

Podcast (David Bishop on mitochondria training, mytophagy etc)

METABOLIC DEMANDS OF “JUNKYARD” TRAINING: PUSHING AND PULLING A MOTOR VEHICLE 

https://pubmed.ncbi.nlm.nih.gov/17685675

The Effects of Kettlebell Mass and Swing Cadence on Heart Rate, Blood Lactate, and Rating of Perceived Exertion during an Interval Training Protocol

http://article.sapub.org/10.5923.j.sports.20170703.05.html#:~:text=8%20kg%20kettlebell.-,No%20significant%20differences%20were%20found%20in%20heart%20rate%20or%20blood,exertion%20increased%20as%20mass%20increased.

High-intensity interval training, solutions to the programming puzzle: Part I: cardiopulmonary emphasis

https://pubmed.ncbi.nlm.nih.gov/23539308

Short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00829.2020

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