Most Energy System Programs Are Wrong
With bioenergetics, we aim to establish order in a system that operates in chaos. Bioenergetics integration into sports primarily involves optimizing for the balance between chaotic bouts of work and rest during competition. There is no predictable manner in which work and rest occur during competition. Sure, there are constraints such as the length of a stop and start to a play. Such as there is in baseball, football, or tennis. But that can vary tremendously in terms of demand by length of play and variables before and after the play.
Chaos of work and rest is even more amplified during mixed sports such as basketball, soccer, lacrosse, and hockey. The constraints here are applied via set variables of time. There can be continuous play occurring with bouts consisting of several short-long sprints, change of directions, transitional jogging and walking, and various other movements such as jumping or collisions. Montgomery (1988) stated: “Peak heart rates during a shift on the ice exceed 90% of HRmax with average on-ice values of about 85% of HRmax. Blood lactate is elevated above resting values confirming the anaerobic nature of the game. Glycogen depletion studies show a preferential utilisation of glycogen from the slow twitch fibres but also significant depletion from the fast twitch fibres.” A coach can use common sense to determine that there are extremely diverse demands during competition. More significantly, bioenergetic demands are rarely uniform during competition.
Most energy system development plans myopically look at work to rest in an orderly fashion. You cannot solve for chaos with order. Your only option is to limit the impact of chaos with the understanding of constraints. Constraints are the key to optimization. This article is the expansion of the limits of those constraints with the use of the supplements Enduro2 and Synapsin. We need to embrace that we have no control over the future. What we can improve is our response to that chaos through thoughtful planning of developing the cardiovascular, respiratory, and autonomic nervous systems.
What this article will dive into is how we approach giving our athletes supplemental support through the usage of Enduro2 and Synapsin to handle variance in work-to-rest during competition.
We will start with Heart Rate Recovery (HRR) and how that is the best proxy to determine our reaction to intense work. We will then review how we can change that response by developing our VO2 Max, more specifically, our mitochondrial adaptations with EndurO2. Finally, we will unpack the response autonomically on heart rate through the vagal nerve and how Synapsin can positively affect our response.
Heart Rate Recovery (HRR)
In order to understand how to train for inevitable chaos, we will need to review Heart rate recovery (HRR). HRR is the rate at which the heart rate declines after exercise, typically measured in the first few minutes of recovery (Haraldsdottir, 1999). We look at HRR in various time increments following bouts of exercise. The most common windows include:
This gives us a platform to understand the interaction between the cardiovascular, respiratory, and nervous systems. Heart rate is controlled by the vagal nerve. As demands go, the need for short-term energy production of ATP from either the phosphogen system or the glycolytic system is activated. The vagal nerve controls conductivity to the heart to facilitate faster heartbeats and greater delivery of oxygenated blood.
Our respiratory rate increases when we have an elevated heart rate to simultaneously need more oxygen to meet the demands of exercise, along with the need to remove carbon dioxide. The respiratory system is controlled by the phrenic nerve. Sympathetic demand from anaerobic energy production increases the conductivity of both the phrenic and vagal nerves.
This is the crux of formulaic energy system development; it ignores the interrelationship of systems to handle the variable demand. Why this is important is that we cannot appreciate the impact of variance with work intensity and rest intervals on performance.
Building off this, we can create phases of HRR that which controlled by the Central Nervous System (CNS). The first phase is the ‘Fast’ phase, the first 30–60 seconds. The fast phase is dominated by parasympathetic/vagal reactivation. We have elevated both heart rate and respiratory rate; now we are reacting to the continued sympathetic state. The first 30-60 seconds of success are predicated on our ability to switch gears to parasympathetic, where we slow our respiration and heart rate. We will refer to this as the ‘Alternator’.
Hirsh et al (2006) showed a moderate correlation between VO2 max and HRR. Haraldsdottir did not find as great of correlation between VO2 Max and HRR, but we can take some from both of their outcomes. The research is very unclear on whether or not improved oxygen delivery rate during exercise improves HRR, but that does not discredit oxygen delivery’s impact on the CNS. The simple fact is that if we can transition to an aerobic state through slower breathing, focused on exhalation, and a slowed heart rate, our HRR will be better. Not only better acutely, but also after multiple exposures to anaerobic exercise. Better conditioning is more related to the ability to switch from yang to yin, sympathetic to parasympathetic, or anaerobic to aerobic.
Goldsmith et al (1997) showed just that. He stated, “VO2max was highly correlated with high frequency power (r = 0.74, P = 0.0001), indicating that physical fitness is strongly associated with vagal modulation.” What this means is that power over multiple bouts of exercise was attributed to vagal tone modulation in individuals with higher VO2 Max levels. In a sense, we are better able to adapt to the acute stress from having a higher functioning alternator of our CNS. For acyclical athletes, preparation is not about driving a particular attribute, such as VO2max; it is about being able to switch more rapidly over a longer period of time.
The second phase is the ‘Slow’ phase, the next 2–5 minutes. The Slow phase involves sympathetic withdrawal, metabolic clearance (lactate, H+), and respiratory recovery. We are now controlled by our ability to remove metabolic wastes and rebuild short-term energy stores for future bouts of exercise.
The key point for the Slow phase is the impact of mitochondrial and capillary density on cardiovascular function. All systems work off feedback loops. Local demand goes up, global responds. When we rapidly utilize local ATP, glucose, and glycogen, the cardiovascular/cardiorespiratory system responds by elevating heart and breathing rate. The level of demand placed globally is based on efficiency locally. If we have a greater level of adaptation through the development of mitochondrial and capillary density, we will respond better to that demand.
Mølmen (2025) showed that mitochondrial density was directly correlated to improved endurance and subsequently the overall response to long, moderate, and short-duration sprinting/running. How this connects to HRR is Rate of Perceived Exertion (RPE). What Mølmen showed with evaluating the impact of mitochondrial density was that in all durations/intensities, RPE was reduced. The perceived difficulty of something is lessened, which facilitates a faster recovery from that specific duration/intensity.
Mølmen also showed that adaptations with increased capillary density allowed for a greater diffusion of oxygen locally. This not only improved performance in all three durations and intensities but also diminished the acute response. The combined effect of having greater mitochondria and capillary density led to an improved RPE, which leads to an improvement during the Slow phase of HRR. This is bioenergetic flexibility. We not only see a sharp decline in Fast HRR, but we continue to see a decline during the Slow HRR.
Yılmaz (2025) showed that improvements in Heart Rate Variability (HRV) improve response to exercise. We can use HRV as our ‘Governor’ in training. If we have a low HRV, we have a low bandwidth to handle acute spikes in heart and respiratory rate. Esco (2010) showed a weak correlation between higher HRV and Fast HRR following maximal intensity anaerobic exercise. So we can conclude that HRV may be more correlated with Slow HRR or more aerobic capacity.
When we break up HRR into Fast or the Alternator combined with Slow or the Governor, we get a clear look at the potential to handle variance with training.
EndurO2 & Synapsin LPT to the rescue
We can look at this in one of two ways:
This is a real causality dilemma. There is no right answer when it comes to determining which of the two interdependent conditions is the cause and which is the effect of an outcome. The answer when deciding to choose one or both is yes.
Testing matters here. If you run a fitness test and you find that the limiting factor is, in fact, fitness, then yes, work on fitness. If you run a comprehensive metabolic panel where the limiting factor is the cardiovascular, immune, and/or endocrine systems is the limiting factor, then yes, work on nutrition and supplementation. But rarely is it one or the other; it is always both.
My advice is to treat everyone as n=1. You always want to run experiments to see the efficacy of our interventions. Use good research methods with a solid hypothesis, research design, planned intervention, and review of data findings. Since this is a causality dilemma, you are better served to treat this as such. This way, you avoid bias and preference. The correct answer is the one that makes the largest difference.
Here is what you are trying to find out to determine needing Enduro2 and/or Synapsin:
What we are trying to determine here is if either our fast or slow recovery ability is compromised as a determinant to use either EndurO2 LPT or Synapsin LPT . This approach is based on removing expanding constraints. If we find that makes acute changes with the utilization of supplements, we have a better platform to react to chaos. The constraints are based on our Governor and/or Alternator not functioning properly. We limit the impact of those constraints with targeted supplementation.
I want to make a disclaimer that these products are not mimetics (exercise mimicking). You have to do the work. The hope is that you get more from said work. That is the essence of performance supplements: a compounding agent that increases the value from the time and effort you are putting into training. There is no replacing the work you will need to do to be successful.
The other disclaimer is that if you have a low governor, you will have a bad alternator. It is always both. This is due to the interdependence of both the CNS and the cardiovascular/respiratory systems at play.
Why Synapsin and Enduro2 work
EndurO2 LPT uses the raw material LANDKIND Pure Salidroside, which is the active compound in Rhodiola Rosea, which requires a lot of raw material. EndurO2 LPT goes through a fermentation process that isolates pure salidroside, ensuring long-term stability of the ingredient without depleting Rhodiola rosea resources. Essentially, EndurO2 LPT isolates and enhances the active component of Rhodiola Rosea related to improved endurance.
Rhodiola and Salidroside in studies has been proven to perform:
With EndurO2 LPT, we are thinking about modulating our Governor with direct improvements to mitochondrial efficiency locally and subsequently better Slow HRR.
Synapsin is ginsenoside Rg3 which is a bioactive compound found in Panax ginseng. It belongs to the class of ginsenosides, which are the primary pharmacologically active components of ginseng. When you think of Syanapsin, you are thinking of a mediated response to high stress and subsequently better CNS performance, such as high output, high focus, or enhanced skill.
Synapsin in studies has been shown to support:
With Synapsin, we are thinking about modulating our Alternator with direct improvements to vagal and phrenic nerve efficiency to respond in better Fast HRR.
Take Home
References
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