Enhancing Human Endurance Performance

Improving fitness levels optimizes sport performance and enhances everyday physical function. Fitness is defined as a set of attributes that people have or achieve relating to their ability to perform physical activity [1]. Fitness is made up of the Five Components of Fitness which are: muscular strength, muscular endurance, cardiovascular endurance, flexibility, and body fat composition [2]. One of the most important components of fitness is endurance, both muscular and cardiovascular endurance, both of which may adapt with endurance training. Endurance is defined as the ability to sustain a prolonged stressful effort (ability to sustain a high percentage of VO2max) throughout an entire effort duration [3]. Cardiovascular endurance is the ability of the heart, lungs, and blood vessels to deliver oxygen to the body's tissues (skeletal muscle) for an extended period of time [4]. Muscular endurance is the muscle’s ability to resist repeated contractions and/or maintain a contraction over a period of time [5]. 

The human body is beautifully and wonderfully made. For instance, the upper and lower extremities are designed strategically with different fiber type distributions. Skeletal muscle fibers are composed of two fiber types: Type I (slow-twitch) and Type II (fast-twitch) fibers. Interestingly enough, upper body muscles have a greater distribution of fast-twitch fibers and lower body muscles have a greater distribution of slow-twitch fibers [6]. So, the upper body is designed for more strength and power while the lower body is designed for more endurance. This makes sense if we take a step back and think on it… We can stand and walk for long periods of time (using our legs) without getting fatigued. However, if we try to do a handstand or walk on our hands, we fatigue much quicker. We were not designed to stand on our hands. Meaning, our lower body was designed for endurance while our upper body for strength and power. However, this does not mean that we cannot train our body to have more central and peripheral endurance (cardiovascular and muscular endurance). 

Through endurance training, both muscular and cardiovascular endurance performance increases [7,8]. But what is endurance training? Endurance training can be accomplished both by lifting weights in a circuit fashion as well as traditional aerobic training (standard cardio) like running or cycling [7,8]. The goal is to enhance overall endurance of the body, that means training must stress the cardiorespiratory and musculoskeletal systems. Research has found that doing circuit resistance training and/or standard cardio, like cycling or running, enhances both muscular and cardiorespiratory fitness by decreasing fatigue as the body undergoes positive physiological adaptations [9]. Consequently, the body becomes more resistant to fatigue and increases its capacity for vigorous exercise or physical activity, thus increasing endurance performance. 

Though traditional methods of endurance training elicits positive benefits, to truly optimize human endurance performance, the use of PowerDot technology is of paramount importance. PowerDot combines the two powerful technologies of transcutaneous electrical nerve stimulation (TENS) and neuromuscular electrical stimulation (NMES). By adding NMES as another training stimulus, the human body has a greater potential to further enhance cardiovascular and muscular endurance performance by further increasing aerobic capacity, exercise economy (exercise becomes easier), and anaerobic threshold [10,11,12,13]. PowerDot takes out all of the guesswork providing endurance protocols that are as easy to follow. To go beyond standard improvements in fitness and to truly optimize human performance and fitness parameters, PowerDot is an essential tool needed by everyone. 

Endurance and The Fick Principle

When examining endurance performance, exercise physiologists examine several variables that are regulated by cardiorespiratory and musculoskeletal endurance. These variables are measured as VO2 expressed in milliliters of oxygen consumed per minute (ml/kg/min). VO2 is a measure of energy expenditure and bodily effort, it has been shown to increase linearly with heart rate, which is why we use heart rate to measure exercise intensity levels [14]. The variables that comprise someone with high cardiovascular and muscular endurance are: anaerobic (lactate) threshold, maximal oxygen consumption (aerobic capacity also known as VO2max), and exercise economy [2,15]. A highly trained endurance athlete will have a high level of all of these variables allowing them to endure long intense training sessions [16]. 

So, why do exercise physiologists, sports scientists, and endurance coaches use VO2 to examine endurance performance? Why use VO2 to measure anaerobic threshold, aerobic capacity, and exercise economy as mentioned above? The answer lies in the fact that there's a VO2 equation (Fick Equation) that incorporates cardiovascular and muscular endurance physiology [17].

Adolf Eugene Fick first presented on the physiological variables that impact VO2 at a conference in 1870 [18]. So, this is not new information. Through his discovery came the infamous Fick Equation. Exercise scientists have used this equation to further understand the physiology of endurance performance. The Fick equation tells us:

VO2 = Cardiac Output (HR x SV) x A-VO2dif

Let’s break this equation down and see how the cardiovascular and musculoskeletal systems work and adapt together to enhance endurance performance. 

Cardiac output is the amount of blood pumped from the heart per minute. It is equal to heart rate (HR) multiplied by stroke volume (SV - which is the amount of blood pumped from the heart per beat). So, the faster the heart beats (HR) and and the more blood that is pumped per beat (SV) the more oxygenated blood that is pumped to the working skeletal muscle (CO - Cardiac Output). The more rich oxygenated blood pumped to the working skeletal muscle the more energy that can be created to meet sustained physical demands. That describes the components that impact cardiovascular system endurance, but where does the musculoskeletal system come into play?

It’s the second part of the equation, A-VO2dif. The “A” stands for arterial. The “V” stands for venous. And “O2dif” is the oxygen difference. Meaning, A-VO2dif is the difference of oxygen between the arteries and veins. Oxygenated blood is pumped from the heart, as mentioned previously, and travels through the arteries reaching the capillaries at the skeletal muscle. Here, the oxygen is “dropped off” for the muscles to use. A muscle fiber with high endurance is going to have a greater content of myoglobin and mitochondria to handle transportation of oxygen into the muscle to generate energy. If not, it will fatigue quickly.

This explains that VO2 (whether VO2max or VO2submax) is dependent on both how well and how much oxygenated blood is pumped to the skeletal muscle as well as the skeletal muscles ability to take and utilize that oxygen. Thus, if we have poor cardiovascular endurance, our heart and circulation do not operate well. If we have poor muscular endurance, our muscles do not have the ability to take and utilize oxygen to meet the demands of long duration exercise. If the muscle cannot receive and utilize the oxygen it needs to meet the demands of long duration, intense exercise, it will rely more on anaerobic metabolism. 

Anaerobic metabolism produces energy quickly to meet the physical demands of long duration exercise, though, it also results in high concentrations of lactic acid, or lactate. This is why a high lactate threshold is a key indicator of endurance performance [16]. Lactate threshold is measured as a percentage of someone’s VO2max (so it’s a VO2 value), meaning, the higher percentage the more intense the exercise has to be to cause lactate to accumulate [3]. For instance, two runners both have a VO2max of 50 ml/kg/min and they hit that max value at 10mph. Runner A, who’s lactate threshold occurs at 50% of their VO2max will not be able to run as fast for as long as Runner B, who’s lactate threshold occurs at 70% of their VO2max. Why? As mentioned, if there’s a lag in the cardiovascular system getting oxygenated blood to the skeletal muscle or the muscles do not have the capacity to fully utilize the oxygen being delivered, the muscle will rely more on anaerobic metabolism (thus, poor cardiovascular or musculoskeletal endurance capacities) [19]. This increases lactic acid or lactate accumulation, which is associated with (not the cause) that burning sensation during exercise [20]. Lactate threshold is an indicator of fatigue because once someone feels that burning sensation they slow down, they cannot endure that pace or intensity [21]. So, to answer the question about Runner A and B, Runner A will start to feel that burning running around 5mph or so, whereas Runner B won’t feel that burning until about 7mph. So, Runner B could endure running at 5mph longer than Runner A, hence, greater endurance performance. 

Now, VO2max is pretty well known in the endurance community, though, let’s look back at the Fick Equation, but in regards to MAX.

VO2max = Cardiac Outputmax (HRmax x SVmax) x A-VO2difmax

What this equation tells us is that a higher amount of oxygenated blood pumped from the cardiovascular system and more oxygen is extracted and utilized at the skeletal muscle the greater endurance capacity that person will have.

Last, but not least, is exercise economy. An athlete that is “economical” will have a lower submaximal VO2 [16]. As previously mentioned, VO2 is a measurement of exercise intensity. So, let’s look at Runners A and B again. Let’s say that Runner B is more economical than Runner A. What this means, is that if both runners are running at 4mph, Runner B will have a lower VO2, meaning that 4mph is not as intense of a pace as it is for Runner A. 

To summarize, greater cardiovascular and muscular endurance can be described using the Fick Equation, by examining VO2. Someone with great cardiovascular endurance is able to pump a lot of oxygenated blood through the circulation. Someone with great muscular endurance will be able to utilize that oxygen efficiently and delay lactate accumulation. This begs the question, how does endurance training physiologically enhance cardiovascular and muscular endurance? 

Physiological Adaptations Improve Endurance Performance

Let’s think back to the Fick Equation… Cardiovascular endurance is going to depend on HR and SV whereas muscular endurance is going to depend on the A-VO2dif [22,23]. Endurance training elicits both central (cardiovascular) and peripheral (muscular) physiological adaptations which are evident in highly trained endurance athletes [16]. Let’s examine these adaptations one by one. 

Looking at heart rate adaptations, heart rate max doesn’t really change. And actually heart rate max declines as a person ages which impairs endurance performance as we get older. However, from endurance training, resting and submaximal heart rate decrease. This is due to increased activity of the parasympathetic nervous system that keeps our heart rate from increasing too quickly which is very beneficial. For instance, you may be a cyclist, and after a few weeks of cycling at a certain wattage, that wattage becomes easier and your heart rate does not elevate as high. This means that intensity is now easier and you can endure it more without feeling fatigued.

Where stroke volume differs from heart rate is that there are multiple physiological adaptations that increase the amount of blood pumped per beat. So, as a result of training, stroke volume increases at rest, submaximal, and maximal intensities. One reason stroke volume increases is due to an increase in heart mass (left ventricular hypertrophy). The cardiac muscle increases in size and now produces a more forceful contraction increasing the amount of blood pumped from the heart. Another physiological mechanism causing stroke volume to increase is our body increases our plasma volume and red blood cell count. This allows more oxygenated blood to flow efficiently through the circulation and increases the amount of blood returned to the heart so more can be pumped back out to the body. However, these cardiovascular adaptations are not as beneficial if our skeletal muscle cannot take it and utilize it. 

Now, there’s many adaptations (bulleted below) that occur at the skeletal muscle that help to take more oxygen up at the skeletal muscle which increases the A-VO2dif:

  • ↑ Capillarization (more capillaries). Capillaries are the site of gas exchange at the skeletal muscle (dropping off oxygen). Having more capillaries allows our body to handle the increased cardiac output.
  • ↑ Mitochondria. The powerhouse of the cell! Within the mitochondria is where the oxidative energy system does it’s thing. More mitochondria are able to handle more oxygenated blood.
  • ↑ Enzymatic Activity. This increased enzymatic activity is within the mitochondria. Enzymes catalyze or speed up reactions. In this case, the increased enzymatic activity increases production of ATP for higher aerobic performance.
  •  Myoglobin. Once oxygen is dropped off to the skeletal muscle, the myoglobin protein takes it deep into the mitochondria. With more oxygenated blood, more myoglobin are able to take all that oxygen to where it needs to go...the more mitochondria.

It is important to keep in mind that these adaptations occur more greatly at the Type I (slow-twitch) fibers [6]. Those adaptations are the reason Type I fibers are more resistant to fatigue and have greater endurance. Meaning, fiber type distribution does play a role. So, to recap...the cardiovascular and skeletal muscle adaptations go hand in hand and work together to distribute and utilize more oxygen, enhancing endurance performance of the human body. 

PowerDot NMES Stimulates and Trains Both Fiber Types

The PowerDot NMES Smart Technology device is designed to specifically target both Type I and Type II fibers and increase circulation. NMES takes a “nonselective approach”, activating both fiber types at the same time [24]! Meaning, both Type I and Type II fibers are activated while your PowerDot is on. Though, the question remains, how can utilizing the updated and new PowerDot 2.0, elevate endurance performance to new heights? 

The NMES technology in the PowerDot smart muscle stimulator not only stimulates both fiber types, but also elicits an increase in oxygen consumption and heart rate [11]. This increased cardiometabolic demand suggests NMES may be used as a supplementary training stimulus to improve endurance performance [11]. Essentially, by incorporating PowerDot, there is the potential to further enhance functional aerobic performance related to ventilation threshold (anaerobic threshold) and aerobic capacity which are key physiological indicators of endurance performance [10]. Lastly, something that is often overlooked in endurance training is incorporating training aimed at improving strength. Muscular strength is imperative for improving endurance performance. Improving strength increases time to exhaustion and improves running economy and power [13]. Adding PowerDot as another training stimulus only further optimizes the variables that make-up a highly trained endurance athlete. 

By utilizing the PowerDot endurance protocol, you may delay the onset of fatigue during workouts and in competition, enhancing your endurance performance.




  1. American College of Sports Medicine. (2013). ACSM's guidelines for exercise testing and prescription. Lippincott Williams & Wilkins. [Link]
  2. Pollock, M. L., Gaesser, G. A., Butcher, J. D., Després, J. P., Dishman, R. K., Franklin, B. A., & Garber, C. E. (1998). ACSM position stand: the recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness, and flexibility in healthy adults. Medicine & Science in Sports & Exercise30(6), 975-991. [Link]
  3. Bosquet, L., Léger, L., & Legros, P. (2002). Methods to determine aerobic endurance. Sports Medicine32(11), 675-700. [Link]
  4. McAuley, P. A., Kokkinos, P. F., Oliveira, R. B., Emerson, B. T., & Myers, J. N. (2010, February). Obesity paradox and cardiorespiratory fitness in 12,417 male veterans aged 40 to 70 years. In Mayo Clinic Proceedings (Vol. 85, No. 2, pp. 115-121). Elsevier. [Link]
  5. Ruiz, J. R., Castro-Piñero, J., Artero, E. G., Ortega, F. B., Sjöström, M., Suni, J., & Castillo, M. J. (2009). Predictive validity of health-related fitness in youth: a systematic review. British Journal of Sports Medicine43(12), 909-923. [Link]
  6. Ørtenblad, N., Nielsen, J., Boushel, R., Söderlund, K., Saltin, B., & Holmberg, H. C. (2018). The muscle fiber profiles, mitochondrial content, and enzyme activities of the exceptionally well-trained arm and leg muscles of elite cross-country skiers. Frontiers in physiology9, 1031. [Link]
  7. Buch, A., Kis, O., Carmeli, E., Keinan-Boker, L., Berner, Y., Barer, Y., ... & Stern, N. (2017). Circuit resistance training is an effective means to enhance muscle strength in older and middle aged adults: a systematic review and meta-analysis. Ageing research reviews37, 16-27. [Link]
  8. Thomas, E. J., Pettitt, R. W., & Kramer, M. (2020). High-Intensity Interval Training Prescribed Within the Secondary Severe-Intensity Domain Improves Critical Speed But Not Finite Distance Capacity. Journal of Science in Sport and Exercise, 1-13. [Link]
  9. Sperlich, B., Wallmann-Sperlich, B., Zinner, C., Von Stauffenberg, V., Losert, H., & Holmberg, H. C. (2017). Functional high-intensity circuit training improves body composition, peak oxygen uptake, strength, and alters certain dimensions of quality of life in overweight women. Frontiers in physiology8, 172. [Link]
  10. Miyamoto, T., Kamada, H., Tamaki, A., & Moritani, T. (2016). Low-intensity electrical muscle stimulation induces significant increases in muscle strength and cardiorespiratory fitness. European journal of sport science16(8), 1104-1110. [Link]
  11. Crognale, D., Crowe, L., DeVito, G., Minogue, C., & Caulfield, B. (2009, September). Neuro-muscular electrical stimulation training enhances maximal aerobic capacity in healthy physically active adults. In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society (pp. 2137-2140). IEEE. [Link]
  12. Mettler, J. A., Magee, D. M., & Doucet, B. M. (2018). High-Frequency Neuromuscular Electrical Stimulation Increases Anabolic Signaling. Medicine and Science in Sports and Exercise50(8), 1540-1548. [Link]
  13. Paavolainen, L., Hakkinen, K., Hamalainen, I., Nummela, A., & Rusko, H. (1999). Explosive-strength training improves 5-km running time by improving running economy and muscle power. Journal of applied physiology86(5), 1527-1533. [Link]
  14. Jakicic, J. M., Donnelly, J. E., Pronk, N. P., Jawad, A. F., & Jacobsen, D. J. (1995). Prescription of exercise intensity for the obese patient: the relationship between heart rate, VO2 and perceived exertion. International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity19(6), 382-387. [Link]
  15. Daniels, J. A. C. K., & Daniels, N. A. N. C. Y. (1992). Running economy of elite male and elite female runners. Medicine and science in sports and exercise24(4), 483-489. [Link]
  16. Joyner, M. J., & Coyle, E. F. (2008). Endurance exercise performance: the physiology of champions. The Journal of physiology586(1), 35-44. [Link]
  17. Yamamoto, J., Harada, T., Okada, A., Maemura, Y., Yamamoto, M., & Tabira, K. (2014). Difference in physiological components of VO2 max during incremental and constant exercise protocols for the cardiopulmonary exercise test. Journal of physical therapy science26(8), 1283-1286. [Link]
  18. Vandam, L. D., & Fox, J. A. (1998). Adolf Fick (1829–1901), Physiologist A Heritage for Anesthesiology and Critical Care Medicine. Anesthesiology: The Journal of the American Society of Anesthesiologists88(2), 514-518. [Link]
  19. Sales, M. M., Sousa, C. V., da Silva Aguiar, S., Knechtle, B., Nikolaidis, P. T., Alves, P. M., & Simões, H. G. (2019). An integrative perspective of the anaerobic threshold. Physiology & behavior205, 29-32. [Link]
  20. Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology287(3), R502-R516. [Link]
  21. Black, M. I., Jones, A. M., Blackwell, J. R., Bailey, S. J., Wylie, L. J., McDonagh, S. T., ... & Bowtell, J. L. (2017). Muscle metabolic and neuromuscular determinants of fatigue during cycling in different exercise intensity domains. Journal of Applied Physiology122(3), 446-459. [Link]
  22. Beere, P. A., Russell, S. D., Morey, M. C., Kitzman, D. W., & Higginbotham, M. B. (1999). Aerobic exercise training can reverse age-related peripheral circulatory changes in healthy older men. Circulation100(10), 1085-1094. [Link]
  23. Saltin, B. (1985). Hemodynamic adaptations to exercise. The American journal of cardiology55(10), D42-D47. [Link]
  24. Gregory, C. M., & Bickel, C. S. (2005). Recruitment patterns in human skeletal muscle during electrical stimulation. Physical therapy85(4), 358-364. [Link]

Ready to take the next step? Explore more below