Muscle Stimulation
for Muscle Recovery

Science & benefits of PowerDot

Muscle Recovery

Utilization of Neuromuscular Electrical Stimulation (NMES) and Transcutaneous Electrical Stimulation (TENS) are the perfect prescription for enhanced muscle recovery and performance. Whether after a workout, long day of travel, or just a long day in general, neck, back, chest, and leg muscles begin to feel sore and fatigued. The combination of NMES and TENS technologies helps sore muscles after a workout or intense day recover faster and perform better. Inflammation, triggering pain receptors, is just one of the causes of sore muscles and fatigue. By incorporating NMES technology as a recovery modality, this technology creates an electro-induced hyperfusion that may help to wash out and clear away cellular debris or metabolites which cause inflammation and trigger pain receptors. TENS technology also decreases pain associated with muscle soreness and fatigue by shutting down or blocking the flow of pain signals from the muscles to the brain. Optimizing muscle recovery is of paramount importance as muscle fatigue and soreness not only result in detriments of physical performance and muscle function, but also mental performance [1,2]. Taking advantage of the NMES and TENS technology offered wirelessly by PowerDot allows the human body to move, compete, train, and exercise with potentially reduced fatigue, soreness, or even injury risks.

Muscle Recovery

Muscle Fatigue and Muscle Recovery Defined

Muscular fatigue is demonstrated as any decline in muscle performance associated with muscle activity [3]. Depending on the mechanism of muscular fatigue, whether peripheral fatigue affecting the actual muscle cell and contractile elements within it and/or central alterations impairing motor unit or muscle fiber activation, recovery from fatigue may take up-to several minutes to several days [4].

Full muscle recovery is displayed as the return to normal physiological conditions after fatigue [5]. Three forms of muscle recovery have previously been defined: immediate recovery, short-term recovery, and training recovery [6]. Immediate recovery is exactly as it sounds, it is instantaneous. An example would be when each leg recovers with each stride while walking or how the hand and finger muscles recover while typing a long email. Short-term recovery refers to recovery during a workout or sporting activity. It is the recovery in-between sets or in-between plays. Lastly, there is training recovery.

Training recovery takes place between multiple workouts, competitions, or activities. NMES and TENS have the capability of mitigating the physiological mechanisms of muscular fatigue enhancing training recovery.

Muscle Recovery

Physiological Mechanisms of Fatigue

Exercise induced muscular fatigue is multifactorial [7]. As previously mentioned, muscle fatigue and soreness may be due to peripheral muscular changes, central alterations, or a combination of both. This is demonstrated by inadequate energy delivery/metabolism, diminished central nervous system (CNS) motor drive, accumulation of metabolites and electrolytes in the blood and within the muscle, as well as structural damage to the muscle [3,8,9].

The human body is fueled by three primary substrates: Carbohydrates, Fat, and Protein. The body’s preferential energy source is carbohydrates as they can easily be broken down into glucose and stored in the muscle as glycogen. Glycogen stored in the muscle is able to provide immediate energy for skeletal muscle during exercise. However, these glycogen stores are limited and as exercise duration and intensity increase, these levels decrease. Diminishing glycogen levels within skeletal muscle results in inadequate energy delivery and metabolism to the working muscle, meaning the body is not able to create energy fast enough for the rising demand, resulting in the feeling of tiredness and fatigue. Consuming carbohydrates has the capability of delaying both physical and mental fatigue enhancing short-term recovery [2].

During and post-exercise, various metabolites and ions accrue both intracellularly and extracellularly contributing to bodily and muscular fatigue. As various substrates are metabolized to create energy (Adenosine Triphosphate - ATP) and as these high energy ATP bonds are broken, lactate and hydrogen ions begin to accumulate. There is also an accrual of inorganic phosphate ions (from the breakdown of ATP)[3]. High-intensity exercise results in the rapid depletion of muscle glycogen and increase in lactate accumulation. Lactic acid or lactate is a product of breaking down glucose or glycogen to create ATP and is associated with a burning sensation felt in the muscles. Though that burning sensation is associated with lactate accumulation, it is important to note the “burn” is caused from anaerobic ATP production and the hydrolysis of that ATP which results in increased proton (hydrogen) release [10]. An accumulation of hydrogen ions decreases the body’s internal pH causing acidosis. This has deleterious effects, inhibiting intracellular glycolytic enzymes and preventing oxygen binding to hemoglobin on red blood cells thus reducing oxygen transport to skeletal muscle and impairing substrate utilization and energy (ATP) production.

Both hydrogen ions and excess inorganic phosphate (accumulated from the breakdown of ATP) directly affect calcium release resulting in impaired muscular contraction. Calcium is an essential component contributing to the muscle contractile mechanism by binding to a protein that ultimately allows contractile filaments of the sarcomere (the basic contractile element of skeletal muscle) to interact and the whole muscle shorten. If calcium release or sensitivity is altered, the strength of a muscular contraction decreases which is an indication of muscular fatigue.

Also contributing to the failure of the muscle contractile mechanism is altered neural control. Failure may occur at the neuromuscular junction (the site of communication between the alpha motor neuron and the muscle cell) preventing muscle activation. Impaired acetylcholine synthesis and release (due to the enzyme cholinesterase breaking down acetylcholine) decreases the concentration of acetylcholine in the neuron. Acetylcholine is an essential neurotransmitter that binds to receptors on the muscle cell membrane provoking an electrical signal that results in a forceful muscular contraction. Though, with exercise induced fatigue, the muscle resting membrane potential decreases even more so it takes more acetylcholine (which our body does not have due to cholinesterase) to reach the threshold stimulus to actually cause a muscle contraction. All this to say, the muscle needs more acetylcholine, the neuron does not have it, which results in impaired or a lack of muscular contraction.

All of these physiological mechanisms at both the muscle and central levels impair muscle function during exercise resulting in immediate muscular fatigue. However, what about fatigue and soreness resulting days later? There is a cause and effect relationship. Due to the intensity of the exercise causing muscular fatigue, muscle soreness is the effect.

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Delayed Onset Muscle Soreness

Delayed onset muscle soreness (DOMS) is the soreness felt days after an intense training session. Side effects of DOMS range from stiffness to severe, restrictive pain one or two days after an exercise bout. Let’s discuss the mechanisms of DOMS and the physiology behind what truly causes muscular soreness.

High tension (having to produce a lot of force… working muscles harder or in a new manner) results in structural damage to the muscle and even connective tissue. The cell membrane damage results in elevated levels of creatine kinase (a marker of muscle damage) as well as disturbs calcium homeostasis resulting in high calcium concentrations that activate enzymes that degrade a structural component of the muscle called, the z-discs. Within a few short hours there is an elevated response in circulating inflammatory cells (neutrophils and macrophages - white blood cells) that participate in the inflammatory response. As a result, other intracellular contents (histamine, kinins, and potassium) begin to accumulate outside of the cells and stimulate free nerve endings in the muscle causing pain. Also, fluid and electrolytes shift into the area creating edema which causes tissue swelling and also activates pain receptors.

Essentially, the inflammation associated with muscle damage triggers pain receptors that results in the muscle soreness feeling [11,12]. DOMS causes fatigue and can affect muscular performance making muscle recovery essential.

Physiology of NMES and Advanced Muscle Recovery

As previously mentioned, an accumulation of metabolites, ions, and inflammatory cells impairs muscular performance by inducing muscular fatigue and soreness. Electric muscle stimulation stimulates both Type I (slow-twitch) and Type II (fast-twitch) muscles to contract, increasing blood flow to skeletal muscle. By evoking muscular contractions, NMES increases the venous blood return to the heart. As more blood is returned to the heart via muscle pumping mechanisms, more oxygenated blood is able to be pumped out to skeletal muscle, therefore increasing cardiac output (the amount of oxygenated blood pumped to the body per minute) [13].

The electric muscle stimulation, in essence, creates an electro-induced flow of oxygenated rich blood that washes away muscle metabolites and inflammatory cells accumulated during the inflammatory response; thereby decreasing the causation of inflammatory associated pain [14].

Physiology of TENS and Advanced Muscle Recovery

Both NMES and TENS reduce muscular fatigue and painful soreness associated with DOMS, though, the way each does this is physiologically unique. As discussed above, NMES increases oxygenated muscular blood flow which removes cellular debris that may stimulate pain receptors associated with DOMS. TENS also provides an electrical current, though at a different frequency and intensity, in which two theories have been developed to explain the mechanisms by which TENS decreases pain and soreness.

The two theories are known as the Gate Control Theory and the Endorphin release theory. Gate Control Theory, suggests that TENS blocks the transmission sent by nociceptive afferent fibers [15]. Nociceptive afferent fibers are sensory nerves that sense painful stimuli and send that signal to the brain. The TENS frequency sends a frequency signal via sensory nerves that blocks the transmission of pain signals to the brain, thus preventing the pain felt with muscle soreness from reaching the brain. The other theory, Endorphin Release, theorizes that TENS stimulates the release of the body’s own endogenous opioids (the body’s natural feel good hormones) which may also block pain messages from reaching the body [15,16]. The figure below demonstrates how both NMES and TENS ultimately lead to the restoration of muscular performance.

Muscle Recovery

NMES and TENS Enhance Performance and Decrease Muscular Pain

Understanding the physiology of how NMES and TENS enhance muscle recovery is one thing, it is another thing to see the practical application of these treatment modalities in enhancing performance and decreasing the pain associated with muscle fatigue and DOMS.

One study [17] examined the benefits of NMES on anaerobic performance, muscle pain, and physiological muscle recovery in professional athletes. Before and after an intense training session, peak power, jump height, muscle soreness, and creatine kinase levels were assessed up to 24-hours post training. Findings indicated that those who’s recovery session incorporated NMES significantly improved their peak power and jump height 24-hours post-training. Also, creatine kinase levels and muscle soreness values were also significantly decreased 24-hours post-training in those that utilized NMES.

Another study [18], further examined similar variables, though in-between a morning and afternoon training session. The amount of time in-between session was less and although no significant STATISTICAL differences in anaerobic performances were reported in this study, electrostimulation was still found to be more beneficial for reducing muscle pain.

Though, let’s not forget about TENS. After undergoing an intensive DOMS protocol, participants that used TENS in their recovery demonstrated also decreased their muscular pain [19].

These findings are further supported in that not only does this technology reduce creatine kinase levels (a marker of muscle damage) but adding electric muscle stimulation elicits both psychosocial and physiological benefits by decreasing creatine kinase levels and enhancing self-assessed energy levels and enthusiasm [20].

This is what athletes are saying about using PowerDot NMES and TENS for their recovery:

“I wish I'd had the PowerDot when I was in the military. If I was able to do some quick muscle therapy and recovery after rucking 100 pounds of gear for 15 miles, that would've been incredible. Everyone should have access to this technology, not just elite athletes.” - Josh Bridges

“Success is absent without recovery. Recovery isn’t an option at this point in my career. At the elite level, we ask so much from our bodies but our bodies are capped off at their capabilities. When I help my body recover, I’m allowing it to not only get stronger by being able to expand its strength capacity but, I am also allowing it to move more efficiently while doing so!” - Georganne Moline

These findings indicate significant training recovery using electrical stimulation promoting optimal muscle recovery and performance day in and day out. PowerDot combines the technology of both NMES and TENS in the pursuit to support optimal muscular recovery from fatigue and soreness.


1. Barnett, A. (2006). Using recovery modalities between training sessions in elite athletes. Sports medicine, 36(9), 781-796. [Link]

2. Welsh, R. S., Davis, J. M., Burke, J. R., & Williams, H. G. (2002). Carbohydrates and physical/mental performance during intermittent exercise to fatigue. Medicine & Science in Sports & Exercise, 34(4), 723-731. [Link]

3. Allen, D. G., Lamb, G. D., & Westerblad, H. (2008). Skeletal muscle fatigue: cellular mechanisms. Physiological reviews, 88(1), 287-332. [Link]

4. Martin, V., Millet, G. Y., Lattier, G., & Perrod, L. (2004). Effects of recovery modes after knee extensor muscles eccentric contractions. Medicine & Science in Sports & Exercise, 36(11), 1907-1915. [Link]

5. Hedayatpour, N., Falla, D., Arendt‐Nielsen, L., & Farina, D. (2010). Effect of delayed‐onset muscle soreness on muscle recovery after a fatiguing isometric contraction. Scandinavian journal of medicine & science in sports, 20(1), 145-153. [Link]

6. Bishop, P. A., Jones, E., & Woods, A. K. (2008). Recovery from training: a brief review: brief review. The Journal of Strength & Conditioning Research, 22(3), 1015-1024. [Link]

7. Babault, N., Cometti, C., Maffiuletti, N. A., & Deley, G. (2011). Does electrical stimulation enhance post-exercise performance recovery?. European journal of applied physiology, 111(10), 2501. [Link]

8. Gandevia, S. C. (2001). Spinal and supraspinal factors in human muscle fatigue. Physiological reviews, 81(4), 1725-1789. [Link]

9. Ament, W., & Verkerke, G. J. (2009). Exercise and fatigue. Sports medicine, 39(5), 389-422. [Link]

10. Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287(3), R502-R516. [Link]

11. Armstrong, R. B. (1984). Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Medicine and science in sports and exercise, 16(6), 529-538. [Link]

12. Smith, L. L. (1991). Acute inflammation: the underlying mechanism in delayed onset muscle soreness?. Medicine and science in sports and exercise, 23(5), 542-551.[Link]

13. Grunovas, A., Silinskas, V., Poderys, J., & Trinkunas, E. (2007). Peripheral and systemic circulation after local dynamic exercise and recovery using passive foot movement and electrostimulation. Journal of sports medicine and physical fitness, 47(3), 335. [Link]

14. Vanderthommen, M., Soltani, K., Maquet, D., Crielaard, J. M., & Croisier, J. L. (2007). Does neuromuscular electrical stimulation influence muscle recovery after maximal isokinetic exercise?. Isokinetics and Exercise Science, 15(2), 143-149. [Link]

15. Cox, P. D., Kramer, J. F., & Hartsell, H. (1993). Effect of different TENS stimulus parameters on ulnar motor nerve conduction velocity. American journal of physical medicine & rehabilitation, 72(5), 294-300. [Link]

16. DeSantana, J. M., Walsh, D. M., Vance, C., Rakel, B. A., & Sluka, K. A. (2008). Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain. Current rheumatology reports, 10(6), 492. [Link]

17. Taylor, T., West, D. J., Howatson, G., Jones, C., Bracken, R. M., Love, T. D., ... & Kilduff, L. P. (2015). The impact of neuromuscular electrical stimulation on recovery after intensive, muscle damaging, maximal speed training in professional team sports players. Journal of Science and Medicine in Sport, 18(3), 328-332. [Link]

18. Tessitore, A., Meeusen, R., Cortis, C., & Capranica, L. (2007). Effects of different recovery interventions on anaerobic performances following preseason soccer training. The Journal of Strength & Conditioning Research, 21(3), 745-750.[Link]

19. Mankovsky-Arnold, T., Wideman, T. H., Larivière, C., & Sullivan, M. J. (2013). TENS attenuates repetition-induced summation of activity-related pain following experimentally induced muscle soreness. The Journal of Pain, 14(11), 1416-1424. [Link]

20. Beaven, C. M., Cook, C., Gray, D., Downes, P., Murphy, I., Drawer, S., ... & Gill, N. (2013). Electrostimulation’s enhancement of recovery during a rugby preseason. International journal of sports physiology and performance, 8(1), 92-98.[Link]

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