Many strength and conditioning programs are primarily built around objective data such as force production, velocity, power, and acceleration. There is an upstream variable that dictates all of those outputs that most training programs overlook: central nervous system (CNS) efficiency.

Without optimal CNS function, athletes cannot recruit motor units at the rate or magnitude their musculoskeletal capacity would otherwise allow. In other words, your athletes may have more strength and speed than they’re currently showing. The limiting factor is not their muscles, it is their nervous system.

The neurological basis of explosive performance

The CNS sends signals to muscles via neurons. Neurons are long, electrically conductive nerve cells that transmit motor commands from the brain to the muscles. The speed and efficiency of that signal determines rate of force development (RFD), reactive strength and overall explosiveness.

Lim and Rasband (2020) explain that the main structural factor that determines signal transmission speed is the myelin sheath. The myelin sheath is a fatty, insulating layer that wraps around axons. Myelin functions similarly to insulation on an electrical wire in that it reduces signal degradation and it increases conduction velocity. Myelin’s primary roles are to “increase conduction velocity to maximal levels” and to “finely tune neuronal network function by synchronizing firing patterns”(Stadelmann et al., 2019). Practically speaking, the thicker the myelin, the faster the signal, the greater the explosiveness.

The Cellular Mechanism: Oligodendrocytes

Myelin can’t get thicker passively. It requires stimulation of a specific kind of glial cell called oligodendrocytes. These oligodendrocytes are responsible for generating, maintaining, and remodeling myelin sheaths throughout the CNS (Stadelmann et al., 2019).

The question for coaches is: “what training stimuli most effectively drive oligodendrocyte activity while managing CNS fatigue?”

Research published in Frontiers of Cellular Neuroscience offers a useful framework. Kujawa and colleagues (2023) found that intense aerobic exercise can induce myelination in regions of the brain associated with that specific activity. Most importantly, they also found that “exposure to physical training of high complexity seems to result in higher myelin content and improved axonal transmission”. Suggesting that neuromotor complexity, not just intensity is a driver of myelination.

Programming Considerations: The Aerobic Paradox

This is where application gets nuanced, mainly for power sport athletes like baseball players.

Aerobic exercise drives myelination. However, consistent, high volume aerobic training promotes type I muscle fiber characteristics which can blunt the fast twitch qualities you’re trying to develop. Long, slow, distance work tells the body to prioritize endurance capacity over explosive output. For most team sport and power athletes, that is a bad trade.

The solution to this paradox is to pursue high intensity, short duration efforts that stress the CNS and drive myelination without the muscle fiber conversion risk of prolonged aerobic work. These reps need to be:

• Maximal or near maximal in intensity: Sub maximal efforts don’t generate sufficient neural demand
• Short in duration: This is to avoid the endocrinological changes that are a byproduct of endurance training.
• High in neuromotor complexity: Multi segment, coordinated efforts produce greater myelination stimulus than isolated movements. For example, rapid vertical jumps will produce a greater stimulus than rapid, banded hamstring curls.

Hill sprints are a practical application of all three of these principles. At 8ctane, we have a 212 yard hill that takes elite athletes under 28 seconds to complete. This exercise demands maximal output from the lower extremities, core and upper body simultaneously. The CNS load is extreme, and the duration is short enough to avoid the downsides of aerobic overreach.

Recovery Protocols: Supporting Neural Adaptation

Training stimulus is only half of the equation. Myelination is a biological process that requires raw materials and adequate recovery time, just like muscular growth. Coaches should address two key variables with their athletes when implementing neural training.

Sleep

Toschi et al. (2021) found significant associations between sleep duration and quality and intracortical myelin levels across multiple brain regions. Although the direct effect on the corticospinal tract specifically requires further study, the data clearly points toward sleep deprivation impairing CNS health and myelination. 8 to 9.5 hours per night should be the target during phases of high neural training load.

Nutrition

Myelin is composed of approximately 70-85% lipids (Poitelon et al., 2020), making dietary fat intake a direct input to myelin growth. Two nutrients are at the forefront of the research.

• Iron: Todorich and colleagues (2009) found that reduced dietary iron is associated with hypomyelination. Athletes in intense training phases should regularly consume iron dense foods like red meat, legumes, leafy greens, and fortified grains.
• Omega-3 Fatty Acids: Given myelin’s lipid heavy composition, getting enough Omega-3s (salmon, walnuts, flaxseed) is a logical and evidence consistent recommendation for supporting myelin synthesis and repair (Poitelon et al., 2020).

Practical Takeaway

Most S&C programs are optimized for the musculoskeletal system. The coaches who start explicitly programming for CNS efficiency through high intensity, high complexity efforts paired with deliberate recovery protocols will produce athletes who can actually express the strength and speed that they have built.

The myelin sheath is trainable. It’s time to start treating it that way.