High-intensity intermittent sprint intervals result in high physiological, metabolic, and neuromuscular demands. Often this type of exercise is accompanied by reversible declines in the force production of the muscles as they contract at or near maximal capacity. This fatigue can be defined as the reversible, exercise-induced reduction in maximal power output or speed. Generally, there is a positive correlation relationship between the power output and speed. One last, yet important, part of the human anatomy and physiology are taxed during these sprints. That area is the central nervous system and the corresponding perception it creates for the athlete. It’s common for the central nervous system to be fatigued during longer-duration exercise. However, the complex interaction of serotonin, noradrenaline, dopamine, and acetylcholine can play a role in central nervous system fatigue. These neurotransmitters each contribute in unique ways to the running ability of the athlete. Serotonin, for example, is higher in the exercising athlete than at rest. This can cause greater perceptions of effort, and greater sensory awareness of peripheral muscle fatigue. Dopamine is lowered during exercise, and can lead to decreases in mental motivation. Acetylcholine drops during exercise as well, and acetylcholine is important for the generation of muscular force. It must be concluded that the central nervous system plays a role in the recovery from fatigue, as well as the onset of it.
The central nervous system might be responsible for more recovery from fatigue than previously expected. However, it’s clear that the peripherally related factors are more scientifically founded than the central nervous system’s relationship to recovery. In situations of extreme weather conditions, the central nervous system plays an important role in that same fatigue recovery that physiological returns to homeostasis contributes. That same role can be duplicated when physiological homeostatic imbalances are mediated by known peripheral recovery factors and the CNS regulates. Controlling this central nervous fatigue has been undertaken by amphetamines, caffeine, carbohydrates, branched-chain amino acids, etc. However, even with optimal supplementation from these sources, it’s apparent that the central nervous system has a response to fatigue of it’s own. Re-focusing on these origins of fatigue primarily associated with the central nervous system could optimize the ability to recover from fatigue. Returning the exerciser to appropriate homeostasis has been previously accomplished by massage, cryotherapy, hydrotherapy, sleep, etc., pharmacological (non-steroidal anti-inflammatory medications), and nutritional supplementation such as carbohydrates. Many peripheral variables lead to reductions in muscular force output. The energy availability to maintain high-intensity sprint intervals is limited, and diminishing returns are noted with each subsequent interval.
Explicit evidence is currently lacking for the well-proven relationship between the central nervous system and exercise-induced fatigue recovery. The understanding of the effects that intermittent sprinting has on the brain, and the role that the central nervous system plays in returning the brain to a place where muscular fatigue is diminished is inconclusive at this time. Further data is needed from recovery interventions that point out the relationship between the PNS and CNS as aids in recovery.
Strengths of the paper include mentioning a potential frontier of science that hasn’t been utilized yet. The possibility of the CNS being involved in the recovery of athletes stimulates questions about the possible applications of the CNS. The weakness of the paper, of course, is that there is no substantial argument that the CNS is involved in an athlete’s recovery at all. Looking towards the future, there are many horizons that could be built if the CNS does in fact prove to be a key regulator of fatigue. However, for now, the application of the paper is best suited for future questions about the relationship that exists between the brain, the spinal cord, and the homeostatic balance they bring post-exercise.