Fatigue is a catchall term that is used in many different contexts. Some view fatigue as a progressive process that begins at the onset of exercise while others view it as the involuntary end point of an exercise bout.
Physiological changes that occur within a muscle in regards to fatigue are termed peripheral fatigue (PF). This is considered the traditional model of fatigue. For example, if when running the quadriceps begin to “burn” and fatigue, this is indicative of a buildup of acidity within the muscle, which slows the runner and possibly causes the runner to stop. In other words, the physiological changes that result in fatigue are isolated to specific, local muscle motor units.
The opposing model of fatigue is termed central fatigue (CF). Central fatigue is the result of events within the brain and spinal cord. Central fatigue and, more specifically, the central governor model (CGM) are discussed below.
CENTRAL GOVERNOR MODEL
The CGM states the brain, not the muscle, is the reason for a decrease in the performance of a muscle. This means that the brain is constantly assessing the body to make sure that we don’t hurt ourselves. In essence, the brain is the body’s control room and thus its safety mechanism. If the brain senses that something is getting to a potentially dangerous level, it acts to decrease the intensity level of that specific area.
In the example used previously regarding a buildup of intramuscular acidity causing a muscle’s function to decrease – under the CGM, this is the result of the brain reducing muscle fiber recruitment of the quadriceps.
SO WHICH MODEL IS RIGHT?
While there are critics of the CGM, primarily due to a lack of proof of a central governor, it is likely that both models of fatigue (central and peripheral) work together to influence and regulate human performance.
EFFECT ON PACING
While there is no absolute proof of a central governor, an individual will pace himself or herself differently when racing a mile versus a marathon, and there is less risk involved with running fast for a mile versus participating in a marathon.
Therefore, it is important to understand that the distance of a race will have a large impact on a runner’s pace.
While the self-selected race pace of a runner can be used as a point of reference, other factors such as formal physiological assessments and past training data (i.e., long-run pace) should also be considered when determining pacing guidelines. In other words, the CGM can likely be overridden to some degree.
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Noakes T D, St Clair Gibson A, Lambert E V. “From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans.” Br J Sports Med 2004. 38511–514.514
Asmussen E. “Muscle fatigue.” Med Sci Sports 1979. 11313–321.321
St Clair Gibson A, Noakes T D. “Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans.” Br J Sports Med 2004. 38797–806.806
Kirkendall DT. “Mechanisms of peripheral fatigue.“ Med Sci Sports Exerc. 1990 Aug;22(4):444-9.
J P Weir, T W Beck, J T Cramer, and T J Housh. “Is fatigue all in your head? A critical review of the central governor model” Br J Sports Med. Jul 2006; 40(7): 573–586. doi: 10.1136/bjsm.2005.023028. PMCID: PMC2564297
Noakes TD. “Is it time to retire the A.V. Hill Model?: A rebuttal to the article by Professor Roy Shephard.” Sports Med. 2011 Apr 1;41(4):263-77. doi: 10.2165/11583950-000000000-00000.
Gandevia S C. “Spinal and supraspinal factors in human muscle fatigue.” Physiol Rev 2001. 811725–1789.1789