Fatigue and Marathon Running
Fatigue and marathon running are almost synonymous in most people’s opinion, and indeed acute fatigue is a natural consequence of any exercise activity.
Fatigue can be defined as a reduction in the ability to produce or maintain the force required for a given activity (Celine et al., 2011), resulting in greater perceived exertion– an increased sensation of effort (Enoka & Stuart, 1992).
The exact causes of fatigue are unclear, although it has been attributed to the central nervous system (brain and spinal cord) and the muscles. These causes are more technically referred to as central and peripheral fatigue (Davis, 1995).
Peripheral fatigue occurs at or past the neuromuscular junction (the area at which a neuron activates a muscle to contract) and is related to biochemical changes within the muscles metabolic environment that lead to reduced responses to activation signals (Amann, 2011).
Potential causes of peripheral fatigue in marathon running include (Kent-Braun, 1999):
- Energy depletion –In order to produce energy (in the form of adenosine tri-phosphate – ATP) during prolonged sub-maximal exercise, the body utilises glucose in the blood stream. Fatigue occurs when blood glucose declines due to a disruption to gluconeogenesis and glycogenolysis in the liver because of a re-distribution of blood flow.
- Acidosis/accumulation of metabolites – During anaerobic exercise (such as bursts of speed during a race) the body will use glucose for fuel; a by-product of this is a build up of lactic acid. This results in a build up of hydrogen ions; these inhibit an enzyme called phosphofructokinase (which affects blood glucose regeneration) and can also interfere with the release of calcium which will impair muscle contraction.
- Excitation-contraction coupling impairment– This refers to a failure of the parts of the muscle fibres needed for muscle contraction and can be linked to the aforementioned decline in calcium release. This impairment has a very slow time course of recovery when compared to the energy depletion mechanism.
Research has suggested that damage to the actual muscle fibres (due to the high volume of eccentric contractions during a marathon (Overgaard et al., 2004) and disruption to the excitation-contraction coupling mechanism is the most likely cause of peripheral fatigue (Ross, 2007).
Peripheral fatigue can also be divided into two subsections due to the stimulation required to elicit fatigue. Low frequency fatigue is demonstrated during electrical stimulation of the muscle at a frequency of 1-20 Hz (roughly equates to exercise such as jogging) whereas high frequency fatigue is shown at 50-100 Hz (activities such as hopping) (Tomazin, Strojnik, & Sarabon, 2002).
Central fatigue is related to the central nervous system which consists of the brain and spinal cord, and is often described as an impairment to the central drive to a muscle (central drive refers to the flow of neural activation signals) (Ross, 2007).
It is effectively a reduction in the voluntary activation of muscle and can be noticed when, towards the end of a marathon, an athlete’s running technique becomes sub-optimal (they appear to have ‘heavy legs’), demonstrating that muscle fibres are not switching on fully due to decreased recruitment and firing frequency.
The extreme of central fatigue in a marathon is seen when an athlete ‘hits the wall’.
The most likely cause of central fatigue is due to the effect prolonged sub-maximal exercise has on serotonin in the brain, a hormone responsible for mood, sleep regulation and feelings of lethargy, also known as 5-HT (Cotel, Exley, Cragg, & Perrier, 2013).
Prolonged (primarily) aerobic exercise such as marathon utilises fat as a fuel source, when this fat is mobilised it causes free fatty acids to be released into the blood stream, which then attach to branched chain amino acids.
The regular function of branched chain amino acids is to ‘hold onto’ tryptophan (the pre-cursor to serotonin) to prevent it crossing the blood-brain barrier and producing serotonin. When free fatty acids prevent branch chain amino acids from doing this, serotonin is produced in the brain and central fatigue occurs.
The Central Governor Theory
The idea that there is a mechanism that prevents an athlete from dangerous over-exertion whilst running was originally suggested by Hill,Long and Lupton in 1924 and then renewed by Noakes in 1997 who gave it the term ‘central governor’.
The central governor theory is a function of multiple brain areas (as opposed to an actual area inside the brain); Noakes (2007) explains it as a neural control system that can reduce the activation levels of muscles in order to enforce homeostasis (steady state) in the body. Noakes and others (Hampson, Gibson, Lambert, & Noakes, 2001; Tucker, Marle, Lambert, & Noakes, 2006) believe that if homeostasis is not controlled the body would be capable of causing catastrophic damage to its vital organs and skeletal muscle.
This theory has been criticised in other research (Shephard, 2009; Weir, Beck, Cramer, & Housh, 2006) for several reasons, specifically in that, if the central governor exists, then it should be impossible for athletes to contract hyperthermia and to induce muscle damage and ischemia. Additionally it has been shown that even when voluntary muscle activation is decreased, maximal activation can still occur with the use of electrical stimulation and it does not result in injury, just additional fatigue (Garland & McComas, 1990).