Models of Fatigue

Original Editor - User Name

Top Contributors - Rebecca Willis and Lucinda hampton  

Introduction

Exercise causes physiological and biochemical adaptations including the development of fatigue . The development of fatigue is the body's mechanism to protect against the harmful effects of exercise, thus it limits the body's ability to perform . Knowledge of the different models of fatigue, resulting from exercise, is important for physiotherapists to understand the training aims of an athlete's programme when improving performance during return from injury. This page outlines the common models used to explain the mechanisms behind fatigue.

Cardiovascular Model

This model suggests that exercise endurance is limited by the heart's ability to pump sufficient blood, and therefore oxygen, to the exercising muscles . When the demand of the skeletal muscle exceeds the cardiac output, fatigue occurs. This is supported by the increase in cardiac output which leads to increases in exercise capacity. However, it is also argued that, if this is the case, then the heart (which also relies on an adequate blood and oxygen supply), would also suffer from oxygen deficiency, which would result in myocardial ischaemia . Therefore, it can be hypothesised that there is a central 'governor' whereby receptors in the heart assess coronary blood flow and oxygen delivery. Before these reach a detrimental limit, the motor cortex reduces skeletal muscle activation, thus resulting in fatigue.

Energy Supply / Energy Depletion Model

This model suggests that fatigue is an inability to supply energy (ATP) at a fast enough rate, or a depletion in energy stores . When endogenous carbohydrate stores are depleted, fatigue occurs. But, similar to the cardiovascular model, if muscle ATP stores are fully depleted, rigor occurs. Therefore it is hypothesised that there is a central 'governor' to defend against skeletal muscle rigor.

Biomechanical Model

This model suggests fatigue is a result of movement inefficiency which results in increased VO2 requirements, increased metabolic accumulation, depletion of energy stores, and increased core body temperature . It is suggested that muscle damage caused during the stretch-shortening cycle reduces the tolerance to move between muscle stretch and muscle contraction (amortization), thus resulting in a reduced force production. It is also suggested that the central nervous system interprets feedback from Golgi tendon organs to provide this protective mechanism, thus a longer amortization phase is felt as fatigue.

Psychological Model

This model suggests exercise is limited by the athlete's conscious effort based on sensory feedback . It is measured by a rating of perceived exertion (RPE) scale and posits that athletes will anticipate the work required and modify their effort accordingly which is supported by the placebo effect .

Muscle Recruitment Model / Central (Nervous System) Fatigue

This model suggests it is the failure of the central nervous system to recruit skeletal muscle that causes fatigue, as shown by reduced motor neuron output in EMG assessment of working muscles .This is brought about by a reduction in excitatory, and/or, an increase in inhibitory neural messaging .This change in neural messaging has several sources; changes in central neurotransmitter concentrations , feedback from rising body temperature, and feedback from skeletal muscle .

Conclusion

Different proponents will advocate different models of fatigue dependent upon their background, but fatigue is a result of several physiological processes that reduces the ability of muscle fibres to generate force . Specific training will produce physiological adaptations that delays the onset of fatigue; the focus of training will depend upon which model is being targeted. This page looks specifically at models as they relate to athletic performance and training, but the related Physiopedia page, Muscle Fatigue, delves further into fatigue as it relates to pathological conditions and the treatment of fatigue.