Effect of Fatigue Protocols on Lower Limb Neuromuscular Function and Implications for Anterior Cruciate Ligament Injury Prevention Training: A Systematic Review

Much is known about the physiological impairments that can cause muscle fatigue. It is known that fatigue can be caused by many different mechanisms, ranging from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex, and that there is no global mechanism responsible for muscle fatigue. Rather, the mechanisms that cause fatigue are specific to the task being performed. The development of muscle fatigue is typically quantified as a decline in the maximal force or power capacity of muscle, which means that submaximal contractions can be sustained after the onset of muscle fatigue. There is even evidence that the duration of some sustained tasks is not limited by fatigue of the principal muscles. Here we review experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue. Selected comparisons of tasks, groups of individuals and interventions with the task-failure approach can provide insight into the rate-limiting adjustments that constrain muscle function during fatiguing contractions.

1. Voluntary activation of elbow flexor muscles can be optimal during brief maximal voluntary contractions (MVCs), although central fatigue, a progressive decline in the ability to drive the muscle maximally, develops during sustained or repeated efforts. We stimulated the motor cortex and motor point in human subjects to investigate motor output during fatigue. 2. The increment in force (relative to the voluntary force) produced by stimulation of the motor point of biceps brachii increased during sustained isometric MVCs of the elbow flexors. Motoneuronal output became suboptimal during the contraction, i.e. central fatigue developed and accounted for a small but significant loss of maximal voluntary force. During 3 min MVCs, voluntary activation of biceps fell to an average of 90.7% from an average of > 99%. 3. The increment in force (relative to the voluntary force) produced by magnetic cortical stimulation was initially small (1.0%) but also increased during sustained MVCs to 9.8% (with a 2 min MVC). Thus, cortical output was not optimal at the time of stimulation nor were sites distal to the motor cortex already acting maximally. 4. A sphygmomanometer cuff around the upper arm blocked blood supply to brachioradialis near the end of a sustained MVC and throughout subsequent brief MVCs. Neither maximal voluntary force nor voluntary activation recovered during ischaemia after the sustained MVC. However, fatigue-induced changes in EMG responses to magnetic cortical stimulation recovered rapidly despite maintained ischaemia. 5. In conclusion, during sustained MVCs, voluntary activation becomes less than optimal so that force can be increased by stimulation of the motor cortex or the motor nerve. Complex changes in excitability of the motor cortex also occur with fatigue, but can be dissociated from the impairment of voluntary activation. We argue that inadequate neural drive effectively 'upstream' of the motor cortex must be one site involved in the genesis of central fatigue.

In soccer one of the most common knee injuries is the anterior cruciate ligament (ACL) tear, which usually occurs through non-contact mechanisms. Female soccer players are at higher risk of sustaining non-contact ACL injuries than male soccer players. A good understanding of ACL loading mechanisms is the basis for a good understanding of the mechanisms of non-contact ACL injuries, which in turn is essential for identifying risk factors and developing prevention strategies. Current literature demonstrates that sagittal plane biomechanical factors, such as small knee flexion angle, great posterior ground reaction force and great quadriceps muscle force, are the major ACL loading mechanisms. A great posterior ground reaction force may be associated with a great quadriceps muscle force, which would cause great anterior draw force at the knee. A small knee flexion is associated with a large patella tendon-tibia shaft angle and ACL elevation angle, which would result in great ACL loading. Current literature also demonstrates that the ACL is not the major structure of bearing knee valgus-varus moment and internal-external rotation loadings. Knee valgus-varus moment and internal-external rotation moment alone are not likely to result in isolated ACL injuries without injuring other knee structures.