Fatigue is a common condition suffered by individuals undergoing chronic illness. The two main factors responsible for fatigue include central and peripheral mechanisms. Central mechanisms largely arise from proximal events such as neuromuscular junction, which is subdivided into supraspinal or spinal. Peripheral fatigue is caused by muscle contraction activities and includes excitation contraction or muscle bioenergetics. The discussion covers some mechanisms involved in fatigue experiences (Gandevia, 1994).
Voluntary muscle activation
This mechanism associated with central fatigue, accounts for about 15% to 20% of the usual and normal fatigue during continuous or sustained fatigue contraction. The voluntary drive of the muscle incurs difference in contraction especially when flexing some muscles like the elbow. The degree of fatigue depends on the muscle being tested. Voluntary contraction may be lesser in diaphragm than in the biceps muscles since there is more twitching force on maximum contraction than in the biceps. Voluntary activation is simultaneously reduced by the by multiple contraction of muscles (Marconnet, 1992).
Transcranial magnetic stimulation (TMS)
It activates the motor cortex neurons while at the same time produces muscle excitatory response (MEP) through muscle twitch force. The latency witnessed between TMS and MEP is mostly determined by the period in which the action is initiated in motor cortex and registered in the electromyographic (EMG). The twitch force and motor-evoked potential are succeeded by electrical silent session caused by motor cortex interneurons which are inhibitory. Spinal alpha neurons turn to be less responsive due to continuous inhibitory period of motor cortex interneurons. The results show fatigue occurs and descending cortical input is required to maintain activation of spinal motor neurons and muscle force (Gandevia, 1994).
Maximum Aerobic Capacity
Usually experienced during exercises where consumption skeletal muscle produces lactate. When low-intensity exercises continue, catabolization of lactate in energy occurs preventing its accumulation in muscles or release into circulation. As the intensity of exercises and consumption of oxygen increases, phosphorylation oxygen is limited leading to accumulation of lactate. Lactate accumulation prompts to fatigue as it is associated with fatigue development and respiratory rates (Marconnet, 1992).
My experience would be associated with maximum aerobic capacity. During my usual exercise sessions, I experienced a state where my oxygen consumption was at a high level. This led to increased lactate production, which resulted in difficulty in the breathing process and fatigue experience witnessed too.
Gandevia, S. C., & Symposium on Neural and Neuromuscular Aspects of Muscular Fatigue (1994, Miami, Fla.). (1995). Fatigue: Neural and muscular mechanisms : [proceedings based in part on the Symposium on Neural and Neuromuscular Aspects of Muscular Fatigue, held November 10-13, 1994, in Miami, Florida]. New York [u.a.: Plenum Press.
Marconnet, P. (1992). Muscle fatigue mechanisms in exercise and training: Proceedings of the 4th International Symposium on Exercise and Sport Biology, Nice, November 1-4, 1990. Basel [u.a.: Karger.