We suggest that during fatigue, the upper limit of motor neuron firing rates which can be sustained by voluntary effort is regulated to match changes in muscle contractile speed such that they never exceed the minimum required for tetanic fusion (maximum force generation); for in a sustained maximum voluntary contraction (MVC) the falling force cannot be increased by tetanic nerve stimulation despite the decline in the integrated surface EMG (IEMG). Under these conditions, force loss cannot be due to muscle contractile failure. For the adductor pollicis muscle, motor neuron firing rates decline in parallel with the slowing of muscle contractile speed. If a similar relationship is now found for other muscles, and when equal amounts of fatigue are induced by other forms of exercise, a muscle-based reflex regulation is suggested. We shall also attempt to identify the range of firing rates, and their changes, for different fiber types by comparing between muscles and by using exercise protocols where each is selectively and/or sequentially recruited. Reflex control could be mediated by free nerve endings within the muscle which respond to many of the mechanical and metabolic changes which accompany fatigue. These metabolic changes will be monitored and related to MVC firing rates during exercise and ischemic and aerobic recovery. Contractile slowing will also be induced in the absence of fatigue. We postulate that one of the sites of muscle contractile failure is impaired excitation/contraction coupling due to extracellular potassium accumulation. This will be tested by relating changes in the evoked action potential to force loss during fatique and ischemic recovery where restoration of other metabolic events is prevented. These studies will provide important information about factors underlying fatigue in normal subjects, athletes, and in the rehabilitation of debilitated patients.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
2R01NS014756-07
Application #
3395747
Study Section
Orthopedics and Musculoskeletal Study Section (ORTH)
Project Start
1978-07-01
Project End
1988-06-30
Budget Start
1985-07-01
Budget End
1986-06-30
Support Year
7
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Quinnipiac University
Department
Type
Sch Allied Health Professions
DUNS #
City
Hamden
State
CT
Country
United States
Zip Code
Thomas, C K; Johansson, R S; Bigland-Ritchie, B (2006) EMG changes in human thenar motor units with force potentiation and fatigue. J Neurophysiol 95:1518-26
Thomas, Christine K; Johansson, Roland S; Bigland-Ritchie, Brenda (2002) Incidence of F waves in single human thenar motor units. Muscle Nerve 25:77-82
Thomas, C K; Johansson, R S; Bigland-Ritchie, B (1999) Pattern of pulses that maximize force output from single human thenar motor units. J Neurophysiol 82:3188-95
Thomas, C K; Tucker, M E; Bigland-Ritchie, B (1998) Voluntary muscle weakness and co-activation after chronic cervical spinal cord injury. J Neurotrauma 15:149-61
Thomas, C K; Zaidner, E Y; Calancie, B et al. (1997) Muscle weakness, paralysis, and atrophy after human cervical spinal cord injury. Exp Neurol 148:414-23
Bigland-Ritchie, B; Rice, C L; Garland, S J et al. (1995) Task-dependent factors in fatigue of human voluntary contractions. Adv Exp Med Biol 384:361-80
Howell, J N; Fuglevand, A J; Walsh, M L et al. (1995) Motor unit activity during isometric and concentric-eccentric contractions of the human first dorsal interosseus muscle. J Neurophysiol 74:901-4
Bigland-Ritchie, B R; Furbush, F H; Gandevia, S C et al. (1992) Voluntary discharge frequencies of human motoneurons at different muscle lengths. Muscle Nerve 15:130-7
Bigland-Ritchie, B; Thomas, C K; Rice, C L et al. (1992) Muscle temperature, contractile speed, and motoneuron firing rates during human voluntary contractions. J Appl Physiol 73:2457-61
Rice, C L; Vollmer, T L; Bigland-Ritchie, B (1992) Neuromuscular responses of patients with multiple sclerosis. Muscle Nerve 15:1123-32

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