A peripheral governor regulates muscle contraction

• Published in: Applied physiology, nutrition, and metabolism Vol. 36; no. 1; pp. 1 - 11
• Main Authors: MacIntosh, Brian R, Shahi, M. Reza S
• Format: Journal Article
• Language: English
• Published: Ottawa Presses scientifiques du CNRC 01.02.2011; NRC Research Press; Canadian Science Publishing NRC Research Press
• Subjects: Adenosine triphosphatase; Adenosine triphosphate; Adenosine Triphosphate - metabolism; Animals; Biological and medical sciences; Calcium - metabolism; Contractile Proteins - metabolism; contractile response; Electromyography; Exercise; exhaustion; Fatigue; Fundamental and applied biological sciences. Psychology; gradation; Humans; Hydrolysis; Muscle Contraction; Muscle Fatigue; Muscle, Skeletal - physiology; Musculoskeletal system; pacing; Physiological aspects; Recruitment, Neurophysiological; Ryanodine Receptor Calcium Release Channel - metabolism; réponse contractile; Sarcoplasmic Reticulum - metabolism; Vertebrates: body movement. Posture. Locomotion. Flight. Swimming. Physical exercise. Rest. Sports; épuisement; United States; Human; Fatigue; Performance; Muscle contraction
• ISSN: 1715-5312; 1715-5320
• DOI: 10.1139/H10-073

Active skeletal muscles are capable of keeping the global [adenosine triphosphate (ATP)] reasonably constant during exercise, whether it is mild exercise, activating a few motor units, or all-out exercise using a substantial mass of muscle. This could only be accomplished if there were regulatory processes in place not only to replenish ATP as quickly as possible, but also to modulate the rate of ATP use when that rate threatens to exceed the rate of ATP replenishment, a situation that could lead to metabolic catastrophe. This paper proposes that there is a regulatory process or "peripheral governor" that can modulate activation of muscle to avoid metabolic catastrophe. A peripheral governor, working at the cellular level, should be able to reduce the cellular rate of ATP hydrolysis associated with muscle contraction by attenuating activation. This would necessarily cause something we call peripheral fatigue (i.e., reduced contractile response to a given stimulation). There is no doubt that peripheral fatigue occurs. It has been demonstrated in isolated muscles, in muscles in situ with no central nervous system input, and in intact human subjects performing voluntary exercise with small muscle groups or doing whole-body exercise. The regulation of muscle activation is achieved in at least 3 ways (decreasing membrane excitability, inhibiting Ca 2+ release through ryanodine receptors, and decreasing the availability of Ca 2+ in the sarcoplasmic reticulum), making this a highly redundant control system. The peripheral governor attenuates cellular activation to reduce the metabolic demand, thereby preserving ATP and the integrity of the cell.