A peripheral governor regulates muscle contraction

Abstract

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 Ca2+ release through ryanodine receptors, and decreasing the availability of Ca2+ 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.

Pacing and Decision Making in Sport and Exercise: The Roles of Perception and Action in the Regulation of Exercise Intensity

“…Since physiological catastrophes can and do occur [1] and a variety of peripheral factors can impair muscle performance [69], it is suggested that the proposed dominant governor could at least be over-ridden. MacIntosh and Shahi [70] proposed a peripheral governor, working at the cellular level, which can reduce the muscle contraction by attenuating activation to avoid metabolic catastrophe. Marcora [71] suggested that deciding when to terminate exercise is done by the conscious brain without the need to include an additional subconscious entity.…”

“…However, the location of-and processes occurring associated with this controller are not understood yet. Different mechanisms are suggested at muscular level [70] as well as within the brain [64].…”

Skeletal muscle fatigue – regulation of excitation–contraction coupling to avoid metabolic catastrophe

“…We have proposed that the cellular regulation of ATP use is the principal mechanism for the decreased contractile response that is associated with acute repetitive muscle use, typically called muscle fatigue (MacIntosh and Shahi, 2011). We also have recognized that regulating Ca 2+ release from the sarcoplasmatic reticulum (SR), and thus the intracellular Ca 2+ concentration ([Ca 2+ ] i ), dictates the rate of ATP use in the muscle cell because it affects Ca 2+ ATPase and myosin ATPase activity, which together account for 90% of ATP use (Box 1).…”

Time to exhaustion at anaerobic threshold in swimming rats: metabolic investigation

“…As a result, the AT is an indirect procedure to determine the aerobic endurance and not always leads to exhaustion, while the time to exhaustion at this intensity (tlim) is adopted as a direct procedure (5). The motives of exhaustion at AT has been investigated since the 1920s, and owing the diffi culty caused by multi factorial characteristic, are still actively researched today (6). Some authors have associated the inability to continue exercise at aerobic required intensity to a lack of energetic substrates, mainly glycogen depletion (7,8).…”