Low Frequency Peripheral Fatigue

In the presence of pure low-frequency fatigue, force generation in response to high-frequency stimulation is unimpaired, indicating that the contractile proteins are capable of generating maximal force provided that sufficient calcium is released by the sarcoplasmic reticulum (SR). As a result, impaired force generation at submaximal frequencies of stimulation may represent either a reduced level of calcium availability due to alterations in SR function or a reduction in the calcium sensitivity of the myofilaments at submaximal calcium concentrations. Both changes have been demonstrated experimentally (16, 17). Reduced myofilament calcium sensitivity can be produced experimentally by increasing hydrogen and phosphate ions (18). The explanation for impaired calcium release by the SR during contractions is less well understood, and a number of theories have been proposed to account for this phenomenon (16, 19-21).

Low-frequency fatigue has been demonstrated in the diaphragm and sternocleidomastoid muscles of normal subjects breathing against high resistive loads (17, 22). Low-frequency fatigue has also been shown to develop in the diaphragm of normal subjects asked to sustain maximum voluntary ventilation for 2 minutes (23).

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