Changes in force and stiffness induced by fatigue and intracellular acidification in frog muscle fibres.

Abstract

1. Changes in force and stiffness were recorded simultaneously during 1 s isometric (fixed ends) tetani of single fibres isolated from the anterior tibialis muscle of Rana temporaria (temperature 1-3 degrees C; sarcomere length, 2.10 micron). Stiffness was measured as the change in force that occurred in response to a 4 kHz sinusoidal length oscillation of the fibre. Some experiments were performed in which stiffness was determined from a fast (0.2 ms) length step that was applied to a 'tendon-free' segment of the muscle fibre during the tetanus plateau. 2. A moderate degree of fatigue was produced by decreasing the time between tetani from 300 s (control) to 15 s. By this treatment the maximum tetanic force (Ftet) was reversibly reduced to 70-75% of the control value. Maximum tetanic stiffness (Stet) was related to Ftet according to the following regression (both variables expressed as percentage of their control values): Stet = 0.369 Ftet + 62.91 (correlation coefficient, 0.95; P less than 0.001). A 25% decrease in isometric force during fatigue was thus associated with merely 9% reduction of fibre stiffness. 3. Whereas the rate of rise of force during tetanus was markedly reduced by fatiguing stimulation, the rate of rise of stiffness was only slightly affected. 4. Intracellular acidification (produced by raised extracellular CO2 concentration) largely reproduced the contractile changes observed during fatigue. However, for a given decrease in tetanic force there was a smaller reduction in fibre stiffness during acidosis than during fatigue. 5. Caffeine (0.5 mM) added to the fibre after development of fatigue and intracellular acidosis greatly potentiated the isometric twitch but did not affect maximum tetanic force. This finding provides evidence that the contractile system was fully activated during the tetanus plateau both in the fatigued state and during acidosis. 6. The results suggest that the decrease in contractile strength after frequent tetanization (intervals between tetani, 15 s) is attributable to altered kinetics of cross-bridge function leading to reduced number of active cross-bridges and, most significantly, to reduced force output of the individual bridge. The possible role of increased intracellular H+ concentration in the development of muscle fatigue is discussed.

Synchronous oscillations of length and stiffness during loaded shortening of frog muscle fibres

“…Tension was recorded by means of a semiconductor strain-gauge element (AE 801, Aksjeselskapet Mikroelektronikk, Horten, Norway). The transducer element had been modified to increase the frequency response of the transducer as described by Edman & Lou (1990). The resonant frequency of the force transducer was 19 kHz when the transducer was submerged in the bathing fluid.…”

“…In some experiments, to be described separately, the fibre was moderately fatigued by reducing the interval between the tetani from 2 min (control) to 15 or 30 s. As the tetanization frequency was increased, the isometric force was steadily reduced and levelled off at approximately 75 % of its original (control) value after 25-30 contractions at the high frequency (for further information, see Edman & Lou, 1990).…”

“…Full details of methods and apparatus used to measure fibre stiffness are given by Edman & Lou (1990) and only an outline is presented here. In these experiments the fibres were mounted between two electromagnetic pullers (motors No.…”

Possible effect of the supplementation of branched chain aminoacids, aspartate and asparagine on anaerobic threshold

“…O terceiro e mais forte nível de inibição ocorre com uma diminuição na disponibilidade de substrato. A fosforilase somente aceitará a forma diiônica do fosfato inorgânico (H P O f') como substrato, e fosfato inorgânico na presença de H+ é convertido em H2PO4* A redução do pH pode alterar de maneira significativa a força exercida pelo músculo, diminuindo 0 número de pontes cruzadas ativadas assim como a força desenvolvida por cada uma delas (Edman & Lou, 1990;Lannergren & Westcrblad, 1991). Possilvemenle a alta concentração de FT reduz a liberação de cálcio (C a^) a partir do retículo sarcoplasmático, competindo pelos sítios dc ativação da troponina.…”

“…Por outro lado, o aumento da intensidade do exercício intensifica a via glicolítica, desviando o piruvato, que seria metabolizado em oxaloacetato, para lactato. Este fato também poderia causar fadiga pelo aum ento das concentrações de lactato, e possivelmente íons H* através da inibição da glicólise, via inibição da enzim a fosfofrutoquinase (Gollnick & Hermansen,1973;Karlsson, 1971) e diminuição do número de pontes cruzadas ativadas dentro do músculo, assim como a força desenvolvida por cada uma delas (Edman & Lou, 1990;Lannergren & Wcsterblad, 1991). b) regulação da produção de serotonina.…”