Abstract
Elevated levels of P(i) are thought to cause a substantial proportion of the loss in muscular force and power output during fatigue from intense contractile activity. However, support for this hypothesis is based, in part, on data from skinned single fibers obtained at low temperatures (< or =15 degrees C). The effect of high (30 mM) P(i) concentration on the contractile function of chemically skinned single fibers was examined at both low (15 degrees C) and high (30 degrees C) temperatures using fibers isolated from rat soleus (type I fibers) and gastrocnemius (type II fibers) muscles. Elevating P(i) from 0 to 30 mM at saturating free Ca(2+) levels depressed maximum isometric force (P(o)) by 54% at 15 degrees C and by 19% at 30 degrees C (P < 0.05; significant interaction) in type I fibers. Similarly, the P(o) of type II fibers was significantly more sensitive to high levels of P(i) at the lower (50% decrease) vs. higher temperature (5% decrease). The maximal shortening velocity of both type I and type II fibers was not significantly affected by elevated P(i) at either temperature. However, peak fiber power was depressed by 49% at 15 degrees C but by only 16% at 30 degrees C in type I fibers. Similarly, in type II fibers, peak power was depressed by 40 and 18% at 15 and 30 degrees C, respectively. These data suggest that near physiological temperatures and at saturating levels of intracellular Ca(2+), elevated levels of P(i) contribute less to fatigue than might be inferred from data obtained at lower temperatures.
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