Oxygen consumption and force development in turtle and trout cardiac muscle during acidosis and high extracellular potassium

Abstract.

Relative to species such as rainbow trout, freshwater turtle shows a high tolerance to challenges involving acidosis and increases in extracellular K⁺. Therefore, the effects of acidosis or high K⁺ on twitch force and oxygen consumption were examined in ventricular ring preparations from these two species. The oxygen consumption associated with force development was estimated by net oxygen consumption (oxygen consumption during twitch force development minus that during rest). For turtle, elevation of CO₂ from 2% (pH 7.7) to 12% (pH 6.9) in the gas equilibrating the muscle bath decreased twitch force by 20% without any effects on oxygen consumption. Decreasing pH from 7.7 to 6.9 with 22 mM lactic acid had similar effects. For trout, CO₂-induced acidosis decreased twitch force by approximately 60%. Furthermore, force development became energetically less efficient as it fell disproportionately more than net oxygen consumption. This was not observed for lactic acidosis. For trout but not for turtle, acidosis resulted in an increase in oxygen consumption during rest. An increase in extracellular K⁺ from 2.5 mM to 10 mM depressed force and oxygen consumption proportionately for both species. Adrenaline (10 µM) increased twitch force for both species and oxygen consumption for trout; it attenuated the effects of high extracellular K⁺. Neither adrenaline nor high K⁺ influenced the ratio of force to net oxygen consumption. As opposed to high extracellular K⁺, acidosis appears to increase the energetic cost of contractility, particularly for the trout heart.