Effects of Anoxia, Acidosis and Temperature on the Contractile Properties of Turtle Cardiac Muscle Strips

The responses to anoxia and acidosis of cardiac ventricular muscle strips from the anoxia-tolerant turtle Chrysemys picta bellii were investigated at 10 °C and 20 °C. Force–velocity curves were determined by quick isotonic releases at 85 % of the time to peak isometric force under control, anoxia, lactate acidosis and anoxic lactate acidosis conditions. The isotonic forces during quick releases spanned 5–95 % of the measured isometric force at each condition. Superfusion solution pH was 7.8 and 7.95 for non-acidosis experiments, and 7.0 and 7.15 for acidosis experiments, at 20 °C and 10 °C, respectively. After normalizing force data to control isometric force, the values of maximum isometric force (P₀), maximum velocity of shortening (V_max) and maximal power output (Power_max) were evaluated by fitting the curves using the hyperbolic Hill equation. The maximum rate of force development (dF/dt_max), time-to-peak force (T_PF) and half-relaxation time (T_1/2) were also determined. At 20 °C, during acidosis, anoxia and anoxic acidosis, P₀ decreased significantly to 81 %, 40 % and 24 % of control values, dF/dt_max decreased significantly to 67 %, 53 % and 23 % of control values, and Power_max decreased significantly to 75 %, 40 % and 14 % of control values, respectively. V_max, however, was not significantly affected by acidosis, anoxia or even anoxic acidosis. T_PF was significantly shortened by anoxia, but prolonged by acidosis. The effects were similar at 10 °C. Temperature did not affect P₀, but V_max decreased by a factor of 1.6–1.8 at all corresponding conditions when temperature was reduced from 20 °C to 10 °C. We conclude that acidosis and anoxia inhibit isometric force production and Power_max of turtle cardiac muscle, but have no effect on V_max, and the insensitivity of V_max indicates that the rate of cross-bridge cycling is not affected by these conditions. Our observations indicate that the reduced power outputs of the hearts of submerged anoxic turtles at low temperature are due in part to inhibition of force production by anoxia and acidosis, and to a reduction of contraction velocity at low temperature.