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 str ips from the anoxia-tolerant turtle Chrysemys picta bellii were invest igated at 10 degrees C and 20 degrees C, Force-velocity curves were de termined by quick isotonic releases at 85% of the time to peak isometr ic force under control, anoxia, lactate acidosis and anoxic lactate ac idosis conditions, The isotonic forces during quick releases spanned 5 -95 % of the measured isometric force at each condition, Superfusion s olution pH was 7.8 and 7.95 for non-acidosis experiments, and 7.0 and 7.15 for acidosis experiments, at 20 degrees C and 10 degrees C, respe ctively, After normalizing force data to control isometric force, the values of maximum isometric force (P-0), maximum velocity of shortenin g (V-max) and maximal power output (Power(max)) were evaluated by fitt ing the curves using the hyperbolic Hill equation, The maximum rate of force development (dF/dt(max)), time-to-peak force (T-PF) and half-re laxation time (T-1/2) were also determined, At 20 degrees C, during ac idosis, anoxia and anoxic acidosis, P-0 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 signific antly to 75%, 40% and 14% of control values, respectively, V-max, howe ver, was not significantly affected by acidosis, anoxia or even anoxic acidosis, T-PF was significantly shortened by anoxia, but prolonged b y acidosis, The effects were similar at 10 degrees C, Temperature did not affect P-0, but Vmax decreased by a factor of 1.6-1.8 at all corre sponding conditions when temperature was reduced from 20 degrees C to 10 degrees C, We conclude that acidosis and anoxia inhibit isometric f orce production and Power(max) of turtle cardiac muscle, but have no e ffect on Vmax, and the insensitivity of V-max indicates that the rate of cross-bridge cycling is not affected by these conditions, Our obser vations indicate that the reduced power outputs of the hearts of subme rged anoxic turtles at low temperature are due in part to inhibition o f force production by anoxia and acidosis, and to a reduction of contr action velocity at low temperature.