1. The relationship between force and intracellular [Ca2+] (monitored using the
protein aequorin) has been investigated in papillary muscles isolated from ferret hearts, under control conditions (superfusate pH (pHo) 7.3) and during
acidosis (pHo 6.8). 2. At pHo 7.3, increasing bathing [Ca2+] from 0.5 mmol l-1 to 8 mmol l-1 led to an increase in the size of the intracellular
calcium transient. At the lower [Ca2+] this was accompanied by an increase in developed force; however, at the higher bathing [Ca2+] developed force reached a plateau. 3.
Acidosis (produced by increasing the [CO2] of the gas with which the muscle superfusate was equilibrated) decreased maximum force and shifted the curve relating peak developed force to peak intracellular [Ca2+] to the right. 4. The mechanisms underlying the apparent decrease in the sensitivity of the
contractile proteins to Ca2+ were investigated by applying rapid length changes to papillary muscles at control pHo, during
acidosis, and after bathing [Ca2+] had been increased to match force during
acidosis to that in control. 5.
Acidosis decreased the change in force produced in response to a given length change (i.e. decreased muscle stiffness) but when bathing [Ca2+] was increased during
acidosis, muscle stiffness returned to control. 6.
Acidosis had no effect on muscle stiffness after the induction of rigor in the muscle (produced by metabolic inhibition). 7. It is suggested that in intact cardiac muscle the major effect of a mild
acidosis is to decrease the sensitivity of the
contractile proteins to Ca2+, hence decreasing the number of bound cross-bridges.