Hypercapnia, serum inorganic phosphorus, and muscle contractility

A marked increase in serum inorganic phosphorus during hypercapnia (+19.4%/10 mm Hg) and the opposite during hypocapnia (-14.3%/10 mm Hg) was observed. Liver and muscle seemed to be the most likely source or sink for the P(i). Continued loss of P(i) from the muscle might reasonably be expected to decrease the force of contraction (P). This was tested on a rat diaphragm phrenic nerve preparation placed in a Krebs Ringer solution at 29°C. The muscle was stimulated either directly or by the phrenic nerve. The bathing medium was equilibrated for 0.5 hr with 95% O₂, 5% CO₂ (control), 90% O₂ + 10% CO₂, or 85% O₂ + 15% CO₂. In 6 experiments the bathing medium was left unbuffered and in 4 experiments it was buffered to prevent the drop in pH. When the muscle was stimulated directly during unbuffered hypercapnia (10%, 15% CO₂) P decreased by 36%, 51% respectively; while during buffered hypercapnia P decreased by 18%, 20% respectively. When the muscle was stimulated by the phrenic nerve during unbuffered hypercapnia (10%, 15% CO₂) P decreased by 40%, 41% respectively; while during buffered hypercapnia P decreased by 9%, 27% respectively. These results are consistent with the hypothesis that P is decreased during hypercapnia by the loss of inorganic phosphorus. They suggest that in the control of respiration one element of the controller (respiratory muscle) can be acted upon directly by the controlled (CO₂) and that the influence of the myoneural junction on P does not seem to be affected in any additional way.