The influence of temperature on neuromuscular performance.

The influence of lowering the temperature, by 10 degrees C increments, from 37 decrees C to 17 degrees C on the twitch )Pt) and tetanic (Po) tension during direct and indirect stimulation, on presynaptic acetylcholine (ACh) release and on muscle acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activity were investigated in vitro on the rat's phrenic-nerve-hemidiaphragm preparation. Decreasing the temperature from 37 degrees C to 17 decrees C caused a progressive increase of the isometric Pt to 195.8 +/- 9.6 (S.E. of mean) and 169.6 +/- 2.9% of control with direct and indirect stimulation respectively. This change in temperature also increased twitch duration and time to peak Pt by factors of about 4 and 6 respectively with both direct and indirect stimulation. The Po/Pt ratio did not change significantly between 37 degrees C and 27 degrees C, but dropped sharply between 27 degrees C and 17 degrees C. With direct stimulation tetanus was only maintained in 50% of the experiments at 37 degrees C and in none at 27 degrees C or 17 degrees C. With indirect stimulation tetanus was maintained in all experiments at 37 degrees C and 27 degress C and in none at 17 degrees C. Post-tetanic facilitation was greater with indirect than direct stimulation and at higher than at lower temperatures. Post-tetanic exhaustion, with both direct and indirect stimulation, was only observed at 37 degrees C. Presynaptic ACh release (pmol . g-1 . min-1) at rest and with stimulation rates of 0.1 to 50 Hz decreased by more than 60% as temperature was lowered from 37 degrees C to 17 degrees C. Cooling from 37 degrees C to 17 degrees C caused a similar decrease in the volley output (pmol . g-1 . volley-1) of ACh. Muscle-AChE and BuChE activities decreased by 34 and 52% respectively when the temperature was lowered from 37 degrees C to 17 degrees C. The findings presented indicate that the site of the facilitating effect of cooling on Pt is the muscle fiber. The facilitation is caused by the delay of the relaxation of the contracted muscle, causing prolongation of the active state and increased tension development. The decreased speed of nerve conduction and ACh release caused by cooling adversely affects neuromuscular transmission. This, however, is partially counteracted by decreased muscle-ChE activity and increased sensitivity of the postjunctional membrane to ACh caused by cooling.