Spike recordings were obtained with preparations of group III and IV fibers from the nervus peroneus of the rat. During the recordings the muscle was stimulated by chemical substances simulating metabolic effects of static exercise: increase of [K+], enhancement of osmolality and increase of concentrations of lactic acid and inorganic phosphates. Two experimental setups were used: in series I application was performed by a perfusion of the circulatorily isolated hindleg, and in series II a single muscle of the hindleg (musculus extensor digitorum longus) was superfused by control or test solutions. Only those fiber preparations were further investigated which did not respond to pressure, tension or squeezing of the muscle. Only few fibers that were exposed to all of our stimuli responded to none of them; from the rest, about the half were selective or only preferential for one stimulus. The majority of the fibers adapted their response after 8 min while the applications still endured. A comparison of all fibers (in series II) proved that all the four stimuli elicited significant increases of activity. The greatest significant effects were found for lactic acid and potassium (in series I and II). Since the concentrations used in the test applications were characteristic for medium and heavy exercise these results support the hypothesis that metabolic muscle receptors participate in the peripheral control of circulatory and respiratory drives during static exercise.
The hypothesis that metabolic receptors in skeletal muscle influence heart-rate during exercise was tested by means of a perfused preparation of the rat's hind legs. The isolated leg was connected to the body only by nerve and bone and was perfused with tyrode solution. The humoral changes of exercise were simulated by perfusing with modified tyrode solutions in which concentration of K+, osmolality, concentrations of lactic acid, and inorganic phosphate were changed to reflect to those occurring during heavy exercise. Only perfusion with a solution enriched with lactic acid elicited a significant increase in heart-rate. The response disappeared when the nerve supply to the leg was cooled or sectioned. 20-60 s after the start of perfusion with solution of high [lactic acid] heart-rate began to increase reaching a maximum (delta HR +/- SE = 20.2 +/- 8.2, n = 7) after about 2 min. The effect on heart-rate increased when the venous concentration of lactic acid was increased the range from 3 to 10 mmol/l. In further experiments, we tried to separate the effects of pH and lactate. Heart-rate responses were induced only at low pH and at low pH the extent to which heart-rate changed increased with increases in lactate concentration.
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