Summary. The regulation of the respiration has been studied in different kinds of muscular exercise, in which the muscles are working under partly anaerobic conditions, viz.: heavy work with the legs, work with the arms and work in light CO‐poisoning. It is shown that a close relationship between the degree of anaerobiosis – as indicated by the concentration of the blood lactates – and a relatively high lung ventilation exists. It is further shown that when the muscles are working under partly anaerobic conditions (increased blood lactate concentration) oxygen breathing lowers the concentration of the blood lactates, and the ventilation, and that the lowering is proportional to the percentage of the oxygen in the inspired air. In rest and during light work (no increased blood lactate concentration) the breathing of oxygen on the other hand tends to produce a slight increase in ventilation and a decrease in alveolar pCO2. The effect of oxygen breathing on the ventilation during partly anaerobic work is not due to a decrease in acidity (see page 180) of the arterial blood or to the elimination of a previously existing arterial unsaturation. It is made probable, that the different effect of oxygen breathing in light and heavy work is due to the circumstance that oxygen breathing acts on the respiration in two different ways, viz. activating on the respiratory centre itself, and depressing on the activity of the chemoreceptors. It is assumed that in rest and during light work in which the activity of the chemoreceptors is only slight the activating effect on the respiratory centre over balances the depressing effect on the chemoreceptors, whereas in heavy work because of an increased chemoreceptor activity the depressing effect of high oxygen tension is able to overbalance considerably the effect on the respiratory centre. The results from the present experiments are best explained by the assumption that in heavy work or other kinds of work in which the muscles are working under partly anaerobic conditions a substance is produced which increases the ventilation reflexly through the chemoreceptors. The effect of oxygen breathing in heavy work then is 1. to decrease the production of this substance and 2. to depress the effect of this substance on the chemoreceptors. An identification of the active substance has not been attempted in this paper, but it is shown that it is not the lactic acid and that it has properties allowing it to appear in and disappear from the blood stream much more rapidly than does lactic acid. On the basis of these and earlier investigations the control of respiration during muscular work can be explained in the following way (see page 185–186): In light work the increase in ventilation is brought about mainly by reflexes from the working limbs. In heavy work (here defined as work in which the blood lactate concentration is increased – in this subject corresponding to oxygen uptakes above 1–1.5 1/min.) the further increase in ventilation is due mainly to an increasing production of the above me...
In the steady state of work on a bicycle ergometer repeated i.v. injections of (+) tubocurarine produced a decrease in handgrip strength. In spite of this the intensity of work was maintained constant for 20 to 30 min. During this time pulse rate and blood pressure increased slightly and irregularity but the ventilation increased, both absolutely and in relation to the oxygen uptake, by up to about 50 %. The cardiac output was uninfluenced by the curarization. By adding CO2 to the inspired air the alveolar PCO2 was maintained at the normal exercise level. It is therefore assumed that all the known humoral factors controlling respiration in exercise must have been normal. The greatly increased ventilation must consequently have been caused by some nervous factors. The origin of these factors, whether central or peripheral, is discussed on the background of earlier experimental findings. A tentative explanation, based on the assumption that bicycle‐work is performed by the mediation of the gamma‐loop, is suggested. According to this the“nervous factor” of respiratory regulation in exercise may be the feed‐back to the reticular formation of afferent impulses from the muscle spindles.
NIELSEN, B. and M. NIELSEN. Body temperature during work at dtyferent environmental temperatures. Acta physiol. scand. 1962. 56. 120-129. -In human subjects it was found that during muscular work only small and unsystematic differences existed between temperatures measured at different depths in the rectum, whereas a steep temperature gradient was found along the upper oesophagus. -The oesophageal temperature measured just above the diaphragm (i. e. close to aorta and left heart) reached during exercise the work level much faster, and, also in the recovery period returned to the resting level much more rapidly than did the rectal temperature. During leg-work the level reached by the oesophageal temperature was considerably lower than that reached by the rectal temperature while during arm-work they were of about the same height. Breathing of air saturated with water vapor at body temperature did not influence the temperature in the lower oesophagus but eliminated the steep temperature gradient in upper oesophagus. Under these conditions the sublingual temperature was equal to the temperature in lower oesophagus. The experiments suggest that the oesophageal temperature measured just above the diaphragm is a good index of the temperature of a large part of the core of the body. -During work both rectal and oesophageal temperatures were practically independent of environmental temperatures between 5 and 30°C.I n earlier studies from this laboratory (NIELSEN 1938) it was shown that rectal temperature during muscular exercise increases to a level higher than that existing during rest. This higher temperature level was dependent o n the intensity of work but over a wide range independent of the environmental temperature. It was, therefore, concluded that the increase in temperature during exercise was not d u e to an insufficiency of heat regulation b u t was d u e to 2 . ''resetting'' of the thermoregulatory centre. 120
Summary. The sensitivity of the respiratory center to CO2 during muscular work at normal and at low oxygen tensions has been studied in three human subjects. It was found that the rectilinear part of the stimulus‐response curves in normal air was displaced to the left of the resting curve and the more so the higher the work intensity. The steepness of the curves was in the majority of cases about the same. In low oxygen the stimulus‐response curves were displaced more to the left and were much steeper than for the same work intensity in normal air. The flattening of the stimulus‐response curves found at higher CO2 concentrations is assumed to be due mainly to a special depressant effect of high CO2 tensions on the respiratory center.
During uninterrupted work on the bicycle ergometer the blood flow to the legs was suddenly interrupted by means of blood pressure cuffs. In the period with blocked circulation CO2 was added to the inspired air in such amounts that the alveolar PCO2 was maintained constant. The excess work O2‐uptake decreased up to 50%. The pulmonary ventilation, the pulse rate and the systolic blood pressure showed a steady and considerable increase. The cardiac output remained nearly constant with a tendency to decrease during the blocking period. The (a—v̄)O2‐difference and the mixed venous PCO2 consequently decreased considerably. These changes in respiratory and circulatory functions were well reproducible and the scattering of the values only small. It was concluded that the observed changes are neurogenic and caused by the increasing anaerobiosis in the blocked muscles. The nervous impulses involved may be elicited from muscle chemoreceptors, or they may stem from mechanoreceptors being activated through an observed recruitment of new motor units necessitated by the anaerobiosis.
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