RESPIRATORY AND CARDIOVASCULAR ADJUSTMENTS DURING EXERCISE OF INCREASING INTENSITY AND DURING RECOVERY IN THOROUGHBRED RACEHORSES

A new design of flowmeter is described and used in a comprehensive stu dy of the respiratory and cardiovascular adjustments that occur during a standardised exercise test in Thoroughbred horses. The flowmeter sy stem and associated lightweight, fibreglass mask (total mass, 0.7 kg) have a maximum dead space of 500 ml and negligible resistance to airfl ow. They have no systematic effect on blood gases and, together with a rapidly responding mass spectrometer, enable an accurate computation of gas exchange to be performed together with breath-by-breath determi nation of other respiratory variables. At the highest level of exercis e (12 m s-1 on a 3-degrees incline), the rate of oxygen uptake (V(02)) and carbon dioxide production (V(CO2)) increased to 29.4 times and 36 .8 times their resting values, respectively. Respiratory minute volume (VE) increased to 27.0 times its resting value, with respiratory freq uency (fR) making the major contribution at the walk and trot. However , with increasing cantering speeds, fR changed little as it was locked in a 1:1 fashion to stride frequency, and tidal volume (VT) then made the major contribution to the increase in VE. The ratio of ventilator y dead space (VD) to VT in resting horses was lower than that previous ly reported in the literature and this could be the result of the diff erent respiratory recording systems that were used. There was a close relationship between VT and stride length at increasing cantering spee ds. Despite the fact that alveolar ventilation (VA) was well matched t o V(O2), there was a significant reduction in arterial P(O2) (Pa(O2)) when the horses cantered at 8 m s-1 and this eventually fell to 34 % b elow the resting value. The present data tend to support the idea that VA/Vb (where Vb is cardiac output) inequalities are important in caus ing this hypoxaemia. However, the reduction in Pa(O2) was more than co mpensated for by an increase in haemoglobin concentration, [Hb], so th e concentration of oxygen in the arterial blood (Ca(O2)) was significa ntly above the resting value at all levels of exercise. Both lactate c oncentration and Pa(CO2) increased during exercise, causing substantia l reductions in pH of both arterial and mixed venous blood. This would have inevitably shifted the oxygen equilibrium curve of the Hb to the right, desaturating the arterial blood and thus exacerbating the effe ct of the hypoxaemia, as would the almost 4-degrees-C rise in blood te mperature. The tight respiratory/locomotor linkage might prevent the a cidosis and hyperthermia having the stimulatory effects on VE that the y have in humans at high work loads. Cardiac output and heart rate (Vb ) were 5 and 6 times their-resting values, respectively, at the highes t level of exercise, while cardiac stroke volume did not change signif icantly. There was both systemic and pulmonary hypertension. with mean pulmonary blood pressure reaching 2.6 times its resting value at the highest level of exercise. It is concluded that the pulmonary hyperten sion does not result from the hypoxaemia and that it could cause pulmo nary oedema, which could contribute to the postulated diffusion limita tion of the lungs during exercise. Although this report confirms some results obtained by other workers, some discrepancies have been found. It is probable that the flowmeter and mask used here have a significa ntly reduced effect on the measured variables compared with methods us ed in many of the previous studies.