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Journal of Experimental Biology, Vol 179, Issue 1 159-180, Copyright © 1993 by Company of Biologists
JOURNAL ARTICLES |
PJ Butler, AJ Woakes, K Smale, CA Roberts, CJ Hillidge, DH Snow and DJ Marlin
School of Biological Sciences, University of Birmingham, Edgbaston, UK.
A new design of flowmeter is described and used in a comprehensive study of the respiratory and cardiovascular adjustments that occur during a standardised exercise test in Thoroughbred horses. The flowmeter system and associated lightweight, fibreglass mask (total mass, 0.7 kg) have a maximum dead space of 500 ml and negligible resistance to airflow. 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 determination of other respiratory variables. At the highest level of exercise (12 ms-1 on a 3 degrees incline), the rate of oxygen uptake (VO2) and carbon dioxide production (VCO2) 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 frequency (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 ventilatory dead space (VD) to VT in resting horses was lower than that previously reported in the literature and this could be the result of the different respiratory recording systems that were used. There was a close relationship between VT and stride length at increasing cantering speeds. Despite the fact that alveolar ventilation (VA) was well matched to VO2, there was a significant reduction in arterial PO2 (PaO2) when the horses cantered at 8 ms-1 and this eventually fell to 34% below the resting value. The present data tend to support the idea that VA/Vb (where Vb is cardiac output) inequalities are important in causing this hypoxaemia. However, the reduction in PaO2 was more than compensated for by an increase in haemoglobin concentration, [Hb], so the concentration of oxygen in the arterial blood (CaO2) was significantly above the resting value at all levels of exercise. Both lactate concentration and PaCO2 increased during exercise, causing substantial 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 effect of the hypoxaemia, as would the almost 4 degrees C rise in blood temperature. The tight respiratory/locomotor linkage might prevent the acidosis and hyperthermia having the stimulatory effects on VE that they have in humans at high work loads.(ABSTRACT TRUNCATED AT 400 WORDS)
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