Although the horse is considered an elite athlete with a specific Vove
r dot(O2max) some 2-4 times higher than man, maximal O-2 transport is
compromised both by moderately severe arterial desaturation and by fai
lure to extract all O-2 from blood perfusing exercising muscle. This p
rompted the present study to ascertain whether correction of arterial
desaturation would proportionally augment Vover dot(O2max) and, if so,
would O-2 extraction behave in a manner predicted by diffusional tran
sport limitation. Six two year old thoroughbreds were exercised to Vov
er dot(O2max) on a treadmill each on three separate occasions breathin
g gases of FIO2 = 0.15, 0.21 and 0.35, each used once in balanced orde
r. Vover dot(O2), ventilation, arterial and pulmonary arterial blood g
ases, pressures and lactate levels were measured both submaximally and
maximally at each FIO2 and cardiac output was computed by mass balanc
e for O-2. At FIO2 = 0.21, Vover dot(O2max) 143.9 +/- 4.8 ml kg(-1) mi
n(-1), arterial saturation (Sa(O2)) was 81.6 +/- 3.3% while venous P-O
2 (PVO2) was 15.3 +/- 1.4 Torr. At FIO2 = 0.35, Vover dot(O2max) was 1
72.6 +/- 8.2 ml kg(-1) min(-1), Sa(O2) reached 97.4 +/- 0.4% and PVO2
was 23.4 +/- 0.7 Torr. Vover dot(O2max) at FIO2 = 0.15 was 109.8 +/- 4
.1 ml kg(-1) min(-1), Sa(O2) fell to 68.1 +/- 2.5% and PVO2 was 10.6 /- 1.0 Torr, all changes being significant, p < 0.01. As FIO2 was vari
ed, Vover dot(O2max) changed proportionally to calculated mean capilla
ry P-O2 as well as to total O-2 delivery. These data confirm substanti
al O-2 supply dependence of Vover dot(O2max) in the horse, and in such
a manner as to be consistent with the hypothesis of combined diffusiv
e and convective transport limitation within muscle.