In three previously reported studies, we had documented that the norma
l exercise hyperventilation in ponies is accentuated by carotid body d
enervation (CBD), not affected by hilar nerve pulmonary vagal denervat
ion (HND), and mildly attenuated by spinal cord ablation of the dorsal
lateral columns at L(2) (SA). In the present study, we hypothesized t
hat if redundancy of control existed in exercising ponies, then multip
le denervations of theoretically important pathways in the same animal
might attenuate the ventilatory response to exercise in a way not pre
dictable by the individual lesion experiments alone. There were three
major findings in the various combinations of CBD, HND, and SA in poni
es during treadmill exercise. First, the combination of CBD with HND o
r SA resulted generally in an accentuation of the hypocapnia during ex
ercise that was predictable on the basis of CBD alone. However, in one
pony that showed a hypercapnic exercise response after SA alone, CBD
subsequently caused a greater exercise hypercapnia. Second, HND in a C
BD or SA pony did not affect the exercise arterial PCO2 response, whic
h is consistent with previous data showing the lack of an HND effect i
n otherwise intact ponies. Third, in ponies with all three denervation
s together, the predominant response was an increase, not a decrease,
in the exercise hyperventilation; this increase was greater than that
predicted from the individual lesions. We conclude that these data do
not provide evidence of redundancy in mechanism for the exercise hyper
pnea other than instances of carotid chemoreceptor error sensing when
hypercapnia occurs during exercise.