Because the oxygen tension (and not oxygen saturation) is
the chemoreflex input signal, this explains why in a previous
study the administration of oxygen in normoxia induced
a significant increase in BRS and parasympathetic activity
despite a small increase in oxygen saturation [25]. Thus, the
increased oxygen absorption may inhibit the chemoreflex
and, by this reciprocal relationship [9, 10], increase BRS.
Bernardi et al. (2001) demonstrated that slow breathing
reduced chemoreflex sensitivity to both hypoxia and hypercapnia,
in part attributing this to an inverse relationship with
BRS [11]. It is well understood that the chemoreflex is amechanism
to stabilize blood pH by increasing ventilation. Possibly,
the increase in oxygen in ujjayi and slow breathing may
inhibit the chemoreflex necessarily stimulating greater BRS.
Our findings of the reciprocal BRS and chemoreflex changes
are in full support of this concept, within the limitations of