Aw. Sheel et al., Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans, J PHYSL LON, 537(1), 2001, pp. 277-289
1. We recently showed that fatigue of the inspiratory muscles via voluntary
efforts caused a time-dependent increase in limb muscle sympathetic nerve
activity (MSNA) (St Croix et at. 2000). We now asked whether limb muscle va
soconstriction and reduction in limb blood flow also accompany inspiratory
muscle fatigue.
2. In six healthy human subjects at rest, we measured leg blood flow ((Q) o
ver dot (L)) in the femoral artery with Doppler ultrasound techniques and c
alculated limb vascular resistance (LVR) while subjects performed two types
of fatiguing inspiratory work to the point of task failure (3-10 min). Sub
jects inspired primarily with their diaphragm through a resistor, generatin
g (i) 60% maximal inspiratory mouth pressure (P-M) and a prolonged duty cyc
le (T-I/T-TOT = 0.7); and (ii) 60% maximal P-M and a T-I/T-TOT of 0.4. The
first type of exercise caused prolonged ischaemia of the diaphragm during e
ach inspiration. The second type fatigued the diaphragm with briefer period
s of ischaemia using a shorter duty cycle and a higher frequency of contrac
tion. End-tidal P-CO2 was maintained by increasing the inspired CO2 fractio
n (F-I,F-CO2) as needed. Both trials caused a 25-40% reduction in diaphragm
force production in response to bilateral phrenic nerve stimulation.
3. (Q) over dot (L) and LVR were unchanged during the first minute of the f
atigue trials in most subjects: however, (Q) over dot (L) subsequently decr
eased (-30%) and LVR increased (50-60%) relative to control in a time-depen
dent manner. This effect was present by 2 min in all subjects. During recov
ery the observed chan es dissipated quickly (< 30 s). Mean arterial pressur
e (MAP; +4-13 mmHg) and heart rate (+16-20 beats min(-1)) increased during
fatiguing diaphragm contractions.
4. When central inspiratory motor output was increased for 2 min without di
aphragm fatigue by increasing either inspiratory force output (95% of maxim
al inspiratory pressure (MIP)) or inspiratory flow rate (5 x eupnoea), (Q)
over dot (L), MAP and LVR were unchanged; although continuing the high forc
e output trials for 3 min did cause a relatively small but significant incr
ease in LVR and a reduction in (Q) over dot (L).
5. When the breathing pattern of the fatiguing trials was mimicked with no
added resistance, LVR was reduced and (Q) over dot (L) increased significan
tly; these changes were attributed to the negative feedback effects on MSNA
from augmented tidal volume.
6. Voluntary increases in inspiratory effort, in the absence of diaphragm f
atigue, had no effecton (Q) over dot (L) and LVR, whereas the two types of
diaphragm-fatiguing trials elicited decreases in (Q) over dot (L) and incre
ases in LVR. We attribute these changes to a metaboreflex originating in th
e diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-
dependent effects on LVR and (Q) over dot (L).