Anthony J. Jacques

Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans

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 al. 2000 ). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2 In six healthy human subjects at rest, we measured leg blood flow (Q̇L) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3‐10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (PM) and a prolonged duty cycle (TI/TTOT= 0.7); and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End‐tidal PCO2 was maintained by increasing the inspired CO2 fraction (FI,CO2) as needed. Both trials caused a 25–40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3 Q̇ L and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, Q̇L subsequently decreased (‐30 %) and LVR increased (50‐60 %) relative to control in a time‐dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (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 diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 × eupnoea), Q̇L, MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in nQ̇L. 5 When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and Q̇L increased significantly; 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 fatigue, had no effect on Q̇L and LVR, whereas the two types of diaphragm‐fatiguing trials elicited decreases in Q̇L and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time‐dependent effects on LVR and Q̇L.

Skeletal muscle pump versus respiratory muscle pump: modulation of venous return from the locomotor limb in humans

The vast majority of quantitative data examining the effects of breathing on venous return have been derived from anaesthetized or reduced animal preparations, making an extrapolation to an upright exercising human problematic due to the lack of a hydrostatic column and an absence of muscular contraction. Thus, this study is the first to quantitatively examine the effects of different breathing mechanics on venous return from the locomotor limbs both at rest and during calf contraction exercise in the semirecumbent human. When subjects inspired using predominantly their ribcage/accessory inspiratory muscles at rest (change in gastric pressure (ΔPGA) = <2 cmH2O, change in oesophageal pressure (ΔPES) =∼−6 cmH2O; inspiratory time/total breath time (TI/TTOT) = 0.5), a slight facilitation of femoral venous return was observed during inspiration (65% of all flow occurred during inspiration), with a slight reduction in femoral venous return during the ensuing expiratory phase of the breath. However, when subjects inspired using a predominantly diaphragmatic breath at rest (ΔPGA= > 5 cmH2O, ΔPES=∼−6 cmH2O; TI/TTOT= 0.5), femoral venous return was markedly impeded (net retrograde flow of 11%) and significantly lower than that observed during ribcage breathing conditions (P < 0.01). During the ensuing expiratory phase of a diaphragmatic breath, there was a large resurgence of femoral venous blood flow. The pattern of modulation during ribcage and diaphragmatic breathing persisted during both mild (peak calf force = 7 kg) and moderate (peak calf force = 11 kg) levels of calf contraction. Despite the significant within‐breath modulation of femoral venous return by breathing, net blood flow in the steady state was not altered by the breathing pattern followed by the subjects. Though popliteal blood flow appeared to be modulated by respiration at rest, this pattern was absent during mild calf contraction where popliteal outflow was phasic with the concentric phase of calf contraction. We conclude that respiratory muscle pressure production is the predominant factor modulating venous return from the locomotor limb both at rest and during calf contraction even when the veins of the lower limb are distended due to the presence of a physiologic hydrostatic column.