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 (.Q(L)) 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 (P(M)) and a prolonged duty cycle (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 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 P(CO2) was maintained by increasing the inspired CO(2) fraction (F(I,CO2)) as needed. Both trials caused a 25-40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. .Q(L) and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, .Q(L) 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 x eupnoea), .Q(L), 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 .Q(L). 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and .Q(L) 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 .Q(L) and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in .Q(L) 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 .Q(L).

Expiratory flow limitation confounds ventilatory response during exercise in athletes.

INTRODUCTION: A significant number of highly trained endurance runners have been observed to display an inadequate hyperventilatory response to intense exercise. Two potential mechanisms include low ventilatory responsiveness to hypoxia and ventilatory limitation as a result of maximum expiratory flow rates being achieved. PURPOSE: To test the hypothesis that expiratory flow limitation can complicate determination of ventilatory responsiveness during exercise the following study was performed. METHODS/MATERIALS: Sixteen elite male runners were categorized based on expiratory flow limitation observed in flow volume loops collected during the final minute of progressive exercise to exhaustion. Eight flow limited (FL) (VO2max, 75.9+/-2.4 mL x kg(-1) x min(-1); expiratory flow limitation, 47.3+/-20.4%) and eight non-flow limited subjects (NFL) (VO2max, 75.6+/-4.8 mL x kg(-1) x min(-1); expiratory flow limitation, 0.3+/-0.8%) were tested for hypoxic ventilatory responsiveness (HVR). RESULTS: Independent groups ANOVA revealed no significant differences between FL and NFL for VO2max, VE max (136.2+/-16.0 vs 137.5+/-21.6 L x min(-1)), VE/VO2, (28.4+/-3.2 vs 27.6+/-2.9 L x lO2(-1)), VE/VCO2 (24.8+/-3.1 vs 24.4+/-2.0 L x lCO2(-1)), HVR (0.2+/-0.2 vs 0.3+/-0.1 L x %SaO2(-1)), or SaO2 at max (89.1+/-2.4 vs 86.6+/-4.1%). A significant relationship was observed between HVR and SaO2 (r = 0.92, P < or = 0.001) in NFL that was not present in FL. Conversely, a significant relationship between VE/VO2 and SaO2 (r = 0.79, P < or = 0.019) was observed in FL but not NFL. Regression analysis indicated that the HVR-SaO2 and SaO2-VE/VO2 relationships differed between groups. DISCUSSION: When flow limitation is controlled for, HVR plays a more significant role in determining SaO2 in highly trained athletes than has been previously suggested.

Ventilation's role in the decline in VO2max and SaO2 in acute hypoxic exercise.

The role of ventilation in the response in aerobic capacity and arterial oxygen saturation (SaO2) to acute hypoxic exercise was studied in 13 healthy active men divided into two groups based on their normoxic maximal exercise VE/VO2 (LOW < or =27.7; HIGH > or = 30.2) and PAO2 estimates (LOW < or = 107 mm Hg; HIGH > or = 110 mm Hg). Groups performed two incremental progressive maximal cycle exercise (VO2max) tests: normoxia (FIO2 = 20.9%) and acute hypoxia (FIO2 = 13.3%). To evaluate the influence of hypoxic ventilatory drive on ventilation, resting hypoxic ventilatory response (rHVR) was measured. LOW demonstrated lower ventilatory responses (VE, VE/VO2, and VE/VCO2) during both normoxic and hypoxic exercise (P < or = 0.05). During maximal hypoxic exercise, LOW had a greater decline in both VO2max (21.6 mL x kg(-1) x min(-1) vs 16.6 mL x kg(-1) x min[-1]) and SaO2 (31.9% vs 22.1%). Modest but significant correlations were identified between normoxic VE/VO2 and the decline in both VO2max (r = -0.62) and SaO2 (r = -0.60). No correlations were identified between rHVR and any ventilatory response or SaO2. In summary, the results from this study suggest that a low exercise-induced hyperventilatory response is a significant mechanism in the arterial desaturation observed during hypoxic exercise and the decline in aerobic capacity associated with this desaturation. However, the ventilatory response to hypoxic exercise is not dependent upon hypoxic ventilatory drive.