At a given steady O2 consumption (VO2) in normoxia, cardiac output (Q) is inversely proportional to arterial O2 concentration (CaO2), so that O2 delivery (QaO2=QCaO2) is kept constant and adapted to VO2. The matching between QaO2 and VO2 keeps O2 return (QvO2=QaO2-VO2) constant and independent of VO2 and haemoglobin concentration ([Hb]). This may not be so in hypoxia: in order for QvO2 to be independent of the inspired O2 fractions (FIO2), the slopes of the Q versus VO2 lines should be greater the lower the CaO2, which may not be the case. Thus, we tested the hypothesis of constant QvO2 by determining QaO2 and QvO2 in acute hypoxia. Thirteen subjects performed steady-state submaximal exercise on the cycle ergometer at 30, 60, 90 and 120 W breathing FIO2 of 0.21, 0.16, 0.13, 0.11 and 0.09. VO2 was measured by a metabolic cart, Q by CO2 rebreathing, [Hb] by a photometric technique and arterial O2, saturation (SaO2) by infrared oximetry. CaO2 was calculated from [Hb], SaO2 and the O2 binding coefficient of haemoglobin. The VO2 versus power relation was independent of FIO2. The relations between Q and VO2 were displaced upward and had higher slopes in hypoxia than in normoxia. However, the Q changes did not compensate for those in CaO2. The slopes of the QaO2 versus VO2, lines tended to decrease in hypoxia. QVO2 was lower the lower the FIO2. A significant relationship was found between QvO2 and SaO2 (QvO2= 1.442 SaO2+0.107, r=0.871, n=24, P<10(-7)), which confutes the hypothesis of constant QvO2 in hypoxia.

At exercise steady state, the lower the arterial oxygen saturation (SaO(2)), the lower the O(2) return (QvO(2)). A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective beta1-adrenergic blockade (BB) would reduce O(2) delivery (QaO(2)) and QvO(2). To test this hypothesis, we studied the effects of BB on QaO(2) and QvO(2) in exercising humans in normoxia and hypoxia. O(2) consumption VO(2), cardiac output Q, CO(2) rebreathing), heart rate, SaO(2) and haemoglobin concentration were measured on six subjects (age 25.5 +/- 2.4 years, mass 78.1 +/- 9.0 kg) in normoxia and hypoxia (inspired O(2) fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150 W without (C) and with BB with metoprolol. Arterial O(2) concentration (CaO(2)), QaO(2) and QvO(2) were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each VO(2), Q was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO(2) and CaO(2) were unaffected by BB. The QaO(2) changes under BB were parallel to those in Q.QvO(2) was unaffected by exercise in normoxia. In hypoxia the slope of the relationship between QaO(2) and VO(2) was lower than 1, indicating a reduction of QvO(2) with increasing workload. QvO(2) was a linear function of SaO(2) both in C and in BB. The line for BB was flatter than and below that for C. The resting QvO(2) in normoxia, lower than the corresponding exercise values, lied on the BB line. These results agree with the tested hypothesis. The two observed relationships between QvO(2) and SaO(2) apply to conditions of predominant sympathetic or vagal activation, respectively. Moving from one line to the other implies resetting of the cardiovascular regulation.

The energy cost of walking (at 3.2 km x h(-1)) per unit distance (J x kg(-1) x m(-1)) at gradients of 0%, +7%, and +12% and during a progressive test (2% increase in gradient every 2 min), as well as the overall (aerobic plus anaerobic) net cumulative energy consumption and the corresponding maximal exercise duration were assessed in 19 patients with peripheral arterial disease (PAD) and in 13 moderately active control subjects. With a 0% gradient, the energy cost of walking was approximately 40% greater in patients with PAD than in controls (2.93+/-0.52 and 2.13+/-0.33 J x kg(-1) x m(-1) respectively; P <0.01). In contrast, at gradients of +7% and +12%, the energy cost of walking was similar in the two groups (+7%: PAD, 4.15+/-0.74 J x kg(-1) x m(-1); controls, 4.18+/-0.54 J x kg(-1) x m(-1); +12%: PAD, 5.59+/-1.03 J x kg(-1) x m(-1); controls, 5.64+/-0.75 J x kg(-1) x m(-1)). In patients with PAD, maximal exercise duration with gradients of 0%, +7% and +12% was 449+/-254, 322+/-200 and 229+/-150 s respectively, whereas the net cumulative energy consumption at fatigue was almost constant at approximately 1100 J x kg(-1) for all gradients. The greater energy cost of walking in PAD patients compared with controls in level, but not uphill, walking is interpreted as being mainly the consequence of an altered mechanical locomotory pattern, and not of lower metabolic efficiency. For a wide range of loads, net cumulative energy consumption appears to be independent of maximal exercise duration, a finding that provides a practical criterion for assessing the degree of functional impairment of patients with PAD on metabolic grounds.

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