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The response of the O2 transport system to acute changes in alveolar ventilation (VA) was analysed. The fractional limitations to maximal O2 consumption (VO2max) imposed by the lungs (ventilation, FV, and lung-blood transfer, FL), the cardiovascular system (FQ), and peripheral O2 diffusion (Fp) were calculated according to a multifactorial model. A reference set of data, describing the status of O2 transport at maximal exercise in normoxia was used. The effects of VA on VO2max were assessed on the assumption of a constant reference O2 flow in mixed venous blood (QVO2). The changes in reference data after given independent changes in VA were calculated by an iterative procedure, until the VO2max value compatible with the constant reference QVO2 was found, at PIO2 values of 150 (normoxia), 130, 110 and 90 Torr. The VO2max changes in normoxia were less than expected assuming a linear O2 transport system, because of the flatness of the O2 dissociation curve around normoxic PO2. This affected the cardiovascular resistance to O2 flow, and its changes counterbalanced the effects on VO2max of induced changes in VA. This phenomenon was reversed in hypoxia, as the steep part of the O2 dissociation curve was approached. The fractional limitations to VO2max in normoxia resulted as follows: FV and FL provided between 5 and 12%, FQ between 59 and 78%, and Fp between 13 and 19% of the overall VO2max limitation. In hypoxia, FV and FL increased and FQ decreased. At PIO2 = 90 Torr, when VA was halved, FV, FL, FQ and Fp amounted to 0.35, 0.31, 0.20 and 0.14, respectively.

This study, aimed at investigating some aspects of breathing control at work, was conducted on 8 heart and lung transplant recipients (HLTR) (age 33 +/- 13 years, mean +/- SD; 10 +/- 6 months post-transplantation) and on two control groups, i.e. 11 heart transplant recipients (HTR) and 11 healthy untrained subjects (C). The patients performed a series of 2 to 6 1-min exercise bouts (at 25 or 50 W, corresponding to about 50% of their VO2max) on a bicycle ergometer, followed by a 5 min 25 or 50 W constant load. C exercised both at 50 W (C1) and at 50% of their VO2max (C2). Inspiratory (VI) and expiratory (VE) ventilation, tidal volume (VT), respiratory frequency (fR), end-tidal O2 and CO2 partial pressures (PETO2 and PETCO2 and gas exchange (VO2 and VCO) were measured breath-by-breath. "Phase I" ventilatory response (ph I) was determined as the mean changes of VI, VE, VT, fR, PETO2 and PETCO2, compared to rest, during the first two respiratory cycles following exercise onset. In HLTR ph I did not significantly differ from that of C1 and C2, whereas the response was lower in HTR. VE, VO2 and VCO2 responses during "phase II" (t 1/2 on-) and "phase III" (steady state exercise) were similar in HLTR and in HTR. t 1/2 on- were longer in HLTR and in HTR compared to C1. In 3 HLTR the ventilatory pattern during the 5 min constant loads was similar to that of HTR and C, whereas 4 HLTR presented higher VT and lower fR values. It is concluded that: 1) The ventilatory response to exercise, in all its phases, is substantially preserved despite lung denervation. When slight alterations are found (i.e. the slower phase II), they are presumably of peripheral origin. 2) The normal ph I in HLTR indicates that cardiac and/or pulmonary inputs to the respiratory centers are not involved in its regulation, or that their role can be subserved by other ventilatory control mechanisms.

The net rate of phosphocreatine hydrolysis [PCr] [symbol; see text], and tissue pH were determined in anaerobic resting frog (Rana Ridibunda Ridibunda) gastrocnemii by 31-P-NMR in the temperature (T) range from 5 to 30 degrees C. Absolute [PCr] [symbol; see text] values from 0.36 to 10.07 mM/h were estimated assuming a resting [PCr] of 26 mM at 20 degrees C. The corresponding Q10 values ranged from 2.1 (30 degrees C) to 17.5 (5 degrees C). Muscle pH was found to be T-dependent with a 10 degrees C drop in T resulting in an increase of 0.1 pH units. At any given T, pH was found to be constant over a period of at least one hour (30 degrees C) from the onset of anaerobiosis. Based on simultaneous [PCr] [symbol; see text] and pH estimates, the contribution of anaerobic glycolysis ([ATPLA]) to the overall rate of ATP resynthesis ([ATPTot]) was estimated assuming a approximately P/La ratio of 1.2. [ATPTot] was then calculated for each investigated T value as the sum of [PCr] and [ATPLa]. [ATPTot] was found to vary between 5 and 30 degrees C from 0.79 mM/h to 22.15 mM/h. The present study, besides proposing a methodology for the assessment of high energy phosphates hydrolysis by 31P-NMR spectroscopy at changing T, provides a comprehensive analysis of the T-dependence of anaerobic metabolism of the resting anaerobic frog gastrocnemius which may be extrapolated to other tissues.

The aim of this study was to test at maximal exercise the hypothesis of the temperature-dependence of the kinetics of O2 consumption (VO2), which predicts a greater O2 deficit as muscle temperature is decreased. Six male subjects underwent 3 min exercise bouts at the minimum power eliciting maximum O2 consumption (VO2max), at normal temperature (A) and after cooling the thigh muscles by water immersion (C). Breath-by-breath VO2 was measured together with muscle blood flow (Qm), blood lactate accumulation ("early lactate", eLa), heart rate and muscle temperature (Tm). The O2 deficit was calculated by standard procedure. Net VO2max was 2.92 +/- 0.85 (SD) and 3.19 +/- 0.71 l center dot min-1 in C and A respectively (P < 0.05). Correspondingly, maximum power was 20 W lower in C than in A. At exercise start, Tm was 35.0 +/- 1.2 and 27.5 +/- 1.8 degrees C in A and C respectively. O2 deficit was 2.25 +/- 0.53 and 3.05 +/- 1.12 l in A and C respectively. The corresponding eLa was 7.7 +/- 2.5 and 13.8 +/- 2.5 mM, (P < 0.05) while Qm was 376 +/- 92 and 290 +/- 50 ml center dot kg-1 center dot min-1 (P < 0.05) in A and C, respectively. The eLa increase in C is associated with an impaired muscle blood flow and decreased muscle O2 unloading, and does not completely explain the greater O2 deficit in C. The unexplained fraction of the latter is perhaps accounted for by a greater net alactic O2 deficit, in agreement with a temperature-dependent decrease of the velocity constants of oxidative reactions, as suggested by the tested hypothesis.

Seven young, healthy male subjects performed maximal exercise on a cycloergometer with central venous and arterial catheters, before and after autologous retransfusion of red blood cells. Maximal oxygen consumption (VO2max), blood gas composition and haemodynamic variables were measured, in order to test the hypothesis of monofactorial vs. polyfactorial VO2max limitation. Autologous blood retransfusion led to significant increases in haemoglobin concentration and consequently arterial oxygen concentration during maximal exercise, while maximal cardiac output, heart rate and stroke volume were not significantly changed. The relationship between maximal oxygen delivery (cardiac output.arterial oxygen concentration; (Q.CaO2)max and maximal oxygen consumption in this study was VO2max (L.min-1) = 0.02 + 0.64.(Q.CaO2)max (L.min-1), the slope being significantly less than unity. These results suggest that (Q.CaO2)max plays but a fractional role in limiting VO2max, in agreement with recent models concerning the resistance to oxygen flow in the respiratory system (di Prampero and Ferretti, Respir. Physiol. 80: 113-128, 1990). The relative increase in VO2max after blood retransfusion matched the relative increase in 'aerobic performance', measured as the maximal power output that could be maintained aerobically for 30 min. Furthermore, the increase in maximal power output (15 +/- 3 watts) could account for almost all of the extra oxygen consumption. This match suggests that there is an inability to fully utilize muscle oxidative capacity in the normocythaemic state.

The kinetics (i.e. the rate of readjustment) of O2 uptake (VO2) at the mouth of muscle blood flow in the vastus lateralis muscle (Qm), and the net accumulation of lactate in the rest-to-exercise transient (early lactate) were assessed in 6 untrained men (age 31 +/- 8 (SD) yrs) during constant-load 5-min duration exercises on the cyclo ergometer of 75 and 125 W, performed at muscle temperatures (Tm) of 35.5 +/- 0.9 degrees C (N) and of 28.0 +/- 1.65 degrees C (C). VO2 was measured breath-by-breath; Qm was assessed from 133Xe clearance; early lactate was calculated as the difference between the venous lactate concentrations observed after and before exercise. At both work loads, steady-state VO2 was slightly higher in N than in C (P less than 0.05 at 75 W; NS at 125 W). The half-times of VO2 kinetics were: in N, 36.2 +/- 6.7 s at 75 W and 41.6 +/- 8.6 s at 125 W; in C, 41.4 +/- 10.0 at 75 W and 43.8 +/- 14.0 at 125 W (NS). Mean steady state Qm was 8.5 ml.min-1.100 g-1 in C, and 13.4 in N at 75 W (NS); at 125 W, Qm was 18.3 ml.min-1.100 g-1 in C vs. 25.0 in N (NS). The half-times of the Qm kinetics tended to be slower in C than in N (NS). At both work loads, early lactate was slightly greater in C than in N (NS). It is concluded that, at submaximal exercise, (a) steady state VO2 and the VO2 kinetics are not affected by Tm, and (b) at the onset of exercise Qm does not affect VO2 kinetics.

The factors limiting VO2max in humans are analyzed according to a multifactorial model derived from the O2 conductance equation. In this context, alveolar ventilation (VA) and lung O2 transfer (GL) are not considered to be limiting, at least at sea level, because changes in VA and/or in GL are not accompanied by changes in VO2max due to the shape of the O2 dissociation curve. Thus, the limits to VO2max are shared between blood O2 transport (FQ') and a peripheral factor. This last includes tissue O2 transfer (Ft') and mitochondrial O2 utilization (Fm'). In untrained subjects at sea level, blood O2 transport is found to be responsible for approximately 70% of the overall limits to VO2max (FQ' = 0.7), the rest depending on the peripheral factors. FQ', as well as the sum of Ft' and Fm', are unchanged after training or upon return to sea level following exposure to chronic hypoxia (altitude higher than 5000 m). In the latter condition, however, since tissue O2 transfer, which sets Ft', is facilitated, and mitochondrial O2 utilization, which sets Fm', is impaired, Ft' is reduced and Fm' increased as compared to control condition and/or after training.