Pulmonary V(O)(2) kinetics at the onset of exercise is faster when actual changes in alveolar O2 stores are considered.

Breath-by-breath (BbB) oxygen uptake rate (V(O)(2)) was measured at the mouth (MO) and at the alveolar level, at the onset of square wave cycling exercise of moderate intensity in six healthy male subjects. Alveolar BbB V(O)(2) values were calculated correcting MO V(O)(2) values by (i) estimating (GR); and (ii) measuring (opto-electronic plethysmography, OEP) BbB lung O(2) store changes.V(O)(2) kinetics was then described by a bi-exponential model. GR yielded larger values of the time constants (tau2) of the primary phase of V(O)(2) kinetics. The mean response times (MRTs) calculated by analysing GR BbB V(O)(2) values were larger than (i) those obtained by using MO and OEP at 90W; and (ii) that by using MO at 120W. OEP corrected V(O)(2) yielded the highest normalised amplitude of the cardiodynamic phase of the V(O)(2) on-response. Correction of BbB V(O)(2) for actual BbB changes of lung O(2) stores by OEP thus seems more appropriate for the study of the early cardiodynamic phase of V(O)(2) kinetics than GR.

Oxygen deficits and oxygen delivery kinetics during submaximal intensity exercise in humans after 14 days of head-down tilt-bed rest.

Beat-by-beat Q(a)O2 and breath-by-breath VO2 were assessed in ten male subjects (24 +/- 3.5 years; 78 +/- 7.7 kg; 182 +/- 5.6 cm) during cycling exercise at 50 W before and after a 14-day period of head-down tilt-bed rest (HDTBR). O2 deficit (DefO2) was calculated as the difference between the volume of O2 that would have been consumed if a steady state had been immediately attained minus that actually taken up during exercise. Q(a)O2 kinetics was described fitting the data with a non-linear mono-exponential model with time delay. Mean response times (MRT) of VO2 and Q(a)O2 kinetics were then calculated. DefO2 and MRT of VO2 response did not change after HDTBR, whereas MRT of Q(a)O2 kinetics increased. The invariance of VO2 kinetics after HDTBR suggests that, although Q(a)O2 response became slower after HDTBR, it did not affect the kinetics of peripheral gas exchange, which probably remained under the control of local muscular mechanisms.

Metabolic and cardiovascular responses during sub-maximal exercise in humans after 14 days of head-down tilt bed rest and inactivity.

VO(2), f (H), Q, SV, [Hb], C(a)O(2), QaO(2), MAP and R (P) were measured in 10 young subjects at rest and during exercise at 50, 100 and 150 W before and after 14 days of head-down tilt bed rest (HDTBR) and of ambulatory (AMB) control period. f (H) was 18 and 8% higher after HDTBR and AMB, respectively. SV dropped by 15% both after HDTBR and AMB, whereas Q did not change. After HDTBR, C(a)O(2) decreased at rest (-8%) and at 50 W (-5%), whereas QaO(2) did not change; MAP was 14 and 6% lower at rest and at 100 W and R (P) decreased by 23% only at rest. Changes in f (H) and SV were larger after HDTBR than after AMB. These results show that, notwithstanding the drop of SV, moderate-intensity dynamic exercise elicited a normal pressure response after 14 days of HDTBR.

Mitochondrial coupling in humans: assessment of the P/O2 ratio at the onset of calf exercise.

Coupling of oxidation to ATP synthesis (P/O2 ratio) is a critical step in the conversion of carbon substrates to fuel (ATP) for cellular activity. The ability to quantitatively assess mitochondrial coupling in vivo can be a valuable tool for basic research and clinical purposes. At the onset of a square wave moderate exercise, the ratio between absolute amount of phosphocreatine split and O2 deficit (corrected for the amount of O2 released from the body O2 stores and in the absence of lactate production), is the mirror image of the P/O2 ratio. To calculate this value, cardiac output (Q), whole body O2 uptake (VO2), O2 deficit (O2(def)) and high-energy phosphates concentration (by 31P-NMR spectroscopy) in the calf muscles were measured on nine healthy volunteers at rest and during moderate intensity plantar flexion exercise (3.44 +/- 0.73 W per unit active muscle mass). Q and VO2 increased (from 4.68 +/- 1.56 to 5.83 +/- 1.59 l min(-1) and from 0.28 +/- 0.05 to 0.48 +/- 0.09 l min(-1), respectively), while phosphocreatine (PCr) concentration decreased significantly (22 +/- 6%) from rest to steady-state exercise. For each volunteer, "gross" O2(def) was corrected for the individual changes in the venous blood O2 stores (representing 49.9 +/- 9.5% of the gross O2(def)) yielding the "net" O2(def). Resting PCr concentration was estimated from the appropriate spectroscopy data. The so calculated P/O2 ratio amounted on average to 4.24 +/- 0.13 and was, in all nine subjects, very close to the literature values obtained directly on intact skeletal muscle. This unfolds the prospect of a non-invasive tool to quantitatively study mitochondrial coupling in vivo.

Factors determining the time course of VO2(max) decay during bedrest: implications for VO2(max) limitation.

The aim of this study was to characterize the time course of maximal oxygen consumption VO2(max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in VO2(max) tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, VO2(max) maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After all periods of HDT, VO2max, Qmax, and QaO2max were significantly lower than before. The VO2max decreased less than qmax after the two shortest bedrests, but its per cent decay was about 10% larger than that of Qmax after 90-day bedrest. The VO2max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max declines after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the VO2max, Qmax, and QaO2max decay during bedrest were less if the bedrest duration were longer, with the exception of that of VO2max in the longest bedrest. The asymptotic VO2max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the VO2max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration.

Alveolar oxygen uptake kinetics with step, impulse and ramp exercise in humans.

The breath-by-breath VO2A of five male subjects (21.2 years +/-3.2; 78.8 kg +/-5.9; 179.6 cm +/-5.8) was measured during a cycling exercise. Starting from a 10 W baseline, the subjects performed (i) ON and OFF step transitions (ST-ON; ST-OFF) to 50, 90, and 130 W; (ii) a ramp (R) exercise with work rate gradually increasing by 20 W min(-1); (iii) impulse transitions (I) to 250 and 410 W lasting 10 and 5 s, respectively. The VO2A data was modelled using non-linear weighted least square regressions. The amplitudes of the VO2A response turned out to be proportional to the input work rate intensities in all the modalities of exercise. Time constants (tau) and time delays (t (d)) of ST-ON and R responses were not significantly different, whereas those of ST-OFF were characterised by longer tau values. tau and t (d) of I responses turned out to be identical to those of ST-ON when the VO2A responses were fitted using a five-component model. These results suggest that: (i) the system controlling alveolar gas exchange behaves linearly when it is forced by ST and R inputs (the ON and OFF phases being considered separate); (ii) the analysis of the I response depends strongly on the models selected to fit the VO2A data. The asymmetry between the ON and OFF responses mirrors that found between the splitting and resynthesis rates of phosphocreatine, and these results support the notion that phosphocreatine could be the main controller of the skeletal muscle respiratory turnover in humans.

New acquisitions in the assessment of breath-by-breath alveolar gas transfer in humans.

We summarise recent results obtained in testing some of the algorithms utilised for estimating breath-by-breath (BB) alveolar O2 transfer (VO2A) in humans. VO2A is the difference of the O2 volume transferred at the mouth minus the alveolar O2 stores changes. These are given by the alveolar volume change at constant O2 fraction (FAiO2 DeltaVAi) plus the O2 alveolar fraction change at constant volume [V(Ai-1)(FAi-F(Ai-1))O2], where V(Ai-1) is the alveolar volume at the beginning of the breath i. All these quantities can be measured BB, with the exception of V(Ai-1), which is usually set equal to the subject's functional residual capacity (FRC) (Auchincloss algorithm, AU). Alternatively, the respiratory cycle can be defined as the time elapsing between two equal O2 fractions in two subsequent breaths (Grønlund algorithm, GR). In this case, FAiO2= F(Ai-1)O2 and the term V(Ai-1)(FAi-F(Ai-1))O2 disappears. BB alveolar gas transfer was first determined at rest and during exercise at steady-state. AU and GR showed the same accuracy in estimating alveolar gas transfer; however GR turned out to be significantly more precise than AU. Secondly, the effects of using different V(Ai-1) values in estimating the time constant of alveolar O2 uptake (VO2A) kinetics at the onset of 120 W step exercise were evaluated. VO2A was calculated by using GR and by using (in AU) V(Ai-1) values ranging from 0 to FRC +0.5 l. The time constant of the phase II kinetics (tau2) of VO2A increased linearly, with V(Ai-1) ranging from 36.6 s for V(Ai-1)=0 to 46.8 s for V(Ai-1)=FRC+0.5 l, whereas tau2 amounted to 34.3 s with GR. We concluded that, when using AU in estimating VO2A during step exercise transitions, the tau2 value obtained depends on the assumed value of V(Ai-1).

Breath-by-breath alveolar oxygen transfer at the onset of step exercise in humans: methodological implications.

The effects of using different algorithms to estimate the time constant of changes in oxygen uptake at the onset of square-wave 120 W cycloergometric exercise were evaluated in seven subjects. The volume of oxygen taken up at the alveoli (VO(2Ai)) was determined breath-by-breath (BB) from the volume of O(2) transferred at the mouth (VO(2mi)) minus the corresponding volume changes in O(2) stores in the alveoli: VO(2Ai)= VO(2mi)-[V(Ai-1)(FO(2Ai)- FO(2Ai-1))+ FO(2Ai) x Delta V(Ai)], where V(Ai-1) is the alveolar volume at the end of the previous breath, FO(2Ai) and FO(2Ai-1) are estimated from the fractions of end-tidal O(2) in the current and previous breaths, respectively, and Delta V(Ai) is the change in volume during breath i. These quantities can be measured BB, with the exception of V(Ai-1) which must be assumed. The respiratory cycle has been defined as the time elapsing between identical fractions of expiratory gas in two successive breaths. Using this approach, since FO(2Ai)= FO(2Ai-1), any assumption regarding V(Ai-1) becomes unnecessary. In the present study, VO(2Ai) was calculated firstly, by using this approach, and secondly by setting different V(Ai-1) values (from 0 to FRC+0.5 l, where FRC is the functional residual capacity). Values for alveolar O(2) flow (VO(2Ai)), as calculated from the quotient of VO(2Ai) divided by breath duration, were then fitted bi-exponentially. The time constant of the phase II kinetics of VO(2Ai) (tau(2)) was linearly related to V(Ai-1), increasing from 36.6 s (V(Ai-1)=0) to 46.8 s (V(Ai-1)=FRC+0.5 l) while tau(2) estimated using the first approach amounted to 34.3 s. We concluded that, firstly, the first approach allowed us to calculate O(2A) during transitions in step exercise; and secondly, when using methods wherein V(Ai-1) must be assumed, tau(2) depended on V(Ai-1).

New perspectives in breath-by-breath determination of alveolar gas exchange in humans.

Alveolar gas transfer over a given breath (i) was determined in ten subjects at rest and during steady-state cycling at 60, 90 or 120 W as the sum of volume of gas transferred at the mouth plus the changes of the alveolar gas stores. This is given by the gas fraction (FA) change at constant volume plus the volume change (deltaVAi) at constant fraction i.e. VAi-1(FAi-FAi-1)+FAi x deltaVAi, where VAi-1 is the end-expiratory volume at the beginning of the breath. These quantities, except for VAi-1, can be measured on a single-breath (breath-by-breath) basis and VAi-1 set equal to the subject's functional residual capacity (FRC, Auchincloss model). Alternatively, the respiratory cycle can be defined as the interval elapsing between two equal expiratory gas fractions in two successive breaths (Grønlund model G). In this case, Ft1 = Ft2 and thus the term VAi-1 (FAi-FAi-1) vanishes. In the present study, average alveolar O2 uptake (VO2,A) and CO2 output (VCO2,A) were equal in both approaches whereby the mean signal-to-noise ratio (S/N) was 40% larger in G. Other approaches yield steady state S/N values equal to that obtained in G, although they are based on the questionable assumption that the inter-breath variability of alveolar gas transfer is minimal. It is concluded that the only promising approach for assessing "true" single-breath alveolar gas transfer is that originally proposed by Grønlund.

Energy cost of front-crawl swimming at supra-maximal speeds and underwater torque in young swimmers.

The energy cost of front-crawl swimming (Cs, kJ x m(-1)) at maximal voluntary speeds over distances of 50, 100, 200 and 400 m, and the underwater torque (T') were assessed in nine young swimmers (three males and six females; 12-17 years old). Cs was calculated from the ratio of the total metabolic energy (Es, kJ) spent to the distance covered. Es was estimated as the sum of the energy derived from alactic (AnA1), lactic (AnL) and aerobic (Aer) processes. In turn, AnL was obtained from the net increase of lactate concentration after exercise, AnA1 was assumed to amount to 0.393 kJ x kg(-1) of body mass, and Aer was estimated from the maximal aerobic power of the subject. Maximal oxygen consumption was calculated by means of the back-extrapolation technique from the oxygen consumption kinetics recorded during recovery after a 400-m maximal trial. Underwater torque (T' x N x m), defined as the product of the force with which the feet of a subject lying horizontally in water tends to sink times the distance from the feet to the center of volume of the lungs, was determined by means of an underwater balance. Cs (kJ x m(-1)) turned out to be a continuous function of the speed (v, m x s(-1)) in both males (Cs = 0.603 x 10(0.228v), r2 =0.991; n = 12) and females (Cs = 0.360 x 10(0.339r), r2 = 0.919; n = 24). A significant relationship was found between T' and Cs at 1.2 m x s(-1); Cs = 0.042T' + 0.594, r = 0.839, n = 10, P<0.05. On the contrary, no significant relationships were found between Cs and T' at faster speeds (1.4 and 1.6 m x s(-1)). This suggests that T' is a determinant of Cs only at speeds comparable to that maintained by the subjects over the longest, 400-m distance [mean (SD) 1.20 (0.07) m x s(-1)].