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New perspectives in breath-by- breath determination of alveolar transmembrane gas exchange
No full textAssessment of breath – to - breath alveolar gas transfer: a comparison of two procedures
No full textNew perspectives in breath-by-breath determination of alveolar gas exchange
No full textAlveolar 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 (F-A) change at constant volume plus the volume change (DeltaV(Ai)) at constant fraction i.e. VAl-1(F-Ai-FAi-1)+F-Ai.(Delta VAi), 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 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 (Gronlund model G). In this case, F-t1=F-t2 and thus the term VAi-1 (F-Ai-FAi-1) vanishes. In the present study, average alveolar O-2 uptake ((V) over dot O-2,O-A) and CO2 output ((V) over dot CO2,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 Gronlund
Metabolic and cardiovascular responses during sub-maximal exercise in humans after 14 days of head-down tilt bed rest and inactivity
No full textEffects of short term bed – rest on exercise response in humans
No full textExposure to real (space flight) or simulated microgravity (e.g., head–down tilt bed rest) induces remarkable alteration of maximal aerobic exercise capacity in humans. Maximal oxygen uptake (V'O2max) drops rapidly during the first 3-6 days to decrease more gradually up to 22 – 17 % of the control values after 30 – 42 days of bed rest (Convertino DA, 1996, Ferretti G et al, 1997, Fortney SM et al, 1996, Saltin B et al, 1968).
The prompt decay of V'O2max is mainly the consequence of the cardiovascular deconditioning ensuing during real and artificial microgravity. The shift of blood and body fluids occurring toward the head and thorax at the onset of microgravity is sensed as a volume overload signal and triggers an integrated cardiovascular-neuro-endocrine response leading to an immediate reduction of total peripheral resistance and to an increased water excretion by the kidney. The consequence is a rapid reduction in circulating volume, which may range from 8.4 % to 16 % in comparison with pre – flight conditions during 4-84 days missions (Convertino DA, 1996).
The observed reduction of circulating blood volume has a detrimental impact on cardiac haemodynamics. Indeed, the decay of and SV seem to be mainly caused by the following cascade of events: the increased elimination of plasma water brings about the reduction in circulating blood volume. This leads, through its effect on venous return, to the reduction of the heart chambers volume and, on longer periods of microgravity exposure, to cardiac atrophy and re–modelling (Levine BD et al, 1997, Perhonen MA et al, 2001), which, in turn, may alter the mechanical functions of cardiac pump in vivo. As a consequence of this chain of events, the volume of blood pumped by the heart at each cardiac cycle drops.
Bed rest campaigns commonly aimed to investigate, in a single group of subjects, the effect of this sort of intervention without considering the possible cross-linked effects of bed-rest and inactivity and/or confinement. In the Short Term Bed Rest – Integrative Physiology (STBR-IP) study, organised at the DLR Institute of Aerospace Medicine in Cologne (D), an experimental protocol was planned to take into considerations the weakness characterising the other similar studies carried out in the past.
To this aim, the same group of subjects was studied before and after confined ambulatory and bed rest periods of identical duration. This allowed us to disentangle the effects of restricted physical activity in a confined environment from those due to bed-rest.
In this paper, the results obtained during sub maximal and maximal exercise in the study at stake are reported. Data deal with oxygen uptake and cardiac output at maximal exercise assessed, in the very same subjects, before and after 14-days of head down bed-rest and ambulatory periods
New acquisitions in the assessment of breath-by-breath alveolar gas transfer in humans
No full textWe summarise recent results obtained in testing some of the algorithms utilised for estimating breath-by-breath (BB) alveolar O-2 transfer (VO2A) in humans. VO2A is the difference of the O-2 volume transferred at the mouth minus the alveolar O-2 stores changes. These are given by the alveolar volume change at constant O-2 fraction (FAiO2 DeltaV(Ai)) plus the O-2 alveolar fraction change at constant volume [VAi-1(F-Ai-FAi-1)O-2], where VAi-1 is the alveolar volume at the beginning of the breath i. All these quantities can be measured BB, with the exception of VAi-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 O-2 fractions in two subsequent breaths (Gronlund algorithm, GR). In this case, FAiO2=FAi-1O2 and the term VAi-1(F-Ai-FAi-1)O-2 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 VAi-1 values in estimating the time constant of alveolar O-2 uptake ((V)over dotO(2A)) kinetics at the onset of 120 W step exercise were evaluated. (V)over dotO(2A) was calculated by using GR and by using (in AU) VAi-1 values ranging from 0 to FRC +0.5 l. The time constant of the phase II kinetics (tau(2)) of (V)over dotO(2A) increased linearly, with VAi-1 ranging from 36.6 s for VAi-1=0 to 46.8 s for VAi-1=FRC+0.5 l, whereas tau(2) amounted to 34.3 s with GR. We concluded that, when using AU in estimating (V)over dotO(2A) during step exercise transitions, the tau(2) value obtained depends on the assumed value of VAi-1
Mitochondrial coupling in humans: assessment of the P/O2 ratio at the onset of calf exercise
No full textCoupling 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 bodyO2 uptake V'O2;O2 deficit O2def 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 _V O2 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’’ O2def was corrected for the individual
changes in the venous blood O2 stores (representing 49.9 +- 9.5% of the gross O2def) yielding the ‘‘net’’ O2def. 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
Alveolar oxygen uptake kinetics with step, impulse and ramp exercise in humans
No full textThe breath-by-breath V’O2A 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; (iii) impulse transitions (I) to 250 and 410 W lasting 10 and 5 s, respectively. The V’O2A data was modelled using non-linear weighted least square regressions. The amplitudes of the V’O2A response turned out to be proportional to the input work rate intensities in all the modalities of exercise. Time constants (s) and time delays (td) of ST-ON and R responses were not significantly different, whereas those of ST-OFF were characterised by longer s values. s and td of I responses turned _ out to be identical to those of ST-ON when the V’O2A 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 V’O2A 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 human
Oxigen deficit and oxygen delivery kinetics during submaximal intensity exercise in humans after 14 days of head down tilt bed rest
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