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.

The relative sensitivity of growth and reproduction in the springtail, Folsomia candida, exposed to xenobiotics in the laboratory: an indicator of soil toxicity.

The Folsomia candida reproduction test [ISO, 1998. Soil quality--Inhibition of reproduction of Collembola (Folsomia candida) by soil pollutants. International Standard Organization Report 11267, 1998, Geneva] is used to evaluate the ecotoxicological risks of contaminants in soils. The aim of this study was to compare the sensitivity of growth and reproduction of F. candida to four xenobiotics: two metals (Cd, Al), one metalloid (As), and one organic compound (pentachlorophenol). We showed that reproduction is a slightly more sensitive parameter than growth: EC(20) for reproduction was 1.25 microg/g dry soil for arsenic, 56 microg/g for cadmium, 97.5 microg/g for aluminum, and 41.7 microg/g for pentachlorophenol. The corresponding EC(20) values for growth were 2.8, 65, 630, and 94.6 microg/g. Keeping in mind that a growth test needs fewer juveniles and less time than a reproduction test, we conclude that the two parameters are complementary and could be used for a better ecotoxicological evaluation of contaminants. However, the relative growth and reproduction sensitivities should be tested with more chemicals before growth could be considered as a good alternative for a faster sublethal test.

Oxygen delivery and oxygen return in humans exercising in acute normobaric hypoxia.

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.

Maximal instantaneous muscular power after prolonged bed rest in humans.

A reduction in lower limb cross-sectional area (CSA) occurs after bed rest (BR). This should lead to an equivalent reduction in maximal instantaneous muscular power (W(p)) if the body segments' lengths remain unchanged. W(p) was determined during maximal jumps off both feet on a force platform before and on days 2, 6, 10, 32, and 48 after a 42-day duration BR. CSA of thigh muscles was measured by magnetic resonance imaging before and on day 5 after BR. Before BR, W(p) was 3.63 +/- 0.43 kW or 48.6 +/- 3.3 W/kg. On days 2 and 6 after BR, W(p) was reduced by 23.7 +/- 6.9 and 22.7 +/- 5.4% (P < 0.01), respectively. Thigh extensors CSA (CSAEXT) was 16.7 +/- 4.7% (P < 0.01) lower than before. When normalized per CSAEXT, W(p) was reduced by only 4.8 +/- 4.5% (P < 0.05). By day 48 of recovery, W(p) had returned to baseline values. Therefore, if W(p) is appropriately normalized for CSA of the extensor muscles, the reduction in CSAEXT explains most of the decrease in W(p) decrease after BR. Other factors such as a deficit in neural activation or a decrease in fiber-specific tension may account for only 5% of the W(p) loss after BR.

Oxygen cost of dynamic leg exercise on a cycle ergometer: effects of gravity acceleration.

A model of the metabolic internal power (Eint) during cycling, which includes the gravity acceleration (ag) as a variable, is presented. This model predicts that Eint is minimal in microgravity (0 g; g=9. 81 m s-2), and increases linearly with ag, whence the hypothesis that the oxygen uptake (VO2) during cycling depends on ag. Repeated VO2 measurements during steady-state exercise at 50, 75 and 100 W on the cycle ergometer, performed in space (0 g) and on Earth (1 g) on two subjects, validated the model. VO2 was determined from the time course of decreasing O2 fraction during rebreathing. The gas volume during rebreathing was determined by the dilution principle, using an insoluble inert gas (SF6). Average VO2 for subject 1 at each power was 0.99, 1.21 and 1.52 L min-1 at 1 g (n=3) and 0.91, 1.13 and 1.32 L min-1 at 0 g (n=5). For subject 2 it was 0.90, 1.12 and 1. 42 L min-1 at 1 g, and 0.76, 0.98 and 1.21 L min-1 at 0 g. These values corresponded to those predicted from the model. Although resting VO2 was lower at 0 g than at 1 g, the net (total minus resting) exercise VO2 was still smaller at 0 g than at 1 g. This difference reflects the lower Eint at 0 g.

Effects of prolonged bed rest on cardiovascular oxygen transport during submaximal exercise in humans.

The hypothesis was tested that prolonged bed rest impairs O2 transport during exercise, which implies a lowering of cardiac output Qc and O2 delivery (QaO2). The following parameters were determined in five males at rest and at the steady-state of the 100-W exercise before (B) and after (A) 42-day bed rest with head-down tilt at -6 degrees: O2 consumption (VO2), by a standard open-circuit method; Qc, by the pressure pulse contour method, heart rate (fc), stroke volume (Qh), arterial O2 saturation, blood haemoglobin concentration ([Hb]), arterial O2 concentration (CaO2), and QaO2. The VO2 was the same in A and in B, as was the resting fc. The fc at 100 W was higher in A than in B (+17.5%). The Qh was markedly reduced (-27.7% and -22.2% at rest and 100 W, respectively). The Qc was lower in A than in B [-27.6% and -7.8% (NS) at rest and 100 W, respectively]. The CaO2 was lower in A than in B because of the reduction in [Hb]. Thus also QaO2 was lower in A than in B (-32.0% and -11.9% at rest and at 100 W, respectively). The present results would suggest a down-regulation of the O2 transport system after bed rest.

The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.

1. Endurance athletes (E) undergo a marked reduction of arterial O2 saturation (Sa,O2) at maximal exercise in normoxia, which disappears when they breathe hyperoxic mixtures. In addition, at a given level of hypoxia, the drop in maximal O2 consumption (VO2,max) is positively related to the individual normoxic VO2,max. 2. These data suggest that the curve relating VO2,max to PI,O2 may be steeper and perhaps less curved in E than in sedentary subjects (S) with low VO2,max values because of the greater hypoxaemia in the latter, whence the hypotheses that (i) the relationship between VO2,max and PI,O2 may be set by the shape of the oxygen equilibrium curve; and (ii) the differences between E and S may be due to the different position on the oxygen equilibrium curve on which these subjects operate. These hypotheses have been tested by performing a systematic comparison of the VO2,max or Sa,O2 vs. PI,O2 relationships in E and S. 3. On ten subjects (five S and five E), VO2,max was measured by standard procedure during cycloergometric exercise. Sa,O2 was measured by finger-tip infrared oximetry. Arterialized blood PO2 (Pa,O2) and PCO2 (Pa,CO2) were determined in 80 microliters blood samples from an ear lobe. The subjects breathed ambient air or a N2-O2 mixture with an inspired O2 fraction (FI,O2) of 0.30, 0.18, 0.16, 0.13 and 0.11, respectively, VO2,max was normalized with respect to that obtained at the highest FI,O2. 4. The relationships between Sa,O2 or normalized VO2,max and FI,O2 (or PI,O2) had similar shapes, the data for E being systematically below and significantly different from those for S. Linear relationships between Sa,O2 and normalized VO2,max, statistically equal between E and S, were found. 5. We conclude that the relationships between either VO2,max or Sa,O2 and FI,O2 (or Pa,O2) may indeed be the mirror images of one another, implying a strict link between the decrease of VO2,max in hypoxia and the shape of the oxygen equilibrium curve, as hypothesized.

Loss of muscle oxidative capacity after an extreme endurance run: the Paris-Dakar foot-race.

We measured changes in maximal oxygen uptake capacity (VO2max), ventilation, heart rate, plasma lactate and speed at the end of an incremental exercise test as a consequence of a relay foot race from Paris to Dakar in 6 subjects. Additionally, anthropometric measurements were taken and muscle biopsies from M. vastus lateralis were obtained before and after the race. The latter were analyzed with morphometric methods for fiber size, capillarity and muscle ultrastructural composition. Weight specific VO2max was significantly reduced from 62.4 to 60.5 ml/min.kg after the race while absolute VO2max and the other endurance related functional variables remained unchanged. Body fat, thigh cross-sectional area and thigh volume showed tendential reduction immediately after the race but regained pre-race values within a few days. Fiber size and capillarity were not affected by the race. Volume density of total mitochondria was significantly reduced from 6.98 to 4.89% of fiber volume. Both subsarcolemmal and interfibrillar mitochondria were significantly reduced by 59 and 21%, respectively. The volume density of satellite cell was increased about three-fold whereas the content of lipofuscin remained constant. It is concluded that extreme endurance events such as a multi-stage relay race may induce a considerable loss of oxidative capacity of skeletal muscle tissue.

Effects of temperature on the maximal instantaneous muscle power of humans.

The maximal instantaneous muscle power (wi,max) probably reflects the maximal rate of adenosine 5'-triphosphate (ATP) hydrolysis (ATPmax), a temperature-dependent variable, which gives rise to the hypothesis that temperature, by affecting ATPmax, may also influence wi,max. This hypothesis was tested on six subjects, whose vastus lateralis muscle temperature (Tmuscle) was monitored by a thermocouple inserted approximately 3 cm below the skin surface. The Wi,max was determined during a series of high jumps off both feet on a force platform before and after immersion up to the abdomen for 90 min in a temperature controlled (T = 20 +/- 0.1 degrees C) water bath. Control Tmuscle was 35.8 +/- 0.7 degrees C, with control Wi,max being 51.6 (SD 8.7) W.kg-1. After cold exposure, Tmuscle decreased by about 8 degrees C, whereas wi,max 27% lower. The temperature dependence of Wi,max was found to be less (Q10 less than 1.5, where Q10 is the temperature coefficient as calculated in other studies) than reported in the literature for ATPmax. Such a low Q10 may reflect an increase in the mechanical equivalent of ATP splitting, as a consequence of the reduced velocity of muscle contraction occurring at low Tmuscle.

Oxygen transport system before and after exposure to chronic hypoxia.

Maximal VO2 on the treadmill (VO2max) and on the bicycle ergometer (VO2peak), maximal cardiac output (Qmax), by a CO2 rebreathing method, maximal heart rate (HRmax), blood hemoglobin concentration (Hb), and hematocrit (Hct) were measured on six subjects before (B) and 3 weeks after (A) prolonged exposure to chronic hypoxia. It was observed that after high-altitude exposure VO2max, VO2peak, and Qmax were lower (P less than 005) than before [A: 4.13 +/- 0.67; 3.28 +/- 0.41 and 16.89 +/- 2.49 (l/min +/- SD); B: 4.39 +/- 0.39; 3.53 +/- 0.34 and 21.81 +/- 1.27, respectively], whereas Hb and Hct were larger (A: 162 +/- 8 g/l and 0.46 +/- 0.02; B: 142 +/- 7 and 0.41 +/- 0.02) and HRmax was unchanged (178 +/- 7 vs 175 +/- 9 bts/min). Thus, the calculated stroke volume of the heart and the Hb flow at VO2 peak were lower in A than in B (95 +/- 15 vs 124 +/- 7 ml and 2,723 +/- 307 vs 3,129 +/- 196 g/min) (P less than 0.05, respectively), whereas the arteriovenous O2 difference was greater in A than in B (195 +/- 16 vs 162 +/- 19 ml O2/l; P less than 0.05). At any given submaximal work load, VO2 and HR were the same in B and in A, whereas Q was lower in A by approximately 2-3 l/min. However, because of the increased Hb, leading to a higher arterial O2 content, at any work load the O2 flow remained unchanged.

Energy cost and efficiency of sculling a Venetian gondola.

Oxygen uptake was measured on four male subjects during sculling gondolas at constant speeds from approximately 1 to approximately 3 m.s-1. The number of scullers on board in the different trials was one, two or four. Tractional water resistance (drag, D, N) was also measured in the same range of speeds. Energy cost of locomotion per unit of distance (C, J.m-1), as calculated from the ratio of O2 uptake above resting to, increased with v according to a power function (C = 155.2.v1.67; r = 0.88). Also D could be described as a power function of the speed: D = 12.3.v2.21; r = 0.94). The overall efficiency of motion, as obtained from the ratio of D to C, increased with speed from 9.2% at 1.41 m.s-1 to 14.5% at 3.08 m.s-1. It is concluded that, in spite of this relatively low efficiency of motion, the gondola is a very economic means. Indeed, at low speeds (approximately 1 m.s-1), the absolute amount of energy for propelling a gondola is the same as that for waking on the level at the same speed for a subject of 70 kg body mass.

The energetics of endurance running.

Maximal O2 consumption (VO2max) and energy cost of running per unit distance (C) were determined on the treadmill in 36 male amateur runners (17 to 52 years) who had taken part in a marathon (42.195 km) or semi-marathon (21 km), their performance times varying from 1.49 to 226 and from 84 to 131 min, respectively. VO2max was significantly (2p less than 0.001) greater in the marathon runners (60.6 vs 52.1 ml . kg-1 . min-1) while C was the same in both groups (0.179 +/- 0.017, S.D., mlO2 . kg-1 . m-1 above resting), and independent of treadmill speed. It can be shown that the maximal theoretical speed in endurance running (vEND) is set by VO2max, its maximal sustainable fraction (F), and C, as described by: vEND = F . VO2max . C-1. Since F was estimated from the individual time of performance, vEND could be calculated. The average speed of performance (vMIG) and vEND (m . s-1) were found to be linearly correlated: vMIG = 1.12 + 0.64 vEND (r2 = 0.72; n = 36). The variability of vMIG explained by vEND, as measured by r2, is greater than that calculated from any one regression between vMIG and VO2max (r2 = 0.51), F . VO2max (r2 = 0.58), or VO2max . C-1 (r2 = 0.63). The mean ratio of observed (vMIG) to theoretical (vEND) speeds amounted to 0.947 +/- 0.076 and increased to 0.978 +/- 0.079 (+/- S.D.; n = 36) when the effects of air resistance were taken into account. It is concluded that vEND = F . VO2max . C-1 is a satisfactory quantitative description of the energetics of endurance running.