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The aim of this paper was to develop a model from experimental data allowing a prediction of the cardiopulmonary responses to steady-state submaximal exercise in varying gravitational environments, with acceleration in the G(z) axis (a (g)) ranging from 0 to 3 g. To this aim, we combined data from three different experiments, carried out at Buffalo, at Stockholm and inside the Mir Station. Oxygen consumption, as expected, increased linearly with a (g). In contrast, heart rate increased non-linearly with a (g), whereas stroke volume decreased non-linearly: both were described by quadratic functions. Thus, the relationship between cardiac output and a (g) was described by a fourth power regression equation. Mean arterial pressure increased with a (g) non linearly, a relation that we interpolated again with a quadratic function. Thus, total peripheral resistance varied linearly with a (g). These data led to predict that maximal oxygen consumption would decrease drastically as a (g) is increased. Maximal oxygen consumption would become equal to resting oxygen consumption when a (g) is around 4.5 g, thus indicating the practical impossibility for humans to stay and work on the biggest Planets of the Solar System.

Bilateral deficit (BLD) occurs when the force (or power) generated by both limbs together is smaller than the sum of the forces (or powers) developed separately by the two limbs. The amount of BLD can be altered by neural adaptations brought about by the repetitive execution of specific motor tasks (training). Prolonged disuse also leads to relevant neural adaptations; however, its effects on BLD are still unknown. Thus, the aim of this study was to investigate the effects of a 35-day bed rest on the BLD of the lower limbs. Ten young healthy volunteers performed maximal explosive efforts on a sledge ergometer with both lower limbs or with the right and the left limb separately. Electromyography (EMG) of vastus lateralis, rectus femoris, biceps femoris and gastrocnemius medialis was also measured. Before bed rest, maximal explosive power and peak force were significantly higher in monolateral than bilateral efforts (+18.7 and +31.0 %, respectively). Conversely, peak velocity was 11.9 % greater in bilateral than monolateral efforts. BLD attained a value of 18.1 % and was accompanied by lower EMG amplitude of knee extensors (−17.0 %) and gastrocnemius medialis (−11.7 %) during bilateral efforts. Bed rest led to a ~28.0 % loss in both bilateral and monolateral maximal explosive power. Neither BLD magnitude nor the difference in EMG amplitudes as well as in peak force and velocity between bilateral and monolateral efforts were affected by bed rest. These results suggest that the neuromuscular factors underlying BLD are unaltered after prolonged disuse.

The aim of the study was to evaluate changes in cardiac troponin I levels (cTnI) and the main biomarkers of skeletal muscle damage after an uphill-only marathon, along with its relationship with athletes’ physiological parameters. Twenty-two runners participated in the “Supermaratona dell’Etna” (43 km, 0–2850 m AMSL). Before and immediately after the race, body mass and hydration status were measured together with blood sampling. At the end of the race, mean cTnI increased significantly in all athletes (mean +900%), and in 52% of them the cTnI values were over the normal range. Mean creatinine and cortisol increased significantly (by 30.5% and 291.4%), while C-reactive protein levels did not change significantly. Then, an uphill-only marathon showed a significant increase in cardiac and skeletal muscle blood biomarkers of injury, and cTnI levels were not significantly correlated with age, body mass index, VO2max, training status, ultra-endurance training experience, race time and blood parameters.

Our objective was to determine the effects of long-lasting endurance events on the energy cost of running (C r), and the role of maximal oxygen uptake (VO2max), its fractional utilisation (F) and C r in determining the performance. Ten healthy runners (age range 26–59 years) participated in an ultra-endurance competition consisting of three running laps of 22, 48 and 20 km on three consecutive days in the North–East of Italy. Anthropometric characteristics and VO2max by a graded exercise test on a treadmill were determined 5 days before and 5 days after the competition. In addition, C r was determined on a treadmill before and after each running lap. Heart rate (HR) was recorded throughout the three laps. Results revealed that mean C r of the individual laps did not increase significantly with lap number (P = 0.200), thus ruling out any chronic lap effect. Even so, however, at the end of lap 3, C r was 18.0% (P

In a comparative study on erythrocytes (RBCs) drawn from mountaineers before and after a high-altitude stay, we observed that upon returning to sea level, their RBCs displayed a senescent-like phenotype as indicated by their density and the partial loss of membrane proteins which are shed by ageing RBCs. The aim of this study was to investigate possible changes in the membrane skeleton of these RBCs and to compare them with pathological RBCs. We analysed the proteins of RBC ghosts obtained from our subjects before and after returning to sea level by two-dimensional electrophoresis and mass spectrometry. We observed lower expression and fragmentation of β-actin after exposure to hypoxia. This suggested an alteration in membrane skeleton structure, which was confirmed by β-actin release in cell lysates during ghost preparation. We observed a similar actin fragmentation and release in RBC lysates from β-thalassaemic patients. In conclusion, these results indicate that after exposure to hypoxia, RBCs display a modification of their actin and cytoskeleton instability.

\( {{\dot{V}O}}_{2} , \)fH, \( \dot{Q}, \) SV, [Hb], CaO2, \( {{\dot{Q}}}_{\text{a}} \)O2, MAP and RP 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. fH was 18 and 8% higher after HDTBR and AMB, respectively. SV dropped by 15% both after HDTBR and AMB, whereas \( \dot{Q} \) did not change. After HDTBR, CaO2 decreased at rest (−8%) and at 50 W (−5%), whereas \( {{\dot{Q}}}_{\text{a}} \)O2 did not change; MAP was 14 and 6% lower at rest and at 100 W and RP decreased by 23% only at rest. Changes in fH and SV were larger after HDTBR than after AMB. These results show that, notwhistanding the drop of SV, moderate-intensity dynamic exercise elicited a normal pressure response after 14 days of HDTBR.

Two forces act on a human body motionless in water: weight (W) and buoyancy (B). They are applied to the center of mass (CM) and to the center of volume (CV) of the subject, respectively. CM and CV do not coincide; this generates a torque that is a measure of the tendency of the upper part of the body to rise, rotating around its center of mass. To quantify this tendency, Pendergast & Craig defined ‘underwater torque’ (T1) as the product of the net force with which the feet of a subject lying horizontally in water tend to sink, times the distance between the feet and the center of volume of the lungs. In this paper we have investigated: (a) the relationships between T1 and body weight (BW), height (H), body surface area (BS), body density (BD) and leg density (LD) in a group of 30 subjects (group A, 14 females and 16 males, age range 16-50 years); and (b) the effect of gender and growth on T1 in a group of 110 subjects (group B, 67 girls and 43 boys, age range 12-17 years). In group A, T1 was found to be linearly related with BW (r= 0.833, P < 0.001), H (r= 0.803, P < 0.001), BS (r= 0.866, P < 0.001), BD (r= 0.617, P < 0.001) and LD (r= 0.549, P < 0.005). A multiple linear regression analysis showed that BS and BD explained about 85% of the variability of T1 (r2= 0.85). In group B, T1 was found to increase linearly with age (r= 0.47, P < 0.01), the increasing rate being three times higher in boys compared with girls. As a consequence, the T1 ratio between boys and girls increased with age, from 1.69 at 13 years to 2.04 at 16 years.

A selective lysis of relatively young erythrocytes (neocytolysis), together with a decrease of erythropoietin (EPO) production, has been described in polycythemic, high altitude acclimatized climbers, after descent to sea level, and in astronauts, soon after exposure to weightlessness (Alfrey CP, Rice L, Udden MM, Driscoll TB. Neocytolysis may represent the physiological down-regulation of red-cell mass. Lancet 349 (1997) 1389-90). To study neocytolysis, we analysed blood samples drawn from 4 mountain climbers at sea level before and after 53 days of high altitude acclimatization (> or = 4500 m). After a 6-day descent to sea level, erythropoietin (EPO) plasma levels were lower than before high altitude acclimatization (mean values: 2.5+/-3.3 versus 10+/-4.5 mIU/ml, p < 0.05). Red blood cell (RBC) populations were separated into low, middle and high density subsets, which, by physical and phenotypical criteria, were characterized as young, middle-aged and old. RBC membrane molecules CD55 and CD59 along with phosphatydylserine and CD47 were measured. The former are partially lost during RBC aging. The latter are involved in the triggering or inhibition of RBC phagocytosis by macrophages. Immunofluorescence and flow cytometry were done on each density subset. Young and middle-aged RBCs largely disappeared after descent from high altitude (from 4.50% (+/-3.10) and 66% (+/-6.90) to 0.19% (+/-0.07) and 1.90% (+/-0.50), respectively). Simultaneously, there was a dramatic increase of high density RBCs (from 29.50% (+/-7) to 97.90% (+/-2.00)). Furthermore, the remaining young and middle-aged RBCs had acquired a senescent-like phenotype, which may account for their increased susceptibility to phagocytosis.

Purpose:To investigate the effects of an uphill marathon (43 km, 3063-m elevation gain) on running mechanics and neuromuscular fatigue in lower-limb muscles.Methods:Maximal mechanical power of lower limbs (MMP), temporal tensiomyographic (TMG) parameters, and muscle-belly displacement (Dm) were determined in the vastus lateralis muscle before and after the competition in 18 runners (age 42.8 ± 9.9 y, body mass 70.1 ± 7.3 kg, maximal oxygen uptake 55.5 ± 7.5 mL · kg−1 · min−1). Contact (tc) and aerial (ta) times, step frequency (f), and running velocity (v) were measured at 3, 14, and 30 km and after the finish line (POST). Peak vertical ground-reaction force (Fmax), vertical displacement of the center of mass (Δz), leg-length change (ΔL), and vertical (kvert) and leg (kleg) stiffness were calculated.Results:MMP was inversely related with race time (r = –.56, P = .016), tc (r = –.61, P = .008), and Δz (r = –.57, P = .012) and directly related with Fmax (r = .59, P = .010), ta (r = .48, P = .040), and kvert (r = .51, P = .027). In the fastest subgroup (n = 9) the following parameters were lower in POST (P < .05) than at km 3: ta (–14.1% ± 17.8%), Fmax (–6.2% ± 6.4%), kvert (–17.5% ± 17.2%), and kleg (–11.4% ± 10.9%). The slowest subgroup (n = 9) showed changes (P < .05) at km 30 and POST in Fmax (–5.5% ± 4.9% and –5.3% ± 4.1%), ta (–20.5% ± 16.2% and –21.5% ± 14.4%), tc (5.5% ± 7.5% and 3.2% ± 5.2%), kvert (–14.0% ± 12.8% and –11.8% ± 10.0%), and kleg (–8.9% ± 11.5% and –11.9% ± 12%). TMG temporal parameters decreased in all runners (–27.35% ± 18.0%, P < .001), while Dm increased (24.0% ± 35.0%, P = .005), showing lower-limb stiffness and higher muscle sensibility to the electrical stimulus.Conclusions:Greater MMP was related with smaller changes in running mechanics induced by fatigue. Thus, lower-limb power training could improve running performance in uphill marathons.

We hypothesized that the third dynamic phase (ϕ3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase (ϕ2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen.Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (fH), stroke volume (SV), cardiac output (Q˙).The fH, SV and Q˙ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady ϕ2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air.The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine ϕ3, the increase in CO2 stores might play a central role in eliciting their activation.

Microgravity leads to a decline of muscle power especially in the postural muscles of the lower limb. Muscle atrophy primarily contributes to this negative adaptation. Nutritional countermeasures during unloading were shown to possibly mitigate the loss of muscle mass and strength. The aim of this study was to investigate the effects of different diet energy intakes during prolonged inactivity on body composition and lower limbs power output. The effects of lower or higher diet energy intake on the decline of maximal explosive power of the lower limbs, as determined on a sledge ergometer before and after 35 days of bed rest, were investigated on two matched groups of young healthy volunteers. Body composition and lean volume of the lower limb were also measured. After bed rest, fat mass increased (+20.5 %) in the higher energy intake group (N = 9), while it decreased (−4.8 %) in the lower energy intake group (N = 10). Also, the loss of body fat-free mass and lean volume of the lower limb was significantly greater in the higher (−4.6 and −10.8 %, respectively) as compared to the lower (−2.4 and −3.7 %, respectively) diet energy intake group. However, the loss of maximal explosive power was similar between the two groups (−25.2 and −29.5 % in the higher and lower energy intake group, respectively; P = 0.440). The mitigation of loss of muscle mass by means of a moderate caloric diet restriction during prolonged inactivity was not sufficient for reducing the loss of maximal explosive power of the lower limbs.

We evaluated the effects of tourniquet application on the cardiovascular system and metabolism in 10 young men undergoing knee surgery with general anesthesia. The duration of inflation was from 75 to 108 min. Heart rate, mean arterial pressure, cardiac index (CI) by pulse contour method, and systemic vascular resistance were measured before, during, and after tourniquet inflation. pH, PaO(2), PaCO(2), and lactate blood concentrations were also measured. VO(2) and VCO(2) were assessed every minute from tracheal intubation up to 15 min after tourniquet deflation and VO(2) in excess of the basal value over the 15 min after deflation (VO(2)exc) was calculated. Mean arterial pressure increased 26% (P:0.05) during inflation and returned to basal values after deflation. CI did not change immediately after inflation; although, thereafter, it increased 18% (P:0.05). Five minutes after deflation, CI further increased to a value 40% higher than the basal value. Therefore, systemic vascular resistance increased 20% suddenly after inflation (P:0.05) and decreased 18% after deflation (P:0.05). VO(2) and VCO(2) remained stable during inflation and increased (P:0.05) after deflation. VO(2)exc depended on duration of tourniquet inflation time (Tisch) (P:0.05). After deflation, PaCO(2) and lactate increased (P:0.05) while Tisch increased. We conclude that tourniquet application induces modifications of the cardiovascular system and metabolism, which depend on tourniquet phase and on Tisch. Whether these modifications could be relevant in patients with poor physical conditions is not known.The clinical effects of tourniquet application were evaluated in 10 young men undergoing knee surgery. Our data indicate that tourniquet application causes hemodynamic and metabolic changes which may become clinically relevant after a long period of tourniquet inflation, particularly in patients with concomitant cardiovascular diseases.

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 aim of this study was to investigate: (1) the role of , the fraction of (F) and the metabolic cost of transport (CoT) in determining performance during an ultra-endurance competition and (2) the effects of the race on several biomechanical and morphological parameters of the lower limbs that are likely to affect CoT. Eleven runners (aged 29-54 years) participated in an ultra-endurance competition consisting of three running stages of 25, 55 and 13 km on three consecutive days. Anthropometric characteristics, body composition, morphological properties of the gastrocnemius medialis, maximal explosive power of the lower limb and were determined before the competition. In addition, biomechanics of running and CoT were determined, before and immediately after each running stage. Performance was directly proportional to (r=0.77) and F (r=0.36), and inversely proportional to CoT (r=-0.30). Low CoT values were significantly related to high maximal power of the lower limbs (r=-0.74) and vertical stiffness (r=-0.65) and low footprint index (FPI, r=0.70), step frequency (r=0.62) and external work (r=0.60). About 50% of the increase in CoT during the stages of the competition was accounted for by changes in FPI, which represents a global evaluation of medio-lateral displacement of the foot during the whole stance phase, which in turn is associated with the myotendinous characteristics of the lower limb. Thus, lower CoT values were related to greater muscular power and lower FPI, suggesting that a better ankle stability is likely to achieve better performance in an ultra-endurance running competition.

Hemodynamic changes, pulmonary CO2 elimination (VECO2) and gas exchange were evaluated during laparoscopic cholecystectomy. An algorithm to calculate inspired ventilation (VI) needed to maintain constant PaCO2 was also developed. In 12 ASA physical status I patients undergoing laparoscopic cholecystectomy, heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), and systemic vascular resistance index (SVRI) were measured by the analysis of a radial artery pressure profile before, during, and after CO2 insufflation. Alveolar-arterial oxygen pressure gradient (P(A-a)O2), physiological and alveolar ventilatory dead space fractions (VDphys/VT; VDalv/VT), and PaCO2 were measured as well. VECO2 was assessed every minute in the patients maintained in the head-up position. HR did not significantly change during pneumoperitoneum, whereas MAP showed a transient increase (24.9%; P0.05) after CO2 insufflation. CI remained stable during pneumoperitoneum, but increased (25.0%; P0.05) after deflation. As a consequence, SVRI transiently increased after CO2 insufflation and decreased by 15.8% (P0.05) 5 min after deflation. P(A-a)O2 increased slightly (P0.05) with increased anesthesia time. VDphys/VT and VDalv/VT did not change after pneumoperitoneum onset, but VDalv/VT decreased after CO2 deflation (13.4%; P0.05). VECO2 increased (decreased) after a monoexponential time course during (after) CO2 insufflation in 8 of 12 patients. The mean time constants (t) of the monoexponential functions were 26.3 and 15.4 min during and after pneumoperitoneum. A monoexponential time course was shown also by PaCO2 during CO2 insufflation (tau = 27.8 min). Finally, the VI needed to maintain PaCO2 at a selected value could be calculated by the following algorithm: VI = [0.448.(1-e(-t/tau) + 2.52].(VA.PaCO2.713)-1, where VA corresponds to alveolar ventilation and t must be chosen according to the pneumoperitoneum phase. We conclude that CO2 insufflation in the abdominal cavity does not induce significant changes in cardiopulmonary function in ASA physical status I patients. The algorithm proposed seems to be a useful tool for the anesthesiologists to maintain constant PaCO2 during all surgical procedures.

The stroke volume of the left ventricle (SV) was assessed in nine young men (mean age 22.2, ranging from 20 to 25 years) during cycle ergometer upright exercise at exercise intensities from 60 to 150 W (about 20% to 80% of individual maximal aerobic power). The SV was calculated from noninvasive tracings of the arterial blood pressure, determined from photoplethysmograph records and compared to the SV determined simultaneously by pulsed Doppler echocardiography (PDE). Given the relationship SV = As.Z-1 in which A(s) is the area underneath the systolic pressure profile (in millimetres of mercury and second), and Z (in millimetres of mercury and second per millilitre) is the apparent hydraulic impedance of the circulatory system, a prerequisite for the assessment of SV from the photoplethysmograph tracings is a knowledge of Z. The experimental value of Z (hereafter defined Z*) was calculated by dividing A(s) (from the finger photoplethysmograph) by SV as obtained by PDE. When the whole group of subjects was considered, Z* was not greatly affected by the exercise intensity: it amounted to 0.089 (SD 0.028; n = 36). The Z was also estimated independently of any parameter other than heart rate (HR), mean (MAP) and pulse (PP) arterial blood pressure obtained from the photoplethysmograph. A computerized statistical method allowed us to interpolate the experimental values of Z*, HR, PP and MAP by the equation Zm = a.(b + c.HR + d.PP + e.MAP)-1, thus obtaining the coefficients a to e. The mean percentage error between Zm (calculated from the coefficients obtained and Z* was 21.8 (SD 14.3)%. However, it was observed that, in a given subject, Z* was significantly affected by the exercise intensity. Therefore, to improve the estimate of Z a second algorithm was developed to update the experimental value of Z determined initially at rest (Zin). This updated value (Zcor) of Z was calculated as Zcor = Zin. [(f/(i + g.(HR/HRin) + h.(PP/PPin) + 1.(MAP/MAPin)], where HRin, PPin, MAPin, HR, PP, MAP are the above parameters at rest and during exercise, respectively. Also in this case, the coefficients f to 1 were determined by a computerized statistical method using Z* as the experimental reference. The values of Zcor so obtained allowed us to calculate SV from arterial pulse contour analysis as SVF = As.Z-1cor. The mean percentage error between the SVF obtained and the values simultaneously determined by PDE, was 10.0 (SD 8.7)%. It is concluded that the SV of the left ventricle, and hence cardiac output, can be determined during exercise from photoplethysmograph tracings with reasonable accuracy, provided that an initial estimate of SV at rest is made by means an independent high quality reference method.

In humans, acute erythroid expansion can lead to maturation of red blood cell (RBC) precursors containing fetal hemoglobin (F red cells). This can occur in patients after recovery from bone marrow transplantation, or in individuals affected by sickle cell or thalassemic syndromes. An accelerated erythroid lineage expansion is also a hallmark of the adaptive response to high altitude hypoxia. To explore the possible effect of this environment on F red cell production, we analyzed RBCs from five subjects during and after 17 days spent at high altitude and investigated the expression of fetal hemoglobin by different methodological approaches. By flow cytometry, we found a moderate increase of circulating F red cells during and after the hypoxia exposure, with respect to control cells analyzed before a stay at high altitude. The increased expression of γ-globin (as the specific subunit contained in F hemoglobin together with α-globin) was further confirmed by immunoblotting of young RBC hemolysates and quantitative RT-PCR of transcripts purified from a reticulocyte-enriched RBC fraction. Thus, in healthy adults the exposure to high altitude hypoxia induces maturation of F red cells at a level higher than under normal condition. The effect appears reduced after return to normoxia.

The mechanical power (Wtot, W·kg−1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO2max)] of 20–40 min duration. The oxygen uptake [VO2 (W·kg−1, 1 ml O2 = 20.9 J)] and venous blood lactate concentration ([la]b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, Wtot decreased linearly with the intensity of the priming exercise (Wtot = 11.9−0.25·VO2). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO2max, Wtot, VO2 and [la]b remained constant until the end of the exercise. For exercise intensities greater than 60% VO2max, VO2 and [la]b showed continuous upward drifts and Wtot continued decreasing. Under these conditions, the rate of decrease of Wtot was linearly related to the rate of increase of V [(d Wtot/dt) (W·kg−1·s−1) = 5.0·10−5 −0.20·(d VO2/dt) (W·kg−1·s−1)] and this was linearly related to the rate of increase of [la]b [(d VO2/dt) (W·kg−1·s−1) = 2.310−4 + 5.910−5·(d [la]b/dt) (mM·s−1)]. These findings would suggest that the decrease of Wtot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO2 (upwards) and of Wtot (downwards) during intense exercise at constant Wtot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).

Beat-by-beat \( \dot{Q} \)aO2 and breath-by-breath \( \dot{V} \)O2 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. \( \dot{Q} \)aO2 kinetics was described fitting the data with a non-linear mono-exponential model with time delay. Mean response times (MRT) of \( \dot{V} \)O2 and \( \dot{Q} \)aO2 kinetics were then calculated. DefO2 and MRT of \( \dot{V} \)O2 response did not change after HDTBR, whereas MRT of \( \dot{Q} \)aO2 kinetics increased. The invariance of \( \dot{V} \)O2 kinetics after HDTBR suggests that, although \( \dot{Q} \)aO2 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.

Time-frequency analysis of the surface electromyographic (EMG) signal is used to assess muscle fiber membrane properties during dynamic contractions. The aim of this study was to compare the direct estimation of average muscle fiber conduction velocity (CV) with instantaneous mean frequency (iMNF) of surface EMG signals in isometric and explosive dynamic contractions. The muscles investigated were the vastus lateralis and medialis of both thighs in 12 male subjects. The isometric contractions were at linearly increasing force (0-100% of the maximal voluntary contraction in 10s). The explosive contractions were performed on a multipurpose ergometer-dynamometer (MED). The subject, sitting on the MED, performed six explosive contractions, separated by 2 min rest, by pushing against two force platforms and thrusting himself backwards with the maximum possible speed, while completely extending his legs. The estimated CV significantly increased with force in both the isometric (mean+/-S.D., from 3.24+/-0.34 to 5.12+/-0.31 m/s for vastus lateralis and from 3.17+/-0.26 to 5.11+/-0.34 m/s for vastus medialis, with force in the range 10-100% of the maximal voluntary contraction level) and explosive contractions (from 4.36+/-0.49 to 5.00+/-0.47 m/s for vastus lateralis, and from 4.32+/-0.46 to 4.94+/-0.44 m/s for vastus medialis, with force in the range 17.5-100% of maximal thrusting force). Moreover, estimated CV was not significantly different at the maximal force in the two exercises. On the contrary, iMNF, computed from the Choi-Williams time-frequency transform, was significantly lower in the explosive (57.7+/-8.2 and 66.5+/-10.3 Hz for vastus laterialis and medialis, respectively) than in the isometric exercises (73.7+/-9.2 and 75.0+/-8.5 Hz for vastus laterialis and medialis, respectively) and did not change with force in any of the conditions. It was concluded that EMG spectral features provide different information with respect to average muscle fiber CV in dynamic contractions. Thus, in general, they cannot be used to infer CV changes during the exertion of a dynamic task. A joint analysis of CV and EMG spectral features is necessary in this type of contractions.

Muscle-fiber conduction velocity (CV) was estimated from surface electromyographic (EMG) signals during isometric contractions and during short (150-200 ms), explosive, dynamic exercises. Surface EMG signals were recorded with four linear adhesive arrays from the vastus lateralis and medialis muscles of 12 healthy subjects. Isometric contractions were at linearly increasing force from 0% to 100% of the maximum. The dynamic contractions consisted of explosive efforts of the lower limb on a sledge ergometer. For the explosive contractions, muscle-fiber CV was estimated in seven time-windows located along the ascending time interval of the force. There was a significant correlation between CV values during the isometric ramp and explosive contractions (R = 0.75). Moreover, CV estimates increased significantly from (mean +/- SD) 4.32 +/- 0.46 m/s to 4.97 +/- 0.45 m/s during the increasing-force explosive task. It was concluded that CV can be estimated reliably during dynamic tasks involving fast limb movements and that, in these contractions, it may provide important information on motor-unit control properties.

The beat-by-beat non-invasive assessment of cardiac output (Q˙ , litre · min−1) based on the arterial pulse pressure analysis called Modelflow® can be a very useful tool for quantifying the cardiovascular adjustments occurring in exercising humans. ˙Q was measured in nine young subjects at rest and during steady-state cycling exercise performed at 50, 100, 150 and 200 Wby using Modelflow® applied to the Portapres® non-invasive pulse wave (˙QModelflow) and by means of the open-circuit acetylene uptake (˙QC2H2 ). ˙Q values were correlated linearly (r=0.784), but Bland–Altman analysis revealed that mean ˙QModelflow − ˙QC2H2 difference (bias) was equal to 1.83 litre · min−1 with an S.D. (precision) of 4.11 litre · min−1, and 95% limits of agreement were relatively large, i.e. from −6.23 to +9.89 litre · min−1. ˙QModelflow values were then multiplied by individual calibrating factors obtained by dividing ˙QC2H2 by ˙QModelflow for each subject measured at 150 Wto obtain corrected˙Q Modelflow (˙Qcorrected) values. ˙Qcorrected values were compared with the corresponding ˙QC2H2 values, with values at 150 Wignored. Data were correlated linearly (r=0.931) and were not significantly different. The bias and precision were found to be 0.24 litre · min−1 and 3.48 litre · min−1 respectively, and 95% limits of agreement ranged from −6.58 to +7.05 litre · min−1. In conclusion, after correction by an independent method, Modelflow® was found to be a reliable and accurate procedure for measuring ˙Q in humans at rest and exercise, and it can be proposed for routine purposes.

Artificial gravity created by the astronauts themselves, without any external power supply, by pedalling on a coupled of couterrotating bicycles along the inner wall of the space module (Twin Bikes System, TBS), was previously suggested (Antonutto et al., 1991) to prevent musculo-skeletal decay and cardiovascular deconditioning during long term space flights. To investigate whether this unusual rotating environment would determine abnormal stimulations of the vestibular system due to Coriolis cross coupled accelerations, thus leading to acute motion sickness (AMS), the conditions of a rotating environment were reproduced in a human centrifuge. A cycloergometer was fixed to the arm of the centrifuge, the rotation speed of which was equal to that yielding 1 g at the feet level in the TBS (i.e. ranging from 19 to 21 RPM). The ergometer position was such that the combination of the horizontal and gravitational acceleration vectors was 1.414 at the inner ear level and was aligned along the head to feet axis. Three subjects, pedalling at 50 W on a cycloergometer during centrifuge's spinning, were asked to move the head following an AMS' provocation protocol. None of them developed any AMS symptoms. This supports the look of the TBS as tool for avoiding musculo-skeletal and cardiovascular deconditioning during long term space flights.

Maximal explosive power during two-leg jumps was measured on four sedentary subjects [mean age 43.0 (SD 10.3) years, mean height 1.74 (SD 0.04) m, mean body mass 73.5 (SD 1.3) kg] using a sledge apparatus with which both force and speed could be directly measured. Different after-loads were obtained by positioning the sledge at five different angles (SA, alpha) in respect to the horizontal so that m x g x sin alpha (where m is the sum of body mass and the mass of the sledge seat, g the acceleration due to gravity) decreased (on average) from 78% body mass at 30 degrees to 27% body mass at 10 degrees, thus simulating conditions of low gravity. The subjects were asked to jump maximally, without counter movement, starting from 70 degrees, 90 degrees, 110 degrees, and 140 degrees of knee angle (KA); the protocol being repeated at 10 degrees, 15 degrees, 20 degrees, 25 degrees and 30 degrees SA. The average (W+(mean)) power output during concentric exercise (CE) was found to decrease when the starting KA was increased, but to be unaffected by SA (i.e. by the after-load, the simulated low g). The higher values of W+(mean) were recorded at 90 degrees KA [15.01 (SD 1.46) W x kg(-1), average for all subjects at all SA]. The subjects were also asked to perform counter movement (CMJ) and rebound jumps (RE) at the same SA as for CE. In CMJ and RE maximal power outputs were also found to be unaffected by the SA; W+(mean) amounted to 16.03 (SD 0.28) W x kg(-1) in CMJ and 16.88 (SD 0.36) W x kg(-1) in RE (average for all subjects at all SA). In CE, CMJ and RE, the instantaneous force at the onset of the positive speed phase (F(i)) was found to increase linearly with SA (i.e. with increasing m x g x sin alpha), and the difference between F(i) in CMJ or RE and F(i) in CE (F(i) in CMJ minus F(i) in CE and F(i) in RE minus F(i) in CE) was unaffected by SA. This indicated that both maximal power and the elastic recoil were unaffected by simulated low g ranging from 1.71 m x s(-2) (at 10 degrees SA) to 4.91 m x s(-2) (at 30 degrees SA).

The maximal explosive power during a two legs jump was measured on four competitive athletes [mean age 24 (SD 4.3) years; height 1.79 (SD 0.09) m; body mass 68.7 (SD 12.8) kg] at different starting knee angles (70, 90, 110, 130 and 150°). The experiments were performed on a newly developed instrument with which both force and speed could be measured using a force platform and a wire tachometer, respectively, and on a conventional force platform. At the smallest knee angle (70°) the mean power output ( $\bar\dot W$ in watts per kilogram) developed during the jump was found not to differ significantly between the two methods (P > 0.1). At the larger knee angles $\bar \dot W$ was 18.4% (90°), 34.5% (110°), 47.4% (130°) and 19.4% (150°) higher using the conventional force platform (P

1. The effects of bed rest on the cardiovascular and muscular parameters which affect maximal O2 consumption (VO2,max) were studied. The fractional limitation of VO2,max imposed by these parameters after bed rest was analysed. 2. The VO2,max, by standard procedure, and the maximal cardiac output (Qmax), by the pulse contour method, were measured during graded cyclo-ergometric exercise on seven subjects before and after a 42-day head-down tilt bed rest. Blood haemoglobin concentration ([Hb]) and arterialized blood gas analysis were determined at the highest work load. 3. Muscle fibre types, oxidative enzyme activities, and capillary and mitochondrial densities were measured on biopsy samples from the vastus lateralis muscle before and at the end of bed rest. The measure of muscle cross-sectional area (CSA) by NMR imaging at the level of biopsy site allowed computation of muscle oxidative capacity and capillary length. 4. The VO2,max was reduced after bed rest (-16.6%). The concomitant decreases in Qmax (-30.8%), essentially due to a change in stroke volume, and in [Hb] led to a huge decrease in O2 delivery (-39.7%). 5. Fibre type distribution was unaffected by bed rest. The decrease in fibre area corresponded to the significant reduction in muscle CSA (-17%). The volume density of mitochondria was reduced after bed rest (-16.6%), as were the oxidative enzyme activities (-11%). The total mitochondrial volume was reduced by 28.5%. Capillary density was unchanged. Total capillary length was 22.2% lower after bed rest, due to muscle atrophy. 6. The interaction between these muscular and cardiovascular changes led to a smaller reduction in VO2,max than in cardiovascular O2 transport. Yet the latter appears to play the greatest role in limiting VO2,max after bed rest (> 70% of overall limitation), the remaining fraction being shared between peripheral O2 diffusion and utilization.

The stroke volume of the left ventricle (SV) was calculated from noninvasive recordings of the arterial pressure using a finger photoplethysmograph and compared to the values obtained by pulsed Doppler echocardiography (PDE). A group of 19 healthy men and 12 women [mean ages: 20.8 (SD 1.6) and 22.2 (SD 1.6) years respectively] were studied at rest in the supine position. The ratio of the area below the ejection phase of the arterial pressure wave (A(s)) to SV, as obtained by PDE, yielded a "calibration factor" dimensionally equal to the hydraulic impedance of the system (Zao = A(s).SV-1). The Zao amounted on average to 0.062 (SD 0.018) mmHg.s.cm-3 for the men and to 0.104 (SD 0.024) mmHg.s.cm-3 for the women. The Zao was also estimated from the equation: Zao = a.(d + b.HR + c.PP + e.MAP)-1, where HR was the heart rate, PP the pulse pressure, MAP the mean arterial pressure and the coefficients of the equation were obtained by an iterating statistical package. The value of Zao thus obtained allowed the calculation of SV from measurements derived from the photoplethysmograph only. The mean percentage error between the SV thus obtained and those experimentally determined by PDE amounted to 14.8 and 15.6 for the men and the women, respectively. The error of the estimate was reduced to 12.3 and to 11.1, respectively, if the factor Zao, experimentally obtained from a given heart beat, was subsequently applied to other beats to obtain SV from the A(s) measurement in the same subject.

Venous blood lactate concentration ([La]b) was measured in five male subjects (age: 30-50 years; BW: 72-84 kg, VO2max:2.2-3.6 l min-1) during cycloergometric exercise in microgravity obtained by parabolic flight maneuvers of approximately 25 s duration. The subject(s) exercised at 30, 60, 90 and 120 W (60 RPM) for at least 7 min at each intensity. Three consecutive parabolas with approximately 3 min interval were performed at each workload. [La]b was determined at rest and immediately after 60, 90 and 120 W exercise. The day after the flight experiments, the subject(s) underwent the same experimental protocol on the ground and the blood samples were taken at the very same time intervals as on the aircraft. [La]b in flight and control didn't show any appreciable difference once the values are plotted as a function of the relative exercise intensities expressed as a percent of the individual VO2max corrected for the moderate hypoxia prevailing inside the aircraft (cabin barometric pressure = 590 mmHg).

Oxygen consumption (VO2) and blood lactate concentration were determined during constant-speed track running on 16 runners of intermediate level competing in middle distances (0.8-5.0 km). The energy cost of track running per unit distance (Cr) was then obtained from the ratio of steady-state VO2, corrected for lactate production, to speed; it was found to be independent of speed, its overall mean being 3.72 +/- 0.24 J.kg-1 x m-1 (n = 58; 1 ml O2 = 20.9 J). Maximal VO2 (VO2max) was also measured on the same subjects. Theoretical record times were then calculated for each distance and subject and compared with actual seasonal best performances as follows. The maximal metabolic power (Er max) a subject can maintain in running is a known function of VO2max and maximal anaerobic capacity and of the effort duration to exhaustion (te). Er max was then calculated as a function of te from VO2max, assuming a standard value for maximal anaerobic capacity. The metabolic power requirement (Er) necessary to cover a given distance (d) was calculated as a function of performance time (t) from the product Crdt-1 = Er. The time values that solve the equality Er max(te) = Er(t), assumed to yield the theoretical best t, were obtained by an iterative procedure for any given subject and distance and compared with actual records.(ABSTRACT TRUNCATED AT 250 WORDS)

The maximal power of the lower limbs was determined in four astronauts (age 37-53 yr) 1) during maximal pushes of approximately 250 ms on force platforms ["maximal explosive power" (MEP)] or 2) during all-out bouts of 6-7 s on an isokinetic cycloergometer [pedal frequency 1 Hz: maximal cycling power (MCP)]. The measurements were done before and immediately after spaceflights of 31-180 days. Before flight, peak and mean values were 3.18 +/- 0.38 and 1.5 +/- 0. 13 (SD) kW for MEP and 1.17 +/- 0.12 and 0.68 +/- 0.08 kW for MCP, respectively. After reentry, MEP was reduced to 67% after 31 days and to 45% after 180 days. MCP decreased less, attaining approximately 75% of preflight level, regardless of the flight duration. The recovery of MCP was essentially complete 2 wk after reentry, whereas that of MEP was slower, a complete recovery occurring after an estimated time close to that spent in flight. In the same subjects, the muscle mass of the lower limbs, as assessed by NMR, decreased by 9-13%, irrespective of flight duration (J. Zange, K. Müller, M. Schuber, H. Wackerhage, U. Hoffmann, R. W. G unther, G. Adam, J. M. Neuerburg, V. E. Sinitsyn, A. O. Bacharev, and O. I. Belichenko. Int. J. Sports Med. 18, Suppl. 4: S308-S309, 1997). The larger fall in maximal power, compared with that in muscle mass, suggests that a fraction of the former (especially relevant for MEP) is due to the effects of weightlessness on the motor unit recruitment pattern.