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Purpose: The three-parameter model of critical power (3-p) implies that in the severe exercise intensity domain time to exhaustion (Tlim) decreases hyperbolically with power output starting from the power asymptote (critical power, ẇcr) and reaching 0 s at a finite power limit (ẇ0) thanks to a negative time asymptote (k). We aimed to validate 3-p for short Tlim and to test the hypothesis that ẇ0 represents the maximal instantaneous muscular power.Methods: Ten subjects performed an incremental test and nine constant-power trials to exhaustion on an electronically braked cycle ergometer. All trials were fitted to 3-p by means of non-linear regression, and those with Tlim greater than 2 min also to the 2-parameter model (2-p), obtained constraining k to 0 s. Five vertical squat jumps on a force platform were also performed to determine the single-leg (i.e., halved) maximal instantaneous power.Results: Tlim ranged from 26 ± 4 s to 15.7 ± 4.9 min. In 3-p, with respect to 2-p, ẇcr was identical (177 ± 26 W), while curvature constant W' was higher (17.0 ± 4.3 vs 15.9 ± 4.2 kJ, p < 0.01). 3-p-derived ẇ0 was lower than single-leg maximal instantaneous power (1184 ± 265 vs 1554 ± 235 W, p < 0.01).Conclusions: 3-p is a good descriptor of the work capacity above ẇcr up to Tlim as short as 20 s. However, since there is a discrepancy between estimated ẇ0 and measured maximal instantaneous power, a modification of the model has been proposed.

We hypothesized that during rapid uptilting at rest, due to vagal withdrawal, arterial baroreflex sensitivity (BRS) may decrease promptly and precede the operating point (OP) resetting, whereas different kinetics are expected during exercise steady state, due to lower vagal activity than at rest. To test this, eleven subjects were rapidly (−1 (SD = 17.1) in S and 16.7 ms·mmHg−1 (SD = 6.4) in U ( P < 0.01), RRi was 901 ms (SD = 118) in S and 749 ms (SD = 98) in U ( P < 0.01), and MAP was 76 mmHg (SD = 11) in S and 83 mmHg (SD = 8) in U ( P < 0.01). During uptilt, BRS decreased promptly [first BRS sequence was 19.7 ms·mmHg−1 (SD = 5.0)] and was followed by an OP resetting (MAP increase without changes in RRi). At exercise, BRS and OP did not differ between supine and upright positions [BRS was 7.7 ms·mmHg−1 (SD = 3.0) and 7.7 ms·mmHg−1 (SD = 3.5), MAP was 85 mmHg (SD = 13) and 88 mmHg (SD = 10), and RRi was 622 ms (SD = 61) and 600 ms (SD = 70), respectively]. The results support the tested hypothesis. The prompt BRS decrease during uptilt at rest may be ascribed to a vagal withdrawal, similarly to what occurs at exercise onset. The OP resetting may be due to a slower control mechanism, possibly an increase in sympathetic activity.

New findings What is the central question of this study? We modelled the alveolar pathway during breath holding on the hypothesis that it follows a hypoventilation loop on the O2 -CO2 diagram. What is the main finding and its importance? Validation of the model was possible within the range of alveolar gas compositions compatible with consciousness. Within this range, the experimental data were compatible with the proposed model. The model and its characteristics might allow predictions of alveolar gas composition whenever the alveolar ventilation goes to zero; for example, static and dynamic breath holding at the surface or during ventilation/intubation failure in anaesthesia. Abstract According to the hypothesis that alveolar partial pressures of O2 and CO2 during breath holding (BH) should vary following a hypoventilation loop, we modelled the alveolar gas pathways during BH on the O2 -CO2 diagram and tested it experimentally during ambient air and pure oxygen breathing. In air, the model was constructed using the inspired and alveolar partial pressures of O2 ( P I O 2 and P A O 2 , respectively) and CO2 ( P IC O 2 and P AC O 2 , respectively) and the steady-state values of the pre-BH respiratory exchange ratio (RER). In pure oxygen, the model respected the constraint of P AC O 2 = - P A O 2 + P I O 2 . To test this, 12 subjects performed several BHs of increasing duration and one maximal BH at rest and during exercise (30 W cycling supine), while breathing air or pure oxygen. We measured gas flows, P A O 2 and P AC O 2 before and at the end of all BHs. Measured data were fitted through the model. In air, P I O 2 = 150 ± 1 mmHg and P IC O 2 = 0.3 ± 0.0 mmHg, both at rest and at 30 W. Before BH, steady-state RER was 0.83 ± 0.16 at rest and 0.77 ± 0.14 at 30 W; P A O 2 = 107 ± 7 mmHg at rest and 102 ± 8 mmHg at 30 W; and P AC O 2 = 36 ± 4 mmHg at rest and 38 ± 3 mmHg at 30 W. By model fitting, we computed the RER during the early phase of BH: 0.10 [95% confidence interval (95% CI) = 0.08-0.12] at rest and 0.13 (95% CI = 0.11-0.15) at 30 W. In oxygen, model fitting provided P I O 2 : 692 (95% CI = 688-696) mmHg at rest and 693 (95% CI = 689-698) mmHg at 30 W. The experimental data are compatible with the proposed model, within its physiological range.

Purpose We analysed the characteristics of arterial baroreflexes during the first phase of apnoea (φ1). Methods 12 divers performed rest and exercise (30 W) apnoeas (air and oxygen). We measured beat-by-beat R-to-R interval (RRi) and mean arterial pressure (MAP). Mean RRi and MAP values defined the operating point (OP) before (PRE-ss) and in the second phase (φ2) of apnoea. Baroreflex sensitivity (BRS, ms·mmHg−1) was calculated with the sequence method. Results In PRE-ss, BRS was (median [IQR]): at rest, 20.3 [10.0–28.6] in air and 18.8 [13.8–25.2] in O2; at exercise 9.2[8.4–13.2] in air and 10.1[8.4–13.6] in O2. In φ1, during MAP decrease, BRS was lower than in PRE-ss at rest (6.6 [5.3–11.4] in air and 7.7 [4.9–14.3] in O2, p 2. After attainment of minimum MAP (MAPmin), baroreflex resetting started. After attainment of minimum RRi, baroreflex sequences reappeared. In φ2, BRS at rest was 12.1 [9.6–16.2] in air, 12.9 [9.2–15.8] in O2. At exercise (no φ2 in air), it was 7.9 [5.4–10.7] in O2. In φ2, OP acts at higher MAP values. Conclusion In apnoea φ1, there is a sudden correction of MAP fall via baroreflex. The lower BRS in the earliest φ1 suggests a possible parasympathetic mechanism underpinning this reduction. After MAPmin, baroreflex resets, displacing its OP at higher MAP level; thus, resetting may not be due to central command. After resetting, restoration of BRS suggests re-establishment of vagal drive.

We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.

To check whether the evolution of alveolar pressures of O2 (PAO2) and CO2 (PACO2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O2. We measured heart rate (fH), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, PAO2 and PACO2 at the end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O2, TPR increase (9 ± 4 mmHg min l−1) and fH decrease (-11 ± 8 bpm) were lower than in air (15 ± 5 mmHg min l−1 and -28 ± 13 bpm, respectively). At end of maximal apnoeas in air, PAO2 and PACO2 were 50 ± 9 and 48 ± 5 mmHg, respectively; corresponding values in O2 were 653 ± 8 mmHg and 55 ± 5 mmHg. At end of phase II, PAO2 and PACO2 in air were 90 ± 13 mmHg and 42 ± 4 mmHg respectively; corresponding values in O2 were 669 ± 7 mmHg and 47 ± 6 mmHg. The PACO2 increase may trigger the AP rise in phase III.

If, as postulated, the end of the steady state phase (φ2) of cardiovascular responses to apnoea corresponds to the physiological breaking point, then we may hypothesize that φ2 should become visible if exercise apnoeas are performed in pure oxygen. We tested this hypothesis on 9 professional divers by means of continuous recording of blood pressure (BP), heart rate (fH), stroke volume (QS), and arterial oxygen saturation (SpO2) during dry maximal exercising apnoeas in ambient air and in oxygen. Apnoeas lasted 45.0 ± 16.9 s in air and 77.0 ± 28.9 s in oxygen (p

Introduction We tested the hypothesis that the alveolar gas composition at the transition between the steady phase II (φ2) and the dynamic phase III (φ3) of the cardiovascular response to apnoea may lay on the physiological breaking point curve (Lin et al., 1974). Methods Twelve elite divers performed maximal and φ2-interrupted apnoeas, in air and pure oxygen. We recorded beat-by-beat arterial blood pressure and heart rate; we measured alveolar oxygen and carbon dioxide pressures (P A O 2 and P A CO 2 , respectively) before and after apnoeas; we calculated the P A CO 2 difference between the end and the beginning of apnoeas (ΔP A CO 2 ). Results Cardiovascular responses to apnoea were similar compared to previous studies. P A O 2 and P A CO 2 at the end of φ2-interrupted apnoeas, corresponded to those reported at the physiological breaking point . For maximal apnoeas, P A CO 2 was less than reported by Lin et al. (1974). ΔP A CO 2 was higher in oxygen than in air. Conclusions The transition between φ2 and φ3 corresponds indeed to the physiological breaking point . We attribute this transition to ΔP A CO 2 , rather than the absolute P A CO 2 values, both in air and oxygen apnoeas.

PURPOSE: The dynamics of the postulated phenomenon of exercise baroreflex resetting is poorly understood, but can be investigated using closed-loop procedures. To shed light on some mechanisms and temporal relationships participating in the resetting process, we studied the time course of the relationship between the R-R interval (RRi) and arterial pressure with a closed-loop approach. METHODS: On ten young volunteers at rest and during light exercise in supine and upright position, we continuously determined, on single-beat basis, RRi (electrocardiography), and arterial pressure (non-invasive finger pressure cuff). From pulse pressure profiles, we determined cardiac output (CO) by Modelflow, computed mean arterial pressure (MAP), and calculated total peripheral resistance (TPR). RESULTS: At exercise start, RRi was lower than in quiet rest. As exercise started, MAP fell to a minimum (MAPm) of 72.8 ± 9.6 mmHg upright and 73.9 ± 6.2 supine, while RRi dropped. The initial RRi versus MAP relationship was linear, with flatter slope than resting baroreflex sensitivity, in both postures. TPR fell and CO increased. After MAPm, RRi and MAP varied in opposite direction toward exercise steady state, with further CO increase. CONCLUSION: These results suggest that, initially, the MAP fall was corrected by a RRi reduction along a baroreflex curve, with lower sensitivity than at rest, but eventually in the same pressure range as at rest. After attainment of MAPm, a second phase started, where the postulated baroreflex resetting might have occurred. In conclusion, the change in baroreflex sensitivity and the resetting process are distinct phenomena, under different control systems.

We hypothesised that phase II time constant (τ2) of alveolar O2 uptake ( [Formula: see text] ) is longer in hypoxia than in normoxia as a consequence of a parallel deceleration of the kinetics of O2 delivery ( [Formula: see text] ). To test this hypothesis, breath-by-breath [Formula: see text] and beat-by-beat [Formula: see text] were measured in eight male subjects (25.4±3.4yy, 1.81±0.05m, 78.8±5.7kg) at the onset of cycling exercise (100W) in normoxia and acute hypoxia ( [Formula: see text] ). Blood lactate ([La]b) accumulation during the exercise transient was also measured. The τ2 for [Formula: see text] was shorter than that for [Formula: see text] in normoxia (8.3±6.8s versus 17.8±3.1s), but not in hypoxia (31.5±21.7s versus 28.4 5.4±5.4s). [La]b was increased in the exercise transient in hypoxia (3.0±0.5mM at exercise versus 1.7±0.2mM at rest), but not in normoxia. We conclude that the slowing down of the [Formula: see text] kinetics generated the longer τ2 for [Formula: see text] in hypoxia, with consequent contribution of anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in [La]b.

The aim of this study was to test the hypothesis that the maximal instantaneous muscular power of humans ( $$ \dot{w} $$ p) is affected by the negative work performed immediately before the jump (w n), possibly due to the recoil of elastic strain energy stored in previously stretched series-elastic elements of the muscle–tendon complex. Twenty-seven Bantu subjects (age 25.1 ± 4.3 years, body mass 67.5 ± 7.8 kg) were investigated. The $$ \dot{w} $$ p, the average power ( $$ \dot{w} $$ a) and w n were determined during maximal vertical jumps off both feet on a force platform. Three jumping conditions were studied: squat jumps (SQ), countermovement jumps (CM), and jumps preceded by a free fall (FF) from a height of 0.3 m above the platform surface. The w n was higher in CM than in SQ and in FF than in CM and SQ. The $$ \dot{w} $$ p was 3.51 ± 0.54 kW in SQ and did not vary in CM and FF. The $$ \dot{w} $$ a increased with increasing w n (1.70 ± 0.30; 1.85 ± 0.34; 1.99 ± 0.31 kW in SQ, CM and FF, respectively, p

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.

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.

We tested whether the kinetics of systemic O2 delivery (Q̇aO2) at exercise start was faster than that of lung O2 uptake (V̇o2), being dictated by that of cardiac output (Q̇), and whether changes in Q̇ would explain the postulated rapid phase of the V̇o2 increase. Simultaneous determinations of beat-by-beat (BBB) Q̇ and Q̇aO2, and breath-by-breath V̇o2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 ± 3.2 years, maximal aerobic power 333 ± 61 W). V̇o2 was determined using Grønlund's algorithm. Q̇ was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate ( fh, electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q̇aO2. The Q̇, Q̇aO2 and V̇o2 kinetics were analyzed with single and double exponential models. fh, Qst, Q̇, and V̇o2 increased upon exercise onset to reach a new steady state. The kinetics of Q̇aO2 had the same time constants as that of Q̇. The latter was twofold faster than that of V̇o2. The V̇o2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q̇ changes fully explained the phase I of V̇o2 increase. We suggest that in unsteady states, lung V̇o2 is dissociated from muscle O2 consumption. The two components of Q̇ and Q̇aO2 kinetics may reflect vagal withdrawal and sympathetic activation.

Interpolation methods circumvent poor time resolution of breath-by-breath oxygen uptake ( $$\dot{V}{\text{O}}_{2}$$ ) kinetics at exercise onset. We report an interpolation-free approach to the improvement of poor time resolution in the analysis of $$\dot{V}{\text{O}}_{2}$$ kinetics. Noiseless and noisy (10 % Gaussian noise) synthetic data were generated by Monte Carlo method from pre-selected parameters (Exact Parameters). Each data set comprised 10 ( $$\dot{V}{\text{O}}_{2}$$ )-on transitions with noisy breath distribution within a physiological range. Transitions were superposed (no interpolation, None), then analysed by bi-exponential model. Fitted model parameters were compared with those from interpolation methods (average transition after Linear or Step 1-s interpolations), applied on the same data. Experimental data during cycling were also analysed. The 95 % confidence interval around a line of parameters’ equality was computed to analyse agreement between exact parameters and corresponding parameters of fitted functions. The line of parameters’ equality stayed within confidence intervals for noiseless synthetic parameters with None, unlike Step and Linear, indicating that None reproduced Exact Parameters. Noise addition reduced differences among pre-treatment procedures. Experimental data provided lower phase I time constants with None than with Step. In conclusion, None revealed better precision and accuracy than Step and Linear, especially when phenomena characterized by time constants of

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.

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.

Morton (J Sport Sci 29:307–309, 2011) proposed a model of the peak power attained in ramp protocol ( $$\dot{w}_{\text{peak}}$$ ) that included critical power (CP) and anaerobic capacity as constants, and mean ramp slope (S) as variable. Our hypothesis is that $$\dot{w}_{\text{peak}}$$ depends only on S, so that Morton’s model should be applicable in all types of ramps. The aim of this study was to test this hypothesis by validating Morton’s model using stepwise ramp tests with invariant step increment and increasing step duration. Sixteen men performed six ramp tests with 25 W increments. Step duration was: 15, 30, 60, 90, 120 and 180 s. Maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ ) and $$\dot{w}_{\text{peak}}$$ were identified as the highest values reached during each test. An Astrand-type test was also performed. We measured oxygen consumption and ventilatory variables, together with lactate and heart rate. $$\dot{V}{\text{O}}_{2\hbox{max} }$$ was the same in all tests; $$\dot{w}_{\text{peak}}$$ was significantly lower the longer the step duration, and all values differed from the maximal power of the Astrand-type test ( $$\dot{w}_{\hbox{max} }$$ ). Morton’s model yielded an excellent fitting, with mean CP equal to 198.08 ± 37.46 W and anaerobic capacity equal to 16.82 ± 5.69 kJ. Morton’s model is a good descriptor of the mechanics of ramp tests. Further developments of Morton’s model demonstrated that, whereas $$\dot{w}_{\text{peak}}$$ is a protocol-dependent variable, the difference between $$\dot{w}_{\hbox{max} }$$ and CP is a constant, so that their values do not depend on the protocol applied.

To define the dynamics of cardiovascular adjustments to apnoea during immersion, beat-to-beat heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures were recorded in six divers during and after prolonged apnoeas while resting fully immersed in 27 degrees C water. Apnoeas lasted 215 +/- 35 s. Compared to control values, HR decreased by 20 beats min(-1) and SBP and DBP increased by 23 and 17 mmHg, respectively, in the initial 20 +/- 3 s (phase I). Both HR and BP remained stable during the following 92 +/- 15 s (phase II). Subsequently, during the final 103 +/- 29 s, SBP and DBP increased linearly to values about 60% higher than control, whereas HR remained unchanged (phase III). Cardiac output (Q') decreased by 35% in phase I and did not further change in phases II and III. Compared to control, total peripheral resistances were twice and three times higher than control, respectively, at the end of phases I and III. After resumption of breathing, HR and BP returned to control values in 5 and 30 s, respectively. The time courses of cardiovascular adjustments to immersed breath-holding indicated that cardiac response took place only at the beginning of apnoea. In contrast, vascular responses showed two distinct adjustments. This pattern suggests that the chronotropic control via the baroreflex is modified during apnoea. These cardiovascular changes during immersed static apnoea are in agreement with those already reported for static dry apnoeas.

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.

To define the dynamics of cardiovascular adjustments to apnoea, beat-to-beat heart rate (HR) and blood pressure and arterial oxygen saturation (SaO(2)) were recorded during prolonged breath-holding in air in 20 divers. Apnoea had a mean duration of 210 +/- 70 s. In all subjects, HR attained a value 14 beats min(-1) lower than control within the initial 30 s (phase I). HR did not change for the following 2-2.5 min (phase II). Then, nine subjects interrupted the apnoea (group A), whereas 11 subjects (group B) could prolong the breath-holding for about 100 s, during which HR continuously decreased (phase III). In both groups, mean blood pressure was 8 mmHg above control at the end of phase I; it then further increased by additional 12 mmHg at the end of the apnoea. In both groups, SaO(2) did not change in the initial 100-140 s of apnoea; then, it decreased to 95% at the end of phase II. In group B, SaO(2) further diminished to 84% at the end of phase III. A typical pattern of cardiovascular readjustments was identified during dry apnoea. This pattern was not compatible with a role for baroreflexes in phase I and phase II. Further readjustment in group B may imply a role for both baroreflexes and chemoreflexes. Hypothesis has been made that the end of phase II corresponds to physiological breakpoint.

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 ± 3.4 yr, 82.1 ± 13.7 kg, maximal aerobic power 330 ± 67 W), we determined beat-by-beat cardiac output (Q̇), oxygen delivery (Q̇aO2), and breath-by-breath lung oxygen uptake (V̇o2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2 = 0.11), because the latter reduces resting vagal activity. We computed Q̇ from stroke volume (Qst, by model flow) and heart rate ( fH, electrocardiography), and Q̇aO2 from Q̇ and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q̇ were higher, and Qst and V̇o2 were unchanged. Q̇aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V̇o2 was unchanged. For fH, Q̇ and Q̇aO2, A1 was lower. Phase I time constant (τ1) for Q̇aO2 and V̇o2 was unchanged. The same was the case for Q̇ at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q̇ and Q̇aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

At exercise steady state, the lower the arterial oxygen saturation (SaO2), the lower the O2 return $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2}).$$ A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective β1-adrenergic blockade (BB) would reduce O2 delivery $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} )$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} .$$ To test this hypothesis, we studied the effects of BB on $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2}$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ in exercising humans in normoxia and hypoxia. O2 consumption $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ),$$ cardiac output $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}, CO_{2}\; \hbox{rebreathing}),$$ heart rate, SaO2 and haemoglobin concentration were measured on six subjects (age 25.5±2.4years, mass 78.1±9.0kg) in normoxia and hypoxia (inspired O2 fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150W without (C) and with BB with metoprolol. Arterial O2 concentration (CaO2), $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2},$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each $$\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ,$$ $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}$$ was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO2 and CaO2 were unaffected by BB. The $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} $$ changes under BB were parallel to those in $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}.$$ $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ was unaffected by exercise in normoxia. In hypoxia the slope of the relationship between $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} $$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} $$ was lower than 1, indicating a reduction of $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ with increasing workload. $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ was a linear function of SaO2 both in C and in BB. The line for BB was flatter than and below that for C. The resting $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ in normoxia, lower than the corresponding exercise values, lied on the BB line. These results agree with the tested hypothesis. The two observed relationships between $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ and SaO2 apply to conditions of predominant sympathetic or vagal activation, respectively. Moving from one line to the other implies resetting of the cardiovascular regulation

Modelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q˙ , litre · min−1). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q˙ .We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q˙ with Modelflow®, so we compared Modelflow® beat-by-beat ˙Q values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0+−2.9 years; weight, 81.2+−12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent ˙Q computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly (P

The costs of walking (Cw) and running (Cr) were measured on 10 runners on a treadmill inclined between −0.45 to +0.45 at different speeds. The minimum Cw was 1.64 ± 0.50 J · kg−1· m−1at a 1.0 ± 0.3 m/s speed on the level. It increased on positive slopes, attained 17.33 ± 1.11 J · kg−1· m−1at +0.45, and was reduced to 0.81 ± 0.37 J · kg−1· m−1at −0.10. At steeper slopes, it increased to reach 3.46 ± 0.95 J · kg−1· m−1at −0.45. Cr was 3.40 ± 0.24 J · kg−1· m−1on the level, independent of speed. It increased on positive slopes, attained 18.93 ± 1.74 J · kg−1· m−1at +0.45, and was reduced to 1.73 ± 0.36 J · kg−1· m−1at −0.20. At steeper slopes, it increased to reach 3.92 ± 0.81 J · kg−1· m−1at −0.45. The mechanical efficiencies of walking and running above +0.15 and below −0.15 attained those of concentric and eccentric muscular contraction, respectively. The optimum gradients for mountain paths approximated 0.20–0.30 for both gaits. Downhill, Cr was some 40% lower than reported in the literature for sedentary subjects. The estimated maximum running speeds on positive gradients corresponded to those adopted in uphill races; on negative gradients they were well above those attained in downhill competitions.

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

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, ifW˙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 theW˙p loss after BR.

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.

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.

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.

Maximal O2 consumption ( $$\dot V_{O_{_2 max} } $$ 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 149 to 226 and from 84 to 131 min, respectively. $$\dot V_{O_{_2 max} } $$ was significantly (2p