Limiting factors to oxygen transport on Mount Everest 30years after: a critique of Paolo Cerretelli's contribution to the study of altitude physiology

In 1976, Paolo Cerretelli published an article entitled "Limiting factors to oxygen transport on Mount Everest” in the Journal of Applied Physiology . The paper demonstrated the role of cardiovascular oxygen transport in limiting maximal oxygen consumption (V̇O2max). In agreement with the predominant view of V̇O2max limitation at that time, however, its results were taken to mean that cardiovascular oxygen transport does not limit V̇O2max at altitude. So it was argued that the limiting factor could be in the periphery, and muscle blood flow was proposed as a possible candidate. Despite this suggestion, the conclusion generated a series of papers on muscle structural characteristics. These experiments demonstrated a loss of muscle oxidative capacity in chronic hypoxia, and thus provided an unambiguous refutation of the then widespread hypothesis that an increased muscle oxidative capacity is needed at altitude to compensate for the lack of oxygen. This analysis is followed by a short account of Cerretelli's more recent work, with a special attention to the subject of the so-called "lactate paradox

An analysis of performance in human locomotion

This paper reports an analysis of the principles underlying human performances on the basis of the work initiated by Pietro Enrico di Prampero. Starting from the concept that the maximal speed that can be attained over a given distance with a given locomotion mode is directly proportional to the maximal sustainable power and inversely proportional to the energy cost of locomotion, we discuss the maximal powers (and capacities) of anaerobic (lactic and alactic) and aerobic metabolisms and the factors that limit them, and the factors affecting the energy cost of various locomotion modes. Special attention is given to the role of air resistance and frictional forces. Finally, computation of performance speed is discussed along the approach originally developed by di Pramper

Maximal oxygen consumption in healthy humans: theories and facts

This article reviews the concept of maximal oxygen consumption ( $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max ) from the perspective of multifactorial models of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation. First, I discuss procedural aspects of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max measurement: the implications of ramp protocols are analysed within the theoretical work of Morton. Then I analyse the descriptive physiology of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max , evidencing the path that led to the view of monofactorial cardiovascular or muscular $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation. Multifactorial models, generated by the theoretical work of di Prampero and Wagner around the oxygen conductance equation, represented a radical change of perspective. These models are presented in detail and criticized with respect to the ensuing experimental work. A synthesis between them is proposed, demonstrating how much these models coincide and converge on the same conclusions. Finally, I discuss the cases of hypoxia and bed rest, the former as an example of the pervasive effects of the shape of the oxygen equilibrium curve, the latter as a neat example of adaptive changes concerning the entire respiratory system. The conclusion is that the concept of cardiovascular $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation is reinforced by multifactorial models, since cardiovascular oxygen transport provides most of the $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation, at least in normoxia. However, the same models show that the role of peripheral resistances is significant and cannot be neglected. The role of peripheral factors is greater the smaller is the active muscle mass. In hypoxia, the intervention of lung resistances as limiting factors restricts the role played by cardiovascular and peripheral factors

NOTA SUI LIMITI FISIOLOGICI DELLE IMMERSIONI PROFONDE IN APNEA

This article discusses the limits of deep breath-hold diving in humans. After a short historical introduction and a discussion of the evolution of depth records, the classical theories of breath-hold diving limits are presented and discussed, namely that of the ratio between total lung capacity and residual volume and that of blood shift, implying an increase in central blood volume. Then the current vision is introduced, based on the principles of the energetics of muscular exercise. The new vision has turned the classical vision upside down, moving the discussion to a different level. A direct consequence of the new theory is the importance of having large lung volumes at the start of a dive, in order to increase body oxygen stores. I finally discuss the role of anaerobic lactic metabolism as a possible mechanism of oxygen preservation, thus prolonging breath-hold duration

Coordination complexes of niobium and tantalum pentahalides with a bulky NHC ligand

The 1 : 1 molar reactions of niobium and tantalum pentahalides with the monodentate NHC ligand 1,3-bis(2,6-diisopropylphenyl)imidazol-2-ylidene (Ipr), in toluene (or benzene) at ca. 80 °C, afforded the complexes NbX5(Ipr) (X = F, 2; Br, 3) and TaX5(Ipr) (X = F, 4; Cl, 5; Br, 6), in generally good yields. Complexes 2–6 represent uncommon cases of stable NHC adducts of metal halides with the metal in an oxidation state higher than +4, and also rare examples of Nb–NHC and Ta–NHC bonding systems. In particular, the X-ray molecular structure determined for 6 provides the unprecedented crystallographic characterization of a tantalum compound with a monodentate NHC ligand. DFT results indicate that the metal–carbon bond in 2–6 is a purely σ one. According to NMR studies (1H, 13C, 93Nb), the formation of 3, 5, 6, as well as the previously communicated NbCl5(Ipr), 1, proceeded with the intermediacy of [MX6]− salts, presumably due to steric reasons. On the other hand, the intermediate formation of MF6− in the pathways to 2 and 4 was not observed, according to 19F (and 93Nb in the case of 2) NMR. DFT calculations were carried out in order to shed light on structural and mechanistic aspects, and allowed to trace possible reaction routes

Lung volumes of extreme breath-hold divers

Achievements in breath-hold diving depend, amongst others, on body oxygen stores at start of dive. A diver with very high lung volumes could increase dive's duration, and attain deeper depths for a given speed. Thus, we hypothesized that extreme breath-hold divers have very high lung volumes. On eight extreme breathhold divers (age 35 + 4 years, height 179 + 7 cm, body mass 76 + 6 kg) and 9 non-diving controls (age 37 + 6 years, height 177 + 4 cm, body mass 81 + 9 kg) residual volume, vital capacity and total lung capacity (TLC) were measured with a body plethysmograph. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were measured with a spirometer. Peak expiratory flow and flow-volume loops were measured with a pneumotachograph. In divers, but not in controls, volumes and capacities were systematically and significantly (p<0.01, paired t-test) higher than predicted from their body size. Consistently, volumes and capacities were significantly higher in divers than in controls, except for residual volume. Divers' TLC was 22% higher than predicted, and 21% higher than in controls. All divers' TLC was higher than 8 L, two had it higher than 9 L. FVC and FEV1 were significantly higher in divers than in controls. The FEV1/FVC ratio was the same in both groups. We conclude that extreme breath-hold divers may constitute a niche population with physiological characteristics different from those of normal individuals, facilitating the achievement of excellent diving performance

Modeling the Power-Duration Relationship in Professional Cyclists During the Giro d'Italia

Vinetti, G, Pollastri, L, Lanfranconi, F, Bruseghini, P, Taboni, A, and Ferretti, G. Modeling the power-duration relationship in professional cyclists during the Giro d'Italia. J Strength Cond Res XX(X): 000-000, 2022-Multistage road bicycle races allow the assessment of maximal mean power output (MMP) over a wide spectrum of durations. By modeling the resulting power-duration relationship, the critical power (CP) and the curvature constant (W') can be calculated and, in the 3-parameter (3-p) model, also the maximal instantaneous power (P0). Our aim is to test the 3-p model for the first time in this context and to compare it with the 2-parameter (2-p) model. A team of 9 male professional cyclists participated in the 2014 Giro d'Italia with a crank-based power meter. The maximal mean power output between 10 seconds and 10 minutes were fitted with 3-p, whereas those between 1 and 10 minutes with the 2- model. The level of significance was set at p &lt; 0.05. 3-p yielded CP 357 ± 29 W, W' 13.3 ± 4.2 kJ, and P0 1,330 ± 251 W with a SEE of 10 ± 5 W, 3.0 ± 1.7 kJ, and 507 ± 528 W, respectively. 2-p yielded a CP and W' slightly higher (+4 ± 2 W) and lower (-2.3 ± 1.1 kJ), respectively (p &lt; 0.001 for both). Model predictions were within ±10 W of the 20-minute MMP of time-trial stages. In conclusion, during a single multistage racing event, the 3-p model accurately described the power-duration relationship over a wider MMP range without physiologically relevant differences in CP with respect to 2-p, potentially offering a noninvasive tool to evaluate competitive cyclists at the peak of training

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

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 regulatio

Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.

We tested whether the kinetics of systemic O2 delivery (Q'aO2) at exercise start was faster than that of lung O2 uptake (V' O2), being dictated by that of cardiac output (Q'), and whether changes in Q' would explain the postulated rapid phase of the V'O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q' and Q' aO2, and breath-by-breath V'O2 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). V'O2 was determined using Grønlund’s algorithm. Q' was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q'aO2. The Q', Q'aO2 and V'O2 kinetics were analyzed with single and double exponential models. fH, Qst, Q', and V'O2 increased upon exercise onset to reach a new steady state. The kinetics of Q'aO2 had the same time constants as that of Q'. The latter was twofold faster than that of V'O2. The V'O2 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 Q' changes fully explained the phase I of V'O2 increase. We suggest that in unsteady states, lung V' O2 is dissociated from muscle O2 consumption. The two components of Q' and Q'aO2 kinetics may reflect vagal withdrawal and sympathetic activation