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

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

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 < 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 < 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

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

Energetics of running in top-level marathon runners from Kenya

On ten top-level Kenyan marathon runners (KA) plus nine European controls (EC, equivalent to KA), we measured maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ ) and the energy cost of running (C r) on track during training camps at moderate altitude, to better understand the KA dominance in the marathon. At each incremental running speed, steady-state oxygen consumption ( $$\dot{V}{\text{O}}_{ 2}$$ ) was measured by telemetric metabolic cart, and lactate by electro-enzymatic method. The speed requiring $$\dot{V}{\text{O}}_{ 2} = \dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ provided the maximal aerobic velocity (v max). The energy cost of running was calculated by dividing net $$\dot{V}{\text{O}}_{ 2}$$ by the corresponding speed. The speed at lactate threshold (v ΘAN) was computed from individual Lâb versus speed curves. The sustainable $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ fraction (F d) at v ΘAN (F ΘAN) was computed dividing v ΘAN by v max. The F d for the marathon (F mar) was determined as F mar=0.92 F ΘAN. Overall, $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ (64.9±5.8 vs. 63.9±3.7mlkg−1min−1), v max (5.55±0.30 vs. 5.41±0.29ms−1) and C r (3.64±0.28 vs. 3.63±0.31Jkg−1m−1) resulted the same in KA as in EC. In both groups, C r increased linearly with the square of speed. F ΘAN was 0.896±0.054 in KA and 0.909±0.068 in EC; F mar was 0.825±0.050 in KA and 0.836±0.062 in EC (NS). Accounting for altitude, running speed predictions from present data are close to actual running performances, if F ΘAN instead of F mar is taken as index of F d. In conclusion, both KA and EC did not have a very high $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ , but had extremely high F d, and low C r, equal between them. The dominance of KA over EC cannot be explained on energetic ground

Effects of acceleration in the Gz axis on human cardiopulmonary responses to exercise

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 Gz axis (a g) ranging from 0 to 3g. 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 4.5g, thus indicating the practical impossibility for humans to stay and work on the biggest Planets of the Solar Syste

Energetics of running in top level marathon runners from Kenya.

On ten top-level Kenyan marathon runners (KA) plus nine European controls (EC, equivalent to KA), we measured maximal oxygen consumption ( _V O2max) and the energy cost of running (Cr) on track during training camps at moderate altitude, to better understand the KA dominance in the marathon. At each incremental running speed, steady-state oxygen consumption ( _V O2) was measured by telemetric metabolic cart, and lactate by electroenzymatic method. The speed requiring _V O2 ¼ _V O2max provided the maximal aerobic velocity (vmax). The energy cost of running was calculated by dividing net _V O2 by the corresponding speed. The speed at lactate threshold (vHAN)was computed from individual Laˆb versus speed curves. The sustainable _V O2max fraction (Fd) at vHAN (FHAN) was computed dividing vHAN by vmax. The Fd for the marathon (Fmar) was determined as Fmar = 0.92 FHAN. Overall, _VO2max (64.9 ± 5.8 vs. 63.9 ± 3.7 ml kg-1 min-1), vmax (5.55 ± 0.30 vs. 5.41 ± 0.29 m s-1) and Cr (3.64 ± 0.28 vs. 3.63 ± 0.31 J kg-1 m-1) resulted the same in KA as in EC. In both groups, Cr increased linearly with the square of speed. FHAN was 0.896 ± 0.054 in KA and 0.909 ± 0.068 in EC; Fmar was 0.825 ± 0.050 in KA and .836 ± 0.062 in EC (NS). Accounting for altitude, running speed predictions from present data are close to actual running performances, if FHAN instead of Fmar is taken as index of Fd. In conclusion, both KA and EC did not have a very high _V O2max, but had extremely high Fd, and low Cr, equal between them. The dominance of KA over EC cannot be explained on energetic grounds