Chest
An Analysis of the Factors Limiting Maximal Oxygen Consumption in Healthy Subjects
Section snippets
THE PATHWAY FOR OXYGEN
The O2 path from the environment to mitochondria can be viewed as a cascade of resistances in series, each resistance being overcome by a specific pressure gradient. If this is so, the O2 flow is set by the overall pressure gradient (ΔPTot) divided by the total resistance (RTot): Since at steady state the O2 flow through each section of the system is the same, the following must also apply: where ΔPi is the pressure gradient across the ith resistance
THE LUNG AS LIMITING STEP
Apart from the above limitations, the model shows that Vo2max is not limited by a single factor, but by a series of physiologic variables whose limiting role can be quantitatively assessed on the basis of the model itself. In addition, if the system behaves linearly, and if the overall pressure gradient from environment to mitochondria is constant, any given change of the ith resistance will lead to a change of Vo2max proportional to the relative magnitude of the resistance in question (Fi).
THE CIRCULATION AND THE MUSCLES AS LIMITING STEPS
Neglecting therefore pulmonary ventilation and diffusion, in the section that follows we will attempt to partition the resistance to O2 transport downstream the lung into 2 fractions: (1) FQ' due to O2 transport and (2) Fp' due to the sum of capillary perfusion and diffusion and mitochondrial O2 utilization (Fp' = Ft' + Fm'). (Note also that whereas FQ and Fp refer to the overall O2 cascade, FQ' and Fp' refer to the portion of the cascade downstream from the lung only.)
FQ' and Fp' will be
CONCLUSIONS
This article discusses and supports the hypothesis that the limits to whole body Vo2max are multifactorial. At least 4 resistances to maximal O2 flow of physiologic relevance are identified: (1) convective and diffusive transfer of O2 from environment to arterial blood; (2) convective O2 transport by the circulation; (3) peripheral O2 transfer from capillaries to mitochondria; and (4) O2 utilization in the mitochondria. The relative role of these resistances in healthy subjects at sea level
REFERENCES (15)
Climbing Mount Everest without oxygen: an analysis of maximal exercise during extreme hypoxia.
Respir Physiol
(1983)- et al.
Model for capillary-alveolar equilibration with special reference to O2 uptake in hypoxia.
Respir Physiol
(1981) Unequal distribution of blood flow in exercising muscle of the dog.
Respir Physiol
(1990)- et al.
Factors limiting maximal oxygen consumption in humans.
Respir Physiol
(1990) - et al.
Exercise induced arterial hypoxaemia in healthy human subjects at sea level.
J Physiol (Lond)
(1984) Limiting factors for aerobic muscle performance.
Acta Physiol Scand
(1970)A non-linear solution, of the oxygen conductance equation: applications to performance at sea level and at an altitude of 7,350 ft.
Int Z Angew Physiol
(1969)
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