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POINT-COUNTERPOINT COMMENTS
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow"
1Cardiovascular Physiology and Rehabilitation Laboratory
University of British Columbia
Vancouver, British Columbia, Canada
e-mail: darren.warburton{at}ubc.ca
2Kinesiology and Health Science
York University
North York, Ontario, Canada
The following letters are in response to the Point:Counterpoint series "In health and in a normoxic environment, O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow" that appeared in the February issue (vol. 100: 744–748, 2006; http://jap.physiol.org/content/vol100/issue2/2006).
To the Editor: We appreciate the invitation to comment on the recent discussions regarding the relative importance of cardiac output (Q) in limiting O2 max. As presented eloquently by Drs. Saltin and Calbet (4), there is a wealth of data to support the contention that Q is the primary (but not the sole) determinant of O2 max in "health and in a normoxic environment" ([Hb] = 15 g% and PaO2 = 90–95 mmHg). On the other hand, there are limited published findings (as opposed to theoretical analyses of potential conditions) to contradict this contention, and those findings are open to interpretation (4). Studies in humans have illustrated clearly that differences in maximal Q account directly for the major differences in O2 max between untrained and endurance-trained individuals (1). Also, numerous researchers have acutely and/or chronically manipulated Q and produced concomitant changes in O2 max. For example, we reported that an acute increase in Q via blood volume expansion was directly associated with a comparable increase in O2 max and an acute decrease in Q was directly associated with a concomitant decrease in O2 max (3). Compelling animal research has likewise demonstrated a direct relationship between Q and O2 max. For example, pericardiectomy in pigs resulted in a 31% increase in O2 max as a result of improvements in end-diastolic volume (33%) and Q (29%) (2). These studies and numerous others support the contention that O2 max is limited primarily by Q (through its central role in oxygen delivery) and this substantial evidence overwhelms other theories that are based on limited data.
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
Department of Anesthesia
The Copenhagen Muscle Research Center
Rigshospitalet
University of Copenhagen
Denmark, Copenhagen
e-mail: nhsecher{at}rh.hosp.dk
To the Editor: The circulation has two operating modes of relevance for flow to the muscles. During vasovagal syncope, as during grave hemorrhage, blood pressure (BP) is kept low by loss of sympathetic tone and flow increases (4). In health, however, the arterial baroreceptors maintain BP mainly by modulating vascular resistance, with the muscles playing an important role, and that control is preserved during exercise (2). The elevated BP during exercise is controlled by resetting the baroreceptors to maintain the BP that is set not only by feed forward, from the central nervous system, and feedback, from the working muscles, but also by the reduced central blood volume in the upright posture.
Two mechanisms elevate BP during exercise. The set increase in BP may be accomplished by the increase in cardiac output, but if that contribution is too small to establish the BP that the baroreceptors are set to control (2), then flow to working muscles (and the brain) is restricted (1, 5).
With the diffusion capacity for oxygen in the muscles (DmO2) varying with flow (5), likely reflecting capillary recruitment, the argument that DmO2 is the key to oxygen transport (3) seems similar to stating that O2 is limited by cardiac output and in turn muscle flow. It may be desirable for the muscles to maintain a high flow during exercise and, therefore, DmO2. Unfortunately, however, the baroreceptor control of BP does not legitimize maximal muscle vasodilatation when a substantial part of the musculature is operative as during various types of "whole body" exercise.
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
1Department for Anatomy
University of Bern
Bern, Switzerland
e-mail: hoppeler{at}ana.unibe.ch;
2Department of Biological Sciences
Northern Arizona University
Flagstaff, Arizona
To the Editor: We have viewed the "battle on the limitation of O2 max" clearly from the perspective of the periphery, having focused our research on the demand-induced plasticity of skeletal muscle tissue for much of the last 30 years. To establish the "bottleneck hypothesis" that O2 max is limited by "cardiac output and locomotor muscle blood flow" implies (as suggested by Bengt Saltin and collaborators; Ref. 4) that 1) phenotypically plastic structures within the muscle (e.g., mitochondria) are over built (have excess capacity) for no apparent reason and 2) oxygen delivery is the critical rate-limiting resistance step to oxygen flow to the periphery. Were this true, it would be demonstrated rather simply because experimentally reducing the resistance of this step (i.e., increasing its transport capacity) would by necessity result in a proportional and quantitatively matched increase of the flow through the entire system (2). This is not what is observed. As shown by Turner et al. (5), under carefully controlled invasive conditions the autologous retransfusion of 900 ml of blood in seven subjects increased O2 max by 0.28 ± 004 l/min, whereas cardiac oxygen delivery increased by 0.57 ± 0.11 l/min. Data reported from four more studies (see Ref. 5) all show that at best 50% of an experimentally induced increase in cardiac O2 delivery can be used by the muscle mitochondria, effectively arguing for significant peripheral resistance or against a "sole" cardiovascular O2 max limitation. Looking at mammals in general (including humans), there is vastly more evidence for a balance of structures and shared limitation in the respiratory system than there is for the bottleneck hypothesis (1, 3).
REFERENCES
O2. J Exp Biol 204: 3195–3199, 2001.[Medline]O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.O2 max in humans after blood retransfusion. Respir Physiol 92: 329–341, 1993.[CrossRef][Web of Science][Medline]
strand Laboratory of Work Physiology
Karolinska Institute and University College of Physical Education and Sports
Stockholm, Sweden
e-mail: Bjorn.Ekblom{at}IHS.se
To the Editor: The 80-year-old Hill-Lupton question has created another well-written debate (game); however, with some player’s insufficiencies (4). Wagner seems to disregard data from pericardioectomy because it was done on dogs (does he expect experiments in humans?), whereas his proof that maximal mitochondrial O2 rate consumption can affect O2 max comes from experiments done on an isolated rat hindlimb preparation. Wagner: "yellow card." Saltin/Calbet could have retorted that combined maximal arm+leg exercise does not enhance peak Q and O2 max compared with maximal leg exercise (5). Thus an increase in total mitochondrial volume will not increase O2 max. Saltin/Calbet argue with solid human experimental data, but miss that the difference in O2 max between well-trained endurance athletes of the same mass is solely due to differences in stroke volume and peak Q (3). Wagner on the other hand builds physiological models, partly on theoretical ground. However, when the model meets reality, it collapses. Increasing Hb concentration enhances O2 max more than the 3.9% mentioned without other effects on the other parameters of the oxygen transport chain (1, 2). Wagner: "red card." He, not Saltin, is blown out of the game.
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.This article has been cited by other articles:
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  D. E. R. Warburton and N. Gledhill Last Word on Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individuals J Appl Physiol, January 1, 2008; 104(1): 285 - 285. [Full Text] [PDF]
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