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POINT-COUNTERPOINT COMMENTS
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow"
Department of Biomedical Sciences and Biotechnologies
School of Medicine
University of Udine
e-mail: pprampero{at}makek.dstb.uniud.it
Department of Biomedical Sciences and Biotechnologies
School of Medicine
University of Brescia, Italy
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.physiology.org/content/vol100/issue2).
To the Editor: The factors limiting O2 max downstream from the lung were estimated viewing the O2 path from arterial blood to mitochondria as a cascade of resistances in series overcome by a specific PO2 gradient (1–3). Three resistances were identified, RQ, Rt, Rm, inversely proportional to 1) cardiovascular O2 transport (
max·
b), where b = (Ca–C
)/(Pa–P) is the average slope of blood O2 dissociation curve, RQ; 2) peripheral perfusion and diffusion estimated from muscle capillary density, Rt; 3) mithocondrial capacity, estimated from succinic dehydrogenase activity or muscle mitochondrial volume density, Rm. For constant PIO2, and mitochondrial PO2 = 0, the relative variation of O2 max caused by changes in any given resistance is given by: O2 max°/O2 max' = 1 + FQ·RQ/RQ + Ft·Rt/Rt + Fm·Rm/Rm, where O2 max°, O2 max' are the values before or after any given manipulation and FQ, Ft, Fm are the ratios of RQ, Rt, Rm to the overall resistance to O2 flow. FQ, Ft, and Fm were estimated from observed O2 max changes induced by changes in RQ, Rt, Rm. It appears that, in exercise with large muscle groups (two legs), RQ is the major (70%) limiting factor downstream from the lung, its role being reduced to 50% during exercise with small muscle groups (one leg). Ft and Fm equally share the remaining 30 or 50% (1–3). Thus our view on the point:counterpoint (4) is that the major factor limiting O2 max in health and normoxia is oxygen transport to active muscles.
REFERENCES
O2 max at the whole animal level. J Exp Biol 115: 319–331, 1985.O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
Health and Integrative Physiology Laboratory
School of Human Kinetics
The University of British Columbia
Vancouver, BC, Canada
e-mail: bsheel{at}interchange.ubc.ca
To the Editor: The limits to maximal O2 consumption (O2 max) have long been debated, and this Point:Counterpoint exchange does little to resolve the question despite creative score keeping by Dr. Wagner (2). Determining the "primary" limit to O2 max is a difficult question to resolve experimentally because manipulation of one pathway step often leads to subsequent changes in other parts of the O2 transport pathway. In turn, this has led to the construction of several models. Disappointingly, but maybe not so surprisingly, different modeling approaches have yielded conflicting results (1, 4). In Dr. Wagner's model (Ref. 3, p. 34) it is assumed that at O2 max "... there is little to suggest impaired cardiac function." This is true during incremental exercise to exhaustion/O2 max but there are in fact several examples in the literature that show significant impaired cardiac function during prolonged exercise (5). The possibility of "cardiac fatigue" is a salient consideration, because it suggests that the properties of the heart during exercise are not limitless. In Figure 1 of Ref. 2, max is theoretically increased acutely by 50%. It is difficult to conceive that increasing max from 40 l/min in a highly trained athlete to 60 l/min is physiologically realistic, and it makes interpreting the corresponding theoretical rise in O2 max difficult. Drs. Saltin, Calbet, and Wagner have provided convincing arguments, but the reader is ultimately left with a choice: to place emphasis on a conceptual scheme or experimental evidence. There are caveats associated with each choice, but I choose to hedge my bets on the available experimental evidence.
REFERENCES
O2 max at the whole animal level. J Exp Biol 115: 319–331, 1985.O2 max at sea level and altitude. Respir Physiol 106: 329–343, 1996.[CrossRef][ISI][Medline]
Abtlg. Sportmedizin
Medizinische Universitaetsklinik Freiburg
79106-Freiburg, Germany
e-mail: olaf{at}msm1.ukl.uni-freiburg.de
To the Editor: As discussed by Saltin and Wagner (4), throughout the last 50 years many approaches have tried to solve the controversy of a central vs. a peripheral limitation of maximal aerobic capacity.
Most if not all approaches are based on the assumption that O2 max is determined by a chain of physiological processes, each of which can represent the "bottle neck" and thereby limit aerobic capacity. On the other hand, most of the components are interacting and might influence each other. From this perspective, it becomes apparent that discrete, well-developed components may be able to compensate for weaker ones, resulting in equally high O2 max. Thisis supported by classical physiological observations in humans, for example, performance-independent exercise-induced arterial hypoxemia or the fact that centrally stimulating substances can increase O2 max without primarily affecting any physiological variable (3). An example from the animal world lends further credence to this issue: myoglobin knockout mice, totally lacking a key factor of oxygen delivery to the energetic system, do not show any difference in aerobic capacity compared with their wild-type counterparts, most likely due to compensating adaptational processes in the adjacent systems affecting O2 max (2).
In heuristic terms, it seems that our comprehension of a "limitation" of O2 max might be improved by adopting an approach considering it as a "dispositional attribute," yielding a variability in response from its components depending on the state of the organism, rather than assuming the O2 max pathway to be a "manifest attribute," predefined in the magnitude of its functional and adaptational capacity (1).
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
The Copenhagen Muscle Research Center
Department of Anesthesia
Rigshospitalet
University of Copenhagen
Copenhagen, Denmark
e-mail: hbay{at}vip.cybercity.dk
To the Editor: Arterial desaturation and the increased alveolar-arterial O2 tension difference reflects that the lungs restrict O2 transport to working skeletal muscles (5). A small decrease in the arterial oxygen tension (PaO2) is, however, of little consequence for arterial hemoglobin O2 saturation (SaO2) due to the S-shaped oxyhemoglobin dissociation curve (1). Thus the influence of a reduced PaO2 on SaO2 increases with development of acidosis. During whole body maximal exercise, such as rowing, pH may reach 6.74 (4), and at a PaO2 of 
75 mmHg, SaO2 drops from 97 to 80%. Immediately after rowing, PaO2 increases to 140 mmHg, whereas pH remains reduced, and the increase in PaO2 allows SaO2 to recover to 93% (2, 4). During exercise, the influences of PaO2 and pH on SaO2 are demonstrated with the administration of an O2-enriched atmosphere or by intravenous administration of sodium bicarbonate. With an inspired O2 fraction of 0.30, PaO2 increases to 165 mmHg with no significant effect on pH, and therefore SaO2 is maintained at 98% (4). Similarly, during exercise with bicarbonate supplementation, acidosis is attenuated and SaO2 remains close to the resting level (3, 4). During exercise with hyperoxia or bicarbonbate infusion, O2 max increases in accordance with SaO2. It is the delicate interaction between the lungs and the oxyhemoglobin dissociation curve that influences the O2 transport to the muscles.
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
German Sport University Cologne
Department Physiology and Anatomy Cologne
Clinic of Thoracic and Cardiovascular Surgery
University Hospital Duesseldorf
Working Group Experimental Surgery
University Hospital Duesseldorf
Duesseldorf, Germany
e-mail: schipke{at}med.uni-duesseldorf.de
To the Editor: To some extent, the controversy derives from interpreting definitions differently: O2 max serves as a convenient example.
O2 max is typically determined spirometrically (at the mouth) but is commonly understood as a measure of maximum aerobic metabolism (maximum working capacity) that results at the end of the transport chain and the end of intracellular metabolic processes. Here, the "theoretical" O2 max should be higher than the spirometric value and can only be assessed spirometrically if all transport processes and the metabolism work at maximum.
CO and perfusion of the exercising muscle are different entities. Muscle perfusion, or locomotor muscle blood flow, is determined by the capillary density only. It is extremely important whether these capillaries can be recruited during exercise to redistribute a large portion of CO toward exercising muscles.
Exercise tests to assess O2 max are frequently unaccounted for "real-life conditions" that include general vasomotor tone and muscle tension. The latter aspect seemingly depends on coordination, i.e., the work movement can be more or less coordinated. Therefore, a comparison of efficiently exercising athletes with sedentary couch people becomes even more complex, because the latter may have a low O2 max and, additionally, may convert oxygen inefficiently into work. In addition to this "coordinative" inefficiency, maximum working capacity could also be limited owing to a "metabolic" inefficiency on the cellular level.
As managers, athletes, physicians, and patients are more interested in maximum working capacity than in O2 max, and, as these two measures are not tightly coupled, any controversy on O2 max limitations will end in a tie.
School of Physiotherapy and Exercise Science
Gold Coast Campus Griffith University
Queensland, Australia
Department of Medicine
University of California, San Diego
La Jolla, California
e-mail: rrichardson{at}ucsd.edu
To the Editor: The rate constant for phosphocreatine (PCr) recovery after submaximal exercise reflects the maximal oxidative rate (i.e., O2 max) attained while restoring the perturbed system (shaken) to resting conditions (3). Of specific relevance to the current debate (5), this assessment also provides a measure of muscle O2 max that, with appropriate experimental design, can be divorced from the convective or muscle blood flow component (not stirred), a prime candidate for limiting oxidative metabolism. The measurement of PCr recovery rate under conditions of altered O2 availability has previously demonstrated that under normoxic conditions O2 availability limits maximal oxidative rate in the skeletal muscle of exercise-trained humans (1) and does not in their untrained counterparts (2). As alterations in muscle blood flow during submaximal exercise either partially or totally compensate, in terms of O2 delivery, for the changes in arterial O2 content induced by breathing hypoxic or hyperoxic gas mixes (4), convective O2 delivery remains relatively constant, whereas the diffusive component of O2 transport is significantly altered. This concept has been highlighted previously (4), where both the Do2 and the convective delivery of O2 were unchanged with alterations in O2 availability, but the PO2 gradient from capillary to myocyte was altered, significantly affecting both myocyte PO2 and skeletal muscle O2 max. Therefore, in summary, the approach of assessing maximal metabolic rate with PCr recovery rate and altered FIO2 (1, 2) highlights both the impact of exercise training status on this parameter and the importance of the diffusive component of O2 transport in determining O2 max.
REFERENCES
O2 max in the exercise-trained human quadriceps. J Appl Physiol 86: 1048–1053, 1999.O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
Center for Sports Medicine and Human Performance
Brunel University, Uxbridge
Middlesex, United Kingdom
Copenhagen Muscle Research Centre
Rigshospitalet
Copenhagen N, Denmark
e-mail: J.Gonzalez-Alonso{at}brunel.ac.uk
To the Editor: The views reflected in the Point:Counterpoint article by Saltin and Calbet vs. Wagner have dominated the debate of the factors limiting O2 max for the last 15 years, with one camp favoring the capacity of the systemic circulation to deliver O2 and the other the muscle diffusive O2 capacity as the primary factors explaining the differences in O2 max between an elite athlete and a couch potato (4). Although the debate is very insightful, it does not answer the key question of whether the circulatory or the muscle diffusive O2 transport and oxidative system reaches its capacity in any human being performing maximal exercise. Results during constant and incremental cycling exercise to exhaustion in trained humans indicate that fatigue is preceded by a fall or a plateau in cardiac output and locomotor muscle blood flow, leading to a blunting in locomotive muscle O2 despite the increasing O2 extraction (1, 2, 3). Importantly, during incremental cycling, systemic and locomotor limb blood flow is only linearly related to O2 up to 50–90% of O2 max, leveling off before O2 max is reached. In the same subjects, muscle O2 was much higher on fatigue when systemic and muscle blood flow did not plateau during one-legged knee-extensor exercise, suggesting that the rates of mitochondrial oxidation and O2 transport from capillary to mitochondrial cytochrome do not reach their capacity during maximal exercise (3). Thus restrictions in blood flow to locomotor muscles before reaching the muscle diffusive O2 capacity is the primary factor limiting O2 max in humans.
REFERENCES
O2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 744–748, 2006.
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