Comment on Point:Counterpoint "In health and in a normoxic environment, VO2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow"

doi:10.1152/japplphysiol.00018.2006

Comment on Point:Counterpoint "In health and in a normoxic environment, O_{2 max} is/is not limited primarily by cardiac output and locomotor muscle blood flow"

Timothy David Noakes

MRC/UCT Research Unit for Exercise Science and Sports Medicine
University of Cape Town and Sports Science Institute of South Africa
Newlands, South Africa
e-mail: tdnoakes{at}sports.uct.ac.za

The following letters are in response to the Point:Counterpointseries "In health and in a normoxic environment, O_{2 max} is/is not limited primarily by cardiac outputand locomotor muscle blood flow" that appeared in the Februaryissue (vol 100: 744–748, 2006; http://jap.physiology.org/content/vol100/issue2).

To the Editor: The common presumption of this debate (5) isthat skeletal muscle function "fails" at O_2max because of inadequate oxygen delivery. If that presumptionis incorrect, this debate is gratuitous.

If cardiac output limits the O_{2 max},then myocardial ischemia will occur before significant skeletalmuscle anerobiosis (2) because the coronary blood flow (dependenton cardiac output) determines myocardial perfusion. A. V. Hillrealized this in 1924 (1; Fig. 2 in Ref. 2). Cardiac outputdoes not "plateau" nor does myocardial ischemia develop at O_{2 max} in health (2).

If oxygen diffusion limits O_{2 max},then all skeletal muscle motor units must be recruited in theexercising limbs. Otherwise, how is the function of nonrecruitedmotor units inhibited by oxygen lack (2)? But if all motor unitsare recruited at O_{2 max}, how doeseach increase its power output three- to fourfold during maximal"anaerobic" exercise? There is no evidence that this is possible.More likely that motor unit recruitment is submaximal at O_{2 max} (2).

If the brain regulates exercise performance to avoid a catastrophicfall in cardiac output leading to myocardial ischemia and skeletalmuscle anerobiosis (2, 4), then exercise will always terminateat submaximal levels of cardiac output, skeletal muscle oxygendiffusion and skeletal muscle recruitment. In which case, noneof these variables "limits" the O_2max. Each is simply a marker of this (protective) regulationoccurring at higher brain centers (4).

As Dr. Wagner states: This debate looks at only part of thestory. As a result, it again (3) provides unsatisfactory answersto the larger question.

REFERENCES

Hill AV, Long CNH, and Lupton H. Muscular exercise, lactic acid and the supply and utilization of oxygen: Parts VII-VIII. Proc Royal Soc Br 97: 155–176, 1924.
Noakes TD and Gibson St Clair A. Logical limitations to the "catastrophe" models of fatigue during exercise in humans. Br J Sports Med 38: 648–649, 2004. doi: 10.1136/bjsm.2004.009761.[Abstract/Free Full Text]
Noakes TD, Calbet JAL, Boushel R, Sondergaard H, Radegran G, Wagner PD, and Saltin B. Central regulation of skeletal muscle recruitment explains the reduced maximal cardiac output during exercise in hypoxia. Am J Physiol Regul Integr Comp Physiol 287: R996–R1002, 2004.[Free Full Text]
St. Clair Gibson A and Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med 38: 797–806, 2004. doi: 10.1136/bjsm.2003.009852.[Abstract/Free Full Text]
Saltin B and Calbet JAL; Wagner PD. Point:Counterpoint: In health and in a normoxic environment, O_{2 max} is/is not limited primarily by the cardiac output and locomotor blood flow. J Appl Physiol 100: 744–748, 2006.[Free Full Text]

Jens Bangsbo

Copenhagen Muscle Research Centre
Institute of Exercise and Sport Science
University of Copenhagen
Copenhagen, Denmark
e-mail: jbangsbo{at}aki.ku.dk

To the Editor: It has been interesting to follow the discussionbetween Saltin/Calbet and Wagner (4). However, the reader appearsto be left with some confusion. To study whether a physiologicalfactor is important in the control of O_2max, the particular factor has to be changed without changingany other components involved. In human studies there will alwaysbe doubts about the outcome of such studies, because compensatorymechanisms may occur or the manipulation may lead to nonphysiologicalconditions. However, the studies brought up by Saltin/Calbetprovide strong evidence that the blood flow delivery is limitingO_{2 max}. Studies manipulating oxygencontent cannot be used to examine whether blood delivery tothe exercising muscles is a limiting factor. However, importantly,such studies clearly show that the O_2max is elevated when oxygen delivery is elevated (2, 3) andprovide evidence that the muscle tissue has the capacity toextract more oxygen. It is also evident that the limitationcan be at the pulmonary level. In particular, Dempsey and coworkers(1) have demonstrated that some highly fit male athletes havea significant exercise induced arterial hypoxemia, and thatpeak O₂ in these subjects could beincreased by inhaling air with an elevated fraction of oxygen,supporting the notion that there are no peripheral limitations.Nevertheless, it appears that under normal conditions the bloodflow to the contracting muscle is the primarily limiting factorin healthy subjects.