.VO2max: what do we know, and what do we still need to know?

Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, Dallas, TX 75231, USA.
The Journal of Physiology (Impact Factor: 4.54). 02/2008; 586(1):25-34. DOI: 10.1113/jphysiol.2007.147629
Source: PubMed

ABSTRACT Maximal oxygen uptake (.VO(2,max)) is a physiological characteristic bounded by the parametric limits of the Fick equation: (left ventricular (LV) end-diastolic volume--LV end-systolic volume) x heart rate x arterio-venous oxygen difference. 'Classical' views of .VO(2,max) emphasize its critical dependence on convective oxygen transport to working skeletal muscle, and recent data are dispositive, proving convincingly that such limits must and do exist. 'Contemporary' investigations into the mechanisms underlying peripheral muscle fatigue due to energetic supply/demand mismatch are clarifying the local mediators of fatigue at the skeletal muscle level, though the afferent signalling pathways that communicate these environmental conditions to the brain and the sites of central integration of cardiovascular and neuromotor control are still being worked out. Elite endurance athletes have a high .VO(2,max) due primarily to a high cardiac output from a large compliant cardiac chamber (including the myocardium and pericardium) which relaxes quickly and fills to a large end-diastolic volume. This large capacity for LV filling and ejection allows preservation of blood pressure during extraordinary rates of muscle blood flow and oxygen transport which support high rates of sustained oxidative metabolism. The magnitude and mechanisms of cardiac phenotype plasticity remain uncertain and probably involve underlying genetic factors, as well as the length, duration, type, intensity and age of initiation of the training stimulus.

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    ABSTRACT: There is unequivocal evidence that exercise results in considerable health benefits. These are the result of positive hormonal, metabolic, neuronal, and structural changes brought about by the intermittent physiological challenge of exercise. However, there is evolving evidence that intense exercise may place disproportionate physiological stress on the right ventricle (RV) and the pulmonary circulation. Both echocardiographic and invasive studies are consistent in demonstrating that pulmonary arterial pressures increase progressively with exercise intensity, such that the harder one exercises, the greater the load on the RV. This disproportionate load can result in fatigue or damage of the RV if the intensity and duration of exercise is sufficiently prolonged. This is distinctly different from the load imposed by exercise on the left ventricle (LV), which is moderated by a greater capacity for reductions in systemic afterload. Finally, given the increasing RV demand during exercise, it may be hypothesized that chronic exercise-induced cardiac remodeling (the so-called athlete's heart) may also disproportionately affect the RV. Indeed, there is evidence, although somewhat inconsistent, that RV volume increases may be relatively greater than those for the LV. Perhaps more importantly, there is a suggestion that chronic endurance exercise may cause electrical remodeling, predisposing some athletes to serious arrhythmias originating from the RV. Thus, a relatively consistent picture is emerging of acute stress, prolonged fatigue, and long-term remodeling, which all disproportionately affect the RV. Thus, we contend that the RV should be considered a potential Achilles' heel of the exercising heart.
    Pulmonary circulation. 09/2014; 4(3):407-16.
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    ABSTRACT: Purpose: The aim of this study was to generate updated Olympic medal benchmarks for V̇O2 max in winter endurance disciplines, examine possible differences in V̇O2 max between medalists and non-medalists, and calculate gender difference in V̇O2 max based on a homogeneous subset of world-leading endurance athletes. Methods: We identified athletes who participated in winter Olympic Games/World Championships in the period 1990-2013. All identified athletes tested V̇O2 max at the Norwegian Olympic Training Center within ±1 yr from their championship performance. Testing procedures were consistent throughout the entire period. Results: For medal winning athletes, the following relative V̇O2 max values (mean: 95% CIs) for men/women were observed (mL∙min-1∙ kg-1): 84:87-81/72:77-68 for cross-country distance skiing, 78:81-75/68:73-64 for cross-country sprint skiing, 81:84-78/67:73-61 for biathlon and 77:80-75 for Nordic combined (men only). Similar benchmarks for absolute V̇O2 max (L∙min-1) in male/female athletes (mean: 95% CIs) are 6.4:6.1-6.7/4.3:4.1-4.5 for cross-country distance skiers, 6.3:5.8-6.8/4.0:3.7-4.3 for cross-country sprint skiers, 6.2:5.7-6.4/4.0:3.7-4.3 for biathletes and 5.3:5.0-5.5 for Nordic combined (men only). The difference in relative V̇O2 max between medalists and non-medalists was large for Nordic combined, moderate for cross-country distance and biathlon, and small/trivial for the other disciplines. Corresponding differences in absolute V̇O2 max were small/trivial for all disciplines. Male cross-country medalists achieve 15% higher relative V̇O2 max values than corresponding females. Conclusions: This study provides updated benchmark V̇O2 max values for Olympic medal level performance in winter endurance disciplines, and can serve as a guideline of the requirements for future elite athletes.
    International journal of sports physiology and performance 02/2015; · 2.68 Impact Factor


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