Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).     

Decline in VO2max with aging in master athletes and sedentary men

Fifteen well-trained master endurance athletes [62.0 +/- 2.3 (SE) yr] and 14 sedentary control subjects (61.4 +/- 1.4 yr) were reevaluated after an average follow-up period of approximately 8 yr to obtain information regarding the effects of physical activity on the age-related decline in maximal O2 uptake capacity (VO2max). The master athletes had been training for 10.2 +/- 2.9 yr before initial testing and continued to train during the follow-up period. The sedentary subjects' VO2max declined by an average of 3.3 ml.kg-1.min-1 (33.9 +/- 1.7 vs. 30.6 +/- 1.6, P less than 0.001) over the course of the study, a decline of 12% per decade. In these subjects maximal heart rate declined 8 beats/min (171 vs. 163) and maximal O2 pulse decreased from 0.20 to 0.18 ml.kg-1.beat (P less than 0.05). The master athletes' VO2 max decreased by an average of 2.2 ml.kg-1.min-1 (54.0 +/- 1.7 vs. 51.8 +/- 1.8, P less than 0.05), a 5.5% decline per decade. The master athletes' maximal heart rate was unchanged (171 +/- 3 beats/min) and their maximal O2 pulse decreased from 0.32 to 0.30 ml.kg-1.beat (P less than 0.05). These findings provide evidence that the age-related decrease in VO2max of master athletes who continue to engage in regular vigorous endurance exercise training is approximately one-half the rate of decline seen in age-matched sedentary subjects. Furthermore our results suggest that endurance exercise training may reduce the rate of decline in maximal heart rate that typically occurs as an individual ages.     

Intensity-controlled treadmill running in rats: VO(2 max) and cardiac hypertrophy

Physiological studies of long-term cardiovascular adaptation to exercise require training regimens that give robust conditioning effects and adequate testing procedures to quantify the outcome. We developed a valid and reproducible protocol for measuring maximal oxygen uptake (VO(2 max)), which was reached at a 25 degrees inclination with a respiratory exchange ratio > 1.05 and blood lactate > 6 mmol/l. The effect of intensity-controlled aerobic endurance training was studied in adult female and male rats that ran 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of VO(2 max) and 2 min at 50-60% of VO(2 max), with adjustment of exercise level according to VO(2 max) every week. After 7 wk, the increase in VO(2 max) plateaued at 60-70% above sedentary controls. Ventricular weights and myocyte length were up 25-30% and 6-12%, respectively. Work economy, oxygen pulse, and heart rate were sufficiently changed to indicate substantial cardiovascular adaptation. The model mimics important human responses to training and could be used in future studies on cellular, molecular, and integrative mechanisms of improved cardiovascular function.     

Crossvalidation of two heart rate-based equations for predicting VO2max in white and black men

The purpose of this investigation was to crossvalidate 2 equations that use the ratio of maximal heart rate (HRmax) to resting HR (HRrest) for predicting maximal oxygen consumption (VO2max) in white and black men. One hundred and nine white (n = 51) and black (n = 58) men completed a maximal exercise test on a treadmill to determine VO2max. The HRrest and HRmax were used to predict VO2max via the HRindex and HRratio equations. Validity statistics were done to compare the criterion versus predicted VO2max values across the entire cohort and within each race separately. For the entire group, VO2max was significantly overestimated with the HRindex equation, but the HRratio equation yielded no significant difference compared with the criterion. In addition, there were no significant differences shown between VO2max and either HR-based prediction equation for the white subgroup. However, both equations significantly overestimated VO2max in the black group. Furthermore, large standard error of estimates (ranging from 6.92 to 7.90 ml·kg(-1)·min(-1)), total errors (ranging from 8.30 to 8.62 ml·kg(-1)·min(-1)), and limits of agreement (ranging from upper limits of 16.65 to lower limits of -18.25 ml·kg(-1)·min(-1)) were revealed when comparing the predicted to criterion VO2max for both the groups. Considering the results of this investigation, the HRratio and HRindex methods appear to crossvalidate and prove useful for estimating the mean VO2max in white men as a group but not for an age-matched group of black men. However, because of inflated values for error, caution should be exercised when using these methods to predict individual VO2max.     

Evaluation of the American College of Sports Medicine submaximal treadmill running test for predicting VO2max

The purpose of this study was to assess the validity of the American College of Sports Medicine's (ACSM's) submaximal treadmill running test in predicting VO2max. Twenty-one moderately well-trained men aged 18-34 years performed 1 maximal treadmill test to determine maximal oxygen uptake (M VO2max) and 2 submaximal treadmill tests using 4 stages of continuous submaximal exercise. Estimated VO2max was predicted by extrapolation to age-predicted maximal heart rate (HRmax) and calculated in 2 ways: using data from all submaximal stages between 110 b·min(-1) and 85% HRmax (P VO2max-All), and using data from the last 2 stages only (P VO2max-2). The measured VO2max was overestimated by 3% on average for the group but was not significantly different to predicted VO2max (1-way analysis of variance [ANOVA] p = 0.695; M VO2max = 53.01 ± 5.38; P VO2max-All = 54.27 ± 7.16; P VO2max-2 = 54.99 ± 7.69 ml·kg(-1)·min(-1)), although M VO2max was not overestimated in all the participants--it was underestimated in 30% of observations. Pearson's correlation, standard error of estimate (SEE), and total error (E) between measured and predicted VO2max were r = 0.646, 4.35, 4.08 ml·kg(-1)·min(-1) (P VO2max-All) and r = 0.642, 4.21, 3.98 ml·kg(-1)·min(-1) (P VO2max-2) indicating that the accuracy in prediction (error) was very similar whether using P VO2max-All or P VO2max-2, with up to 70% of the participants predicted scores within 1 SEE (～4 ml·kg(-1)·min(-1)) of M VO2max. In conclusion, the ACSM equation provides a reasonably good estimation of VO2max with no difference in predictive accuracy between P VO2max-2 and P VO2max-All, and hence, either approach may be equally useful in tracking an individual's aerobic fitness over time. However, if a precise knowledge of VO2max is required, then it is recommended that this be measured directly.     

Cold exposure increases running VO(2max) and cost of transport in goats

We inadvertently subjected a group of goats to 5 mo of cold exposure (mean minimum temperature less than -13 degrees C) during an experiment designed to examine the effects of training by daily running on one member of each sibling pair. During the three coldest months, the sedentary but cold-exposed goats experienced a 34% increase in maximal oxygen uptake (VO(2 max), P < 0.01) and a 29% increase in running speed at maximal (P < 0.05). When temperatures increased in the spring, both oxygen uptake and running speed decreased. We interpret these findings as evidence that cold is a sufficient stimulus to invoke the development of aerobic structures in muscle and that these structures subsequently can be utilized for the novel task of running. When the experiment was subsequently repeated without the cold exposure, running speed and VO(2 max) of trained animals increased less than in either group of cold-exposed animals. However, the cost of transport of these warm runners was lower than either group of cold-exposed animals (from 13-19%, P < 0. 0001). Thus, although aerobic capacity was increased with acclimation to severe winter weather, cold-acclimated goats operated with lower efficiency during locomotion.     

Effect of hindlimb suspension on VO2 max and regional blood flow responses to exercise

Male rodents were studied before and after undergoing one of three treatment conditions for 9 days: 1) cage control (n = 15, CON), 2) horizontal suspension (n = 15, HOZ), and 3) head-down suspension (n = 18, HDT). Testing included measurements of maximal O2 uptake (VO2 max) and select cardiovascular responses to graded treadmill exercise. VO2 max expressed on an absolute basis (ml/min) was significantly decreased after HOZ (-14.1 +/- 2.5%) and HDT (-14.3 +/- 2.0%), while being essentially unchanged in CON (-1.0 +/- 3.3%). Significant reductions in body weight were observed after both HOZ (-10.1 +/- 4.2 g) and HDT (-22.5 +/- 3.3 g), whereas CON animals exhibited a significant increase in weight (10.4 +/- 3.8 g). As a result, when VO2 max was normalized for body weight, all groups exhibited similar significant reductions of 6-7%. Although no differences in heart rate and blood pressure response to graded exercise were observed, the HDT group exhibited greater increases in mesenteric resistance at the same absolute exercise intensity. Furthermore, both suspended groups had higher iliac resistance values during exercise at similar relative exercise conditions, suggesting that muscle blood flow during treadmill running may have been reduced after suspension. In general, the decrements associated with the HOZ and HDT conditions were similar. It was concluded that reduction in exercise capacity and altered cardiovascular responses to exercise observed after 6-9 days of suspension were attributable to a combination of hypokinesia, lack of hindlimb weight bearing, or restraint, rather than to hydrostatic influences associated with HDT.     

Exercise-induced prostacyclin release positively correlates with VO(2max) in young healthy men

In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI(2)), assessed as plasma 6-keto-PGF(1alpha) concentration in young healthy men. Eleven physically active - untrained men (mean +/- S.D.) aged 22.7 +/- 2.1 years; body mass 76.3 +/- 9.1 kg; BMI 23.30 +/- 2.18 kg . m(-2); maximal oxygen uptake (VO(2max)) 46.5 +/- 3.9 ml . kg(-1) . min(-1), performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF(1alpha), lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF(1alpha) concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO(2max) (r=0.78, p=0.004) as well as with the net VO(2) increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-alpha concentrations). The exercise-induced increase in 6-keto-PGF(1alpha) concentration?? was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO(2max) when compared to the group of subjects with the lowest VO(2max), in which no increase in 6-keto-PGF(1alpha) concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exercise-induced release of PGI(2) in young healthy men correlates with VO(2max), suggesting that vascular capacity to release PGI(2) in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI(2) leads to the increased cardiovascular hazard of vigorous exercise.     

Reproducibility of an incremental treadmill VO(2)max test with gas exchange analysis for runners

The evaluation of performance through the application of adequate physical tests during a sportive season may be a useful tool to evaluate training adaptations and determine training intensities. For runners, treadmill incremental VO(2)max tests with gas exchange analysis have been widely used to determine maximal and submaximal parameters such as the ventilatory threshold (VT) and respiratory compensation point (RCP) running speed. However, these tests often differ in methodological characteristics (e.g., stage duration, grade, and speed increment size), and few studies have examined the reproducibility of their protocol. Therefore, the aim of this study was to verify the reproducibility and determine the running speeds related to maximal and submaximal parameters of a specific incremental maximum effort treadmill protocol for amateur runners. Eleven amateur male runners underwent 4 repetitions of the protocol (25-second stages, each increasing by 0.3 km·h in running speed while the treadmill grade remained fixed at 1%) after 3 minutes of warm-up at 8-8.5 km·h. We found no significant differences in any of the analyzed parameters, including VT, RCP, and VO(2)max during the 4 repetitions (p > 0.05). Further, the results related to running speed showed high within-subject reproducibility (coefficient of variation < 5.2%). The typical error (TE) values for running speed related to VT (TE = 0.62 km·h), RCP (TE = 0.35 km·h), and VO(2)max (TE = 0.43 km·h) indicated high sensitivity and reproducibility of this protocol. We conclude that this VO(2)max protocol facilitates a clear determination of the running speeds related to VT, RCP, and VO(2)max and has the potential to enable the evaluation of small training effects on maximal and submaximal parameters.     

Effect of the modality of exercise on the VO2 max]

1. Maximum oxygen consumption has been measured by means of three different exercises: cycle ergometry, treadmill running and uphill walking with a 20 kg-load. 2. Loaded walking allowed to reach a VO2 max level in average 2% greater than running and 13% greater than bicycling. 3. This finding suggest that VO2 max may depend on peripheral factors.     

Oxygen transport to skeletal muscle working at VO(2)max in acute hypoxia: theoretical predictions

The influence of acute hypoxia (30 < or = PaO(2) < or = 100 mmHg) on the values of VO(2)max and parameters of oxygen transport in muscle working at VO(2)max was studied. We investigated muscle working under different values of blood flow F (60 < or = F < or = 120 ml/min per 100 g), blood pH (7.0-7.6), and different diffusion conditions. Investigations were performed on a computer model of O(2) delivery to and O(2) consumption in the working muscle. VO(2)max, PvO(2), pO(2)- and VO(2)-distribution in muscle fiber were calculated. It was shown that the greater the degree of arterial hypoxemia, the lower the muscle VO(2)max and blood pO(2) values. When working at VO(2)max, the average and minimal values of tissue pO(2) depend on PaO(2). The greater the blood flow through muscle, the greater the VO(2)max. However, with an increasing degree of arterial hypoxemia, the effect of F and blood pH on the value of VO(2)max is weakened. The diffusion conditions produced a powerful influence on the VO(2)max value. At reduced PaO(2) they are the most important limiting factors of O(2) supply to muscle working at maximal effort.     

Relationship between angiotensin-converting enzyme ID polymorphism and VO(2max) of Chinese males

Several studies have shown that the angiotensin-converting enzyme (ACE) I allele is associated with enhanced physical performance. We investigated whether this phenomenon is observed in a cohort of 67 Chinese men in Singapore. Angiotensin-converting enzyme ID polymorphism was typed with PCR method and maximal oxygen uptake (VO(2max)) of the DD, ID, and II genotypes was compared. Analysis of covariance revealed that VO(2max) was significantly higher (p<0.05) for the DD genotype (57.86 +/- 3.5 ml.kg.(-1)min(-1)) versus the ID (50.58 +/- 1.80 ml.kg.(-1)min(-1)) or II (50.48 +/- 1.58 ml.kg.(-1) min(-1)) genotype. Our findings suggest that the ACE DD genotype in young adult Chinese males is associated with higher levels of VO(2max).     

Effects of incomplete pulmonary gas exchange on VO2 max

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)     

The ergogenic effect of recombinant human erythropoietin on VO2max depends on the severity of arterial hypoxemia

Treatment with recombinant human erythropoietin (rhEpo) induces a rise in blood oxygen-carrying capacity (CaO(2)) that unequivocally enhances maximal oxygen uptake (VO(2)max) during exercise in normoxia, but not when exercise is carried out in severe acute hypoxia. This implies that there should be a threshold altitude at which VO(2)max is less dependent on CaO(2). To ascertain which are the mechanisms explaining the interactions between hypoxia, CaO(2) and VO(2)max we measured systemic and leg O(2) transport and utilization during incremental exercise to exhaustion in normoxia and with different degrees of acute hypoxia in eight rhEpo-treated subjects. Following prolonged rhEpo treatment, the gain in systemic VO(2)max observed in normoxia (6-7%) persisted during mild hypoxia (8% at inspired O(2) fraction (F(I)O(2)) of 0.173) and was even larger during moderate hypoxia (14-17% at F(I)O(2) = 0.153-0.134). When hypoxia was further augmented to F(I)O(2) = 0.115, there was no rhEpo-induced enhancement of systemic VO(2)max or peak leg VO(2). The mechanism highlighted by our data is that besides its strong influence on CaO(2), rhEpo was found to enhance leg VO(2)max in normoxia through a preferential redistribution of cardiac output toward the exercising legs, whereas this advantageous effect disappeared during severe hypoxia, leaving augmented CaO(2) alone insufficient for improving peak leg O(2) delivery and VO(2). Finally, that VO(2)max was largely dependent on CaO(2) during moderate hypoxia but became abruptly CaO(2)-independent by slightly increasing the severity of hypoxia could be an indirect evidence of the appearance of central fatigue.     

Evidence for tissue diffusion limitation of VO2max in normal humans

We recently found [at approximately 90% maximal O2 consumption (VO2max)] that as inspiratory PO2 (PIO2) was reduced, VO2 and mixed venous PO2 (PVO2) fell together along a straight line through the origin, suggesting tissue diffusion limitation of VO2max. To extend these observations to VO2max and directly examine effluent venous blood from muscle, six normal men cycled at VO2max while breathing air, 15% O2 and 12% O2 in random order on a single day. From femoral venous, mixed venous, and radial arterial samples, we measured PO2, PCO2, pH, and lactate and computed mean muscle capillary PO2 by Bohr integration between arterial (PaO2) and femoral venous PO2 (PfvO2). VO2 and CO2 production (VCO2) were measured by expired gas analysis, VO2max averaged 61.5 +/- 6.2 (air), 48.6 +/- 4.8 (15% O2), and 38.1 +/- 4.1 (12% O2) ml.kg-1.min-1. Corresponding values were 16.8 +/- 5.6, 14.4 +/- 5.0, and 12.0 +/- 5.0 Torr for PfVO2; 23.6 +/- 3.2, 19.1 +/- 4.2, and 16.2 +/- 3.5 Torr for PVO2; and 38.5 +/- 5.4, 30.3 +/- 4.1, and 24.5 +/- 3.6 Torr for muscle capillary PO2 (PmCO2). Each of the PO2 variables was linearly related to VO2max (r = 0.99 each), with an intercept not different from the origin. Similar results were obtained when the subjects were pushed to a work load 30 W higher to ensure that VO2max had been achieved. By extending our prior observations 1) to maximum VO2 and 2) by direct sampling of femoral venous blood, we conclude that tissue diffusion limitation of VO2max may be present in normal humans. In addition, since PVO2, PfVO2, and PmCO2 all linearly relate to VO2max, we suggest that whichever of these is most readily obtained is acceptable for further evaluation of the hypothesis.     

Role of muscle loss in the age-associated reduction in VO2 max

A progressive decline in maximal O2 consumption (VO2max) expressed traditionally as per kilogram body weight generally occurs with advancing age. To investigate the extent to which this decline could be attributable to the age-associated loss of metabolically active tissue, i.e., muscle, we measured 24-h urinary creatinine excretion, an index of muscle mass, in 184 healthy nonobese volunteers, ages 22-87 yr, from the Baltimore Longitudinal Study of Aging who had achieved a true VO2max during graded treadmill exercise. A positive correlation was found between VO2max and creatinine excretion in both men (r = 0.64, P less than 0.001) and women (r = 0.47, P less than 0.001). As anticipated, VO2max showed a strong negative linear relationship with age in both men and women. Creatinine excretion also declined with age in men and women. When VO2max was normalized for creatinine excretion, the variance in the VO2max decline attributable to age declined from 60 to 14% in men and from 50 to 8% in women. Thus comparing the standard age regression of VO2max per kilogram body weight with that in which VO2max is normalized per milligram creatinine excretion, the decline in VO2max between a hypothetical 30 yr old and a 70 yr old was reduced from 39 to 18% in men and from 30 to 14% in women. We conclude that in both sexes, a large portion of the age-associated decline in VO2max in non-endurance-trained individuals is explicable by the loss of muscle mass, which is observed with advancing age.     

Predicting maximal aerobic capacity (VO2max) from the critical velocity test in female collegiate rowers

The objective of this study was to examine the relationship between the critical velocity (CV) test and maximal oxygen consumption (VO2max) and develop a regression equation to predict VO2max based on the CV test in female collegiate rowers. Thirty-five female (mean ± SD; age, 19.38 ± 1.3 years; height, 170.27 ± 6.07 cm; body mass, 69.58 ± 0.3 1 kg) collegiate rowers performed 2 incremental VO2max tests to volitional exhaustion on a Concept II Model D rowing ergometer to determine VO2max. After a 72-hour rest period, each rower completed 4 time trials at varying distances for the determination of CV and anaerobic rowing capacity (ARC). A positive correlation was observed between CV and absolute VO2max (r = 0.775, p < 0.001) and ARC and absolute VO2max (r = 0.414, p = 0.040). Based on the significant correlation analysis, a linear regression equation was developed to predict the absolute VO2max from CV and ARC (absolute VO2max = 1.579[CV] + 0.008[ARC] - 3.838; standard error of the estimate [SEE] = 0.192 L·min(-1)). Cross validation analyses were performed using an independent sample of 10 rowers. There was no significant difference between the mean predicted VO2max (3.02 L·min(-1)) and the observed VO2max (3.10 L·min(-1)). The constant error, SEE and validity coefficient (r) were 0.076 L·min(-1), 0.144 L·min(-1), and 0.72, respectively. The total error value was 0.155 L·min(-1). The positive relationship between CV, ARC, and VO2max suggests that the CV test may be a practical alternative to measuring the maximal oxygen uptake in the absence of a metabolic cart. Additional studies are needed to validate the regression equation using a larger sample size and different populations (junior- and senior-level female rowers) and to determine the accuracy of the equation in tracking changes after a training intervention.     

Familial aggregation of VO(2max) response to exercise training: results from the HERITAGE Family Study.

The aim of this study was to test the hypothesis that individual differences in the response of maximal O(2) uptake (VO(2max)) to a standardized training program are characterized by familial aggregation. A total of 481 sedentary adult Caucasians from 98 two-generation families was exercise trained for 20 wk and was tested for VO(2max) on a cycle ergometer twice before and twice after the training program. The mean increase in VO(2max) reached approximately 400 ml/min, but there was considerable heterogeneity in responsiveness, with some individuals experiencing little or no gain, whereas others gained >1.0 l/min. An ANOVA revealed that there was 2.5 times more variance between families than within families in the VO(2max) response variance. With the use of a model-fitting procedure, the most parsimonious models yielded a maximal heritability estimate of 47% for the VO(2max) response, which was adjusted for age and sex with a maternal transmission of 28% in one of the models. We conclude that the trainability of VO(2max) is highly familial and includes a significant genetic component.