Changes in body temperature influence the scaling of VO2max and aerobic scope in mammals

Debate on the mechanism(s) responsible for the scaling of metabolic rate with body size in mammals has focused on why the maximum metabolic rate (VO2max ) appears to scale more steeply with body size than the basal metabolic rate (BMR). Consequently, metabolic scope, defined as VO2max/BMR, systematically increases with body size. These observations have led some to suggest that VO2max, and BMR are controlled by fundamentally different processes, and to discount the generality of models that predict a single power-law scaling exponent for the size dependence of the metabolic rate. We present a model that predicts a steeper size dependence for VO2max than BMR based on the observation that changes in muscle temperature from rest to maximal activity are greater in larger mammals. Empirical data support the model's prediction. This model thus provides a potential theoretical and mechanistic link between BMR and VO2 max.     

Ambulatory estimates of maximal aerobic power from foot -ground contact times and heart rates in running humans.

Seeking to develop a simple ambulatory test of maximal aerobic power (VO(2 max)), we hypothesized that the ratio of inverse foot-ground contact time (1/t(c)) to heart rate (HR) during steady-speed running would accurately predict VO(2 max). Given the direct relationship between 1/t(c) and mass-specific O(2) uptake during running, the ratio 1/t(c). HR should reflect mass-specific O(2) pulse and, in turn, aerobic power. We divided 36 volunteers into matched experimental and validation groups. VO(2 max) was determined by a treadmill test to volitional fatigue. Ambulatory monitors on the shoe and chest recorded foot-ground contact time (t(c)) and steady-state HR, respectively, at a series of submaximal running speeds. In the experimental group, aerobic fitness index (1/t(c). HR) was nearly constant across running speed and correlated with VO(2 max) (r = 0.90). The regression equation derived from data from the experimental group predicted VO(2 max) from the 1/t(c). HR values in the validation group within 8.3% and 4.7 ml O(2) x kg(-1) x min(-1) (r = 0.84) of measured values. We conclude that simultaneous measurements of foot-ground constant times and heart rates during level running at a freely chosen constant speed can provide accurate estimates of maximal aerobic power.     

The effect of epistasis on the excess of the additive and nonadditive variances after population bottlenecks

The effect of population bottlenecks on the components of the genetic variance generated by two neutral independent epistatic loci has been studied theoretically (VA, additive; VD, dominant; VAA, additive x additive; VAD, additive x dominant; VDD; dominant x dominant components of variance). Nonoverdominance and overdominance models were considered, covering all possible types of marginal gene action at the single locus level. The variance components in an infinitely large panmictic population (ancestral components) were compared with their expected values at equilibrium, after t consecutive bottlenecks of equal size N (derived components). Formulae were obtained in terms of allele frequencies and effects at each locus and the corresponding epistatic value. An excess of VA after bottlenecks can be assigned to two sources: (1) the spatiotemporal changes in the marginal average effects of gene substitution alpha(i), which are equal to zero only for additive gene action within and between loci; and (2) the covariance between alpha2(i) and the heterozygosity at the loci involved, which is generated by dominance, with or without epistasis. Numerical examples were analyzed, indicating that an increase in VA after bottlenecks will only occur if its ancestral value is minimal or very small. For the nonoverdominance model with weak reinforcing epistasis, that increase has been detected only for extreme frequencies of the negative allele at one or both loci. With strong epistasis, however, this result can be extended to a broad range of intermediate frequencies. With no epistasis, the same qualitative results were found, indicating that dominance can be considered as the primary cause of an increase in VA following bottlenecks. In parallel, the derived total nonadditive variance exceeded its ancestral value (V(NA) = V(D) + V(AA) + V(AD) + V(DD)) for a range of combinations of allele frequencies covering those for an excess of VA and for very large frequencies of the negative allele at both loci. For the overdominance model, an increase in V(A) and V(NA) was respectively observed for equilibrium (intermediate) frequencies at one or both loci or for extreme frequencies at both loci. For all models, the magnitude of the change of V(A) and V(NA) was inversely related to N and t. At low levels of inbreeding, the between-line variance was not affected by the type of gene action. For the models considered, the results indicate that it is unlikely that the rate of evolution may be accelerated after population bottlenecks, in spite of occasional increments of the derived V(A) over its ancestral value.     

Anatomic and energetic correlates of divergent selection for basal metabolic rate in laboratory mice

The aerobic capacity model postulates that high basal metabolic rates (BMR) associated with endothermy evolved as a correlated response to the selection on maximum, peak metabolic rate Vo2max. Furthermore, the model assumes that BMR and Vo2max are causally linked, and therefore, evolutionary changes in their levels cannot occur independently. To test this, we compared metabolic and anatomical correlates of selection for high and low body mass-corrected BMR in males of laboratory mice of F18 and F19 selected generations. Divergent selection resulted in between-line difference in BMR equivalent to 2.3 phenotypic standard deviation units. Vo2max elicited by forced swimming in 20 degrees C water was higher in the low BMR than high BMR line and did not differ between the lines when elicited by exposure to heliox at -2.5 degrees C. Moreover, the magnitude of swim- and heliox-induced hypothermia was significantly smaller in low BMR mice, whereas their interscapular brown adipose tissue was larger than in high BMR mice. Our results are therefore at variance with the predictions of aerobic capacity model. The selection also resulted in correlated response in food consumption (C) and masses of metabolically active internal organs: kidneys, liver, small intestine, and heart, which fuel maximum, sustained metabolic rate (SusMR) rather than Vo2max. These correlated responses were strong enough to claim the existence of positive, genetic correlations between BMR and the mass of viscera as well as C. Thus, our findings support the suggestion that BMR evolved as a correlated response to selection for SusMR, not Vo2max. In functional terms BMR should therefore be interpreted as a measure of energetic costs of maintenance of metabolic machinery necessary to sustain high levels of energy assimilation rate.     

L-arginine enhances aerobic exercise capacity in association with augmented nitric oxide production.

We tested whether supplementation with L-arginine can augment aerobic capacity, particularly in conditions where endothelium-derived nitric oxide (EDNO) activity is reduced. Eight-week-old wild-type (E(+)) and apolipoprotein E-deficient mice (E(-)) were divided into six groups; two groups (LE(+) and LE(-)) were given L-arginine (6% in drinking water), two were given D-arginine (DE(+) and DE(-)), and two control groups (NE(+) and NE(-)) received no arginine supplementation. At 12-16 wk of age, the mice were treadmill tested, and urine was collected after exercise for determination of EDNO production. NE(-) mice demonstrated a reduced aerobic capacity compared with NE(+) controls [maximal oxygen uptake (VO(2 max)) of NE(-) = 110 +/- 2 (SE) vs. NE(+) = 122 +/- 3 ml O(2). min(-1). kg(-1), P < 0.001]. This decline in aerobic capacity was associated with a diminished postexercise urinary nitrate excretion. Mice given L-arginine demonstrated an increase in postexercise urinary nitrate excretion and aerobic capacity in both groups (VO(2 max) of LE(-) = 120 +/- 1 ml O(2). min(-1). kg(-1), P < 0.05 vs. NE(-); VO(2 max) of LE(+) = 133 +/- 4 ml O(2). min(-1). kg(-1), P < 0.01 vs. NE(+)). Mice administered D-arginine demonstrated an intermediate increase in aerobic capacity in both groups. We conclude that administration of L-arginine restores exercise-induced EDNO synthesis and normalizes aerobic capacity in hypercholesterolemic mice. In normal mice, L-arginine enhances exercise-induced EDNO synthesis and aerobic capacity.     

Maximal oxygen consumption test during arm exercise--reliability and validity.

The reliability and validity of a continuous progressive arm test, in which maximal 02 consumption (V02 max arm) is determined, were analyzed. Forty-one men (28.2 +/- 8.8 yr) performed the test twice. Eighteen additional men (22.6 +/- 5.6 yr) performed the arm test, as well as the treadmill run, in which maximal O2 consumption VO2max leg) was determined. The validity of the VO2 max arm test was computed, using VO2 max leg as a criterion for the individual's aerobic capacity. The reliability coefficients of VO2 max arm, VEmax arm, and HRmax arm were 0.94, 0.98, and 0.76, respectively, indicating a high reliability of the testmthe validity coefficient of VO2max arm was only 0.74. The regression equation of VO2max leg on VO2max arm was y = 24.4 + 0.9 +/- 4.4 (Syx). These findings indicate that, following the suggested protocol, the individual repeatedly uses the same muscles and does reach an all-out stage. However, different individuals apparently are aided by their trunk and leg muscles to different degrees, which lowers the validity of this test as a predictor of aerobic capacity.     

Mathematical analysis of running performance and world running records

The objective of this study was to develop an empirical model relating human running performance to some characteristics of metabolic energy-yielding processes using A, the capacity of anaerobic metabolism (J/kg); MAP, the maximal aerobic power (W/kg); and E, the reduction in peak aerobic power with the natural logarithm of race duration T, when T greater than TMAP = 420 s. Accordingly, the model developed describes the average power output PT (W/kg) sustained over any T as PT = [S/T(1 - e-T/k2)] + 1/T integral of T O [BMR + B(1 - e-t/k1)]dt where S = A and B = MAP - BMR (basal metabolic rate) when T less than TMAP; and S = A + [Af ln(T/TMAP)] and B = (MAP - BMR) + [E ln(T/TMAP)] when T greater than TMAP; k1 = 30 s and k2 = 20 s are time constants describing the kinetics of aerobic and anaerobic metabolism, respectively, at the beginning of exercise; f is a constant describing the reduction in the amount of energy provided from anaerobic metabolism with increasing T; and t is the time from the onset of the race. This model accurately estimates actual power outputs sustained over a wide range of events, e.g., average absolute error between actual and estimated T for men's 1987 world records from 60 m to the marathon = 0.73%. In addition, satisfactory estimations of the metabolic characteristics of world-class male runners were made as follows: A = 1,658 J/kg; MAP = 83.5 ml O2.kg-1.min-1; 83.5% MAP sustained over the marathon distance. Application of the model to analysis of the evolution of A, MAP, and E, and of the progression of men's and women's world records over the years, is presented.     

Familial resemblance in maximal heart rate, blood lactate and aerobic power

There are considerable interindividual differences in maximal oxygen uptake per kilogram of body weight (VO2 max/kg), maximal heart rate (max HR) and maximal blood lactate (max blood La) measured during a progressive exercise test. The aim of the study was to quantify the familial relationships for these variables. Parents and children of 38 families of French-Canadian descent were submitted to a modified Balke treadmill test. VO2 max/kg and max HR were the highest values reached during the test for 1 min. Max blood La was obtained from a blood sample taken 2 min after the test. The effects of age and sex were significant for max blood La and VO2 max/kg in each generation. Scores were thus adjusted through multiple regression procedures (age + sex + age X sex + age2), yielding residuals which were submitted to further analysis. Intraclass correlations (ri) were significant in pairs of sibs for max blood La and max HR, i.e. 0.28 (p less than 0.01) and 0.43 (p less than 0.05), respectively. For VO2 max/kg, pairs of spouses and sibs were about similarly correlated (ri = 0.20 and 0.15; p less than 0.05). Data suggested that children were more related to their mother than to their father for VO2 max/kg, VO2 max/kg of fat-free weight, and particularly for max HR. It was concluded that familial resemblance and heritability estimates for maximal aerobic power, max HR and max blood La were quite low and generally nonsignificant. Correlations between biological sibs were, however, consistently significant for max HR and max blood La. The suggestion of a maternal effect in maximal aerobic power should be further investigated.     

Energetics of kayaking at submaximal and maximal speeds

The energy cost of kayaking per unit distance (C(k), kJ x m(-1)) was assessed in eight middle- to high-class athletes (three males and five females; 45-76 kg body mass; 1.50-1.88 m height; 15-32 years of age) at submaximal and maximal speeds. At submaximal speeds, C(k) was measured by dividing the steady-state oxygen consumption (VO(2), l x s(-1)) by the speed (v, m x s(-1)), assuming an energy equivalent of 20.9 kJ x l O(-1)(2). At maximal speeds, C(k) was calculated from the ratio of the total metabolic energy expenditure (E, kJ) to the distance (d, m). E was assumed to be the sum of three terms, as originally proposed by Wilkie (1980): E = AnS + alphaVO(2max) x t-alphaVO(2max) x tau(1-e(-t x tau(-1))), were alpha is the energy equivalent of O(2) (20.9 kJ x l O(2)(-1)), tau is the time constant with which VO(2max) is attained at the onset of exercise at the muscular level, AnS is the amount of energy derived from anaerobic energy utilization, t is the performance time, and VO(2max) is the net maximal VO(2). Individual VO(2max) was obtained from the VO(2) measured during the last minute of the 1000-m or 2000-m maximal run. The average metabolic power output (E, kW) amounted to 141% and 102% of the individual maximal aerobic power (VO(2max)) from the shortest (250 m) to the longest (2000 m) distance, respectively. The average (SD) power provided by oxidative processes increased with the distance covered [from 0.64 (0.14) kW at 250 m to 1.02 (0.31) kW at 2000 m], whereas that provided by anaerobic sources showed the opposite trend. The net C(k) was a continuous power function of the speed over the entire range of velocities from 2.88 to 4.45 m x s(-1): C(k) = 0.02 x v(2.26) (r = 0.937, n = 32).     

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.     

Effects of genetic drift on variance components under a general model of epistasis

We analyze the changes in the mean and variance components of a quantitative trait caused by changes in allele frequencies, concentrating on the effects of genetic drift. We use a general representation of epistasis and dominance that allows an arbitrary relation between genotype and phenotype for any number of diallelic loci. We assume initial and final Hardy-Weinberg and linkage equilibrium in our analyses of drift-induced changes. Random drift generates transient linkage disequilibria that cause correlations between allele frequency fluctuations at different loci. However, we show that these have negligible effects, at least for interactions among small numbers of loci. Our analyses are based on diffusion approximations that summarize the effects of drift in terms of F, the inbreeding coefficient, interpreted as the expected proportional decrease in heterozygosity at each locus. For haploids, the variance of the trait mean after a population bottleneck is var(delta(z)) = sigma(n)k=1 FkV(A(k)), where n is the number of loci contributing to the trait variance, V(A(1)) = V(A) is the additive genetic variance, and V(A(k)) is the kth-order additive epistatic variance. The expected additive genetic variance after the bottleneck, denoted (V*(A)), is closely related to var(delta(z)); (V*(A)) = (1 - F) sigma(n)k=1 kFk-1V(A(k)). Thus, epistasis inflates the expected additive variance above V(A)(1 - F), the expectation under additivity. For haploids (and diploids without dominance), the expected value of every variance component is inflated by the existence of higher order interactions (e.g., third-order epistasis inflates (V*(AA. This is not true in general with diploidy, because dominance alone can reduce (V*(A)) below V(A)(1 - F) (e.g., when dominant alleles are rare). Without dominance, diploidy produces simple expressions: var(delta(z)) = sigma(n)k=1 (2F)kV(A(k)) and (V(A)) = (1 - F) sigma(n)k=1 k(2F)k-1V(A(k)). With dominance (and even without epistasis), var(delta(z)) and (V*(A)) no longer depend solely on the variance components in the base population. For small F, the expected additive variance simplifies to (V*(A)) approximately equal to (1 - F)V(A) + 4FV(AA) + 2FV(D) + 2FC(AD), where C(AD) is a sum of two terms describing covariances between additive effects and dominance and additive X dominance interactions. Whether population bottlenecks lead to expected increases in additive variance depends primarily on the ratio of nonadditive to additive genetic variance in the base population, but dominance precludes simple predictions based solely on variance components. We illustrate these results using a model in which genotypic values are drawn at random, allowing extreme and erratic epistatic interactions. Although our analyses clarify the conditions under which drift is expected to increase V(A), we question the evolutionary importance of such increases.     

Comparison of body water turnover in endurance runners and age-matched sedentary men

This study compared the body water turnover in endurance athletes and age-matched sedentary men. Eight competitive endurance athletes (20.8+/-1.9 yr) and age-matched eight sedentary men (21.6+/-2.5 yr) participated in this study. Total body water and body water turnover were measured using the deuterium (D(2)O) dilution technique. Urine samples were obtained every day for 10 days after oral administration of D(2)O. The day-by-day concentrations were used to calculate the biological half-life of D(2)O and body water turnover. Maximal oxygen uptake (VO(2max)) and oxygen uptake corresponding to ventilatory threshold (VO(2VT)) as an index of aerobic capacity were determined during a graded exercise test. Both VO(2max) and VO(2VT) were higher in the exercise group than in the sedentary group (P<0.05). The biological half-life of D(2)O was significantly shorter in the exercise group than in the sedentary group (5.89+/-0.81 days vs. 7.52+/-0.77 days, P<0.05), and the percentage of the body water turnover was significantly higher in the exercise group than in the sedentary group (11.99+/-1.96% vs. 9.39+/-1.21%, P<0.05). The body water turnover was correlated with VO(2max) and VO(2VT), respectively (P<0.05). Based on these findings, this study speculates that a level of physical activity may induce a body water turnover higher in the healthy state, since the better trained subjects have a higher body water turnover.     

Effects of habitual smoking on cardiorespiratory responses to sub-maximal exercise

The effects of habitual cigarette smoking on cardiorespiratory responses to sub-maximal and maximal work were evaluated in nine adult nonsmokers and nine smokers with a mean age of 33 yr. A maximal treadmill test was followed by three tests at 45, 60 and 75% of each subject's VO(2)max. Compared to nonsmokers, the habitual smokers had a non-significantly lower VO(2)max in L/min and per lean body mass (9 and 6%, respectively), but had higher %fat (p<0.01), resulting in a significantly lower VO(2)max per kg body wt (13%, p<0.03). Maximal exercise ventilation (V(E)) was 16% lower in smokers. During sub-maximal work at equivalent exercise stress levels in the two groups, the V(E)/VO(2) ratio was higher in smokers by an average of 11% because VO(2) was lower and the respiratory exchange ratio values were significantly elevated in smokers at 75% of VO(2)max. Blood lactate concentrations in smokers were higher as workloads increased and O(2) pulse (VO(2)/HR) was significantly lower throughout, indicating reduced O(2) extraction, probably due to carbon monoxide. The resting HR was significantly higher in smokers and the HR recovery following all three submaximal exercises was significantly slower in smokers. These results show that detrimental cardiorespiratory effects of chronic cigarette smoking in apparently healthy individuals are evident at moderate exercise levels as reduced gas exchange efficiency in lungs and muscles.     

Assessment of aerobic and anaerobic capacity of athletes in treadmill running tests.

The criteria of max VO2 and max O2D which are traditionally used in studying aerobic and anaerobic work capacity, have the different dimensions. While max VO2 is an index of the power of aerobic energy output, max O2D assesses the capacity of anaerobic sources. For a comprehensive assessment of physical working capacity of athletes, both aerobic and anaerobic capabilities should be represented in three dimensions, i.e. in indexes of power, capacity and efficiency. Experimental procedures have been developed for assessing these three parameters in treadmill running tests. It is proposed to assess anaerobic power by measuring excess CO2, concurrently with determination of max VO2. Maximal aerobic capacity is established as the product of max VO2 by the time of max VO2 maintenance determined in a special test with running at critical speed. The erogmetric criteria derived on the basis of the tests proposed, may be used for systematization of various physical work loads.     

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists.

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O(2) = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O(2) consumption (VO(2 max)) and arterial oxyhemoglobin saturation (Sa(O(2)), Ohmeda Biox ear oximeter) under normoxic (VO(2 max) = 4.88 +/- 0.43 l/min and Sa(O(2)) = 90.2 +/- 0.9, means +/- SD) and hypoxic (VO(2 max) = 4.24 +/- 0.49 l/min and Sa(O(2)) = 75.5 +/- 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO(2 max), under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO(2) (Pa(O(2))), arterial PCO(2), and Sa(O(2)) were determined, and the alveolar-arterial difference for PO(2) (A-aDO(2)) was calculated. Measurements of Pa(O(2)) and Sa(O(2)) were significantly lower and A-aDO(2) was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for Pa(O(2)), Sa(O(2)) and A-aDO(2) (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.     

Study of the circadian variation of different circulatory and respiratory functions at submaximal and maximal ergometer work (author's transl)]

The maximal aerobic power of six highly trained young cyclist, mean age 16.3 years and mean VO2max 4.9 l/min, was directly measured at intervals of 4 hrs. A Latin square design was used for the test order. At submaximal work of O2-consumption 2.4 to 4.4 l/min no circadian variation of any single function was found. However, at maximal work load the differences between the maxima and minima values were 12.4% for maximal work output (W max), 7.8% for expiratory minute volume (V Emax), 5.7% for maximal aerobic power (VO2max) and 3.4% for maximal heart rate (H Rmax). All the functions--with the exception of VO2max-had their minima at 0300 hrs; the minima of VO2max was reached already at 2300 hours. The maxima-values of V Emax and VO2max were measured at 1500 hrs, of W max and H Rmax at 0700 and of H Rrest at 1900 hrs correspondingly. A one-tailed test showed significant differences between the maxima and minima values of all variables (P less than 0.05). The results suggest a decreased cardiopulmonary working capacity at night. However, this impairment is only of practical importance if the work will be done near the limit of endurance capacity. Besides it will suggest, that the indirect methods for assessing the cardiopulmonary capacity based on VO2max and W170 are not useful at nighttime, because the presuppositions for these methods are limited of the time of day.     

Development of a submaximal test to predict elliptical cross-trainer VO2max

The purpose of this study was to develop an equation to predict VO2max from a submaximal elliptical cross-trainer test. Fifty-four apparently healthy subjects (25 men and 29 women, mean +/- SD age: 29.5 +/- 7.1 years, height: 173.3 +/- 12.6 cm, weight: 72.3 +/- 7.9 kg, percent body fat: 17.3 +/- 5.0%, and elliptical cross-trainer VO2max: 43.9 +/- 7.2 ml x kg(-1) x min(-1)) participated in the study and were randomly assigned to an original sample group (n = 40) and a cross-validation group (n = 14). Each subject completed an elliptical cross-trainer submaximal (3 5-minute submaximal stages) and a VO2max test on the same day, with a 15-minute rest period in between. Stepwise multiple regression analyses were used to develop an equation for estimating elliptical cross-trainer VO2max from the data of the original sample group. The accuracy of the equation was tested by using data from the cross-validation group. Because there was no shrinkage in R2 between the original sample group and the cross-validation group, data were combined in the final prediction equation (R2 = 0.732, standard error of the estimate = 3.91 ml x kg(-1) x min(-1), p < 0.05): VO2max = 73.676 + 7.383(gender) - 0.317(weight) + 0.003957(age x cadence) - 0.006452(age x heart rate at stage 2). The correlation coefficient between the predicted and measured VO2max values was r = 0.86. Dependent t-tests resulted in no significant differences (p > 0.05) between predicted (43.8 ml x kg(-1) x min(-1)) and measured (43.9 ml x kg(-1) x min(-1)) VO2max measurements. Results indicate that the protocol and equation developed in the current study can be used by exercise professionals to provide acceptably accurate estimates of VO2max in non-laboratory-based settings.     

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).     

A physiological description of critical velocity

Although critical velocity (CV) provides a valid index of aerobic function, the physiological significance of CV is not known. Twelve individuals performed exhaustive runs at 95% to 110% of the velocity at which VO2max was attained in an incremental test. VO2max was elicited in each run. Using the time to exhaustion at each velocity, CV was calculated for each participant. Using the time to achieve VO2max at each velocity, which was shorter at higher velocities, a parameter we have designated as CV' was calculated for each participant. During exercise at or below CV', VO2max cannot be elicited. CV (238+/-24 m x min(-1)) and CV' (239+/-25 m x min(-1)) were equal (t = 0.60, p = 0.56) and correlated (r = 0.97, p < 0.01). These results demonstrate that CV is the threshold intensity above which exercise of sufficient duration will lead to attainment of VO2max.