Genomic scan for maximal oxygen uptake and its response to training in the HERITAGE Family Study.

This study aimed to identify human genomic regions that are linked to maximal oxygen uptake (VO(2 max)) in sedentary individuals or to the responsiveness of VO(2 max) to a standardized endurance training program. The results of a genomic scan based on 289 polymorphic markers covering all 22 pairs of autosomes performed on the Caucasian families of the HERITAGE Family Study are presented. The mean spacing of the markers was 11 cM, and a total of 99 families and 415 pairs of siblings were available for the study. VO(2 max) in the sedentary state was adjusted for the effects of age, sex, body mass, fat mass, and fat-free mass, whereas the VO(2 max) response was adjusted for age and baseline level of the phenotype. Two analytic strategies were used: a single-point linkage procedure using all available pairs of siblings (SIBPAL) and a multipoint variance components approach using all the family data (SEGPATH). Results indicate that linkages at P values of 0.01 and better are observed with markers on 4q, 8q, 11p, and 14q for VO(2 max) before training and with markers on 1p, 2p, 4q, 6p, and 11p for the change in VO(2 max) in response to a 20-wk standardized endurance training program. These chromosomal regions harbor many genes that may qualify as candidate genes for these quantitative traits. They should be investigated in this and other cohorts.     

Endurance training of older men: responses to submaximal exercise.

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.     

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.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

The Na(+)-K(+)-ATPase alpha2 gene and trainability of cardiorespiratory endurance: the HERITAGE family study.

The Na(+)-K(+)-ATPase plays an important role in the maintenance of electrolyte balance in the working muscle and thus may contribute to endurance performance. This study aimed to investigate the associations between genetic variants at the Na(+)-K(+)-ATPase alpha2 locus and the response (Delta) of maximal oxygen consumption (VO(2 max)) and maximal power output (W(max)) to 20 wk of endurance training in 472 sedentary Caucasian subjects from 99 families. VO(2 max) and W(max) were measured during two maximal cycle ergometer exercise tests before and again after the training program, and restriction fragment length polymorphisms at the Na(+)-K(+)-ATPase alpha2 (exons 1 and 21-22 with Bgl II) gene were typed. Sibling-pair linkage analysis revealed marginal evidence for linkage between the alpha2 haplotype and DeltaVO(2 max) (P = 0.054) and stronger linkages between the alpha2 exon 21-22 marker (P = 0.005) and alpha2 haplotype (P = 0.003) and DeltaW(max). In the whole cohort, DeltaVO(2 max) in the 3.3-kb homozygotes of the exon 1 marker (n = 5) was 41% lower than in the 8.0/3.3-kb heterozygotes (n = 87) and 48% lower than in the 8.0-kb homozygotes (n = 380; P = 0.018, adjusted for age, gender, baseline VO(2 max), and body weight). Among offspring, 10.5/10.5-kb homozygotes (n = 14) of the exon 21-22 marker showed a 571 +/- 56 (SE) ml O(2)/min increase in VO(2 max), whereas the increases in the 10.5/4.3-kb (n = 93) and 4.3/4.3-kb (n = 187) genotypes were 442 +/- 22 and 410 +/- 15 ml O(2)/min, respectively (P = 0.017). These data suggest that genetic variation at the Na(+)-K(+)-ATPase alpha2 locus influences the trainability of VO(2 max) in sedentary Caucasian subjects.     

Major gene effects on exercise ventilatory threshold: the HERITAGE Family Study.

This study investigates whether there are major gene effects on oxygen uptake at the ventilatory threshold (VO(2VT)) and the VO(2VT) maximal oxygen uptake (VT%VO(2 max)), at baseline and in response to 20 wk of exercise training by using data on 336 whites and 160 blacks. Segregation analysis was performed on the residuals of VO(2VT) and VT%VO(2 max). In whites, there was strong evidence of a major gene, with 3 and 2% of the sample in the upper distribution, that accounted for 52 and 43% of the variance in baseline VO(2VT) and VT%VO(2 max), respectively. There were no genotype-specific covariate effects (sex, age, weight, fat mass, and fat-free mass). The segregation results were inconclusive for the training response in whites, and for the baseline and training response in blacks, probably due to insufficient power because of reduced sample sizes or smaller gene effect or both. The strength of the genetic evidence for VO(2VT) and VT%VO(2 max) suggests that these traits should be further investigated for potential relations with specific candidate genes, if they can be identified, and explored through a genome-wide scan.     

Influence of resistance training on cardiorespiratory endurance and muscle power and strength in young athletes

The purpose of this study was to investigate the influence of additional resistance training on cardiorespiratory endurance in young (15.8 ± 0.8 yrs) male basketball players. Experimental group subjects (n=23) trained twice per week for 12 weeks using a variety of general free-weight and machine exercises designed for strength acquisition, beside ongoing regular basketball training program. Control group subject (n=23) participated only in basketball training program. Oxygen uptake (VO(2max)) and related gas exchange measures were determined continuously during maximal exercise test using an automated cardiopulmonary exercise system. Muscle power of the extensors and flexors was measured by a specific computerized tensiometer. Results from the experimental group (VO(2max) 51.6 ± 5.7 ml.min(-1).kg(-1) pre vs. 50.9 ± 5.4 ml.min(-1).kg(-1) post resistance training) showed no change (p>0.05) in cardiorespiratory endurance, while muscle strength and power of main muscle groups increased significantly. These data demonstrate no negative cardiorespiratory performance effects on adding resistance training to ongoing regular training program in young athletes.     

Interactive effects of body posture and exercise training on maximal oxygen uptake

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

Changes in maximal aerobic capacity with age in endurance-trained women: 7-yr follow-up.

On the basis of cross-sectional data, we previously reported that the absolute, but not the relative (%), rate of decline in maximal oxygen consumption (VO(2 max)) with age is greater in endurance-trained compared with healthy sedentary women. We tested this hypothesis by using a longitudinal approach. Eight sedentary (63 +/- 2 yr at follow-up) and 16 endurance-trained (57 +/- 2) women were reevaluated after a mean follow-up period of 7 yr. At baseline, VO(2 max) was ~70% higher in endurance-trained women (48.1 +/- 1.7 vs. 28.1 +/- 0.8 ml. kg(-1). min(-1). yr(-1)). At follow-up, body mass, fat-free mass, maximal respiratory exchange ratio, and maximal rating of perceived exertion were not different from baseline in either group. The absolute rate of decline in VO(2 max) was twice as great (P < 0.01) in the endurance-trained (-0.84 +/- 0.15 ml. kg(-1). min(-1). yr(-1)) vs. sedentary (-0.40 +/- 0.12 ml. kg(-1). min(-1). yr(-1)) group, but the relative rates of decline were not different (-1.8 +/- 0.3 vs. -1.5 +/- 0.4% per year). Differences in rates of decline in VO(2 max) were not related to changes in body mass or maximal heart rate. However, among endurance-trained women, the relative rate of decline in VO(2 max) was positively related to reductions in training volume (r = 0.63). Consistent with this, the age-related reduction in VO(2 max) in a subgroup of endurance-trained women who maintained or increased training volume was not different from that of sedentary women. These longitudinal data indicate that the greater decrease in maximal aerobic capacity with advancing age observed in middle-aged and older endurance-trained women in general compared with their sedentary peers is due to declines in habitual exercise in some endurance-trained women. Endurance-trained women who maintain or increase training volume demonstrated age-associated declines in maximal aerobic capacity not different from healthy sedentary women.     

A program of moderate physical training for Wistar rats based on maximal oxygen consumption

Moderate physical training is often associated with improved cardiorespiratory fitness in athletes and the general population. In animals, studies are designed to investigate basic physiology that could be invasive and uncomfortable for humans. The standardization of an exercise training protocol for rats based on maximal consumption of oxygen (VO(2)max) is needed. This study validated a program of moderate physical training for Wistar rats based on VO(2)max determined once a week. A 10-stage treadmill running test was developed to measure VO(2)max through an indirect, open circuit calorimeter. Thirty male Wistar rats (210-226 g) were randomly assigned to either a nontrained group or a trained group. The animals were evaluated weekly to follow their VO(2)max during 8 weeks of moderate training and to adjust the intensity of the protocol of training. The soleus muscle was removed for determination of citrate synthase activity. Trained animals maintained their values of VO(2)max during a moderate running training and showed a significant less body weight gain. An increase of 42% in citrate synthase activity of the soleus muscle from trained rats was found after the training program. Our study presents a protocol of moderate physical training for Wistar rats based on VO(2)max. Peripheral adaptations such as the values of citrate synthase activity also responded to the moderate training program imposed as observed for VO(2)max. Other studies can use our protocol of moderate training to study the physiologic adaptations underlying this specific intensity of training. It will provide support for study with humans.     

Muscle morphological and biochemical adaptations to training in obese Zucker rats

The purposes of the present study were to characterize the histochemical and enzymatic profiles of various hindlimb skeletal muscles, as well as to determine maximal O2 consumption (VO2max) and respiratory exchange ratios (R) during steady-state exercise in the obese Zucker rat. The changes that occurred in these parameters in response to a 6-wk training program were then assessed. Obese rats were randomly assigned to a sedentary or training group. Lean littermates served as a second control. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 day/wk for 6 wk. During week 6, VO2max and R during a steady-state run (74% max) were determined. After 2 days of inactivity, hindlimb muscles were excised, stained for fiber type and capillaries, and assayed for hexokinase, citrate synthase, cytochrome oxidase, and beta-hydroxyacetyl-CoA dehydrogenase. The obese sedentary rats demonstrated greater oxidative enzyme activities per gram of muscle tissue than their lean littermates, greater R values during submaximal exercise of the same relative intensity, and greater absolute VO2max values. Training resulted in a 20-56% increase in oxidative enzymes, a 10% increase in VO2max, and an increase in capillary density in the soleus and plantaris. There was no alteration in R values during exercise at 74% VO2max or in fiber type composition in response to exercise training. Results suggest that the muscle of the obese Zucker rat manifests a greater oxidative capacity than the muscle of its lean littermates. The apparent inability of the obese rat to increase its use of fat during submaximal exercise of the same relative intensity in response to training remains to be elucidated.     

Ventilatory chemosensitive adaptations to intermittent hypoxic exposure with endurance training and detraining.

The present study was performed to clarify the effects of intermittent exposure to an altitude of 4,500 m with endurance training and detraining on ventilatory chemosensitivity. Seven subjects (sea-level group) trained at sea level at 70% maximal oxygen uptake (VO2 max) for 30 min/day, 5 days/wk for 2 wk, whereas the other seven subjects (altitude group) trained at the same relative intensity (70% altitude VO2 max) in a hypobaric chamber. VO2 max, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response, as an index of central hypercapnic chemosensitivity (HCVR) and as an index of peripheral chemosensitivity (HCVRSB), were measured. In both groups VO2 max increased significantly after training, and a significant loss of VO2 max occurred during 2 wk of detraining. HVR tended to increase in the altitude group but not significantly, whereas it decreased significantly in the sea-level group after training. HCVR and HCVRSB did not change in each group. After detraining, HVR returned to the pretraining level in both groups. These results suggest that ventilatory chemosensitivity to hypoxia is more variable by endurance training and detraining than that to hypercapnia.     

Fifteen-day cessation of training on selected physiological and performance variables in women runners

This study examined the effects of a 15-day cessation of training on maximal oxygen consumption and selected physiological variables (maximal heart rate, cardiac output [Q], stroke volume [SV], arteriovenous oxygen difference [(a-v)O2 diff], blood plasma concentration) in 15 women middle-distance competitive runners (.VO2max: 49.8 +/- 1.1 ml.kg(-1).min(-1)). Subjects were randomly assigned to a cessation training (CT, n = 7) or maintenance training (MT, n = 8) group and tested every 5 days. Q was measured by CO2 rebreathing from which SV and (a-v)O2 diff were calculated. No significant changes were found at day 5. After 10 days there was a significant decrement in .VO2max (3.8 ml.kg(-1).min(-1)) in the CT group, being significantly lower than MT but no changes thereafter in any physiological variables. Performance (2,400 m) times did not change for MT but was significantly slower (21.5 +/- 7.1 seconds) for the CT group after 15 days, corresponding to the 7.8% decrease in .VO2max. These findings suggest that in competitive women middle-distance runners, actual performance decrements found after 15 days of CT most likely are due to declines in .VO2max.     

Effect of endurance training on oxygen uptake kinetics during treadmill running.

The purpose of this study was to examine the effect of endurance training on oxygen uptake (VO(2)) kinetics during moderate [below the lactate threshold (LT)] and heavy (above LT) treadmill running. Twenty-three healthy physical education students undertook 6 wk of endurance training that involved continuous and interval running training 3-5 days per week for 20-30 min per session. Before and after the training program, the subjects performed an incremental treadmill test to exhaustion for determination of the LT and the VO(2 max) and a series of 6-min square-wave transitions from rest to running speeds calculated to require 80% of the LT and 50% of the difference between LT and maximal VO(2). The training program caused small (3-4%) but significant increases in LT and maximal VO(2) (P<0.05). The VO(2) kinetics for moderate exercise were not significantly affected by training. For heavy exercise, the time constant and amplitude of the fast component were not significantly affected by training, but the amplitude of the VO(2) slow component was significantly reduced from 321+/-32 to 217+/-23 ml/min (P<0.05). The reduction in the slow component was not significantly correlated to the reduction in blood lactate concentration (r = 0. 39). Although the reduction in the slow component was significantly related to the reduction in minute ventilation (r = 0.46; P<0.05), it was calculated that only 9-14% of the slow component could be attributed to the change in minute ventilation. We conclude that the VO(2) slow component during treadmill running can be attenuated with a short-term program of endurance running training.     

A new approach to assessing maximal aerobic power in children: the Odense School Child Study

In two experiments maximal aerobic power (VO2max) calculated from maximal mechanical power (Wmax) was evaluated in 39 children aged 9-11 years. A maximal multi-stage cycle ergometer exercise test was used with an increase in work load every 3 min. In the first experiment oxygen consumption was measured in 18 children during each of the prescribed work loads and a correction factor was calculated to estimate VO2max using the equation VO2max = 12.Wmax + 5.weight. An appropriate increase in work rate based on height was determined for boys (0.16 W.cm-1) and girls (0.15 W.cm-1) respectively. In the second experiment 21 children performed a maximal cycle ergometer exercise test twice. In addition to the procedure in the first experiment a similar exercise test was performed, but without measurement of oxygen uptake. Calculated VO2max correlated significantly (p less than 0.01) with those values measured in both boys (r = 0.90) and girls (r = 0.95) respectively, and the standard error of estimation for VO2max (calculated) on VO2max (measured) was less than 3.2%. Two expressions of relative work load (%VO2max and %Wmax) were established and found to be closely correlated. The relative work load in %VO2max could be predicted from the relative work load in %Wmax with an average standard error of 3.8%. The data demonstrate that calculated VO2max based on a maximal multi-stage exercise test provides an accurate and valid estimate of VO2max.     

Effects of sprint training on maximal stroke volume of rats with a chronic myocardial infarction.

The hemodynamic response to maximal exercise was determined in rats with a chronic myocardial infarction (MI) that were subjected to 6-8 wk of high-intensity sprint training (HIST) or limited exercise activity (sedentary control). Training was performed 6 days/wk and consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animal's maximal O2 uptake (VO2max). The left ventricular infarct size for the HIST and sedentary control rats was 35 +/- 4 and 34 +/- 3% of the total endocardial circumference, respectively. VO2max was significantly greater for MI rats subjected to the HIST paradigm than for sedentary control rats. This increase in VO2max was due to an increase in the maximal stroke volume that could be generated by the HIST rat during exercise, inasmuch as the maximal heart rate response and the ability to extract O2 from the blood were similar between the two groups of rats. Citrate synthase activities measured in the plantaris muscle of the HIST and sedentary control rats were similar. These results suggest that the increase in VO2max produced with HIST in MI rats may be linked to changes in central cardiac function, as indicated by the increase in maximal stroke volume that could be generated by the MI rat during maximal exercise conditions.     

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.     

Frequency and duration of interval training programs and changes in aerobic power.

This study was designed to ascertain whether 7- and 13-wk interval training programs with training frequencies of 2 days/wk would produce improvement in maximal aerobic power (VO2max) comparable to that obtained from 7- and 13-wk programs of the same intensity consisting of 4 training days/wk. Sixty-nine young healthy college males were used as subjects. After training, there was a significant increase in VO2max (bicycle ergometer, open-circuit spirometry) that was independent of both training frequency and duration. However, there was a trend for greater gains after 13 wk. Maximal heart rate (direct lead ECG) was significantly decreased following training, being independent of both training frequency and duration. Submaximal VO2 did not change with training but submaximal heart rate decreased significantly with greater decreases the more frequent and longer the training. Within the limitations of this study, these results indicate that: 1) maximal stroke volume and/or maximal avO2 difference, principle determinants of VO2max, are not dependent on training frequency nor training duration, and 2) one benefit of more frequent and longer duration interval training is less circulatory stress as evidenced by decreased heart rate, during submaximal exercise.