Decline In VO2max Research Articles

Prescribing exercise intensity for older women.

For the purpose of prescribing exercise intensity, the American College of Sports Medicine (ACSM) provides guidelines for relating the perceived level of exertion and the heart rate (HR) response during exercise, expressed either as a percentage of maximal HR or of HR reserve, to a percentage of maximal aerobic power (VO2max). However, because maximal HR and VO2max decline with age, it is possible that these guidelines are not appropriate for an older population. The purpose of this study was to evaluate in 60- to 72-year-old women the relationships among the common methods of prescribing exercise intensity. Participants were 112 healthy but sedentary women, aged 66 +/- 4 years, who performed treadmill walking at four speeds. Subjects were recruited from the community, and exercise tests were performed at a university laboratory facility. VO2max and maximal HR were determined during treadmill walking. The HR and VO2 responses to walking 6 minutes at each of four speeds ranging from 67 to 107 m/min, along with ratings of perceived exertion (RPE) and plasma lactate levels, were determined on a separate day. The exercise bouts required an average of 55 +/- 10%, 64 +/- 12%, 77 +/- 12%, and 91 +/- 9% of VO2max. Corresponding HR values were 64 +/- 8%, 70 +/- 9%, 81 +/- 10%, and 92 +/- 7% of maximal HR, and they were within the expected ranges based on ACSM guidelines. HR values as a percentage of HR reserve were much lower than expected based on the guidelines. RPE values were lower than expected at a given %VO2max, and plasma lactate levels were also relatively low, suggesting that older women are able to exercise at a higher percentage of VO2max than levels currently recommended. The results indicate that HR expressed as a percentage of maximal HR is an appropriate method of prescribing exercise intensity in healthy, sedentary 60- to 72-year-old women. The HR reserve method is not recommended in this population because it will likely result in the exercise being performed at a higher than expected percentage of VO2max.

Age-related changes in the microcirculation of skeletal muscle.

The age-related reduction in exercise capacity is associated with a reduction in cardiac output and maximal oxygen consumption (VO2max). The loss of muscle mass explains a large portion of the age-related decline in VO2max. The capillary supply to a muscle fibre is primarily determined by its size, but also by its metabolic profile and the metabolic profile of surrounding fibres. Thus the age-related fibre atrophy and changes in the fibre type composition are expected to be accompanied by changes in the capillarisation. The exchange of oxygen, blood-borne energy sources, metabolites and heat between the blood and muscle tissue takes place in the microcirculation. Changes in the microcirculation may thus affect the functioning and viability of the muscle. The resting blood flow is minimally affected by age, but blood flow during or following exercise is generally reduced. This may in part be due to a reduced vasodilatory capacity and a decreased capillarisation. However, the coupling between capillary supply to a fibre and its metabolic profile or the profile of the surrounding fibres is maintained. There are some changes in ultrastructure of the endothelium. The age-related changes in the microcirculation are associated with a reduced VO2max and exercise capacity. The adaptability of the microcirculation is maintained at old age.

A model of oxygen transport capacity changes for independently living older men and women.

The purpose of the present investigation was to describe, for a subset of a large random survey of men and women, restricted to the ages of 55 to 85 years, the physiological decay pattern for aerobic fitness and contributing factors of cardiovascular and pulmonary function. The time course of the age-related changes in maximal oxygen uptake (VO2max), ventilatory threshold (TVE), maximal ventilation (VEmax), maximal heart rate (HRmax), and O2 pulse (VO2max/HRmax) were examined by fitting the data to a decaying exponential model by use of a least-squares parameter estimation technique. The time constant (tau) was used to describe the rate of decline. The women showed a much slower decline in VO2max (tau = 47.4 years) and TVE (tau = 83.3 years) than the men (tau = 20.8 and 15.4 years, respectively). There was a significant age-related decrease in body weight (0.45 kg.yr-1) in the men, whereas the women showed no change. Pulmonary function did not limit performance based on the very slow decline in VEmax and the normal FEV1.0. The decay in HRmax was better described by a linear model, resulting in an extremely slow tau. Maximal O2 pulse clearly exhibited an exponential decay, with a shorter tau (tau men = 13.5 years; tau women = 28.5 years) than any other variable.

Change in aerobic fitness of patients with multiple sclerosis during a 6‐month training program

Twenty‐three individuals with multiple sclerosis (MS) participated in a 6‐month exercise training program; 11 ambulatory (AMB) and 8 semi‐ambulatory (SEMI). Four persons with MS served as non‐exercising controls (C). A test of maximal aerobic power (VO2max) was administered at baseline to all subjects. AMB and SEMI subjects exercised on alternating days for 30 minutes, at 55‐60% VO2max using either a commercially available recumbent or upright combination leg/arm bicycle ergometer. At the end of 12 and 24 weeks, exercising subjects were re‐evaluated. The C group was only re‐evaluated at 24 weeks. The results show that the AMB and SEMI groups experienced a +20% and +5% improvement in VO2max, respectively. The C group averaged a 12% decline in VO2max during the 6 months. These data demonstrate the possibility that although exercise improves cardiovascular fitness of some persons with less severe MS, this beneficial response may not apply to the more severely impaired patient. Nevertheless, improved cardiovascular health at any level may enhance the overall rehabilitation outcome of many individuals in this patient population.

Exercise-induced hypoxaemia in elite endurance athletes. Incidence, causes and impact on VO2max.

Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50% of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max. The mechanism(s) to explain this exercise-induced hypoxaemia (EIH) remain controversial. However, hypoventilation and venoarterial shunt do not appear to be involved. By elimination, this suggests that ventilation-perfusion inequality and/or pulmonary diffusion limitations must contribute to EIH in this population. Theoretical and direct experimental evidence exists to support the notion that both ventilation-perfusion inequality and diffusion disequilibrium contribute to EIH; however, the relative contribution of each factor remains to be determined. In athletes who exhibit a profound EIH, the exercise-induced decline in arterial oxygenation results in a limitation of VO2max. Further, athletes who exhibit EIH at sea level suffer more severe gas exchange impairments during short term exposure to altitude than athletes or nonathletes who do not exhibit EIH at sea level. This finding explains much of the observed variance in the decline in VO2max among individuals during short term altitude or hypoxia exposure.

Multivariate Model for Defining Changes in Maximal Physical Working Capacity of Men, Ages 25 to 70 Years

The purpose of this study was to develop a multivariate model with cross-sectional data that defined the decline in VO2max over time, and cross-validate the model with longitudinal data. The cross-sectional sample consisted of 1,608 healthy men who ranged in age from 25 to 70 years. VO2max was directly measured during a maximum Bruce treadmill stress test. Regression analysis showed that the cross-sectional age and VO2max relationship was linear, r = 0.45 and the age decline in VO2max was 0.48 ml/kg/min/year. Multiple regression developed the multivariate model from age, percent body fat (%fat), self-report physical activity (SR-PA), and the interaction of SR-PA and %fat (R = 0.793). Accounting for the variance in percent body fat and exercise habits decreased the influence of age on the decline of VO2max to just −0.27 ml/kg/min/year. This showed that much of decline in maximal physical working capacity was due to physical activity level and percent body fat, not aging. The multivariate equation was applied to the data of the longitudinal sample of 156 men who had been tested twice (Mean AgeΔ = 3.1 ± 1.2 years). The correlation between the measured and estimated change in VO2max over time (ΔVO2max) was 0.75. The results of the study showed that changes in body composition and exercise habits had more of an influence on changes in maximal physical working capacity than aging. The developed model provides a useful way to quantify the changes in physical working capacity with aging.

Aging, fitness and muscular performance

A decrease in habitual physical activity accompanies old age in mammalian species and in healthy man.74,142 This is not simply a consequence of a parallel decline in exercise capacity, and factors other than those which limit aerobic capacity and endurance performance must be involved.143 Moreover, most old people remain at least moderately active.144 Everyday activities may require cardiorespiratory and muscle performance which is much nearer the maximum in elderly individuals than in younger people and further reduction in reserves by, for example, illness, will more readily cause disability.Regular moderate activity is sufficient to mitigate declining exercise capacity and muscle performance and conditioning programmes may well confer additional benefits even at advanced ages. Exercise remains good for you regardless of age. A suitable programme is one of moderate to high workrates, involving large muscle groups and performed for 15–30 minutes every other day.145 The intensity is best guided by heart rate, for which a variety of formulae have been proposed.146The complex interaction of physiological factors influencing muscular performance has been illustrated. Only when these physiological processes are disentangled and better defined will we elucidate the molecular mechanisms which underlie age-associated changes. It is not yet possible to define the relative importance of intrinsic and extrinsic influences, but the proportion of the decline in VO2 max which is directly attributable to intrinsic aging is smaller than is usually assumed, probably less than 50%.147 While the most critical determinant of VO2 max in young subjects is probably cardiac output,148 we now recognize that in elderly people the balance shifts; muscle performance, changes in blood distribution and peripheral microvascular capacity become ever more important determinants of exercise performance and should command increasing research interest.

Slowing the Aging Process with PHYSICAL ACTIVITY

1. Functional capacity declines 0.75% to 1.0% per year after the age of 30. Exercise is an intervention that will help maintain and enhance functional ability as chronological age increases. 2. Exercise reduces the age-related decline in VO2 max, reduces mean blood pressure and systemic vascular resistance, preserves lean body mass and decreases fat deposits, increases HDL and decreases triglycerides, increases bone mineral content, improves basal metabolic rate, increases muscle strength, and increases cognitive functioning. 3. Exercise programs can be designed to maintain or improve the cardiovascular system without the demands and dangers of an exhaustive workout. 4. The exercise prescription should include aerobic exercise at 60% of maximal heart rate at least every other day.

Fatigue of mammalian skeletal muscle in situ during repetitive contractions

When the gastrocnemius-plantaris muscle group of the dog is stimulated to contract repetitively for 30 min at frequencies high enough to generate VO2 levels at or near VO2 max, VO2 and mechanical performance decline with time. This decline with time is fatigue, and it occurs during twitch and tetanic contractions that are isometric or isotonic. There is oxidation of the mitochondrial electron transport system, and net lactic acid output is transient, ending after 20 min of contractions. Energy and substrate stores and intracellular pH are only moderately changed and do not appear to be well correlated with the development of fatigue. Blood flow through the muscle is well correlated with the development of fatigue and decreases as fatigue develops in a manner that keeps the blood arteriovenous O2 difference nearly constant. Changing the blood flow alters the rate of development of fatigue as an inverse relation, and this response does not appear to be related to changes in the availability of O2 in the mitochondria. Nerve-muscle transmission of excitation does not seem to be involved in the development of fatigue. Excitation-contraction coupling is well accepted to be at least part of the genesis of the development of fatigue. Metabolic limitations and control may affect excitation-contraction coupling by one or more changes in the internal environment. Blood flow affects this system by an unknown mechanism. The role of blood flow in fatigue deserves further consideration.

Long-term effects of physical training on aerobic capacity: controlled study of former elite athletes

We studied 15-yr changes in physical training, subcutaneous fat, and maximal oxygen consumption (VO2 max) in male former elite athletes (27 long-distance runners and 9 bobsledders) and in a control group of 23 normal men. In 1973, elite athletes all trained vigorously, whereas in 1988 there was a great interindividual variation in physical training. In the lowest tertile of runners' training activity in 1988 (n = 9), the rate of decline in VO2max during the 15 yr was 1.11 +/- 0.15 (SE) ml.kg-1.min-1.yr-1, or 16% per decade, whereas the most active quintile of runners (n = 5) tended to increase VO2max (NS). The remaining 13 runners showed a rate of decline in VO2max of 0.54 +/- 0.14 ml.kg-1.min-1.yr-1, or 7% per decade. The rates of decline were 0.22 +/- 0.12 and 0.56 +/- 0.10 ml.kg-1.min-1.yr-1, or 5 and 11% per decade, in bobsledders and controls, respectively. When normalized for lean body mass instead of body weight, VO2max showed a reduced variability in the rate of decline, with values ranging from 0.00 +/- 0.27 (most active runners) to 0.69 +/- 0.15 ml.kg lean body mass-1.min-1.yr-1 (least active runners). In multiple linear regression analysis, 15-yr changes in mileage, running pace, and truncal fat together explained 51% of variance in the 15-yr change of VO2max normalized for body weight in runners and 41% in all study men. In runners, change in truncal fat was dependent on changes in both mileage and running pace. In the presence of physical training and anthropometric variables in the regression equation, the 15-yr decrease in maximum heart rate was only modestly predictive of the change in VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

Maximal O2 uptake of in situ dog muscle during acute hypoxemia with constant perfusion

We investigated the relationships among maximal O2 uptake (VO2max), effluent venous PO2 (PvO2), and calculated mean capillary PO2 (PCO2) in isolated dog gastrocnemius in situ as arterial PO2 (PaO2) was progressively reduced with muscle blood flow held constant. The hypothesis that VO2max is determined in part by peripheral tissue O2 diffusion predicts proportional declines in VO2max and PCO2 if the diffusing capacity of the muscle remains constant. The inspired O2 fraction was altered in each of six dogs to produce four different levels of PaO2 [22 +/- 2, 29 +/- 1, 38 +/- 1, and 79 +/- 4 (SE) Torr]. Muscle blood flow, with the circulation isolated, was held constant at 122 +/- 15 ml.100 g-1.min-1 while the muscle worked maximally (isometric twitches at 5-7 Hz) at each of the four different values of PaO2. Arterial and venous samples were taken to measure lactate, pH, PO2, PCO2, and muscle VO2. PCO2 was calculated using Fick's law of diffusion and a Bohr integration procedure. VO2max fell progressively (P less than 0.01) with decreasing PaO2. The decline in VO2max was proportional (R = 0.99) to the fall in both muscle PvO2 and calculated PCO2 while the calculated muscle diffusing capacity was not different among the four conditions. Fatigue developed more rapidly with lower PaO2, although lactate output from the muscle was not different among conditions. These results are consistent with the hypothesis that resistance to O2 diffusion in the peripheral tissue may be a principal determinant of VO2max.

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.

Maximal Oxygen Uptake Relative to Plasma Volume Expansion

Controversy exists as to whether plasma volume (PV) expansion has the potential to increase maximal oxygen uptake (VO2max). In the present study, VO2max and exercise time to fatigue were measured in nine untrained men when plasma volume (PV) was normal and then again on the next day following two levels of PV expansion. Resting PV was expanded (via intravenous infusion of a 6% dextran solution) by 282 +/- 16 ml (i.e., PVX-1) and then by 624 +/- 26 ml (i.e., PVX-2). PVX-1 increased stroke volume (CO2 rebreathing) during submaximal exercise by 15% (P less than 0.05) above normal levels. VO2max following PVX-1 was increased 4% (P less than 0.05; 3.78 to 3.92 l/min) despite a 4% reduction in hemoglobin concentration. Exercise time to fatigue was also increased (P less than 0.05). PVX-2 resulted in an 11% (P less than 0.05) reduction in hemoglobin concentration during maximal exercise and a return of VO2max and exercise time to normal levels. In summary, we have observed in untrained men that 200-300 ml of PV expansion increases SV, measured during submaximal exercise, yet causes only a small amount of hemodilution. As a result, VO2max is increased slightly and performance is improved. Further PV expansion to levels 500-600 ml above normal results in an excessive hemodilution and a subsequent decline in VO2max and performance to normal levels. There is an optimal PV for eliciting VO2max in untrained men which appears to be approximately 200-300 ml above their normal levels.

The effect of detraining and reduced training on the physiological adaptations to aerobic exercise training.

In previously sedentary individuals, regularly performed aerobic exercise results in significant improvements in exercise capacity. The development of peak exercise performance, as typified by competitive endurance athletes, is dependent upon several months to years of aerobic training. The physiological adaptations associated with these improvements in both maximal exercise performance, as reflected by increases in maximal oxygen uptake (VO2max), and submaximal exercise endurance include increases in both cardiovascular function and skeletal muscle oxidative capacity. Despite prolonged periods of aerobic training, reductions in maximal and submaximal exercise performance occur within weeks after the cessation of training. These losses in exercise performance coincide with declines in cardiovascular function and muscle metabolic potential. Significant reductions in VO2max have been reported to occur within 2 to 4 weeks of detraining. This initial rapid decline in VO2max is likely related to a corresponding fall in maximal cardiac output which, in turn, appears to be mediated by a reduced stroke volume with little or no change in maximal heart rate. A loss in blood volume appears to, at least partially, account for the decline in stroke volume and VO2max during the initial weeks of detraining, although changes in cardiac hypertrophy, total haemoglobin content, skeletal muscle capillarisation and temperature regulation have been suggested as possible mediating factors. When detraining continues beyond 2 to 4 weeks, further declines in VO2max appear to be a function of corresponding reductions in maximal arterial-venous (mixed) oxygen difference. Whether reductions in oxygen delivery to and/or extraction by working muscle regulates this progressive decline is not readily apparent. Changes in maximal oxygen delivery may result from decreases in total haemoglobin content and/or maximal muscle blood flow and vascular conductance. The declines in skeletal muscle oxidative enzyme activity observed with detraining are not causally linked to changes in VO2max but appear to be functionally related to the accelerated carbohydrate oxidation and lactate production observed during exercise at a given intensity. Alternatively, reductions in submaximal exercise performance may be related to changes in the mean transit time of blood flow through the active muscle and/or the thermoregulatory response (i.e. degree of thermal strain) to exercise. In contrast to the responses observed with detraining, currently available research indicates that the adaptations to aerobic training may be retained for at least several months when training is maintained at a reduced level. Reductions of one- to two-thirds in training frequency and/or duration do not significantly alter VO2max or submaximal endurance time provided the intensity of each exercise session is maintained.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiopulmonary fitness in a sample of Malaysian population.

Lung capacity and maximum oxygen uptake (VO2max) were measured directly in 167 healthy males, from all the main races in Malaysia. Their ages ranged from 13 to 59 years. They were divided into five age groups (A to E), ranging from the second to the sixth decade. Lung capacities were determined using a dry spirometer and VO2max was taken as the maximum rate of oxygen consumption during exhaustive exercise on a cycle ergometer. Mean forced vital capacity (FVC) was 3.3 +/- 0.5 l and it correlated negatively with age. Mean VO2max was 3.2 +/- 0.2 l.min-1 (56.8 +/- 3.5 ml.kg-1.min-1) in Group A (13-19 years) compared to 1.7 +/- 0.2 l.min-1 (28.9 +/- 2.9 ml.kg-1.min-1) in Group E (50-59 years). Regression analysis revealed an age-related decline in VO2max of 0.77 ml.kg-1.min-1.year-1. Multiple regression of the data gave the following equations for the prediction of an individual's VO2max: VO2max (l.min-1) = 1.99 + 0.035 (weight)-0.04 (age), VO2max (ml.kg-1.min-1) = 67.7-0.77 (age), where age is in years, weight in kg. In terms of VO2max as an index of cardiopulmonary performance. Malaysians have a relatively lower capacity when related to the Swedish norms or even to those of some Chilean workers. Malaysians were, however, within the average norms of the American Heart Association's recommendations. Age-related decline in VO2max was also somewhat higher in the Malaysians.

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.

Exercise and the Elderly

Data from cross-sectional studies suggest that VO2max declines in adulthood at a rate of 0.40-0.45 ml.kg-1.min-1 per year in males and 0.30 ml.kg-1.min-1 per year in females. Longitudinal studies suggest that the loss is much greater for males, approximating 1.0 ml.kg-1.min-1 per year or more. The rate of loss may be greater in sedentary compared to active individuals. The decline in VO2max with age appears to be inevitable, and a major contributing factor may be the decline in maximal cardiac output. A reduced maximal heart rate is a consistent finding, and this may be due to decreased end-organ sensitivity to catecholamines. Maximal stroke volume may or may not decrease, and physical training status may be a determining factor. The most recent evidence suggests increased dependence upon the Frank-Starling mechanism, resulting in an increased stroke volume to offset the decline in maximal heart rate. Cardiac output is thought to be maintained in this manner. Use of this mechanism may depend upon the absence of underlying disease. Therefore, investigators who vigorously screen potential subjects for occult coronary disease may report findings different from those who do not. Maximal a-vO2 difference may or may not decline in the elderly. The research is divided, and there is support for both beliefs. Several factors typical of the elderly, including a decline in muscle mass, increased blood distribution to the skin during exercise, and a potentially lower capillary/fiber ratio, would contribute to a lower a-vO2 difference. On the other hand, in those subjects with reduced cardiac output, there may be greater dependence upon a-vO2 difference during maximal exercise. Pulmonary function does not appear to limit VO2max, although the elderly may be less efficient while breathing during exercise. However, the higher ventilation and higher ventilatory equivalent for oxygen observed during submaximal exercise could be due to higher relative stress in the elderly. Elderly males and females are capable of demonstrating a training effect in response to endurance training regardless of previous physical activity patterns and current training status. The degree of change with training, expressed in relative terms, appears to be comparable to that demonstrated by younger subjects. Physiological factors contributing to an increased VO2max as a result of training appear to be similar in elderly and younger subjects, with the possible exception of no change in maximal a-vO2 difference in the elderly. This point is somewhat controversial.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of water-training in the maintenance of cardiorespiratory endurance of athletes.

The effectiveness of water-training in maintaining cardiorespiratory endurance was investigated in 16 cross country athletes, 18--24 years. Following a competitive season, subjects were stress-tested (T1) and divided into three equated groups based on VO2 max. Group I (n=5) continued training as it had during the competition season. Group II (n=5) underwent an experimental period of water-training, and Group III (n=6) let their training lapse. Subjects in the water-training group exercised in deep water for 40 minutes, 6 days/week for 3 weeks, supported by a flotation device which permitted them to engage in a running type activity, resembling their natural running form. All subjects were retested after 3 weeks (T2). A non-significant F ratio from an analysis of variance at T1 confirmed the equality of the three groups in terms of VO2 max. Analysis of covariance at T2 using T1 VO2 max values as covariates revealed a significant (p less than .05) F ratio reflecting a significant (p less than .05) difference between the regular training group and the group which let its training lapse. The water-training group did not differ significantly from the regular training group indicating that the water-training programme prevented a significant decline in VO2 max.

Age and Aerobic Power in Women: A Longitudinal Study

Thirty-six women from an original cross-sectional population of 81 were retested after an average time span of 6.1 years to determine the longitudinal effects of aging on aerobic power. Women in their 20s maintained a constant level of VO2max. All other age groups showed a decrease in aerobic power (l . min-1 and ml . kg-1 . min-1) similar to that observed in the cross-sectional study. Although the decline in VO2max was similar for both groups, active women increased walk time on the treadmill, while sedentary women decreased in endurance time. Maximal heart rate also decreased with age but the rate of decrease was not constant across time. HRmax remained relatively steady during the middle years and then declined at a faster rate in the 50- and 60-year-old age groups. The results of the present study suggest that cross-sectional studies can provide valid information about the effect of age on response to maximal exercise provided that close attention is paid to the limitations underlying regression therapy. The data also indicate a need to consider alternatives to linear regression analysis of aging effects, since the rate of change of some variables is not constant across age.

Physiological variables during 10 years of endurance exercise

The reported decline in Physical Working Capacity (PWC) max is from 9-15 percent during the ages of 45 to 55 years. The use of vigorous physical activity to prevent this decline and to possibly protect against fatal myocardial infarction has been suggested. The purpose of this study was to investigate the effect of an endurance type exercise program on the maximal PWC of middle-aged men during a 10 year span. Sixteen men, initially 32-56 years (M-44.6), were trained with running or swimming at an intensity above 60 percent of VO2 max during a 10 year period. The average weekly running distance was 15 miles (25 km). The criterion for PWC was directly measured VO2 using the Douglas Bag/Scholander technique. No changes were observed in body weight, resting heart rate (HR), or resting blood pressure (BP). Maximal HR declined 7 beats per minute in 10 years. Pulmonary ventilation (STPD) increased approximately 18 percent. Mean VO2 max was essentially unchanged, 3.376 and 3.303 1/min STPD. VO2 max related to body weight was 43.7 initially and 44.4 ml/min-kg after 10 years. It was concluded that the usual 9-15 percent decline in PWC or VO2 max from age 45 to 55 years can be forestalled by regular endurance exercise. The results may have implications for protecting against heart attacks.