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A 20-yr longitudinal study of Olympic oarsmen


Medicine & Science in Sports & Exercise: September 1996 - Volume 28 - Issue 9 - p 1150-1156

Nine 1972 silver-medalist oarsmen were studied before the Olympic Games and 10 and 20 yr later. Peak power, metabolic responses, and heart rate were recorded during rowing ergometry; blood lactate was measured following exercise. The skinfold equation yielded percent body fat. The average change(multiple analysis of variance) among measurements from 1972 to 1992 was 37.5± 3% (P < 0.01). Average changes between 1972 and 1982 and between 1982 and 1992 were similar, 17 and 18%, respectively (P < 0.01). The most significant change between 1972 and 1992 was decreased peak blood lactate (106%). Decreases in peak power, ˙VE, and˙VO2 (ml·kg-1·min-1) were all similar, approximately 40%, and were significant. Body fat increased (from 12.3 to 15.6%), and absolute ˙VO2 and relative ˙VO2 (lean body mass) decreased 30% (P < 0.01). Only body weight, heart rate, and O2 pulse showed smaller changes, but these changes were still significant (P < 0.05). Relative peak ˙VO2 decreased from 65.5 to 46.8 ml·kg-1·min-1 from 1972 to 1992 and at a rate of 10%·decade-1. The most significant changes between 1972 and 1982 were increases in percent body fat (from 12.3 to 16.3%) and decreases in ˙VO2 values (P < 0.01). There was less change in body fat between 1982 and 1992, but lactate significantly decreased (P < 0.01), as did peak power and absolute and relative˙VO2 and ˙VE. Although fitness levels in former elite oarsmen decreased each decade, these declines were somewhat arrested by regular aerobic training. Body fat increased and metabolic capacity decreased rapidly during the first decade, whereas anaerobic capacity decreased more significantly in the second decade. Anaerobic capacity diminished at a significantly greater rate than aerobic capacity, probably as a result of the aging process and emphasis on aerobic training in post-competitive years.

Department of Biological Sciences, Ohio University, Athens, OH 45701-2979; and Human Physiology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111

Submitted for publication September 1995.

Accepted for publication February 1996.

Current addresses: W. J. Evans, 119 Noll Lab, Penn State University, University Park, PA 16801; R. A. Fielding, Department of Health Sciences, Boston University, 635 Commonwealth Avenue, Boston, MA 02215; D. T. Kirkendall, Duke University Medical Center, Duke University, Durham, NC 27710; and K. E. Ragg, Student Health Services, Ohio University, Athens, OH 45701.

Address for correspondence: F. C. Hagerman, Department of Biological Sciences, Irvine Hall, Ohio University, Athens, OH 45701-2979.

Aging is associated with numerous metabolic and physiological changes. Declines in function of several major organ systems have been observed (10). Of particular importance are the well-described changes in body composition that occur with advancing age. Based on 24-h creatinine excretion, Tzankoff and Norris(40) confirmed that skeletal muscle mass decreased on average 6%·decade-1 and that this decrease in muscle mass is largely responsible for the age-related decline in resting metabolic rate. Changes in cardiovascular and muscular performance associated with advancing age can affect functional capacity and impinge on an individual's ability to perform activities of daily living. Maximal oxygen consumption declines at a rate of about 1% · yr-1 after the third decade of life(1,20), and muscle strength and cross-sectional area decrease significantly between the second and seventh decades(25,32). The decline in ˙VO2max with age has been attributed to the age-related decline in maximal cardiac output(22). However, Flegg and Lakatta(9) have also demonstrated that the decline in muscle mass observed with age as measured by 24-h urinary creatinine excretion could explain about 40% of the variance of the age-related decline in maximal oxygen uptake. It is unclear whether these changes are an inevitable consequence of aging or simply a result of age-related declines in voluntary physical activity. The decreased cardiorespiratory function and reduced muscle mass and strength observed with advancing age closely resemble the declines in these parameters that are noted with bed rest or inactivity(3,36). These findings suggest that alterations in body composition, especially declines in skeletal muscle mass, may have profound effects on functional exercise capacity.

The sport of rowing requires outstanding physiological attributes and places excessive demands on muscular power, cardiorespiratory transport, and aerobic and anaerobic capacities(11-16,27,28). It is well known that the aging process and disuse can dramatically influence these functions.

Our group of subjects presented a unique opportunity to conduct a longitudinal study with the same group of athletes because they have met each year since 1972 to row a competitive effort and because for most this has represented their only competition since that time. In addition, this yearly competitive effort is of a low intensity and part of a largely low-key recreational regatta. The racing distance is approximately 6000 m, three times the normal racing distance for elite competitive crews. It was therefore the purpose of this study to periodically compare specific performance, cardiorespiratory, and metabolic responses of aging elite oarsmen over a 20-yr period.

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Nine 1972 Olympic silver-medalist oarsmen were studied prior to the Olympic Games and 10 and 20 yr later. Both verbal and written informed consent were obtained before each testing session. This study was approved by the Ohio University Institutional Review Board for Human Subjects and the Tufts University-New England Medical Center Human Investigation Review Committee. Anthropometric measurements, including a six-site skinfold analysis for estimation of percent body fat (11), were determined prior to each exercise test using the same procedure for all three determinations. Pertinent physical characteristics appear inTable 1.

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Activity History

Activity levels were determined for each subject based on average exertional patterns during the 10-yr period before each test. These exertional levels were defined using the following criteria: very high, training at least 7 d·wk-1 and rowing competitively on a regular basis; high, training at least 5 d·wk-1 and rowing competitively on a regular basis; moderate, training at least 3 d·wk-1 and little or no competitive rowing; and low, training at least 1 d·wk-1 and little or no competitive rowing. Competition on a regular basis was defined as at least six competitions per year, while little or no competition meant one competition or less per year. Each training level was arbitrarily assigned a numerical equivalent based on days per week of training.

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Exercise Testing

All physiological responses were observed continuously during each of the three simulated 2000-m competitive efforts. This simulated exercise was originally selected because it provided important applied data at critical stages of racing not otherwise produced using a standard ˙VO2max ramp protocol or graded exercise (14). This simulated protocol is still used effectively to determine fitness and effects of training among elite rowers. Instead of maximal values, we have chosen to refer to the highest values recorded during this type of exercise protocol aspeak values. This seemed appropriate because ˙VO2max, for example, is usually reported only for a standardized graded exercise rather than during a simulated competitive effort such as we used. Because of our earlier studies (13,14), in which a simulated 2000-m ergometer exercise protocol produced the highest ˙VO2, we initially described these responses as maximal. However, journal reviewers suggested we use some other description since we did not use a standard max exercise protocol. Therefore, the values we observed are referred to as peak but in reality are maximal. In addition, the highest physiological values reported for this protocol often occur before the end of exercise(12). Although several studies have measured˙VO2max for rowers, these values were consistently lower than the peak ˙VO2 measurements and other peak physiological responses we have reported (12).

Power output and cardiorespiratory and metabolic responses were measured at each test session during a 6-min simulated 2000-m (the standard competitive distance for international rowing) competitive effort on a rowing ergometer. The 1972 tests were conducted utilizing a Lyons-type mechanical ergometer(14), while the 1982 and 1992 tests were conducted with Concept II ergometers, models A and B, respectively(12,17). Although some differences exist among these ergometers, similarity of test data obtained from each supports our comparisons of test results (12). The older Lyons-type ergometer is a fixed-resistance ergometer utilizing a brake shoe mechanism and presents the rower with a heavier load than the more contemporary variable-resistance Concept II. According to experienced rowers both ergometers adequately simulate rowing conditions on the water, but since the Lyons-type offers slightly higher resistance, the experience is like rowing in a slight head-wind or rough water and thus the highest ˙VO2 values occur earlier in the exercise. In addition, the Lyons-type ergometer was the only suitable choice in 1972, whereas the Concept II ergometer has been the instrument most frequently used in contemporary rowing testing, including several of our previous studies(5,12,17,18).

Ergometer power output, pulmonary ventilation (˙VE), oxygen consumption (˙VO2), and heart rate (HR) were measured continuously and recorded at the end of each minute of exercise. ˙VE and˙VO2 were measured using semiautomated open-circuit spirometry. All ventilations were appropriately corrected to BTPS (body temperature and ambient pressure and saturated with water vapor) and STPD (standard temperature and pressure with no water vapor). In 1972 and 1982, Fe02 and FeC02 were analyzed by Beckman models E-2 and OM-11 and LB-1 and LB-2 analyzers, respectively, while in 1992 fractional concentrations were determined using an applied electrochemistry SA-2 02 analyzer and a Beckman LB-2 C02 analyzer. Calibration gases were Scholandered for accuracy. Heart rate and cardiac cycle events were monitored using 12-lead electrocardiography (ECG) for all tests, and oxygen pulse was calculated from peak absolute ˙VO2 and HR. Power output was recorded continuously in watts. Capillary blood samples were obtained 5 min following exercise via finger prick for determination of blood lactic acid (LA) concentrations(spectrophotometrically in 1972 and using Yellow Springs Instruments instrumentation, model 23L, in 1982 and 1992).

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Statistical Analysis

The BMDP statistical package was used to produce a multiple analysis of variance to compare all responses among the three test periods. Significance was accepted at an alpha level of 0.05.

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Physical Characteristics and Activity Levels

Body weight increased from 87.4 to 93.8 kg (P < 0.05) from 1972 to 1992, and the rate of increase per decade was 4.8% for 1972-1982 and 2.4% for 1982-1992, the former significant at P < 0.05 and the latter representing no significant change (Table 1). Percent body fat increased significantly (P < 0.01) from 12.3 to 15.6% between 1972 and 1992 and in 1982 reached its highest mean value, 16.3%, which is also significantly different (P < 0.01) from the 1972 mean value. There was no significant change between 1982 and 1992 (from 16.3 to 15.6%).

Because training frequency, duration, and intensity were unusually high for all subjects prior to the 1972 Olympic Games (seven of the subjects had also competed in the 1968 Olympic Games), their training intensity during this period could be described as very high and averaged almost 7 d·wk-1. In addition to consistently high-quality off-season and in-season training by the subjects ranging between 5 and 7 yr before 1972, there were only minor differences in the routine of two daily training sessions, 7 d·wk-1, most at relatively high intensities from June until Olympic competition in early September. Training also included 3 wk of altitude exposure at 2300 m in August, and the crew competed in several international pre-Olympic regattas during 3 months of training in Europe. Because training levels were reduced for most subjects during subsequent 10-yr periods, training during these periods was categorized as either high, moderate, or low. The most dramatic change in activity level for this group for any 10-yr period occurred between 1972 and 1982, from an average of 7 d·wk-1 in 1972 to 3.6 d·wk-1 in 1982 and further to 3.1 d·wk-1 in 1992. Both the 1982 and 1992 values were significantly different from the 1972 value (P < 0.01); there was no significant difference between 1982 and 1992 for activity levels.

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Metabolic Responses and Exercise Tolerance

Peak relative ˙VO2 - body weight (BW) decreased significantly(P < 0.01) from 65.5 to 46.8 ml·kg-1·min-1) between 1972 and 1992 and at a rate of about 20%·decade-1 (Fig. 1c) or 0.935 ml·kg-1·min-1·yr-1. Decreases in peak absolute ˙VO2 and relative ˙VO2 - lean body mass(LBM) were also significant (P < 0.01) and are shown inFigure 1. Absolute ˙VO2 and relative˙VO2 - LBM decreased approximately 30% over the 20-yr test period, while absolute ˙VO2 decreased approximately 20% between 1972 and 1982 and 10% between 1982 and 1992, with relative ˙VO2 - LBM decreasing 17% the first decade and 13% the second decade; all of these changes were significant (P < 0.01). Training frequency, duration, and intensity declined dramatically between 1972 and 1992, decreasing from very high to moderate, for all but one subject. Between 1972 and 1982 this subject reduced his training to a moderate level and then increased it to a high level between 1982 and 1992, and the fluctuation in his test data for these periods reflects these changes: peak relative˙VO2 - BW declined from 69.8 to 57.8 ml·kg-1·min-1 in the first post-Olympic decade and went back up to 63.2 ml·kg-1·min-1 following a decade of increased training. In contrast, the subject who trained the least(lowest levels since 1972), showed consistent decreases in peak relative˙VO2 - BW: 1972, 48.9 ml·kg-1·min-1; 1982, 34.2 ml·kg-1·min-1; and 1992, 28.9 ml·kg-1·min-1.

Peak pulmonary ventilation and power output decreased at about the same rate as aerobic capacity between 1972 and 1992, about 40%(Figs. 1a and 2a). Average peak power in 1972 was 472 W, decreasing to 419 W in 1982 and finally to 339 W in 1992; these were all significant changes (P < 0.01). ˙VE decreased 27 l·min-1 between 1972 and 1982 and 30.2 l·min-1 between 1982 and 1992. These decrements, along with the total decrease of 57 l·min-1 between 1972 and 1992 (from 190 to 133 l·min-1), were all significant at P < 0.01(Fig. 1a).

The most significant change between 1972 and 1992 was a 106% decrease in peak lactate (P < 0.001), from 14.4 to 7.0 mmol·l-1 (Fig. 2d). Lactate concentrations decreased 25% between 1972 and 1982 (from 14.1 to 11.5 mmol·l-1) and decreased another 64% between 1982 and 1992 (from 11.5 to 7.0 mmol·l-1). All 10-yr LA decrements were significant (1972-1982, P < 0.05; 1982-1992,P < 0.01).

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Cardiovascular Responses

Peak HR decreased significantly between 1972 and 1992 from 186 to 171 beats·min-1 (P < 0.05), with an average decrement of about 7%·decade-1 during the 20-yr study(Fig. 2b). Peak oxygen pulse decreased 19% between 1972 and 1992, and this was significant at P < 0.01(Fig. 2c). Significant changes were also observed for peak 02 pulse for each decade (P < 0.05), as it decreased from 30.6 to 27.1 ml·beat-1 from 1972 to 1982 and finally to 25.7 ml·beat-1 in 1992.

Although 12-lead ECG analysis in 1992 indicated normal cardiac rhythm and vascular integrity in the hearts of most subjects at rest and during exercise, two of the subjects in 1992 did exhibit some ECG alterations during exercise consistent with ischemia. Despite their possible genetic advantages and history of vigorous training, it appears that even former elite athletes in their mid-40s are susceptible to cardiovascular changes usually associated with a more sedentary population.

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Physiological factors important to aerobic performance decline with age(1,2,19,20,29-31), and this decline is suppressed by regular endurance training and enhanced by physical inactivity(23,24,29,30,33,34). Former elite aerobic athletes are also susceptible to this decline if inactivity is evident among them(29,30,41). Although the effects of aging have been studied previously on elite athletes and described by Saltin and Grimby (35) and Sutton and Brock(39), longitudinal comparisons of the same subjects over several years, especially exercise responses, are rare(8,31).

Although most of our subjects continued to perform some type of aerobic exercise training on a regular basis during their post-Olympic years, significant declines in fitness still occurred. This is in agreement with data reported in previous longitudinal studies in which the rate of decline was consistently higher in aging elite athletes than those reported for both active and nonactive subjects (see Table 2). This is in contrast with cross-sectional data reported by Rogers and Evans(32) suggesting that aging athletes can maintain maximal aerobic capacities by a constant training stimulus or at the very least show only minimal rates of decline (33). These and other mostly cross-sectional studies(4,19,29,30,41) have reported a rate of decline in masters runners between 1 and 5%·decade-1. Dill et al. (8) studied 16 highly competitive middle-distance runners at peak conditioning and again 18-50 yr after their competitive running careers had ended. Data from these studies revealed that these former elite athletes showed significantly greater deterioration in resting and exercise cardiovascular and metabolic responses than untrained subjects of the same age (Table 2). Robinson et al.(31) studied 13 of these same subjects again 8-9 yr after the first restudy and observed over the course of follow-up a 12% decline in ˙VO2max, which is considerably greater than the decline reported for sedentary individuals. These rates of decline seem to be the normal response of aging distance runners and are slightly higher than the decline reported for our subjects. However, it must be remembered that the former elite runners were all much older than our subjects at the time of final testing and, for the most part, had not trained following initial testing.

In addition to observing more accelerated rates of declines in˙VO2 when compared with earlier studies, declines among our subjects showed far less individual variability. Thus, it was possible to observe reasonable group homogeneity throughout the study, probably owing to, at least in part, similar training regimens maintained by most subjects during the 20-yr period. The only exceptions to this observation were two subjects, one of whom trained at a relatively very high level, especially during the last decade of this study, and another representing the other extreme by training at a relatively very low level throughout the 20-yr post-Olympic period. It is also noteworthy that initial cardiorespiratory and metabolic responses of our subjects exceeded those reported for other endurance athletes(6,12,19,29-31,35,41). Elite rowers are unique among endurance athletes because they generate extraordinary muscular power (≥500 W), achieve very high pulmonary ventilations (≥200 l·min-1) and absolute oxygen consumptions(≥6 l·min-1), and exhibit a large proportion of Type I muscle fibers with unusually large cross-sectional areas in a primary power agonist used in rowing (11,12,37). These responses relate to several interactive stimuli, including genetics, anthropometry, high-intensity training, and competitive efforts. A reduction in training and competition along with changes in anthropometry associated with aging no doubt accounted for an almost 40% decrease in performance factors between 1972 and 1992, with an average rate of decline consistent over each decade (17-18%). These data are somewhat skewed as peak LA decreased 106% from 1972 to 1992(Fig. 2d). However, other than values determined for BW, percent body fat, and peak HR, all other physiological responses showed similar declines ranging between 30 and 40% for the 20-yr period. Although masters athletes tend to have substantially more fat and less LBM than their younger counterparts, hereditary advantages, conscious dietary monitoring, and habitual aerobic training among our subjects over the 20-yr period no doubt discouraged accumulation of excess fat (from 12.3% in 1972 to 15.6% in 1992). This final value is well below the norm reported for this age group. Previous studies showed a 9% reduction per decade in ˙VO2max in sedentary adults after age 25 (7,19), while other studies indicated ˙VO2max for active individuals was reduced to less than 5% for the same time period (4,7,19). Costill (6) has suggested that records for the 10-km run slow about 1%, or about 14 s, per year up to the age of 60 and then slow significantly more than a minute, or about 4%, per year thereafter. These data suggest that endurance performance decrements are small during middle age, and power decreases for our subjects during the first decade, 12.6% from 1972 to 1982, show similar changes. However, a 23.6% decrement in ergometric power among our subjects from 1982 to 1992 suggests that rowing athletes may respond more significantly as the effects of a high-intensity training stimulus diminish over time. It appears that the change from a training program of very high intensity and frequency and long duration was more drastic for the elite rowers as declines in performance factors doubled those of even sedentary adults after age 25. It is also interesting that these declines were consistent over each decade and occurred despite participation in some form of regular aerobic training.

It has been suggested that individuals with a high initial˙VO2max from genetic endowment and/or training effects and who become less active exhibit a higher rate of decline in ˙VO2max with age (4). Only one of our subjects was able to achieve a significant proportion of his original peak aerobic capacity after 20 yr, but that was possible only after he began training again in 1982 at a very high level. His original peak relative ˙VO2 - BW was 69.8 ml·kg-1·min-1, and this decreased to 57.8 ml·kg-1·min-1 in 1982 following a decade of reduced training. However, increasing training and competitive participation from 1982 to 1992 to very high levels resulted in a considerable increment to 63.2 ml·kg-1·min-1. The most rapid decline in mean aerobic capacity occurred in the first decade following Olympic competition(22% as opposed to 14.5% from 1982 to 1992. These changes were accompanied by rather small but significant declines in peak HR that were similar for both decades (4.5% from 1972 to 1982 and 4.1% from 1982 to 1992). One of the most notable changes with aging is a steady decline in HRmax. Our subjects were not immune to this change, as peak HR decreased 15 beats·min-1 in the 20-yr period, 8 beats·min-1 from 1972 to 1982, and 7 beats·min-1 from 1982 to 1992. These responses are comparable to declines in HRmax reported previously for masters athletes (41). Decreases in HRmax appear to be similar in both the athletic and sedentary aging populations(41), and although both groups experience a reduction in˙VO2max with aging, it is significantly less in the athletic group, who had a markedly higher stroke volume and therefore a larger maximal cardiac output. Although cardiac output was not measured, 02 pulse declined 13% the first decade and just 5% the second. 02 pulse is only an estimate of cardiac efficiency, but these data suggest that the decrease in aerobic capacity may have been due more to the declining ability of the muscles to utilize oxygen rather than the deficiency of transport mechanisms. However, recent studies have suggested that aging causes an increase in peripheral vascular resistance, primarily as a result of the loss of vascular anatomical and functional integrity. This is compensated for in the aging athlete by a greater oxygen extraction and a higher stroke volume; thus, far less reduction in ˙VO2max occurs in the aging athlete (41). Body weight also exhibited its greatest increment in the first decade and thus inflated relative declines in aerobic capacity. The most extreme increase in percent body fat occurred in the same subject whose peak ˙VO2 declined the most; his very low level of activity during the first post-Olympic decade resulted in an 86% increase in body fat (from 16.7 to 31.0%). More attention to exercise and diet during the last decade of the study no doubt helped this subject, as his percent body fat decreased to 28%. All other subjects were considerably more active and showed far less increase in body fat.

Although the magnitude of peak power and lactate changes were comparable to other physiological responses during the first decade, these values almost doubled and tripled, respectively, during the next decade(Figs. 2a, 2d). To our knowledge these are the largest decrements reported for these responses in former elite endurance athletes and emphasize the importance of the absence of high-intensity anaerobic training. Because the anaerobic energy component is so important in measurements relating to power development and lactate production during rowing(14), it was not surprising to observe these findings. Anaerobic training represented a critical phase of preparation for Olympic competition and reached its zenith for our subjects in 1972. With each successive decade the need and willingness to engage in high-intensity training became less important for our subjects, and examination of individual training regimens indicated a preponderance to train more submaximally and at low aerobic steady-state intensities. As a result, anaerobic capacity became significantly impaired, a finding consistent with retired endurance athletes(12,38). A decrease in muscle mass, another observation in our study, could also account for a diminished power output and lactate response, as well as a possible age-selective loss of fast-twitch(Type II) muscle fibers. Even the most aerobically fit of our subjects, who after 20 yr achieved 90% of his initial aerobic capacity, showed a 43% decrease in power and a 66% decline in peak LA over the same period.

In summary, fitness levels in former elite oarsmen decreased significantly every 10 yr following Olympic competition, and this was arrested somewhat by relatively consistent aerobic training. Percent body fat and metabolic capacity decreased rapidly during the first decade, whereas anaerobic capacity decreased more significantly in the second decade. Anaerobic capacity diminished at a significantly faster rate than aerobic capacity, probably owing to the aging process and emphasis on lower-intensity, decreased-duration, and less frequent training sessions in the post-competition years. Our data not only demonstrate that these declines can be slowed with activity but also raise the possibility of protective genetic effects for elite endurance athletes. Despite the reductions in training specificity, duration, and intensity and the accumulative effects of the aging process, our subjects still exhibited fitness levels or physical attributes far exceeding those of men of their age. Thus, physiological deterioration in the aging elite athlete seems to be a function of several factors whose relative contribution is not known but includes alterations in habitual levels of physical activity.

Figure 1-a) ˙VEBTPS in l·min-1 ([horizontal bar over]X ± SD). * P < 0.01 between 1972 and 1982, between 1982 and 1992, and between 1972 and 1992. b) ˙VO2 STPD in l·min-1 ([horizontal bar over]X ± SD). *

Figure 1-a) ˙VEBTPS in l·min-1 ([horizontal bar over]X ± SD). * P < 0.01 between 1972 and 1982, between 1982 and 1992, and between 1972 and 1992. b) ˙VO2 STPD in l·min-1 ([horizontal bar over]X ± SD). *

Figure 2-a) Power output in W ([horizontal bar over]X ± SD).*

Figure 2-a) Power output in W ([horizontal bar over]X ± SD).*

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1. Åstrand, I. Aerobic work capacity in men and women with special reference to age. Acta Physiol. Scand. Suppl. 169:1-92, 1983.
2. Åstrand, I., P. O. Åstrand, I. Hallback, and A. Kilbom. Reduction in maximal oxygen uptake with age. J. Appl. Physiol. 35:649-654, 1973.
3. Bortz, W. M. Disuse and aging. J.A.M.A. 248:1203-1208, 1982.
4. Buskirk, E. R. and J. L. Hodgson. Age and aerobic power: the rate of change in men and women. Fed. Proc. 46:1824-1829, 1987.
5. Chance, B., M. T. Dait, C. Zhang, T. Hamaoka, and F. C. Hagerman. Recovery from exercise-induced desaturation in the quadriceps muscles of elite competitive rowers. Am. J. Physiol. 262:C766-C775, 1992.
6. Costill, D. L. Inside Running, Basics of Sports Physiology. Indianapolis, IN: Benchmark Press, Inc., 1986, p. 167.
7. Dehn, M. M. and R. A. Bruce. Longitudinal variations in maximal oxygen intake with age and activity. J. Appl. Physiol. 33:805-807, 1972.
8. Dill, D. B., S. Robinson, and J. C. Ross. A longitudinal study of 16 championship runners. J. Sports Med. Phys. Fitness 7:1-27, 1967.
9. Flegg, J. L. and E. G. Lakatta. Role of muscle loss in the age-associated reduction in Vo 2 max. J. Appl. Physiol. 65:1147-1151, 1988.
10. Goldman, R. Decline in organ function with aging. In:Clinical Geriatrics, I. Rossman (Ed.). Philadelphia: Lippincott, 1979.
11. Hagerman, F. C. Teamwork in the hardest pull in sports.Physician Sports Med. 1:303-326, 1984.
12. Hagerman, F. C. Physiology and nutrition for rowing.In: Perspectives in Exercise Science and Sports Medicine, Vol. 7: Physiology and Nutrition for Competitive Sport, D. R. Lamb, et al. (Eds.). Carmel, IN: Cooper Publishing Group, 1994, pp. 221-302.
13. Hagerman, F. C., W. W. Addington, and E. A. Gaensler. A comparison of selected physiological variables among outstanding competitive oarsmen. J. Sports Med. Phys. Fitness 12:12-22, 1972.
14. Hagerman, F. C., M. C. Connors, J. A. Gault, G. R. Hagerman, and W. J. Polinski. Energy expenditure during simulated rowing.J. Appl. Physiol. 45:87-93, 1978.
15. Hagerman, F. C., G. R. Hagerman, and T. C. Mickelson. Physiological profiles of elite rowers. Physician Sports Med. 7:74-81, 1979.
16. Hagerman, F. C. and R. S. Staron. Season variations among physiological variables in elite rowers. Can. J. Appl. Sport Sci. 8-3:143-148, 1983.
17. Hagerman, F. C., R. A. Lawrence, and M. C. Mansfield. A comparison of energy expenditure during rowing and cycling ergometry.Med. Sci. Sports Exerc. 20:479-488, 1988.
18. Hagerman, F. C. and K. Korzeniowski. Applied rowing ergometer testing. FISA Colloque des Entraineurs 19:115-133, 1989.
19. Heath, G. W., J. M. Hagberg, A. A. Ehsani, and J. O. Holloszy. A physiological comparison of young and older endurance athletes.J. Appl. Physiol. 51:634-640, 1981.
20. Hodgson, J. L. and E. R. Buskirk. Physical fitness and age, with emphasis on cardiovascular function in the elderly. J. Am. Geriatr. Soc. 25:385-392, 1977.
21. Hollman, W. Körperliches Training zur Prävention von Herz-Kreislauf-Krankheiten. Stuttgart, West Germany: Hippokrates-Verlag; 1965. Cited by Dehn, M. M., and R. A. Bruce. Longitudinal variations in maximal oxygen intake with age and activity. J. Appl. Physiol. 33:805-807, 1972.
    22. Julius, S., A. Amery, L. Whitlock, and J. Conway. Influence of age on the hemodynamic response to exercise.Circulation 36:222-230, 1967.
    23. Kasch, F. W. and J. P. Wallace. Physiological variables during 10 years of endurance exercise. Med. Sci. Sports Exerc. 8:5-8, 1976.
    24. Kasch, F. W., J. P. Wallace, and S. P. Van Camp. Effects of 18 years of endurance exercise on physical work capacity of older men. J. Cardiopulmonary Rehabil. 5:308-312, 1985.
    25. Larsson, L. Histochemical characteristics of human skeletal muscle during aging. Acta Physiol. Scand. 117:469-471, 1983.
    26. MacKeen, P. C., J. L. Rosenberger, J. S. Slater, W. C. Nicholas, and E. R. Buskirk. A 13-year follow-up of a coronary heart disease risk factor screening and exercise program for 40- to 59-year old men: exercise habit maintenance and physiological status. J. Cardiac Rehabil. 5:510-523, 1985.
    27. Mahler, D. A., W. N. Nelson, and F. C. Hagerman. Mechanical and physiological evaluation of exercise performance in elite national rowers. J.A.M.A. 252:496-499, 1984.
    28. Mickelson, T. C. and F. C. Hagerman. Anaerobic threshold measurement of elite oarsmen. Med. Sci. Sports. Exerc. 14:440-444, 1982.
    29. Pollock, M. L., C. Foster, J. Rod, J. Hare, and D. H. Schmidt. Ten year follow-up on the aerobic capacity of champion master's track athletes. Med. Sci. Sports Exerc. 14:105, 1982.
    30. Pollock, M. L., C. Foster, D. Knapp, J. L. Rod, and D. H. Schmidt. Effect of age and training on aerobic capacity and body composition of master's athletes. J. Appl. Physiol. 62:725-731, 1987.
    31. Robinson, S., D. B. Dill, R. D. Robinson, S. P. Tzankoff, and J. A. Wagner. Physiological aging of champion runners. J. Appl. Physiol. 41:46-51, 1976.
    32. Rogers, M. A. and W. J. Evans. Changes in skeletal muscle with aging: effects of exercise training. In: Exercise and Sports Sciences Reviews, J.O. Holloszy (Ed.). Baltimore: Williams and Wilkins, 1993, pp. 65-102.
    33. Rogers, M. A., J. M. Hagberg, W. H. Martin III, A. A. Ehsani, and J. O. Holloszy. Decline in VO2max with aging in master athletes and sedentary men. J. Appl. Physiol. 68:2195-2199, 1990.
    34. Saltin, B., G. Blomqvist, J. Mitchell, R. L. Johnson, K. Wildenthal, and C. B. Chapman. Response to exercise after bed rest and after training. Circulation 37/38(Suppl. 7):1-78, 1968.
    35. Saltin, B. and G. Grimby. Physiological analysis of middle-aged and old former athletes. Circulation 38:1104-1115, 1968.
    36. Saltin, B. and L. B. Rowell. Functional adaptations to physical activity and inactivity. Fed. Proc. 39:1506-1513, 1980.
    37. Secher, N. H. The physiology of rowing. J. Sports Sci. 1:23-53, 1983.
    38. Shepherd, R. J. Physical Activity and Aging. Chicago: Year Book Medical Publishers, Inc., 1978, p. 85.
    39. Sutton, J. R. and R. M. Brock. Sports Medicine for the Mature Athlete. Indianapolis, IN: Benchmark Press, Inc., 1986, pp. 59-89.
    40. Tzankoff, S. P. and A. H. Norris. Effect of muscle mass decrease on age-related BMR changes. J. Appl. Physiol. 43:1001-1006, 1978.
    41. Wilmore, J. H. and D. L. Costill. Training for Sport and Activity, 3rd Ed. Champaign, IL: Kinetics Publishers, 1988, pp. 303-317.


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