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Comparison of Measures of Maximal and Submaximal Fitness in Response to Exercise


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Medicine & Science in Sports & Exercise: April 2017 - Volume 49 - Issue 4 - p 711-716
doi: 10.1249/MSS.0000000000001164
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Cardiorespiratory fitness measured as maximal exercise capacity (mCRF; V˙O2peak) is an established marker of cardiovascular disease and all-cause mortality (8,20). It is well established that regular moderate-intensity exercise is associated with increases in mCRF (12,23). However, increasing evidence suggests that substantial interindividual variation in mCRF occurs in response to a standard exercise dose (3,5,6,28–30). We (25) and others (6) have recently reported that approximately 20% to 40% of individuals do not improve mCRF beyond the error of measurement in response to exercise consistent with consensus recommendations.

Improvements in mCRF are explained in large measure through central adaptations (stroke volume), whereas peripheral adaptations (oxygen uptake and oxidative capacity) contribute far less (19). By contrast, improvement in submaximal cardiorespiratory fitness (sCRF) is strongly associated with peripheral adaptations (11,14,16). We reasoned that individuals who adhere to physical activity (PA) guidelines and perform exercise at moderate intensity (50% to 65% of mCRF) may experience peripheral adaptations more readily captured by a sCRF test performed at exercise intensities similar to that performed during exercise. Accordingly, we also posited that improvements in sCRF may be observed despite no change in mCRF. Were this true, it would provide a basis for inclusion of tests that assess exercise-induced improvement in exercise tolerance in addition to exercise capacity.

Previous trials have considered the association between changes in mCRF and sCRF (2,13,15,22,31) but in large measure have employed highly trained individuals performing high-intensity exercise training. Therefore, we sought to determine, in a high-risk group of physically inactive, primarily overweight-to-obese men, the associations between changes in sCRF and mCRF consequent to exercise consistent with current recommendations. We also considered the interindividual variation of response in both sCRF and mCRF. We hypothesized that a 4-wk, carefully controlled exercise trial consistent with guideline recommendations would lead to individual improvements in sCRF independent of changes in mCRF in previously physically inactive men.


Participant characteristics

Thirty inactive (no more than 1 h·wk−1 of self-reported exercise) men between the ages of 30 and 60 yr were recruited using mass media from the Kingston area. Inclusion criteria required that the men be weight stable (weight change no more than ±2 kg for 6 months before the start of the study) and nonsmokers. Exclusion criteria included having a body mass index greater than 40 kg·m−2, any physical impairment that would make performing exercise difficult or unsafe, or a history of cardiovascular disease (myocardial infarction, stroke, angioplasty, coronary bypass surgery, unstable angina, ischemia, or peripheral artery disease) in the past 6 months. All participants provided informed written consent before participant. This study was approved by the Queen's University Health Sciences Research Ethics Board.

Measurement of mCRF

mCRF (V˙O2peak) was measured using a maximal graded treadmill test in combination with open-circuit spirometry (SensorMedics Corp., Yorba Linda, California). For each test, a constant speed was set at 3.7 mph. After 3 min at zero grade, the incline was increased by 2% every 3 min until volitional fatigue. Heart rate (HR) was monitored at 20-s intervals throughout each test using a Polar HR monitor (Polar Oy, Kempele, Finland). V˙O2peak was established as the highest average oxygen uptake recorded during a 20-s interval. The participant had to achieve three of four of the following criteria for the V˙O2peak test to be valid: 1) RER ≥1.1, 2) HR greater than or equal to the age-predicted maximum, 3) plateau in oxygen uptake with an increase in work rate, and/or 4) a rate of perceived exertion equal to 10 on the BORG Scale. V˙O2peak was measured twice at baseline and twice after the exercise intervention to determine the repeatability of the V˙O2peak measures. A minimum of 24 h separated all CRF testing procedures during which the participants were asked not to perform any structured exercise. CRF testing was performed within 24–48 h of the last exercise session. The values of the two V˙O2peak tests performed pre- and postintervention were averaged unless the absolute difference in maximal oxygen uptake (V˙O2peak) between tests was greater than 5%. If the difference in V˙O2peak was greater than 5%, the test with the higher value was taken to be V˙O2peak.

Measurement of sCRF: exercise tolerance

sCRF as estimated by exercise tolerance was measured as the total distance traveled during a 12-min time trial on a motorized treadmill. This protocol simulates the Cooper test, an established submaximal test used to predict oxygen uptake (7). Participants walked or jogged at a self-selected speed, which could be self-adjusted throughout the duration of the time trial. The grade remained at 0% throughout the test. Participants were blinded to distance traveled and HR achieved during the test. Participants were encouraged to reach the point of exhaustion by the completion of the time trial. HR was monitored continuously throughout the test using a Polar HR monitor (Polar Oy) and recorded at 20-s intervals for the duration of the test. Speed was also measured at 20-s intervals along with HR. The values of the two tests at pre- and postintervention were averaged to obtain final values unless the distance traveled at 12-min between tests showed a difference of greater than 5%. In this case, the test result with the higher value was used as the measure of exercise tolerance.

Measurement of sCRF: submaximal HR

sCRF as estimated by submaximal HR was calculated as the average HR recorded during the final 40 s of treadmill exercise at three incline levels during the mCRF (V˙O2peak) test. Inclines of 2%, 4%, and 6% during the mCRF test were chosen for analysis because all participants reached work rates greater than 6% at both baseline and follow-up. The values for submaximal HR were calculated as an average of the HR values recorded for a given incline during the two mCRF tests performed pre- and postexercise. In cases where the absolute difference in mCRF between tests was greater than 5%, the sCRF HR values were taken from the mCRF test with the higher V˙O2peak.

Measurement of PA

Daily PA was measured using the GT3X accelerometer (ActiGraph, Pensacola, FL) for a 7-d period at baseline and during the final week of the exercise intervention. The accelerometers collected data continuously for the full 7 d while worn on the front of the right hip. Participants wore the monitors during waking hours and removed the device before sleep. Participants also completed a log to record the time at which they woke up in the morning, went to bed at night, and if they removed the device for any water-based activities. A minimum of 10 h of wear time was required for a complete day to be registered (17). For this analysis, at least four complete days of data (3 weekdays and 1 weekend day) was required for inclusion (32). Wear time was determined by extended periods of zero counts, which was evaluated by visual examination in conjunction with the participant logs. The interpretation of the accelerometry data was conducted using threshold values as described by Freedson et al. (10). To compare the baseline values of moderate- to vigorous-intensity physical activity (MVPA) to those obtained during the final week of exercise, the 30-min supervised exercise time and the 5-min warm-up were subtracted from the total MVPA on days in which participants completed an exercise session.

Exercise intervention

Participants were asked to complete 4 wk of supervised aerobic exercise on a motorized treadmill five times per week for 30 min per session at 65% of their V˙O2peak. The duration of this exercise trial was based on data from our recently completed randomized controlled trial (27). From that data, we observed that 54% of the total change in V˙O2peak observed in completers of our low-amount–low-intensity group (approximately 150 min·wk−1 at 50% of V˙O2peak, for 6 months) occurred by the end of the first 4 wk. The exercise prescribed in this study was at a slightly higher intensity than what was prescribed in the prior trial, providing further confidence that we would observe a change in mCRF after 4 wk. HR was monitored continuously throughout each exercise session using a polar HR monitor (Polar Oy) and recorded along with treadmill speed and grade at 5-min intervals. Speed and grade were adjusted throughout each session to maintain HR within 3 bpm of the target prescribed.

Anthropometric measurements

Body weight was measured to the nearest 0.1 kg on a calibrated beam scale. Standing height was obtained to the nearest 0.1 cm using a wall-mounted stadiometer. Waist circumference was obtained at the waist at the level of the iliac crest as previously described (26).

Statistical analysis

All data are presented as mean and SD. Differences between repeated measures obtained pre- and postexercise were compared using paired sample t-tests. Average changes of all measured variables pre- and postintervention were also compared using paired sample t-tests. The effect size of the change was described using Cohen's effect size (d). mCRF and sCRF nonresponse levels were identified using a technical error (TE) measure based on the methods originally outlined by Bouchard et al. (3). TE is a conservative measure of assessor error and day-to-day variation when conducting an exercise test. TE is calculated by taking the square root of the sum of squared differences of repeat measures divided by the total number of paired samples multiplied by 2. Any individual whose change in CRF was within ±1 TE was considered a nonresponder. The TE determined in our laboratory is 0.2 L·min−1 for mCRF, 0.07 km for exercise tolerance (sCRF), and 3.9 bpm for submaximal HR (sCRF). Thus, participants at 4 wk whose change in mCRF was less than 0.2 L·min−1, less than 0.07 km for exercise tolerance, and less than 3.9 bpm for submaximal HR were considered nonresponders.

The association between mCRF and sCRF (exercise tolerance and change in submaximal HR) was examined using two-tailed bivariate correlations. All continuous variables were standardized by conversion to z-scores. The standardized values were used in a forced-entry linear regression analysis to determine the variables that significantly predicted change in mCRF. The results of the model are interpreted such that a significant b score of 1.5 represents a 1.5-fold increase in mCRF for each unit increase in the predictor variable. As a result of the standardized scale, a unit change is equal to a change of 1 SD. Differences between changes of sCRF (exercise tolerance and change in submaximal HR) between responders and nonresponders of mCRF were determined using independent t-tests. All statistical analysis was performed using the Statistical Package for the Social Sciences for Windows (version 23; SPSS Inc., Chicago, IL).


Descriptive characteristics

Five participants did not complete the intervention as prescribed and are not included in the analysis. Two participants withdrew because of injuries unrelated to exercise incurred outside the laboratory while the remaining three withdrew citing lack of time. Characteristics of the 25 male participants who completed the intervention are shown in Table 1. The men were middle-age (mean ± SD = 44.3 ± 9.1 yr), and all but three had a BMI greater than 25 kg·m−2. Baseline mCRF varied considerably (29.0 to 58.3 mL·kg−1·min−1) with a mean value of 41.9 (7.7) mL·kg−1·min−1.

Participant descriptive data of completers.

Adherence to exercise intervention

Participants who completed the intervention attended 94% (18.8 of 20 sessions prescribed) of the exercise sessions and completed the exercise at the target intensity of 65% (64.5 ± 1.3 mCRF). There was no change in objectively measured unstructured MVPA, light-intensity PA, or total PA performed outside the exercise sessions throughout the 4-wk intervention (P > 0.05) (Table 1).

Anthropometric measures

No change in body weight was observed at 4 wk (P > 0.05, d = −0.02; Table 1); however, a small decrease in waist circumference (preexercise: 107.5 ± 16.6 cm; postexercise: 106.3 ± 15.9 cm; P < 0.05, d = −0.07) was observed.

Change in unstructured PA and sedentary time

Daily PA and sedentary time at baseline is shown in Table 1. At 4 wk, PA data were not obtained for three participants, and therefore the data for these participants are not included in the analysis of unstructured PA. We observed no difference in light-intensity PA (P > 0.05, d = 0.004, n = 22) or total PA (P > 0.05, d = 0.02, n = 22) between measures at baseline and week 4. When the MVPA was adjusted for the prescribed exercise, no significant change in MVPA (P > 0.05, d = 0.12, n = 22) was observed at 4 wk. Sedentary time decreased significantly from baseline to week 4 (P < 0.05, d = −0.48, n = 22), where the difference in sedentary time from baseline to week 4 is approximately the same as the amount of time spent performing the prescribed exercise.

Exercise-induced change in mCRF and sCRF

mCRF values pre- and postexercise are shown in Table 2. A significant increase in both absolute (P = 0.009, d = 0.41) and relative mCRF (P = 0.002, d = 0.31) was observed.

Changes in V˙O2peak, exercise tolerance, and submaximal adaptations.

sCRF as measured by exercise tolerance (km) improved significantly at 4 wk (P < 0.001, d = 0.35, Table 2). The average HR maintained during the exercise tolerance test did not change (P > 0.05, d = −0.06). sCRF measured by steady-state HR during the treadmill test decreased by 10–13 bpm compared with baseline at 2%, 4%, and 6% grade (P < 0.001, d = −0.97, d = −0.93, d = −0.92).

Associations between mCRF and sCRF (exercise tolerance)

Baseline mCRF (L·min−1) was not associated with the total distance (km) achieved during the baseline exercise tolerance test (R2 = 0.08, P > 0.05). The change in absolute (L·min−1) and relative (mL·kg−1·min−1) mCRF was not associated with the change in sCRF as measured by change in exercise tolerance (km) (absolute R2 = 0.006, P > 0.05, relative R2 = 0.009, P > 0.05).

A secondary analysis was completed to determine whether changes in exercise tolerance differed between mCRF responders and nonresponders (Fig. 1). There were 13 nonresponders (52%) for mCRF. The group identified as nonresponders for mCRF showed a significant increase in exercise tolerance at 4 wk (0.18 ± 0.15 km, P < 0.001). There was no significant difference in exercise tolerance between mCRF responders (0.12 ± 0.10 km, n = 12) and nonresponders (0.18 ± 0.15 km, n = 13, P > 0.05; Fig. 1A and B). All but four nonresponders for mCRF improved in exercise tolerance (Fig. 1A–C).

Response across all three measures of cardiorespiratory fitness. A, Maximal oxygen uptake; 13 participants (52%) were nonresponders for mCRF after 4 wk of aerobic PA. TE = 0. 204 L·min−1. B, Exercise tolerance; eight participants were nonresponders for exercise tolerance. TE = 0.07 km. C, Submaximal HR; two participants were nonresponders for submaximal HR. TE = 3.9 bpm at 6% incline. The gray bar indicates the TE for each measure. Bar 1 represents the results for the same individual in every subsequent graph. Favorable outcomes for each variable are as follows: increase in mCRF, increase in distance traveled, and decrease in submaximal HR.

Associations between mCRF and sCRF (submaximal exercise HR)

Change in mCRF was not associated with change in sCRF measured as steady-state HR for submaximal exercise at 2% (R2 = 0.004, P > 0.05), 4% (R2 = 0.046, P > 0.05), or 6% grade (R2 = 0.035, P > 0.05). As a group, mCRF nonresponders significantly decreased submaximal exercise HR values at 2%, 4%, and 6% grade after 4 wk (2%: −10.65 ± 5.69 bpm; 4%: −10.98 ± 7.74 bpm; 6%: −13.52 ± 9.09 bpm; P < 0.001). There was no significant difference in the change in submaximal HR at 2%, 4%, or 6% grade between mCRF responders (2%: −9.2 ± 5.38 bpm; 4%: −11.81 ± 6.76 bpm; 6%: −13.42 ± 6.60 bpm; n = 12) and nonresponders (2%: −10.65 ± 5.69 bpm; 4%: −10.98 ± 7.74 bpm; 6%: −13.52 ± 9.09 bpm; n = 13, P > 0.05; Fig. 1A and C). Similarly to exercise tolerance, all but two nonresponders for mCRF improved in submaximal exercise HR (Fig. 1A–C).


The primary finding of this study is that improvements in mCRF in response to exercise training consistent with the consensus recommendation are not associated with improvements in sCRF among previously physically inactive, overweight men. That all participants demonstrated an increased exercise capacity at submaximal exercise levels (sCRF) with or without a corresponding improvement in mCRF is encouraging given the strong inverse association between PA and cardiovascular disease. Practitioners and researchers are encouraged to include measures of sCRF to determine exercise-induced improvements in submaximal exercise capacity.

To our knowledge, no other study has examined the association between changes in mCRF and measures of sCRF in response to exercise training consistent with current guidelines in previously sedentary men. However, our finding that individual measures of sCRF are not significantly associated with mCRF is consistent with previous trials (2,9,22,24,31) in young, highly active, high-intensity trained individuals. Together, these findings suggest that regardless of age, fitness level, or exercise intensity, change in sCRF is unrelated to corresponding change in mCRF.

In this study, the interindividual changes for mCRF and sCRF measures were considered in light of the biological or day-to-day variability of measurement. More than 50% of our participants did not improve (e.g., nonresponse) mCRF which is slightly higher than the levels of nonresponse for mCRF reported previously (25). However, of those mCRF nonresponders, all improved in at least one measure of sCRF, suggesting that the exercise-induced physiological adaptations in mCRF and sCRF are independent of one another. In support of this hypothesis, we did not observe a significant association between change in sCRF HR and change in mCRF. If the change in sCRF HR were associated with the change in mCRF, it would imply a common mechanism. That the changes in sCRF HR and mCRF were not associated suggests that not only are adaptations in sCRF and mCRF independent of each other but that sCRF changes are likely due to peripheral adaptations. This observation confirms our a priori hypothesis that mCRF and sCRF tests capture distinct adaptations to exercise, wherein mCRF more readily captures central adaptations (19) and sCRF better captures peripheral adaptations (11,14).

Our findings suggest that after 4 wk of exercise, all individuals who improved in at least one variable reduced their health risk by either increasing mCRF (8,20) or by increasing their ability to perform regular PA vis-à-vis improvements in submaximal exercise performance (12,23). Although the health benefits associated with improving mCRF are established, the benefits of increasing submaximal exercise performance on health outcomes are unclear. However, submaximal exercise performance is indicative of the ability to perform PA, where increasing PA is an established method for reducing morbidity and mortality risk (1,4). The results of our study reinforce the notion that individuals of any age looking to improve their health should focus on increasing the level of PA, where PA is viewed as a behavior to improve, and not simply a conduit to improve mCRF.

Strengths of our study include objective measures of 24-h PA, which helped us isolate the effects of the prescribed exercise on CRF from improvements consequent to increases in daily PA performed outside the laboratory (18). All exercise sessions were supervised to ensure that participants adhered to the prescribed intensity and amount of exercise. Finally, our study population was inactive and overweight, which is representative of a large majority of the adult male population in developed countries worldwide. Limitations of our study include the relatively small sample size and our exclusion of women. It would be of interest to measure ventilatory threshold, blood lactate, and other metabolic markers during mCRF and sCRF tests to better understand the mechanisms involved in the adaptations observed. Finally, whether improvements in measures of sCRF predict health outcomes in a manner similar to mCRF is unknown.


Submaximal measures of CRF capture adaptations to exercise consistent with consensus guidelines independent of change in mCRF. Submaximal tests of CRF may be useful for measuring improvements not captured by V˙O2peak such as the ability to do PA and perform activities of daily living. This is especially encouraging for individuals unable to improve CRF and for populations whose health limits their ability to exercise at maximal effort. These results bolster the growing body of work establishing the benefits of structured MVPA with or without corresponding improvement in mCRF.

This study received financial support from the Canadian Institutes of Health Research (grant no. OHN-63277). The authors thank the staff and students of the Lifestyle and Cardiometabolic Research Unit at Queen's University for their support in the completion of this study. They also acknowledge the volunteers who participated in this study.

No authors report any conflicts of interest. The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. Also, the results of this study do not constitute endorsement by the American College of Sports Medicine.


1. Archer E, Blair SN. Physical activity and the prevention of cardiovascular disease: from evolution to epidemiology. Prog Cardiovasc Dis. 2011;53(6):387–96.
2. Billat V, Demarle A, Paiva M, Koralsztein JP. Effect of training on the physiological factors of performance in elite marathon runners (males and females). Int J Sports Med. 2002;23(5):336–41.
3. Bouchard C, Blair SN, Church TS, et al. Adverse metabolic response to regular exercise: is it a rare or common occurrence? PLoS One. 2012;7(5):e37887.
4. Bouchard C, Blair SN, Katzmarzyk PT. Less sitting, more physical activity, or higher fitness? Mayo Clin Proc. 2015;90(11):1533–40.
5. Bouchard C, Rankinen T. Individual differences in response to regular physical activity. Med Sci Sports Exerc. 2001;33(6 Suppl):S446–51; discussion S452-3.
6. Church TS, Earnest CP, Skinner JS, Blair SN. Effects of different doses of physical activity on cardiorespiratory fitness among sedentary, overweight or obese postmenopausal women with elevated blood pressure: a randomized controlled trial. JAMA. 2007;297(19):2081–91.
7. Cooper KH. A means of assessing maximal oxygen intake. Correlation between field and treadmill testing. JAMA. 1968;203(3):201–4.
8. DeFina LF, Haskell WL, Willis BL, et al. Physical activity versus cardiorespiratory fitness: two (partly) distinct components of cardiovascular health? Prog Cardiovasc Dis. 2015;57(4):324–9.
9. Esfarjani F, Laursen PB. Manipulating high-intensity interval training: effects on V˙O2max, the lactate threshold and 3000 m running performance in moderately trained males. J Sci Med Sport. 2007;10(1):27–35.
10. Freedson PS, Melanson E, Sirard J. Calibration of the Computer Science and Applications, Inc. accelerometer. Med Sci Sports Exerc. 1998;30(5):777–81.
11. Goodman JM, Pallandi DV, Reading JR, Plyley MJ, Liu PP, Kavanagh T. Central and peripheral adaptations after 12 weeks of exercise training in post-coronary artery bypass surgery patients. J Cardiopulm Rehabil. 1999;19(3):144–50.
12. Grundy SM, Blackburn G, Higgins M, Lauer R, Perri MG, Ryan D. Physical activity in the prevention and treatment of obesity and its comorbidities: evidence report of independent panel to assess the role of physical activity in the treatment of obesity and its comorbidities. Med Sci Sports Exerc. 1999;31(11):1493–500.
13. Gurd BJ, Giles MD, Bonafiglia JT, et al. Incidence of nonresponse and individual patterns of response following sprint interval training. Appl Physiol Nutr Metab. 2016;41(3):229–34.
14. Henriksson J. Training induced adaptation of skeletal muscle and metabolism during submaximal exercise. J Physiol. 1977;270(3):661–75.
15. Lortie G, Simoneau JA, Hamel P, Boulay MR, Landry F, Bouchard C. Responses of maximal aerobic power and capacity to aerobic training. Int J Sports Med. 1984;5(5):232–6.
16. Maiorana AJ, Briffa TG, Goodman C, Hung J. A controlled trial of circuit weight training on aerobic capacity and myocardial oxygen demand in men after coronary artery bypass surgery. J Cardiopulm Rehabil. 1997;17(4):239–47.
17. Mâsse LC, Fuemmeler BF, Anderson CB, et al. Accelerometer data reduction: a comparison of four reduction algorithms on select outcome variables. Med Sci Sports Exerc. 2005;37(11 Suppl):S544–54.
18. McGuire KA, Ross R. Incidental physical activity is positively associated with cardiorespiratory fitness. Med Sci Sports Exerc. 2011;43(11):2189–94.
19. Murias JM, Kowalchuk JM, Paterson DH. Time course and mechanisms of adaptations in cardiorespiratory fitness with endurance training in older and young men. J Appl Physiol (1985). 2010;108(3):621–7.
20. Myers J, McAuley P, Lavie CJ, Despres JP, Arena R, Kokkinos P. Physical activity and cardiorespiratory fitness as major markers of cardiovascular risk: their independent and interwoven importance to health status. Prog Cardiovasc Dis. 2015;57(4):306–14.
21. Noonan V, Dean E. Submaximal exercise testing: clinical application and interpretation. Phys Ther. 2000;80(8):782–807.
22. Paavolainen L, Häkkinen K, Hämäläinen I, Nummela A, Rusko H. Explosive-strength training improves 5-km running time by improving running economy and muscle power. J Appl Physiol (1985). 1999;86(5):1527–33.
23. Paffenbarger RS Jr, Blair SN, Lee IM, Hyde RT. Measurement of physical activity to assess health effects in free-living populations. Med Sci Sports Exerc. 1993;25(1):60–70.
24. Ramsbottom R, Williams C, Fleming N, Nute ML. Training induced physiological and metabolic changes associated with improvements in running performance. Br J Sports Med. 1989;23(3):171–6.
25. Ross R, de Lannoy L, Stotz PJ. Separate effects of intensity and amount of exercise on interindividual cardiorespiratory fitness response. Mayo Clin Proc. 2015;90(11):1506–14.
26. Ross R, Hudson R, Day AG, Lam M. Dose-response effects of exercise on abdominal obesity and risk factors for cardiovascular disease in adults: study rationale, design and methods. Contemp Clin Trials. 2013;34(1):155–60.
27. Ross R, Hudson R, Stotz PJ, Lam M. Effects of exercise amount and intensity on abdominal obesity and glucose tolerance in obese adults: a randomized trial. Ann Intern Med. 2015;162(5):325–34.
28. Scharhag-Rosenberger F, Walitzek S, Kindermann W, Meyer T. Differences in adaptations to 1 year of aerobic endurance training: individual patterns of nonresponse. Scand J Med Sci Sports. 2012;22(1):113–8.
29. Sisson SB, Katzmarzyk PT, Earnest CP, Bouchard C, Blair SN, Church TS. Volume of exercise and fitness nonresponse in sedentary, postmenopausal women. Med Sci Sports Exerc. 2009;41(3):539–45.
30. Skinner JS, Jaskólski A, Jaskólska A, et al. Age, sex, race, initial fitness, and response to training: the HERITAGE Family Study. J Appl Physiol (1985). 2001;90(5):1770–6.
31. Vollaard NB, Constantin-Teodosiu D, Fredriksson K, et al. Systematic analysis of adaptations in aerobic capacity and submaximal energy metabolism provides a unique insight into determinants of human aerobic performance. J Appl Physiol (1985). 2009;106(5):1479–86.
32. Ward DS, Evenson KR, Vaughn A, Rodgers AB, Troiano RP. Accelerometer use in physical activity: best practices and research recommendations. Med Sci Sports Exerc. 2005;37(11 Suppl):S582–8.


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