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APPLIED SCIENCES: Physical Fitness and Performance

Heart rate and performance parameters in elite cyclists: a longitudinal study.

LUCÍA, ALEJANDRO; HOYOS, JESÚS; PÉREZ, MARGARITA; CHICHARRO, JOSÉ L.

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Medicine & Science in Sports & Exercise: October 2000 - Volume 32 - Issue 10 - p 1777-1782
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Abstract

In endurance sports, the prescription of training loads is often based on heart rate (HR) data (13,14,18,21). HR is an indicator of exercise intensity up to levels close to maximum oxygen uptake (V̇O2max) (13), and it is currently possible to use reliable telemetric HR monitors during training sessions for immediate feedback to the athlete and for later analysis (13,16). Nevertheless, target HR recommendations are often based on the results of previous laboratory exercise tests. The blood lactate response during incremental exercise, i.e., the lactate threshold, or LT, is considered to be a good predictor of performance (10,15,33,34). Both the first (VT1) and second ventilatory threshold (VT2), which may be determined during progressive exercise testing (3,6,7), have also been shown to be important determinants of performance and fitness level in endurance exercise (22,24). VT1 represents the first increase in minute ventilation (V̇E) that is proportional to the increase in CO2 output (V̇CO2) generated by the HCO3− buffering of lactic acid (6). As a result, the ventilatory equivalent for oxygen (V̇E·V̇O21) increases with no change in the ventilatory equivalent for carbon dioxide (V̇E·V̇CO21) (6). VT2, in turn, represents a high work intensity at which blood lactic accumulation increases considerably (i.e., production exceeds clearance) and is accompanied by a additional hyperventilation in an attempt to buffer acidosis (20,31). At this exercise intensity, both V̇E·V̇O2−1 and V̇E·V̇CO2−1 show a marked increase whereas end-tidal partial pressure of carbon dioxide (PETCO2) starts to decrease (6). Thus, determination of the specific HR associated with one or more of these parameters is of great use in prescribing adequate training loads based on HR data. This methodology is in fact frequently employed by elite endurance athletes (e.g., professional cyclists) to evaluate the level of intensity attained during training sessions and competitions (24).

As the result of changes in training loads, the workload (i.e., power output) eliciting such lactate or ventilatory markers may vary considerably throughout the sports season (8,10,17,19,26,27,32,33,37). However, surprisingly few research efforts (11) have focused on determining the longitudinal stability of HR associated with lactate or ventilatory parameters. If target HR were shown to be stable during the sports season, a single laboratory study might be sufficient to establish adequate training prescription. This would be of use to many athletes and coaches. Foster and coworkers (11) recently demonstrated that both the values of HR and the rate of perceived exertion (RPE) associated with lactate markers (lactate concentrations of 2.5 and 4.0 mmol·L1) remain stable over the training year in competitive speed skaters.

It would be of particular interest to corroborate the findings reported by Foster and coworkers (11) in other types of elite athletes for whom exercise prescription is mainly based on target HR. In addition, it remains to be established whether HR values related to ventilatory parameters also remain stable. In professional road cycling, one of the most physically demanding endurance sports, it is general practice to base training prescription on HR data (24). This requires frequent visits to the same laboratory by athletes who need to travel constantly (i.e., to complete 90 or more competition days in many different countries). On the other hand, both VT1 and VT2 (especially the latter) have been shown to be important determinants of performance and fitness level in top-level cycling (22,24).

It was therefore the purpose of our investigation to evaluate the stability of target HR values corresponding to LT, VT1, and VT2 during the course of a sports season in a group of professional road cyclists.

METHODS

Subjects.

Thirteen professional road cyclists participated in this study. The subjects’ mean (±SD) age, height, and weight (at the beginning of the study) were 24 ± 2 yr, 180.2 ± 2.2 cm, and 70.8 ± 5.2 kg, respectively. A previous physical examination (including ECG and echocardiographic evaluation within the same year) was used to ensure that each participant was in good health. With a professional competition experience of 4 ± 2 yr, some of these athletes are considered among the best cyclists in the world (i.e., top 20 in the 1998 ranking of the “Union Cycliste Internationale” or U.C.I.). The following are the most outstanding awards obtained in professional races: first in the 1995 and 1998 World Championships (road race and time-trial respectively); second in the 1995 Time Trial World Championships; second in the 1996 Olympic Games (time trial); second and first in the 1995 and 1998 “Vuelta a España”; third in the 1996 “Giro d’Italia”; fourth and eighth in the 1997 “Tour de France”; sixth in the 1997 “Vuelta a España”; and first in several stages (including time trials) of the “Tour de France” and “Vuelta a España,” etc.

Study protocol.

Informed consent was obtained from each participant in accordance with the guidelines of the Complutense University. Each subject reported to the laboratory three times during the study for an exercise testing session. Each session corresponded to the “active” rest (fall: November), precompetition (winter: January), or competition periods (spring: May) of the sports season. Subjects adopted an almost sedentary lifestyle (with no cycling exercise at all) during the first 2–3 wk of the “active” rest period. Training volume, expressed as the average number of km cycled per week during each of the three periods, was as follows (mean ± SD): 267 ± 60 km (rest), 713 ± 46 km (precompetition), and 810 ± 30 km (competition). When expressed as the total number of km accumulated during the season (from the beginning of November) before each evaluation, training volume averaged ∼ 500 ± 200 km (end of November), 7430 ± 800 km (end of January), and 12,770 ± 2,042 km (end of April), respectively.

Exercise tests.

Each test was performed on a bicycle ergometer (Ergometrics 900; Ergo-line, Barcelona, Spain) after a ramp protocol until exhaustion. This type of protocol has been used for the physiological evaluation of professional cyclists in several previous studies conducted in our laboratory (4,22–26). Starting at 0 W, the workload was increased by 25 W·min1 (5 WA12 s1), and pedaling cadence was kept constant at 70–90 revolutions·min1. A pedal-frequency meter was used by the subject to maintain this cadence. Each exercise test was terminated either: 1) voluntarily by the subjects, 2) when pedaling cadence could not be maintained at 70 revolutions·min1 at least, or 3) when established criteria of test termination were met (1). During the tests, subjects adopted the conventional (upright) cycling posture. This posture was characterized by a trunk inclination of ∼ 75° and by the subject placing his hands on the handlebars with elbows slightly bent (flexion ∼ 10°). Each test was performed at the same time of day (13:00–16:00) under similar environmental conditions (21–24°C and 45–55% relative humidity). Each subject was well rested before testing and had not performed hard physical work during the previous 24 h. All of them followed a similar type of high-carbohydrate (CHO) diet during the days previous to testing, and the last meal (breakfast, with a mean intake of ∼ 150 g of CHO) was ingested 4 h before the beginning of testing sessions. Finally, any drugs that could influence heart rate were avoided on the morning of testing.

HR (beats·min1) was continuously recorded throughout the tests and during the first 5 min postexercise from modified 12-lead ECG tracings (EK56, Hellige; Freiburg, Germany). Gas exchange data were collected continuously using an automated breath-by-breath system (CPX; Medical Graphics; St. Paul, MN). The measuring instruments were calibrated before each test and the necessary environmental adjustments were made. The following parameters were recorded (average of each 15 s interval) during the tests: oxygen consumption (V̇O2, in L·min −1 STPD), V̇CO2 (L·min1 STPD), V̇E (L·min 1 BTPS), V̇E·V̇O21, V̇E·V̇CO21, and end-tidal partial pressure of oxygen (PETO2) and carbon dioxide (PETCO2).

The workloads (W and W·kg1) corresponding to ventilatory thresholds 1 and 2 (VT1 and VT2, respectively) were also identified. VT1 was determined using the criteria of an increase in both V̇E·V̇O21 and PETO2 with no concomitant increase in V̇E·V̇CO21 (6) (Fig. 1). In our experience with the present type of ramp-like protocol for testing professional cyclists (22,24–26), VT1 is easily detectable because the first marked increase in V̇E·V̇O21 with no concomitant increase in V̇E·V̇CO21 coincides in most cases with the point of “optimal ventilatory efficiency” (i.e., lowest value of V̇E·V̇O21 during exercise). VT2 was determined using the criteria of an increase in both the V̇E·VO21 and V̇E·V̇CO21 and a decrease in PETCO2 (6). With our protocol, this decrement of PETCO2 which starts at VT2 is particularly evident until the end of the test. VT1 and VT 2 were detected by two independent observers. If there was disagreement, the opinion of a third investigator was sought.

Figure 1
Figure 1:
Example of determination of lactate threshold (LT), and first (VT1) and second ventilatory threshold (VT2) in one test. Each gas-exchange data point (middle and lower figures) corresponds to a 15-s interval. V̇E·V̇O2 −1, ventilatory equivalent for oxygen; V̇E·V̇CO2 1, ventilatory equivalent for carbon dioxide; PETO2, end-tidal pressure of oxygen; end-tidal pressure of carbon dioxide (PETCO2).

Blood samples (50 μL) for the measurement of blood lactate (YSI 1500; Yellow Springs Instruments; Yellow Springs, OH) were taken from fingertips at rest every 2 min during the test and immediately after termination of exercise. The LT was determined by examining the “lactate concentration-workload (W)” relationship during the tests according to the methodology described by Weltman and coworkers (35) (Fig. 1). This method defines the workload corresponding to LT as the highest workload not associated with a rise in lactate concentration above baseline. This always occurred just before the curvilinear increase in blood lactate observed at subsequent exercise intensities. An increase of at least 0.2 mM blood lactate concentration was required for the determination of the LT.

Statistical analysis.

Data were compared by one-way repeated measures ANOVA. Comparison was made of heart rates recorded during the three periods at VT1, VT2, and LT, respectively. HRs recorded at maximal intensities and at 3 and 5 min postexercise were also compared, as were the power outputs (W and W·kg1) eliciting VT1, VT2, and LT during each of the three periods of study. When the ANOVA tests indicated a significant difference, the post hoc Scheffé test was applied. Confidence intervals for mean HR values at VT1, VT2, and LT throughout the three evaluations were also calculated.

Further analysis of the longitudinal stability of target HR values (corresponding to LT and VT2) was undertaken by applying the procedures suggested by Bland and Altman (2). For this analysis, the mean differences (bias) and standard deviation (SD) of the differences between the mean values (in beats·min1) obtained in the three evaluations (rest vs precompetition, rest vs competition, and precompetition vs competition) were calculated. The data were presented graphically to compare the difference between HR values corresponding to two of the evaluations versus their average value in beats·min1. The mean difference (bias) plus and minus two standard deviations (2SD) are indicated in the graph.

The level of significance was set at 0.05. Results are expressed as means ± standard error of the mean (SEM).

RESULTS

The V̇O2max of the subjects averaged ∼ 75.0 mL·kg1·min1 throughout the study (72.6 ± 1.5, 74.4 ± 1.3, and 75.2 ± 1.6 mL·kg1·min1 for the rest, precompetition, and competition periods, respectively). VT1, VT2, and LT were detected in 100% of the cases. Both independent researchers were in agreement for VT1 and VT2 detection in 33 (−85%) of the tests. In those six cases where the opinion of a third observer was assessed for VT1 and/or VT2 detection, there always existed agreement with one of the two other researchers. VT1 and/or VT2 were then detected based on this agreement. The VT1 and VT 2 values recorded at each of the three evaluations are shown in Table 1. The power output (expressed as both W and W·kg1) at which VT1 occurred was significantly higher during the competition than during the rest period (P < 0.05 and P < 0.01, respectively). Significant differences were also observed in VT2 (only when expressed as W·kg1) between the later two periods (P < 0.05) and in LT (W and W·kg1) between each of the three periods (P < 0.01).

Table 1
Table 1:
Power output corresponding to VT1, VT2, and LT.

Mean values of target HR recorded during the three evaluations are shown in Table 2. No significant differences were found, except for a higher HR at VT2 at rest compared with precompetition (P < 0.05) and at 3 and 5 min postexercise at rest compared with the remaining periods (P < 0.01). Confidence intervals for mean values of target HR (VT1, VT2, and LT) during the three periods are shown in Table 3.

Table 2
Table 2:
HR values (beats·min−1) recorded during the three evaluation periods.
Table 3
Table 3:
Confidence intervals (at 0.05 level of significance) of mean HR values for the three evaluation periods at VT1, VT2, and LT.

The results of the graphical analysis performed as suggested by Bland and Altman (2) are shown in Figures 2 and 3. The HR values recorded at VT2 were in close agreement throughout the study because more than 90% of data points were within the limits of agreement (bias ± 2SD) when comparing each of the three periods to another period. Similar findings were obtained for the HR values registered at LT because at least 90% of data points were within the limits of agreement with the exception of rest versus precompetition (∼ 84% of data points within agreement limits).

Figure 2
Figure 2:
Agreement between HR values corresponding to the second ventilatory threshold (VT2) during the three periods of study.
Figure 3
Figure 3:
Agreement between HR values corresponding to the lactate threshold (LT) during the three periods of study.

DISCUSSION

The main finding of our study was that mean HR values corresponding to several physiological markers of performance (LT, VT1, and VT2) remain stable during the course of a training year despite significant training-induced adaptations (i.e., shifts in LT, VT1, and VT2 toward higher workloads). Furthermore, the graphical analysis suggested by Bland and Altman (2) showed close agreement between HR values corresponding to LT and VT2 (both well documented markers of performance) during the sports season. This implies that a single laboratory study (i.e., at the beginning of the season) might be sufficient to adequately prescribe training loads based on HR data. The latter would no doubt simplify the testing schedule of endurance athletes such as professional cyclists and avoid the need for periodic readjustments to target HR values.

Previous research (17,30) has centered on the stability of HR at reference blood lactate values in untrained subjects. Both these reports by Hurley et al. (17) and Saltin et al. (30) have shown a slight decrease in HR associated with blood lactate concentrations of 2.5 and 4.0 mmol·L1, respectively, after an 8–12-wk training program in healthy, previously sedentary individuals. To the best of our knowledge, however, only one previous study by Foster and coworkers (11) focuses on the stability of HR values related to reference markers of performance (blood lactate concentrations of 2.5 and 4.0 mmol·L1) in well-trained athletes (ice speed skaters). The present study provides novel data to the body of knowledge in this area. First, in contrast to the incremental laboratory test (workload increases at 5-min intervals) used by Foster’s team, we tested a group of professional cyclists using a different type of protocol (ramp test involving gradual, continuous workload increases of 5 W·12 s1 or 25 W·min1). This type of protocol is frequently used to evaluate professional road cyclists (4,22–26). Indeed, ramp protocols (i.e., eliciting increases in HR values lower than 8 beats·min1 of exercise) are recommended by Italian exercise physiologists (5) and are commonly also applied to evaluate European professional riders. Moreover, previous research has shown the superiority of ramp-like protocols over graded steady-state protocols to detect ventilatory threshold(s) in healthy individuals (29). Secondly, the present investigation assesses the longitudinal stability of other documented markers of endurance performance such as VT1 and VT2 (22,24). This permits the quantification of training corresponding to three phases of different intensity (phase I or “low intensity”: < VT1; phase II or “moderate intensity”: between VT1 and VT2; and phase III or “high intensity”: > VT2) according to a methodology described elsewhere (31). Specifically, VT2 represents a high work intensity at which blood lactic accumulation increases considerably (i.e., production exceeds clearance) and is accompanied by a marked increase in ventilation in an attempt to buffer acidosis (20,31). Physical activity performed above VT2 mainly involves anaerobic metabolism and may be described as “hard” or “high intensity” exercise (13,14,31). Thus, the reference HR at VT2 represents a useful tool for adequate training prescription in elite endurance athletes. The percentage of V̇O2max (∼ 90%) corresponding to VT2 is considerably high in professional riders (22,24). This parameter represents an important performance factor even during extreme endurance events such as 3-wk races (Tour de France, etc.) (24). Indeed, during the most strenuous parts of these races (mountain passes and time trials), successful performance requires that the athletes tolerate a level of exercise intensity at or above VT2 over long periods of time (>30 min). Finally, in the present investigation, maximal and recovery HR values were also analyzed.

Although maximal HR did not significantly change during the season, 3- and 5-min postexercise values showed a consistent decrease. Surprisingly, few investigators have analyzed the possible training adaptations of HR values recorded after progressive exercise to exhaustion. Although speculative, the decrease in HR may be attributed to an increase in stroke volume (28) or to a decrease in sympathetic tone (9,36). These are well-known adaptations to endurance training. Our data suggest that both decreased HR during recovery from gradual exercise protocols and increased workloads eliciting performance (lactate or ventilatory) markers are two adaptations to endurance training which can be detected by repeated testing over the season. For practical purposes (i.e., training prescription based on HR); however, a single laboratory test should suffice. Recent technological developments have made it possible to measure power output (W) on a bicycle with a power measuring device (i.e., the SRM Training System) and thus to prescribe training loads based on power output eliciting ventilatory or lactate markers (18). Moreover, power output may be the most direct indicator of exercise intensity (12,18). In contrast, when training is based on HR data, training orientation requires periodic readjustment of target power output (i.e., at LT or VT2) by repeated testing during the season. Power output during actual cycling is much more variable than heart rate (18) that limits its use for training prescription. To date, HR is the most useful parameter for evaluating the level of intensity attained during training sessions and competition in professional cycling.

In summary, values of target HR for training orientation generally remain stable in professional cyclists during the course of the season. Thus, a single laboratory study (i.e., at the beginning of the season) might be sufficient to adequately prescribe training loads for elite endurance athletes based on HR data.

The authors acknowledge Ana Burton for her linguistic assistance. This study was financed as the result of a formal agreement between the Asociación Deportiva Banesto and the Complutense University of Madrid and is dedicated to professional cyclists in general for their generous efforts undertaken on roads throughout the world.

REFERENCES

1. American College of Sports Medicine. Guidelines for Exercise Testing and Prescription. Philadelphia: Lea and Febiger, 1986, pp. 95–96.
2. Bland, J. M., and K. Altman. Statistical methods for assessing agreement between methods of clinical measurement. Lancet 1: 307–310, 1986.
3. Caiozzo, V. J., J. F. Davis, J. E. Ellis, J. Azus, R. Vandagrill, and C. A. Prietto. A comparison of gas exchange indices used to detect the anaerobic threshold. J. Appl. Physiol. 53: 1184–1189, 1982.
4. Chicharro, J. L., A. Carvajal, J. Pardo, M. Pérez, and A. Lucía. Physiological parameters determined at OBLA vs. a fixed heart rate of 175 beats·min−1 in an incremental test performed by amateur and professional cyclists. Jpn. J. Physiol. 49: 63–69, 1999.
5. Conconi, F., G. Grazzi, C. Casoni, et al. The Conconi test: methodology after 12 years of applications. Int. J. Sports Med. 17: 509–519, 1996.
6. Davis, J. A. Anaerobic threshold: a review of the concept and directions for future research. Med. Sci. Sports Exerc. 17: 6–18, 1985.
7. Davis, J. A., P. Vodak, J. H. Wilmore, J. Vodak, and P. Kurtz. Anaerobic threshold and maximal aerobic power for three modes of exercise. J. Appl. Physiol. 41: 554–550, 1986.
8. Denis, C., R. Fouquet, P. Poty, A. Geyssant, and J. R. Lacour. Effect of 40 weeks of endurance training on the anaerobic threshold. Int. J. Sports Med. 3: 208–214, 1982.
9. Ekblom, B., A. Kilblom, and J. Sottysiak. Physical training, bradycardia and autonomic nervous system. Scand. J. Clin. Lab. Invest. 32: 251–256, 1973.
10. Evans, S. L., K. P. Davy, E. T. Stevenson, and D. R. Steals. Physiological determinants of 10-km performance in highly trained female runners of different ages. J. Appl. Physiol. 78: 1931–1941, 1995.
11. Foster, C., D. J. Fitzgerald, and P. Spatz. Stability of the blood lactate-heart rate relationship in competitive athletes. Med. Sci. Sports Exerc. 31: 578–582, 1999.
12. Gaesser, G. A., and G. A. Brooks. Muscular efficiency during steady-rate exercise: effects of speed and work rate. J. Appl. Physiol. 38: 1132–1138, 1975.
13. Gilman, M. B. The use of heart rate to monitor the intensity of endurance training. Int. J. Sports Med. 21: 73–79, 1996.
14. Gilman, M. B., and C. L. Wells. The use of heart rates to monitor exercise intensity in relation to metabolic variables. Int. J. Sports Med. 14: 339–344, 1993.
15. Hills, A. P., N. M. Byrne, and A. J. Ramage. Submaximal markers of exercise intensity. J. Sports Sc. 16: S71–S76, 1998.
16. Hopkins, S. R., and D. C. McKenzie. The laboratory assessment of endurance performance in cyclists. Can. J. Appl. Physiol. 19: 266–274, 1994.
17. Hurley, B. F., J. M. Hagberg, W. K. Allen, et al. Effect of training on blood lactate levels during submaximal exercise. J. Appl. Physiol. 56: 1260–1264, 1984.
18. Jeukendrup, A., and A. Van Diemen. Heart rate monitoring during training and competition in cyclists. J. Sports Sci. 16: S91–S99, 1998.
19. Keith, S. P., I. Jacobs, and T. M. McLellan. Adaptations to training at the individual anaerobic threshold. Eur. J. Appl. Physiol. 65: 316–323, 1992.
20. Kinderman, W., G. Simon, and J. Keul. The significance of the aerobic-anaerobic transition for the detection of work load intensities during endurance training. Eur. J. Appl. Physiol. 52: 25–34, 1979.
21. Lambert, M.I., Z.H. Mbambo, and A. St Clair Gibson, Heart rate during training and competition for long-distance running. J Sports Sci 16: S85–S90, 1998.
22. Lucía, A., J. Pardo, A. Durántez, J. Hoyos, and J. L. Chicharro. Physiological differences between professional and elite road cyclists. Int. J. Sports Med. 19: 342–348, 1998.
23. Lucía, A., A. Carvajal, A. Alfonso, F. J. Calderón,and J. L. Chicharro. Breathing pattern in highly competitive cyclists during incremental exercise. Eur. J. Appl. Physiol. 79: 512–521, 1999.
24. Lucía, A., J. Hoyos, A. Carvajal, and J. L. Chicharro. Heart rate response to professional road cycling: the Tour de France. Int. J. Sports Med. 20: 167–172, 1999.
25. Lucía, A., O. Sánchez, A. Carvajal, and J. L. Chicharro. Analysis of the aerobic-anaerobic transition in elite cyclists during incremental exercise with the use of electromyography. Br. J. Sports Med. 33: 178–185, 1999.
26. Lucía, A., A. Carvajal, A. Boraita, L. Serratosa, J. Hoyos, and J. L. Chicharro. Heart dimensions may influence the occurrence of the heart rate deflection point in highly trained cyclists. Br. J. Sports Med. 33: 387–392, 1999.
27. Martin, D. E., D. M. Vroon, A. F. May, and S. P. Pilbean. Physiological changes in elite male distance runners training for olympic competition. Physician Sportsmed, 14: 152–171, 1986.
28. Meyer, K., H. S. Westbrooks, L. Samek, et al. Ventilatory and lactate threshold determinations in healthy normals and cardiac patients: methodological problems. Eur. J. Appl. Physiol. 72: 387–393, 1996.
29. Rowell, L. B. Cardiovascular adjustments to exercise and thermal stress. Physiol Rev. 54: 75–159, 1974.
30. Saltin, B., L. H. Hartley, A. Kilbom, and I. Astrand. Physical training in sedentary middle aged and older men: II. Oxygen uptake, heart rate and blood lactate concentration at submaximal and maximal exercise. Scand J Clin Lab Invest. 24: 323–334, 1969.
31. Skinner, J. S., and T. H. McLellan. The transition from aerobic to anaerobic metabolism. Res. Q. Exerc. Sport 51: 234–238, 1980.
32. Tanaka, K., H. Watanabe, and Y. Konishi. Longitudinal associations between anaerobic threshold and distance running performance. Eur. J. Appl. Physiol. 55: 248–252, 1986.
33. Tanaka, K., N. Takashema, T. Kato, S. Nihata, and K. Ueda. Critical determinants of endurance performance in middle aged and elderly endurance runners with heterogeneous training habits. Eur. J. Appl. Physiol. 59: 443–449, 1990.
34. Weltman, A. (Ed.). The Blood Lactate Response to Exercise. Champaign, IL: Human Kinetics, 1995, pp. 49–58.
35. Weltman, A., D. Snead, R. Seip, R. Schurrer, S. Levine, and R. Rutt. Reliability and validity of a continuous incremental treadmill protocol for the determination of lactate threshold, fixed blood lactate concentrations, and VO2max. Int. J. Sports Med. 11: 26–32, 1990.
36. Wilmore, J. H., P. R. Stanforth, J. Gagnon, et al. Endurance exercise training has a minimal effect on resting heart rate: The Heritage Study. Med. Sci. Sports Exerc. 28: 829–835, 1996.
37. Yoshida, T., Y. Suda, and N. Takeuchi. Endurance training regimen based upon arterial blood lactate: effects on anaerobic threshold. Eur. J. Appl. Physiol. 49: 223–230, 1982.
Keywords:

TRAINING; CYCLING; VENTILATORY THRESHOLD; LACTATE THRESHOLD

© 2000 Lippincott Williams & Wilkins, Inc.