The anaerobic threshold during exercise-based cardiac rehabilitation

Coronary Health Care (1999) 3, 81-86 9 1999 Harcourt Brace & Co. Ltd

ORIGINAL A R T I C L E

The anaerobic threshold during exercise-based cardiac rehabilitation D. Brodie*, X. Liut, P. Bundred:~ *Professor, Department of Movement Science, 7-PhDStudent, Department of Movement Science, ,tReader, Department of Primary Care, University of Liverpool, Liverpool, UK SUMMARY. The purposes of this study were (a) to examine the concept of an anaerobic threshold (AT) based upon a change in the slope of blood lactate (BL) and the volume of expired air (~'E) during incremental exercise, (b) to examine the relationship between BL and VE, and (c) to establish the level of AT in terms of the percentage of peak oxygen uptake (% VO2pk) for post myocardial infarction patients (PMIP). Thirty-two male recent non-blockade PMIP, aged 60.2+6.2 years, performed a graded exercise test on a motorized treadmill until volitional cessation or reaching any of the American College of Sports Medicine (ACSM) criteria. Oxygen uptake and T2E were recorded every 30 seconds during the exercise. Blood lactate was measured before, during exercise (at the end of each stage) and in recovery for the third and the sixth minute. The results showed that the inflection point for both BL and VE in relation to % VO2pk was easily determined and corresponded to 72% and 70% respectively. A correlation of 0.93 (P < 0.001) was shown between I;'E and BL expressed in terms of % VO2pk. The results provided evidence that 70% VO2pk represents the mean onset of metabolic acidosis, an undesirable intensity of exercise for cardiac rehabilitation. Health professionals, unable to measure oxygen uptake, can monitor respiratory changes and use these as a valuable indicator of aerobic limits during exercise. This will assist in setting a programme that maximizes the training benefits whilst minimizing the risk.

INTRODUCTION

heart rates than normal subjects of the same age and may even have lower heart rates than normal subjects at very low workloads (Amundsen 1981). The ventilation break point is the level of exercise at which a marked increase in ventilation that is out of proportion to oxygen uptake is observed (Lamb 1984). Respiratory exchange ratio is the amount of carbon dioxide production relative to the amount of oxygen uptake (Fox et al. 1989). During incremental exercise, it appears that a work rate is reached that alters the demand-supply relationship for oxygen, thus increasing energy release from anaerobic metabolism with a subsequent increase in lactate formation (Wasserman & Whipp 1975). This onset of blood lactate (BL) accumulation was labelled as anaerobic threshold (AT) by Sjodin & Jacobs (1981). The feasibility of measuring the AT has been advanced considerably with the description of a noninvasive procedure by Wasserman et al. (1973) who defined the AT as the work rate just below the point of a non-linear increase in volume of expired gas (VE). This relationship has yet to be established in post

There are two general metabolic pathways in the muscle to provide the energy for work. One pathway requires oxygen (aerobic metabolism) and yields large quantities of adenosine 5'-triphosphate (ATP) per mol of glucose. The other does not require oxygen (anaerobic metabolism) and yields small quantities of ATP per mol of glucose or muscle glycogen. Blood lactate is the end product of anaerobic metabolism in the blood (Lamb 1984). Peak oxygen uptake is the highest single oxygen uptake value seen in an exercise test (Rowland 1993). The heart rate normally increases linearly with work rate within the physiological range. Healthier and more active individuals will usually have a lower heart rate at a given work rate. Cardiac patients, however, will have lower maximum

Correspondenceto: ProfessorD. A. Brodie,Departmentof MovementScienceand PhysicalEducation,Universityof Liverpool,Liverpool,L69 3BX,UK. 81

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myocardial infarction patients (PMIP). However, if the AT is detectable using blood lactate (BL) and IkE, it will provide one more useful reference for an optimal training zone that avoids anaerobic metabolism during cardiac rehabilitation. The purposes of this study were (a) to examine the concept of an AT based upon a change in the slope of BL and the t;'E during incremental exercise, (b) to examine the relationship between BL and I2E, and (c) to establish the level of AT in terms of the percentage of peak oxygen uptake (%FO2pk) for PMIR The stage of the incremental exercise protocol in which the mean AT occurs will additionally become evident.

MATERIALS AND M E T H O D S Supers Thirty-two male recent non-blockade PMIP undertook a graded exercise test on a motorized treadmill (Marquette, Manchester, UK). The details of this study were described to the subjects and their written, informed consent was obtained. Ethical approval was provided by the Wirral and West Cheshire Community Healthcare Trust. Patients were selected sequentially as they completed the Phase III programme (12 weeks of exercise-based cardiac rehabilitation). They had already undertaken the full exercise protocol previously and were therefore familiar with the modified Bruce protocol and the use of the gas collection system. As the subjects had exercised regularly for 12 weeks they were moderately trained and were totally habituated to the treadmill. Protocol The modified Bruce treadmill protocol (Bruce & Horsten 1969) was used for the graded exercise test. The criteria to end the exercise test followed the American College of Sports Medicine guidelines (American College of Sports Medicine 1991) and included any abnormal electrocardiogram, reaching the age-predicted heart rate maximum (HRmax), any abnormal blood pressure readings, a rating of perceived exertion (RPE) of 17 and a respiratory exchange ratio (RER) of above 1.15. The patients were questioned throughout the study and could stop the exercise at any time, even if the above criteria were not evident. The modified Bruce protocol is highly reproducible both from a practical perspective and in terms of repeat reliability of measurements. The speed and inclination of the treadmill is computer controlled by the Marquette Centra system so it is impossible for human error to occur. This guarantees absolute consistency between and within subjects. In a typical cardiac rehabilitation programme it is difficult to assess the repeat reliability of the measurements because subjects usually only repeat the Coronary Health Care (1999) 3 (2), 81-86

protocol following a training programme. However, in a separate experiment 20 subjects were re-tested at an interval of 1 week. No significant differences were found between any of the measures. The modified Bruce protocol is preferred with cardiac patients because the increments are smaller than the Bruce protocol. In spite of this when physiological data are plotted against treadmill stage, significant differences are usually demonstrated. Measurements RPE were measured using the 15 point scale (Borg 1982). It was presented as a large wall chart directly in front of the subject so continuous reference could be made to it. It was recorded during the last minute of every exercise stage (i.e. every 3 minutes) by placing the scale just in front of the subject and requesting the subject to point to the relevant number. Both systolic and diastolic blood pressure were also measured immediately before RPE using a mercury sphygrnomanometer (Baum, Copiague, USA). Oxygen uptake (IYO2), I~E, heart rate (HR) and RER were measured every 30 seconds using a totally integrated metabolic analyser (Brodie et al. 1994). Maximum oxygen uptake values were unlikely to be achieved in the present study because of prior exercise cessation, so in place of maximum oxygen uptake the term peak oxygen uptake was used. The percentage of peak oxygen uptake (%VO2pk) was derived from this. A 12-lead electrocardiogram was observed continuously (Marquette, Centra, Manchester, UK) by a clinician and summary recordings made every 3 minutes. Following micropuncture of the finger tip (Autoclix, Boehringer Mannheim, Germany), a 20 gL blood sample was taken for BL analysis (Accusport, Boehringer Mannheim, Germany) by dry chemistry before, during exercise (at the end of each stage) and in recovery for the third and the sixth minutes. This measurement has previously been established as reliable (P<0.01) (Liu & Brodie 1998), and showed a high correlation (r=0.85, P<0.01) with values measured by an alternative analyzer (GM7, Analox Instrument Ltd, UK). A four level angina and dyspnea scale (Cornett & Watson 1984) was also presented immediately after the RPE measurement to establish whether the subjects were experiencing any chest pain or breathing difficulties. The patients were required to point to the appropriate descriptors on the scale should any of these occur. AT was determined at the point when BL and VE appeared from graphical analysis to change the slope of the association with %VOo. (Davis et al. 1976), and they were called BLAT and VE-AT respectively. zp~

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Statistics The raw data were analysed using the Arcus statistics package on an Opus Technology 386 computer at the 9 1999 Harcourt Brace & Co. Ltd

The anaerobic threshold

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Computing Services Department, the University of Liverpool. The results were expressed as means and standard deviations (SD). The relationship between the estimated AT derived from both BL and I;'E inflection was established through regression analysis using the linear model of y=a+bx. A paired t-test with two-tailed model was used to examine the difference between the intensities established according to BL-AT and I;'E-AT. A probability of P<0.05 was regarded as statistically significant. RESULTS The 32 male subjects were 60.2 (_+6.2) years old, were 174.9 (+6.2) cm in height, had a body mass of 78.4 (-+11.3) kg and exercised for a mean time of 15.7 (+1.3) minutes. Figures 1 and 2 show the BL and I;'E values relative to % I;'O2pk during exercise, in which a non-linear increase can be seen for both variables. Figure 3 demonstrates the comparability o f the BL-AT and I;'E-AT. The r value is 0.93 (r 2 = 86%, P<0.001) for the regression line, which has the linear equation o f y = - 11.65 + 1.17><. It is noted that all the 9 1999 Harcourt Brace & Co. Ltd

data points lie within the 95% confidence limits (as expressed by the dotted lines on Fig. 3) and the standard error o f the estimate is only 2.6%. The % I;'O2pk values for BL-AT and I?E-AT were 72.0-+7.0 and 69.9-&_5.7 respectively. The equivalents for exercise stage were 3.6_+0.7 and 3.7_+0.7. There was a non-significant difference between the two AT values f o r 0//0~rO2pk, and between the two stages (P>0.05). In addition to the above, the equivalent values for RPE, % H R m a x and % H R peak are shown for both BL-AT and I;'E-AT as follows: for BL-AT, RPE = 11.5+1.5, % H R m a x = 67.0i-_8.5 and % H R peak = 77.2+7.1; for rTE-AT, RPE = 11.6+1.6, % H R m a x = 67.3+8.8 and % H R peak = 78.0-k_7.0. Once again the consistency o f the values is noted. DISCUSSION Sport scientists utilize the AT to monitor training adaptations (Ready & Quinney 1982) and to prescribe exercise intensities that elicit maximal aerobic performance (Whipp & Ward 1980). The intensity of exercise at the AT is highly correlated with long distance Coronary Health Care (1999) 3 (2), 81-86

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Fig. 3 Regressionof the BL-ATon the VE-AT.

aerobic activity (Costill et al. 1973; Farrell et al. 1979; Rhodes & McKenzie 1984; Maffulli et al. 1991) and is representative of an individual's endurance capacity (Weltman et al. 1978; Rusko et al. 1980; Tanaka et al. 1983; Peronnet et al. 1987). Based upon this evidence, the AT has gained acceptance as a critical determinant of optimal performance. If AT could also be applied to specific unhealthy populations, it could become a routine laboratory measure with broad applications. The AT is useful in assessing the presence and severity of cardiovascular disease (Wasserman & Mcllroy 1964; Weber & Janicki 1985) and may be useful in rehabilitation programmes (Casaburi et al. 1989). In practice, the exercise intensity at which AT will occur is usually expressed by work rate or by percentage of maximum oxygen uptake (Skinner & McLellan 1980; Lamb 1984). However, a less precise inflection point was shown when BL and VE was compared with exercise stage (work rate). Percentage of maximum oxygen uptake, besides representing exercise intensity, can also provide information about the performance capability. For example, elite endurance athletes must be capable of exercising efficiently for prolonged times at high percentages of maximum oxygen uptake without accumulating large amounts of lactic acid in their blood (Pollock 1977). Maximum oxygen uptake is potentially a dangerous measure to establish in PMIP because it would require increasing the exercise intensity to a point that the 1202 plateaus. Thus, % 1202pk was chosen in place of percentage of maximum oxygen uptake to examine changes of both BL and 12E during exercise in the present study. One of the purposes of this study was to determine the feasibility of detecting the AT using BL and 12E measurement for PMIR This has been achieved and is verified by the clear point of departure from linearity in BL and lYE responses to % 1202pk as shown in Figures 2 and 3. The fact that these measures are highly correlated and occur at the same point means that the detection of the AT can be made using no more laboratory equipment than is normally used for the measurement of VE. Coronary Health Care (1999) 3 (2), 81-86

Much of the research to date has concluded that the two mechanisms driving the ventilatory and lactic acid accumulating responses are associated in some way. This relationship lies in the increase in ventilation driven by an elevated carbon dioxide production, which results from the buffering of protons (Wasserman et al. 1973). Despite the widely accepted causal relationship between lactic acid accumulation and increasing ventilation, suggestions of a coincidental relationship also exist (Simon et al. 1983; Cecca et al. 1986; Gaesser & Poole 1986). This could result in a significant difference between the work rate just below BL-AT and 12E-AT. In the present study, a correlation of r = 0.93 (r ~ = 86%, P < 0.001) was observed after plotting %VO 2pk scores for VE-AT versus BL-AT methods. This result, combined with the low standard error of estimate (2.6%), tends to support the above causal relationship hypothesis yet the coincidental possibility must be examined as a viable alternative. The maximum lactate steady state is considered by Jones & Doust (1998) to be the highest BL at which a balance exists between lactate production and removal. This level 'theoretically demarcates the exercise intensity above which anaerobic metabolism makes an increasingly important contribution to ATP resynthesis' (Jones & Doust 1998). Their study, although based on trained male runners, demonstrates the clear statistical association between BL-AT and I)'E-AT with a non-significant difference between the velocities at these thresholds. The present study provides further evidence in an unhealthy population of this coincidental association. Spurway (1992) also accepts the coincidence of these two measures with the breakpoints often being at a sufficiently similar intensity for one to be used as an analogue for the other. However, the close association in healthy subjects (Wasserman et al. 1973; Davis 1985) is not observed in glycogen depletion (Hughes et al. 1982) as a result of training (Gaesser & Poole 1986; Londeree 1997) and in patients with McArdle's syndrome (Hagberg et al. 1989). If a dissociated relationship is accepted, then the question remains as to what may be the coincidental, non-mechanistic cause. Acidic products and elevation of plasma potassium concentration have been suggested by Spurway (1992) but the more important question is concerned with the meaning of the lactate threshold. In answering this question, Spurway (1992) hypothesizes that elevation of BL during an incremental test is due to sympathetic vasoconstriction of visceral blood flow. This could have serious implications for an already compromised cardiovascular system, as is often the case in PMIR Although muscle metabolism during elevated BL does not appear to be curtailed by a lack of oxygen, at BL-AT when large muscle masses are involved, some deprivation appears to be beginning (Spurway 1992). Oxygen deprivation may not enhance lactate production until very close to maximum oxygen uptake. A justification for this is the 9 1999 Harcourt Brace & Co. Ltd

The anaerobic threshold observation that in cardiac rehabilitation a normal BL-AT may be associated with a severely reduced cardiac output and maximum oxygen uptake. Some studies (Coyle et al. 1983; Weltman 1989) have even shown maximum oxygen uptake and BL-AT to be coincident. The results of this study have shown no such coincidence and demonstrate that the 72+7% figure is a more consistent finding in well-trained cardiac rehabilitees. The mode of exercise should be aerobic for coronary heart disease patients during rehabilitation (Coats et al. 1995). Any movement into anaerobic metabolism could be detrimental as a general training principle and more specifically for patients suffering from a compromised cardiovascular system. The regular measurement of lactic acid to establish anaerobosis is unlikely in a practical context. However, the contribution of the present study has been the observation of a clear elevation of lactate above resting levels at 70% of the peak oxygen uptake level in patients with coronary heart disease. It could be argued that to make this measurement is also an unlikely scenario in many cardiac rehabilitation clinics, but the more frequently measured analogues such as HR, RPE and rate pressure product can provide useful and sensitive alternative measures. AT is usually expressed as a percentage of maximum oxygen uptake or % l)'O2pk. In this study the AT related intensities were also provided in terms of exercise stage. This is because (a) the modified Bruce treadmill protocol is commonly used in cardiac rehabilitation; (b) the measurement of I;'O2 can be distressing to some patients; and (c) very few clinics have the capacity to measure VO z. A nonsignificant difference was observed between the stage at which AT was measured whether from VE or blood lactate concentration. On average, AT occurred for BL at 3.6_+0.7 stages and for/;'E at 3.7_+0.7 stages. Thus, in general terms the target intensity of aerobic training should be between stage 3 and stage 4 on modified Bruce treadmill protocol for cardiac rehabilitation, It is recognized that this is based on mean values and this is for guidance only, not taking into account specific individual differences. It is also recognized that our measure of AT, an abrupt increase in BL, is only an indirect index of lactate production by the working muscle itself. The muscle begins to produce lactate much earlier in the process and this lactate is removed as rapidly as it is produced. Therefore, the 'anaerobic threshold' that we observe reflects the point where lactate production exceeds removal. The deleterious effect of any lactate production in PMIP is unknown and it has to be assumed that it is only when lactate production exceeds removal that consequences of anaerobic metabolism become evident. A further practical contribution from this study is the close relationship between lactate increase and I;'E. This reinforces the importance for a health professional in cardiac rehabilitation observing closely 9 1999 Harcourt Brace & Co. Ltd

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the breathing rate and depth of patients. Should breathing become laboured during exercise it would suggest strongly that a patient is near to the anaerobic threshold. The intensity of exercise should then be reduced to permit controlled breathing to re-occur. Londeree's (1997) meta-analysis of the effects of training on the lactate/ventilatory thresholds concluded that training at an intensity near to the BL or VE thresholds will provide a training stimulus for sedentary subjects Although his study did not include any post myocardial infarction patients, this conclusion is likely to be particularly relevant to such patients who are normally sedentary at the time of their infarction. Even though it is dangerous to extrapolate from one population to another it would seem that Londeree's conclusion would give an additional rationale for the health professional to be able to set an exercise intensity related to either the BL or VE threshold. Health professionals in cardiac rehabilitation may additionally wish to make use of the RPE and %HRmax or %HR peak values. As the values for f'EAT and BL-AT are so close, for practical purposes it is legitimate to provide a single figure. The RPE value at AT is 11.5 + 1.5 and as such an RPE value of 12 is probably a safe recommended maximum for AT. For % HRmax the equivalent value is 67% and for %HR peak 77%. These will provide guidelines to calculate heart rate maxima on an age-related basis.

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Rhodes EC, McKenzie DC 1984 Predicting marathon times from anaerobic threshold measurements. Physician and Sportsmedicine 12:95-99 Rowland TW 1993 Aerobic Exercise Testing Protocols. In: Rowland TW (Ed.) Pediatric Laboratory Exercise Testing: Clinical Guidelines. Human Kinetics, Champaign II Rusko H, Rahkila P, Karvinen E 1980 Anaerobic threshold, skeletal muscle enzymes and fiber composition in young female cross country skiers. Acta Psychiatrica Scandinaviea. 108:263-268 Simon J, Young JL, Gutin B, Blood DK, Case RB 1983 Lactate accumulation relative to the anaerobic and respiratory compensation thresholds. Journal of Applied Physiology 54: 13-17 Sjodin B, Jacobs I 1981 Onset of blood lactate accumulation and marathon running performance. International Journal of Sports Medicine 2:23-26 Skinner JS, McLellan TH 1980 The transition from aerobic to anaerobic metabolism. Research Quarterly for Exercise and Sport. 51:234--248 Tanaka Y, Matsuura Y, Kumagai S, Matsuzaka A, Hirakoba K 1983 Relationship of anaerobic threshold and onset of blood lactate accumulation with endurance performance. European Journal of Applied Physiology 52:51-56 Wasserman K Mcllroy 1964 Detecting the threshold of anaerobic metabolism in cardiac patients during exercise. American Journal of Cardiology 14:844-852 Wasserman K, Whipp B J, Koyal SN, Beaver WL 1973 Anaerobic threshold and respiratory gas exchange during exercise. Journal of Applied Physiology 35:236-243 Wasserman K, Whipp BJ 1975 Exercise physiology in health and disease. American Review of Respiratory Diseases 112: 219-249 Weber KT, Janicki JS 1985 Cardiopulmonary exercise testing for evaluation of chronic cardiac failure. American Journal of Cardiology 55:22A-31A Weltman A 1989 The lactate threshold and endurance performance. Advances in Sports Medicine 2:91-116 Weltman A, Katch V, Sady S, Freedson P 1978 Onset of metabolic acidosis (anaerobic threshold) as a criterion measure of submaximal fitness. Research Quarterly for Exercise and Sport 49:117-218 Whipp BJ, Ward SA 1980 Ventilatory control dynamics during muscular exercise in man. International Journal of Sports Medicine 1:146-159

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