A Conceptual Framework for Performance Diagnosis ...

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T. Meyer1 A. Lucía2 C. P. Earnest3 W. Kindermann1

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A Conceptual Framework for Performance Diagnosis and Training Prescription from Submaximal Parameters ± Theory and Application n?

Abstract The first part of this article intends to give an applicable framework for the evaluation of endurance capacity as well as for the derivation of exercise prescription by the use of two gas exchange thresholds: aerobic (AerTGE) and anaerobic (AnTGE). AerTGE corresponds to the first increase in blood lactate during incremental exercise whereas AnTGE approximates the maximal lactate steady state. With very few constraints, they are valid in competitive athletes, sedentary subjects, and patients. In the second part of the paper, the practical application of gas exchange thresholds in cross-sectional and longitudinal studies is

Introduction Maximal oxygen uptake (VÇO2peak/max) and maximal power output (Pmax) attained during ergometric testing are the most frequently applied indicators of endurance capacity. After recognizing the disadvantages arising from peak ergometric measurements (necessity of maximal effort, dependency on motivation/ attitude of subject/investigator, difficulty to guarantee measurement precision during high intensity exercise, or lacking sensitivity for small changes in endurance capacity) several working groups have developed alternative models utilizing submaximal parameters. As a result, within the last two decades, performance diagnoses and training prescriptions in endurance sport have often relied upon blood lactate curves from incremental ex-

described, thereby further validating the 2-threshold model. It is shown that AerTGE and AnTGE can reliably distinguish between different states of endurance capacity and that they can well detect training-induced changes. Factors influencing their relationship to the maximal oxygen uptake are discussed. Finally, some approaches of using gas exchange thresholds for exercise prescription in athletes, healthy subjects, and chronically diseased patients are addressed. Key words nplease add

ercise tests [68]. However, irrespective of their longer history of application [149], submaximal indicators derived from gas exchange measurements have gained less attention although their noninvasive nature renders them attractive. Together with sports medicine, cardiology and pneumology represent medical disciplines that traditionally apply cardiopulmonary exercise testing. Therefore, an ideal framework for performance diagnosis and exercise prescription should be also valid for patients with impaired function of the heart or lungs. This is particularly important because endurance exercise has been implemented as a therapeutic measure in several cardiac and pulmonary disease entities, e.g. obstructive airway disease (COPD), coronary artery disease (CAD), or chronic heart failure (CHF). Obvi-

Affiliation Institute of Sports and Preventive Medicine, University of Saarland, Saarbrücken, Germany Department of Morphological and Physiological Sciences, Universidad Europea de Madrid, Madrid, Spain 3 Cooper Institute Center for Human Performance and Nutrition Research, Dallas, Texas, USA 1

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Correspondence T. Meyer, M. D., Ph.D ´ Institute of Sports and Preventive Medicine, University of Saarland, Faculty of Clinical Medicine ´ Campus, Bldg. 39.1 ´ 66123 Saarbrücken ´ Germany ´ Phone: + 49 (0) 6813 02 37 50 ´ Fax: + 49 (0) 6813 02 42 96 ´ E-mail: [email protected] Accepted after revision: n Bibliography Int J Sports Med 2005; 26: 1 ± 11  Georg Thieme Verlag KG ´ Stuttgart ´ New York ´ DOI 10.1055/s-2004-830514 ´ ISSN 0172-4622

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ously, in these patients there are several other (disease-specific) aspects to be considered prior to the commencement of training. But in the absence of contraindications, prescription of exercise (intensity) might be done according to the framework outlined below which is based on submaximal ªthresholdº concepts.

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It is acknowledged that the term ªthresholdº does not perfectly reflect the physiological processes which form the basis for the endurance indicators discussed below [17,106]. Some readers might prefer ªtransitionº instead. However, as this article is primarily intended to give outlines for practical applications, the more common term ªthresholdº was chosen. It emphasizes that the thresholds represent important landmarks within the spectrum of workloads. For purposes of endurance capacity assessment and exercise prescription, this is undoubtedly the most important aspect.

Lactate Threshold Concepts

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The use of blood lactate concentrations for ergometric evaluations and exercise prescriptions is based on the simple and reliable determination of this glucose metabolite from capillary blood and on its property to increase exponentially during incremental exercise. Available lactate models almost exclusively fit into one of two categories [62, 89], i.e., they approximate either 1. the first increase in blood lactate concentrations above resting values during incremental exercise (termed ªanaerobicº threshold by Wasserman [152]; but ªaerobicº threshold by Kindermann [62]) or 2. the maximal lactate steady state (MLSS) representing the exercise intensity above which a continuous increase in blood lactate is unavoidable (ªanaerobicº threshold according to Kindermann and McLellan [62, 89,134]). Within this paper the thresholds will be called aerobic lactate threshold (AerTLA) and anaerobic lactate threshold (AnTLA), respectively. (Unfortunately, there has been a lot of confusion concerning the terms ªaerobicº and ªanaerobicº. It was argued that there is no complete absence of anaerobic metabolism even at rest. In addition, the rather transitional nature of changes in metabolic processes from very low to high intensities was emphasized. However, we would like to lead the readers attention to the application-oriented background of the models. Apart from the naming, no real disagreement exists that at least for clinicians and coaches the first rise in blood lactate during incremental exercise and the maximal lactate steady state represent two clearly discernible phenomena each with a different meaning [32, 57]. The reason to adopt the Kindermann/McLellan terminology with in this review is that it covers both ªthresholdsº ± although it does not solve all problems. Consequently, it is acknowledged that the terms ªaerobicº and ªanaerobicº do not precisely represent the physiological process that underlie these thresholds.) When the assessment of a threshold models validity is intended with regard to performance prediction and exercise prescription, studies have to consider the described physiological back-

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grounds. Correlation analyses between one threshold and competition results alone touch only one aspect [14, 56, 66,124,139]. Almost uniformly, satisfactory relationships between various submaximal lactate indices and performance measures have been documented [142]. But additional constant-load tests of long duration are usually warranted to investigate the metabolic meaning of the thresholds ± i.e. their applicability for purposes of training categorisation [13,144]. Theoretically, such tests should lead to blood lactate concentrations in the range of resting values for intensities corresponding to the aerobic threshold. Small increases of the workload above this intensity are expected to elicit slightly elevated lactate levels without an exponential rise. Intensities corresponding to the anaerobic threshold give the highest possible equilibrium between lactate release and uptake. Thus, small further increases of the workload will unavoidably induce rising lactate concentrations. Training studies demonstrating the sensitivity of a threshold model for changes in endurance capacity should ideally complete the set of validation steps [1, 34]. Surprisingly, an acceptable validation along these lines has been done for very few models only [143]. The results from sound investigations utilizing constant-load tests of sufficient duration substantiate the 2-threshold frame described above. As early as 1986, Ribeiro et al. documented only slight increases in blood lactate concentrations at an intensity corresponding to the aerobic threshold whereas cycling at the anaerobic threshold (ªsecond break pointº in lactate curve) elicited average steady-state lactate values of 5 mmol ´ l±1 [119]. A workload between anaerobic threshold and VÇO2max was not sustainable for the majority of 8 subjects for more than 15 minutes, and lactate concentrations approached 10 mmol ´ l±1. However, the authors failed to rule out that there are intensities more closely above the anaerobic threshold that could have been maintained under steady lactate conditions. Smaller differences between investigated workloads were chosen by another working group [145] who intended to validate the model of the ªindividual anaerobic thresholdº (IAT; [135]). And it was shown that even workloads only 5% above the IAT led to increasing lactate concentrations and premature cessations of constant exercise before the intended duration of 45 min was reached. These findings correspond well to the results from other investigators who used similar graphical models to determine aerobic and anaerobic threshold and applied constant-load tests of 30 [16, 90] or 45 min duration [111], respectively. In addition, these studies indicate that the critical power [105] does not necessarily represent the maximal lactate steady state. Although representing the earliest and most frequently cited approach [81], fixed lactate concentrations ± usually 2 and 4 mmol ´ l±1 ± do not appropriately determine aerobic [111] or anaerobic thresholds [16,134]. However, it has to be mentioned that even for the well-validated model of Stegmann et al. [134] for unknown reasons there exist some results which point out that it might overestimate the intensity of the individual maximal lactate steady state in single subjects [69, 92]. The most likely explanation is that there occur false threshold determinations due to the somewhat complicated graphical procedure.

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Aerobic Gas Exchange Threshold (AerTGE)

Graphical determination of AerTGE is usually done by the V-slope method [9] which depicts VÇCO2 on the y-axis and VÇO2 on the xaxis (Fig. 1). After an initial linear relationship, there appears a sudden upward bend indicating the excess CO2 being exhaled. The intersection of two regression lines for the upper and the lower part of the function indicates AerTGE which is, by definition, an oxygen uptake. If the corresponding workload during incremental exercise is to be determined the time constant for oxygen has to be considered. A modification of the V-slope method ± detection of the workload where the slope of the relation VÇCO2/ VÇO2 becomes larger than 1 ± has been proposed by the same working group, thereby further eliminating investigator bias [137]. Computerized solutions are available for a long time already [108]. There are three other criteria suggested in the literature to detect AerTGE: ± the first rise in the ventilatory equivalent for O2 (VE/VÇO2) without a concomitant rise in the ventilatory equivalent for CO2 (VE/VÇCO2) ± not really different from plotting VE vs. VÇO2 because no new data are added ± the first overproportional increase in the respiratory exchange ratio (RER = VÇCO2/VÇO2) ± just another expression of the original V-slope method and often difficult to detect ± the first increase in the expiratory fraction of O2 ± it represents the consequence of hyperpnea, adds a new parameter, but is still primarily dependent on ventilation and not on metabolic parameters It can be recommended to rely mainly on the V-slope method as the most direct approach [9] utilizing only measurements of VÇCO2 and VÇO2 [4]. The employment of ventilation data adds a source of variance because the individual sensitivity of chemoreceptors to the partial pressure of carbon dioxide together with the central processing of their afferences becomes relevant [106]. Therefore, it might be the best solution to use the courses of VE and EqO2 in a supportive manner only for cases of indeterminate AerTGE from the sole application of the V-slope method.

Fig. 1 Determination of AerTGE by the V-slope method in one cardiac ÇO2 at AerTGE. patient. The arrow indicates the V

Due to technical constraints, precise measurements of VE were available earlier than determinations of VÇCO2. These circumstances might partly explain why there is a number of studies which support the view that the physiological link between AerTLA and AerTGE is absent or coincidental although the sequence of events from the appearance of lactate to an enhanced ventilation seems attractive and evident. Not surprisingly, it is a striking feature of most of these studies that they used only ventilation data for the determination of AerTGE [40, 42, 51, 53,107, 114,128]. But exercise ventilation is controlled by numerous factors other than lactate appearance and its resulting increase in the partial pressure of CO2 which renders these procedures more unreliable than V-slope [51,106,154,155]. Therefore, such studies can detect incongruencies between exercise-induced hyperpnea and the lactate increase, but hardly between AerTGE and AerTLA. Recognizing these shortcomings an influential review arrived at the conclusion that ª¼little doubt should exist that the (aerobic) blood lactate and ventilatory responses are causally linkedº [68]. However, even when perfectly complying with the above described determination schedule for AerTGE, the inherent variation of gas exchange measurements can lead to inaccuracies. Objectivity (= inter-observer reliability) and reproducibility (= repeatability) of AerTGE have been questioned as well as the percentage of indeterminate thresholds [49, 94,127,159]. Computerized procedures [108] as well as data transformation enabling easier decisions [8] have been suggested without finally solving the methodological problems. Therefore, duplicate determinations only from experienced observers, utilization of multiple criteria, and plausibility controls for computer results have become scientific standard. In 1996, a list of procedural recommendations was published from a group that mainly works with cardiac patients [94]. It can be regarded as useful for healthy individuals, too. If all these precautions are met, AerTGE determinations can be regarded as valid [10, 38, 48, 67, 85, 95,138] even if there seems to remain a small number of indeterminate thresholds for varying and sometimes unknown reasons, particularly in unfit subjects [38, 61, 94]. When, in contrast to the above given recommendations, ventilatory data are mainly used for the determination there is a danger of mixing up the AerTGE with the respiratory compensation

Meyer T et al. Submaximal Gas Exchange Parameters ¼ Int J Sports Med 2005; 26: 1 ± 11

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During incremental exercise, the first rise in blood lactate concentration leads to an overproportional increase of carbon dioxide output (ªexcess CO2º; [4]) as related to oxygen uptake due to the bicarbonate buffering of the proton resulting from the dissociation of lactic acid [152]. As a consequence of a slightly rising carbon dioxide partial pressure, there is a compensatory increased stimulus for ventilation mediated via the carotid bodies [151]. Thus, minute ventilation (VE) is also increasing overproportionally. And this is why the workload corresponding to these events is sometimes termed ªventilatory thresholdº or ªventilatory threshold 1º although it is primarily a metabolic phenomenon as reflected in Wassermans choice to call it ªanaerobic thresholdº [149,152]. However, as indicated by the physiological basis, this intensity reflects the ªaerobicº lactate threshold [22, 35, 36, 91,129,140,160] as it was described in the preceding chapter. Consequently, we will use the term ªaerobic gas exchange thresholdº (AerTGE) for the rest of the text.

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threshold (see next chapter). In a knowledgeable review McLellan called this ª¼the single most common methodological error in the literatureº [89]. Unfortunately, this evaluation was published in a journal with low impact and not widely spread. And it failed to change the facts as evidenced by an own survey being conducted in 2002 on 49 papers from the four most influential sports medicine journals. They were elected from the years 1991 ± 2000 provided they reported values for AerTGE as well as for VÇO2max. A thorough review revealed that almost 50% of these articles reported values which were hardly in agreement with the physiological basis of AerTGE, i.e. most times too high absolute values or too high percentages of VÇO2peak. Beneath inadequate exercise protocols (too slow increment, too large steps, breaks between stages, and inadequate degree of effort spent at maximal exercise) an obvious mixing up with the respiratory compensation threshold (= anaerobic gas exchange threshold = AnTGE) ± most often on the basis of using only ventilation data ± was the most common mistake (own unpublished data). The latter might even occur when VÇCO2 is utilized on the y-axis because of a noticeable increase in VÇCO2 close to MLSS. Due to the steepening characteristic of the lactate curve in this region, the first increase in blood lactate might be ªoverlookedº by inexperienced observers. Nevertheless, the best solution to obtain reliable results is the consequent application of the V-slope method [9] and of ramp exercise protocols (also appropriate for VÇO2peak determination) although they are not optimal for the simultaneous determination of lactate thresholds.

Anaerobic Gas Exchange Threshold (AnTGE)

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The anaerobic gas exchange threshold (AnTGE) represents the onset of exercise-induced hyperventilation, i.e. an overproportional increase of VE as related to VÇCO2 [9,117,129]. By definition, it is a ªventilatoryº phenomenon, and this is reflected in the term ªrespiratory compensation pointº (RCP) which is most often used in the literature. However, for the purposes of this review we will consistently use AnTGE to maintain uniform terminology. Graphically, AnTGE is determined similar to V-slope but with VE on the y-axis and VÇCO2 on the x-axis (Fig. 2). Two regression lines are fitted for the upper and the lower part of the relation, and their intersection represents AnTGE. The first systematic increase in the ventilatory equivalent for CO2 or the first decrease in the expiratory fraction of CO2 can be taken as alternative indicators. However, they do not provide new information beyond a different representation of the onset of exercise-induced hyperventilation. When VE is plotted against VÇO2 the AnTGE represents a second upward bending of the graph above AerTGE, which led to the naming ªventilatory threshold 2º [2]. The physiological basis of AnTGE is less clear than that of AerTGE because there are several stimuli for ventilation during exercise. It was hypothesized that the metabolic acidosis resulting from insufficient buffering of lactic acid might be the main responsible factor. The workloads between AerTGE and AnTGE were consequently termed the zone of ªisocapnic bufferingº [150] ± or aerobic-anaerobic transition by others [62]. However, experimental correction of the pH to resting levels did not completely prevent hyperventilation but was sufficient to delay it [96]. Additional

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Fig. 2 Determination of AnTGE in an endurance athlete. The arrow inÇO2 at AnTGE. dicates the V

non-humoral stimuli have to be considered as partly responsible for the occurrence of AnTGE, e. g. core temperature [155], potassium [21] and local ªmetaboreceptorsº [87,133], or mechanical receptors [57] in the muscles. There are some cross-sectional studies that describe the location of AnTGE more closely by comparing it with known indicators of endurance capacity. In 11 subjects being tested on a treadmill, Dickhuth et al. [35] observed AnTGE slightly (0.8 km´h±1 when expressed as running speed) above their AnTLA (baseline lactate concentration + 1.5 mmol ´ l±1, [124]). This is substantiated by findings from another working group which found AnTGE on average 49 W above the maximal lactate steady state (= 239 W) in 11 young students on a cycle ergometer [33]. And during 30-min constant power tests ªjust belowº AnTGE in only 3 untrained subjects the resulting lactate concentrations were not compatible with a steady state whereas cycling ªjust aboveº AnTGE led to exhaustion after 10 min and a lactate increase to approximately 11 mmol ´ l±1 in a single subject [129]. Only Ahmaidi et al. reported no significant differences between AnTLA and AnTGE in 11 subjects of fair endurance capacity [2]. But it was surprising that in one of their participants the difference between both workloads reached 100 W (AnTLA higher). Taken together, published results indicate that AnTGE might slightly overestimate the maximal lactate steady state and, therefore, be located slightly above AnTLA. This results in a performance diagnosis model as depicted in Fig. 3. Unfortunately, in contrast to AerTGE there exist very few scientific investigations about methodological problems of the AnTGE determination. Two studies indicate sufficient reproducibility [5, 35] in 33 and 11 subjects, respectively. Objectivity could not be addressed in one of these studies [35] because a computer calculated the thresholds. But the other authors reported significant but (in absolute terms) small inter-investigator differences [5]. And nothing is known about the percentage of indeterminate AnTGEs. One reason for the low number of investigations might be the high degree of effort being necessary to reach intensities above AnTGE which is a prerequisite for its determination [109]. Patients with a low endurance capacity often cannot reach these stages because symptoms or subjective exhaustion occur earlier.

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Fig. 3 Model for the delineation of exercise intensities (= training zones) by use of gas exchange thresholds. Typical values for endurance-trained and untrained subjects as well as for chronically diseased patients are shown in the squares.

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Application of the Gas Exchange Thresholds in Cardiopulmonary Exercise Testing and Training Prescription Athletes and other healthy populations Several studies have reported the AerTGE and/or AnTGE in subjects with different fitness levels using mostly ramp-like gradual tests with short-duration (~ 1 min) workloads. Extensive research has been conducted in professional road cyclists. In these athletes, AerTGE and AnTGE correspond to 70 ± 75% VÇO2max and 85 ± 90 % VÇO2max, respectively [73]. In other competitive endurance athletes, AnTGE is located at comparable or slightly lower intensities, i.e. ~ 85% VÇO2max in marathon/long-distance runners, canoeists, rowers or pentathletes [19], ~ 80 % VÇO2max in middle-distance runners, and between 80 and 85% VÇO2max in long- and short-distance top-level triathletes during cycling exercise [103], at ~ 80 % VÇO2max in younger triathletes on a treadmill [18], or at ~ 90% VÇO2max in endurance swimmers (vs. 60% in sprinters) [131]. In trained triathletes, AerTGE occurs at different oxygen uptakes for each discipline, i.e. ~ 74% VÇO2max in treadmill running vs. ~ 63% in ergometer cycling [126]. In paraplegic athletes (VÇO2peak ~ 40 ml ´ kg±1 ´ min±1) evaluated during incremental wheelchair exercise, AerTGE occurred at 56% of VÇO2peak [148]. Both AerTGE and AnTGE as percentages of VÇO2peak/max reflect, at least partly, the degree of adaptation of humans to endurance exercise and their fitness level. Compared with highly endurancetrained humans, AerTGE and/or AnTGE occur at considerably lower intensities in subjects with inferior endurance training background (AerTGE in non-professional well-trained cyclists at 65% VÇO2max vs. 70 ± 75 % VÇO2max in professionals; [28]). In only moderately trained cyclists, AerTGE and AnTGE were found to be located at 58 and 75% VÇO2max, respectively [7]. In rhythmic gymnasts or dancers (AerTGE at ~ 60 and ~ 45% VÇO2max, respectively; [6]), physically fit adults (non-athletes; AnTGE at 79% VÇO2max; [141]) or healthy sedentary adults (AerTGE at ~ 50 ± 58% VÇO2peak; [29, 50, 79]) AerTGE rarely reaches or surpasses 60 % VÇO2peak [82]. Research within large population samples has elicited no remarkable gender differences in the intensity (% VÇO2max) corresponding to AerTGE in sedentary adults [50,152]. The same seems to be true in endurance-trained individuals, where no major difference is observed for AnTGE between males and females [58].

Older subjects Some research has been conducted in healthy elderly people not engaged in regular endurance training and on the possible effects of ageing on the AerTGE [3, 84,112,115]. In individuals with a mean age between 55 and 75 y (VÇO2peak ~ 25 ml ´ kg±1 ´ min±1), AerTGE has often been reported to occur at ~ 60% VÇO2peak, corresponding to a VÇO2 value of 15 ± 17 ml ´ kg±1 ´ min±1 [3,115], although it has also been observed to approach 20 ml ´ kg±1 ´ min±1 in elderly subjects under 75 y of age [112] and in physically active octogenarians [84]. Even 28 ml ´ kg±1 ´ min±1 at AerTGE have been reported in physically active sexagenarians [84]. In a cross-sectional study aiming at indirectly assessing the effects of ageing on aerobic fitness, Paterson and co-workers determined the AerTGE by use of a ramp-like treadmill protocol in a large sample of healthy men (n = 124) and women (n = 97) ranging in age from 55 to 85 yrs [112]. As expected, the absolute workload eliciting AerTGE decreased significantly with age in both sexes. However, the rate of age-decline in VÇO2peak was greater than that of AerTGE, which resulted in AerTGE occuring at a considerably higher proportion of VÇO2peak, i.e. 77 vs. 84% VÇO2peak in the youngest and oldest men, and 80 vs. 90 % VÇO2peak in the youngest and oldest women, respectively. Furthermore, less than 11% of variance in AerTGE (expressed as ml ´ kg±1 ´ min±1) was explained by the ageing process itself. In agreement with the aforementioned findings, the AerTGE of healthy, untrained older people (mean: 68 y) occurred at considerably higher relative intensities than in their younger controls (mean: 23 y), i.e. 60 vs. 50 % VÇO2peak [115]. Malatesta and coworkers have recently reported the AerTGE to occur at very high submaximal intensities (~ 80 % VÇO2peak) in physically active sexagenarians and octogenarians [84]. Taken together, these findings would suggest that the age-decline in (absolute) VÇO2peak is partly compensated for by an increase in the % VÇO2peak at which AerTGE occurs. In endurance-trained elderly men (i.e., master marathoners with a mean age of 62 y and a mean VÇO2max of ~ 50 ml ´ kg±1 ´ min±1), AerTGE and AnTGE occurred at similar relative intensities than those reported in young endurance athletes, i.e. at ~ 65 and ~ 85% VÇO2max, respectively [71]. These findings might indicate that habituation to high degrees of effort enables

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higher maximal ergometric measurements and, consequently, lower relative values for AerTGE and AnTGE.

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Children and adolescents Compared with sedentary adults, AerTGE occurs at slightly higher relative workloads in healthy children from 5 to 16 yrs of age, i.e. at a VÇO2 of 25 ± 40 ml ´ kg±1 ´ min±1 and 60 ± 65% VÇO2max on average [30, 46, 54, 82, 83,113,117,122]. Healthy untrained adults reach 50 ± 58% VÇO2peak [29, 50, 79] and rarely surpass 60 % VÇO2peak [82]. Furthermore, in endurance-trained male children (11 ± 13 yrs), AerTGE was reported to occur at very high relative intensities, i.e., ~ 80 % VÇO2max [147]. This might indicate a less well-developed acidosis tolerance in the young [39,157] ± particularly marked after predominantly aerobic endurance training ± which leads to comparably lower maximal lactate concentrations [26]. Diseased populations Extensive research has been conducted on subjects with various chronic diseases associated with abnormally low VÇO2peak (usually < 15 ± 20 ml ´ kg±1 ´ min±1) and poor exercise tolerance (e.g. peak power output < 100 W during cycle ergometer tests) due to impaired cardiac output, altered gas exchange in the lung, and/or severe muscle deconditioning, namely: patients with chronic heart failure [47, 63, 86,130,153,156], cardiac transplant recipients [80], patients with primary pulmonary hypertension [31,121] or coronary artery disease [45,125], cancer patients [104] and survivors [15], and others [12, 23, 65,102,120]. VÇO2 (ml´min±1 or ml ´ kg±1 ´ min±1) at AerTGE is considerably lower in these patients than in healthy controls and tends to decrease with the severity of the disease, which renders AerTGE a valid indicator of functional capacity in these patients. For instance, the AerTGE of patients with chronic heart failure decreases progressively as New York Heart Association functional class (NYHA) advances [64, 86]: 33 ml ´ kg±1 ´ min±1 in healthy controls vs. 23, 17, and 13 ml ´ kg±1 ´ min±1 in class I, II, and III patients, respectively [86]. Furthermore, in this population (different etiologies) the risk of early death was shown to increase considerably if the VÇO2 at AerTGE was < 11 ml ´ kg±1 ´ min±1 [47]. It must be emphasized, however, that although in healthy subjects deconditioning is associated with a lower % VÇO2peak at the AerTGE [132], in many of the aforementioned patients the % VÇO2peak at AerTGE is quite high [86,121], e.g. ~ 74% in patients with primary pulmonary hypertension vs. 60 % VÇO2peak in healthy controls [121] or ~ 72% VÇO2peak in chronic heart failure patients [47]. In addition, patients with congestive heart failure demonstrate increases in the relative intensity at AerTGE with the severity of the disease reaching 75% VÇO2peak in patients of NYHA class IV (mean VÇO2peak: 9.2 ml ´ kg±1 ´ min±1). This apparently paradoxical phenomenon is likely due to an attenuated rise of VÇO2 above AerTGE and/or the fact that in many of these patients exercise tolerance is remarkably low. This means that any increase in VÇO2 above resting values (~ 3.5 ml ´ kg±1 ´ min±1) represents a rather high percentage of the subjects VÇO2peak [121]. In liver transplant recipients with chemotherapy-induced severe muscle atrophy (mean VÇO2peak of 22 ml ´ kg±1 ´ min±1), AerTGE occurred at low workloads in absolute terms (VÇO2 of 1.2 l´min±1) but at high relative intensities (nearly ~ 73% actual VÇO2peak; [136]).

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In summary, relative intensities of AerTGE and AnTGE vary with (and are largely determined by) endurance training and subsequent fitness level, health status, or age. When thresholds are reported relative to VÇO2max, a sufficient degree of effort is a prerequisite for appropriate interpretation. Diminished acidosis tolerance (children, elderly) as well as submaximal cessation of exercise (lacking motivation), and symptom limitation (disease) lead to increasing percentages. In severely ill patient populations this can render relative values almost meaningless. The highest workloads eliciting both thresholds have been reported in toplevel endurance athletes. In these subjects, it is not uncommon to detect AerTGE and AnTGE at ~ 75 % and 90% VÇO2max, respectively. In sedentary subjects average values of 55% for AerTGE and 75% for AnTGE are representative. It is of particular interest that absolute values of AerTGE expressed in ml ´ kg±1 ´ min±1 have prognostic power in chronically diseased humans. Thresholds reflect differences in endurance capacity (cross-sectional and longitudinal studies) Both AerTGE and AnTGE reflect endurance capacity, i.e. the adaptation of humans to endurance exercise. For instance, when comparing professional with elite amateur cyclists (~ 35 000 vs. 24 000 km covered during both training and competition each year), it appears that VÇO2max is not sensitive enough to reflect the small differences in endurance capacity that exist between these subjects. VÇO2max approached a similar mean value of ~ 75 ml ´ kg±1 ´ min±1 in both groups despite obvious differences in fitness and performance level [78]. Significant differences, however, were found for the workload (W, W ´ kg±1 or % VÇO2max) eliciting both AerTGE and AnTGE. The high values of both thresholds in professional riders, particularly that of AnTGE (~ 386 W on average or ~ 90% VÇO2max) was thought to reflect the ability of these riders to tolerate very high workloads (= 350 W) during long time intervals (= 20 min) without intolerably high lactate concentrations in the blood. However, it is obvious that longitudinal studies are the most appropriate methodological approach to investigate if gas exchange thresholds reflect adaptations to endurance training. In a meta-analysis that covered the years from 1967 to 1994 and 34 studies performed mostly with non-athletes (of which 13 reported values for AerTGE), Londeree [70] calculated that AerTGE was on average less responsive to training than AerTLA. Obviously, no standardization of training loads was available. Also, threshold determination methodology varied between studies. These problems, together with the independency of the pooled samples, made meaningful comparisons between AerTGE and AerTLA difficult. However, similar findings were reported in two studies from one working group that measured training effects on both AerTLA and AerTGE (determined by use of ventilation data alone) in one sample of subjects, suggesting that metabolic adaptations at the muscle level occur more readily than subsequent changes in ventilatory control [42,114]. Their discrepant findings for both types of thresholds might be explained by the sole use of ventilation for the determination of AerTGE (see chapter ªAerobic gas exchange thresholdº). This is not to say that AerTGE and AnTGE do not show significant improvements with endurance training. In a classic study, Davis et al. [32] reported a marked improvement in the workload eliciting AerTGE (44% increase when expressed as absolute VÇO2 and 15% when expressed

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relative to VÇO2peak) after a 9-wk training program (4 d ´ wk±1) in previously sedentary middle-aged men. Comparable findings were obtained by Smith and ODonnell [132] in physically active middle-aged men.

In middle-distance runners, the improvement induced by an endurance training program including highly intense sessions has been reported to be more marked for AnTGE than for AerTGE [110]. In elite 400-meter runners, Röcker et al. [123] reported a longer isocapnic buffering phase (the distance between AerTGE and AnTGE) compared with (non-elite) endurance runners and sedentary subjects. Taken together, both findings suggest that very intense training sessions (such as those performed by 400meter runners) induce an improvement in buffering capacity rather than in muscle oxidative capacity. As a result, the training-associated improvements in AnTGE are more marked than those of AerTGE. In professional road cyclists, however, yearly training (~ 30 000 km ´ year±1) is based mostly on long sessions of moderate intensity involving mainly aerobic pathways that induce similar improvements in both thresholds [27].

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ing [125]. Similar findings (26 % improvement) have been reported in elderly humans after a 3-month interval training program: two weekly sessions consisting of walking/jogging bouts alternating with rest periods until achieving a total exercise time of 1 h by the end of the program [3]. Even in chronic heart failure patients AerTGE is responsive to training. After 12 weeks of endurance training on a cycle ergometer (45 min, 4 ± 5 days per week), moderate improvements of 11% were noted [98,100, 101]. This is in accordance with other studies which used AerTGE as a secondary parameter only [11, 37, 53]. Application of AerTGE and AnTGE in exercise prescription As early as 1978, the validity of the ªrelative percent conceptº, i.e. prescribing training intensities as percentages of maximal ergometric values, was substantially criticized [60] and instead the use of AerTGE as reference recommended. A more recent investigation concerning the metabolic meaning of given percentages of VO2max and HRmax substantiates these findings [97]. AerTGE and AnTGE can be used to delineate intensity ªzonesº for endurance training (Fig. 3). These are usually prescribed by means of ªtargetº heart rates or running velocities. However, meanwhile in competitive cycling more sophisticated technical solutions exist. Athletes have their own bicycle equipped with a portable powermeter. This device measures the actual power output directly at the crank which enables prescribing intensities in W. In an attempt to quantify competition intensity, Lucía et al. (1999) used a simple model derived from a preceding ramp test: zone 1 or ªlow intensityº, zone 2 or ªmoderate intensityº, and zone 3 or ªhigh intensityº ± that is, below AerTGE, between AerTGE and AnTGE, and above AnTGE, respectively [72]. This approach has been used to quantify exercise loads in one of the most extreme endurance exercises undertaken by humans: the Tour de France [72, 76, 77]. During the 1997 Tour de France (total duration of ~ 100 h for the 7 subjects being studied), the % time spent in zones 1, 2, and 3 was 70, 23, and 7%, respectively [72]. This approach has also been used to quantify the training loads of elite endurance athletes over a sports season. For example, research with professional cyclists has shown that, from fall (pre-competition) to spring (competition period) the percentage contribution of high-intensity training (zone 3) increased from 1 to 8% whereas that of low-intensity workloads (zone 1) decreased from 88 to 77%, respectively [73].

Using 432 previously sedentary subjects of both sexes (aged 17 to 65 y), Gaskill et al. in 2001 evaluated the effects of 20 weeks exercise training intensity relative to the AerTGE on the degree of improvements in a) the workload (VÇO2) eliciting AerTGE and b) VÇO2peak [44]. Supervised cycle ergometer training was performed 3 times per week. Exercise training progressed from the HR corresponding to 55 % VÇO2max for 30 min to the HR associated with 75% VÇO2max for 50 min for the final 6 weeks. The subjects were retrospectively divided into groups based on whether exercise training was initiated below, at, or above AerTGE. Training intensity (relative to AerTGE) accounted for about 26 % of the improvement in the VÇO2 level at the AerTGE but had no effect on VÇO2max. That is, higher intensities (> AerTGE) resulted in larger gains in the VÇO2 at the AerTGE but not in VÇO2max. Researchers from this multi-centre project have shown that there exists a strong familial [43] and genetic contribution to both the workload eliciting the AerTGE and its response to training [41]. Future research might determine specific candidate genes associated with the trainability of AerTGE.

In a training study within a more sedentary population (n = 432), Gaskill et al. [44] categorized intensity similarly: below, at, or above AerTGE. Another working group used different training targets: 50% and 70 or 75 % of the difference between AerTGE and VÇO2max in 10 and 9 healthy individuals, respectively [25, 32]. McLellan and Skinner noted significantly larger training effects after 8 weeks of cycle ergometry when AerTGE was the training reference compared with VÇO2max [93]. However, the number of tested subjects (n = 6 vs. n = 8, respectively) was very low, and VÇO2max was chosen as criterion variable.

Some studies have also confirmed significant increases in the AerTGE induced by training in individuals with low functional capacity. As an example, in patients with coronary artery disease, the VÇO2 (in ml ´ kg±1 ´ min±1) at AerTGE increased by as much as ~ 25% after 1 y of aerobic training combined with strength train-

As endurance exercise has gained importance for rehabilitative purposes after chronic disease, the assessment of appropriate exercise intensities becomes important. However, physicians are often reluctant to exercise these patients to the maximum. This is why the AerTGE represents an attractive reference particularly

Meyer T et al. Submaximal Gas Exchange Parameters ¼ Int J Sports Med 2005; 26: 1 ± 11

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In studies with top-class endurance athletes, both thresholds were highly responsive to training. In world-class cyclists, the power outputs eliciting AerTGE and AnTGE significantly increased from the start of the season to the competition months (spring) by ~ 8% and 6%, respectively [75]. Corresponding findings have been obtained when analysing the AerTGE response to training in another group of professional cyclists [55]. Similarly, in topclass endurance runners the running velocity eliciting AerTGE significantly increased by ~ 10% during the season [20]. In contrast, there are indications that the VÇO2max of world-class endurance athletes is insensitive to training interventions over the competitive season despite significant improvements in AerTGE/AnTGE [74, 75].

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in this population. This has been acknowledged by some in cardiac rehabilitation [88] but has more often been considered by pneumologists. Guidelines for rehabilitation in pulmonary patients have adopted corresponding intensity recommendations [158]. Not surprisingly, AnTGE was not used for prescription purposes because too many patients do not reach sufficiently high intensities during exercise testing to allow its determination.

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The most often cited study is one from Casaburi et al. [24] which demonstrated that 11 COPD (chronic obstructive pulmonary disease) patients who trained for 8 weeks at a workload corresponding to 60% of the difference AerTGE ± VÇO2max had larger training gains than 8 similar patients who trained at 90 % of the AerTGE only. This was interpreted in a way that AerTGE represents an intensity to be surpassed for ensuring training effect. Such interpretations led Puente-Maestu et al. (2000) to the choice of an intensity of AerTGE plus 25% of the difference to VÇO2max for their 8-week training program [116]. Another training study used the heart rate at AerTGE as intensity prescription for 20 COPD patients [146], but other investigators questioned the justification of this approach [60,161]. In the last decade several training studies were conducted in chronic heart failure (CHF) patients. In this population, AerTGE seems to be an attractive reference, too, but has only been used for evaluation of the functional capacity for a long time [99]. Two very recent publications shed light on the usefulness of AerTGE also for CHF patients [99,101]. The authors were able to demonstrate that AerTGE serves well for exercise prescription and the evaluation of training effects without causing undue health risks. In accordance with Katch et al. [60] intensity prescription was given to the patients as a workload.

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Conclusions An applicable framework has been outlined for the evaluation of endurance capacity as well as for the derivation of exercise prescription by use of gas exchange thresholds. With very few constraints, it is valid for competitive athletes, sedentary subjects, and recreational patients. After summarizing the relationship between blood lactate, acid-base status, and gas exchange during incremental exercise, the existence of two meaningful gas exchange thresholds (AerTGE and AnTGE) was explained and a model for intensity prescription introduced. Then the validity of both thresholds for the evaluation of fitness differences (cross-sectional view) and changes in endurance capacity (longitudinal) was documented. Finally, some approaches of using gas exchange thresholds for exercise prescription in athletes, healthy and chronically diseased subjects were addressed.

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