For years, the concept of threshold-based exercise intensity has been used to assess and stratify cardiorespiratory fitness and health, for exercise prescription, and to quantify the outcomes of specific interventions (28). Yet, numerous physiological “thresholds” exist in the literature (each with unique nomenclature and methodology for determination), creating ambiguity regarding their physiological bases and relevance. To date, a popular model for prescribing exercise is the “intensity domain” model (outlined by Whipp et al. (38)), which partitions intensity into ranges (or clusters) of power outputs (PO) that elicit common pulmonary O2 uptake (V˙O2p) response characteristics (i.e., moderate, heavy, very heavy, and severe domains, although alternative classifications exist (17)). In this schema, the “threshold” separating heavy from very heavy exercise (i.e., sustainable from unsustainable constant-power exercise) is critical power (CP) (32). However, other “thresholds” that have also been considered to represent this important physiological “boundary” exist. Among the most common are maximal lactate steady state (MLSS), respiratory compensation point (RCP), and more recently, the deoxyhemoglobin breakpoint ([HHb]BP) (15,31). Each of these paradigms uses different methods of measurement and may be preferred on the basis of consistencies with previous work, available instruments, and the test population, lending to confusion regarding which one represents (or should represent) the “ceiling” of tolerable endurance exercise and whether they are physiologically equivalent.
Previous studies have attempted to examine the association between these indices of intensity by comparing the PO associated with each “threshold” (5,13,31). The attractiveness of this approach resides in the simplicity of obtaining a PO associated with CP and MLSS while avoiding the necessity of i) measuring gas exchange during prolonged constant-load exercise (at both CP and MLSS) and ii) assigning a V˙O2p value during exercise where a V˙O2p slow component is manifest. Using this design, the measurement of gas exchange and ventilatory variables is only required for determination of RCP. However, it has previously been demonstrated that the PO associated with RCP can vary (whereas the V˙O2p associated with RCP does not) depending on the selection of incremental exercise protocol (33). Furthermore, because the change in V˙O2p (L·min−1) for a unit change in PO (W) is 0.01 (i.e., 100 times smaller) and V˙O2p is also associated with an intrinsic measurement error between 2.5% and 5%, relatively small changes in metabolic rate (i.e., V˙O2p) may be interpreted as large changes in exercise intensity (i.e., PO). In addition, Broxterman et al. (7) showed that the intrasubject variability between RCP and critical speed (a surrogate of CP) was greatest when the parameters were expressed in speed compared with absolute V˙O2p. Therefore, the methodological approaches previously used to compare CP, MLSS, and RCP may have precluded the ability to detect their agreement.
Interestingly, it was recently demonstrated in a series of studies (using near-infrared spectroscopy (NIRS)) that the V˙O2p at which deoxygenated hemoglobin ([HHb]) begins to “plateau” during incremental exercise (i.e., [HHb]BP) is strongly associated with both the V˙O2p at RCP (15,25) and at MLSS (3). Together, these studies suggest the existence of a link between MLSS, RCP, and [HHb]BP, yet correspondence between all three indices of exercise intensity has not previously been evaluated in a single group of subjects.
Each of the mentioned “thresholds” may be the result of similar underlying physiological and metabolic processes reflecting a common level of aerobic metabolism beyond which there is a progressive loss of homeostasis. For example, the physiological characterization of exercising slightly above CP includes accumulation of fatigue-inducing metabolites (20), precipitous increases in intramuscular and arterial hydrogen ion concentration ([H+]) (9,29), and disproportionate increases in muscle blood flow and motor unit recruitment (11). It could be argued that the physiological consequences of exercising at CP include the criteria for MLSS (i.e., the highest metabolic rate at which [La−] can achieve a steady state (4)), RCP (i.e., the highest metabolic rate at which ventilatory compensation is able to maintain an elevated but stable metabolic acidosis (37)), and [HHb]BP (i.e., the metabolic rate at which there is a reduction in the O2 delivery-to-O2 utilization relation); however, before the mechanisms underlying these indices of exercise intensity can be examined, it first must be determined whether the intensity at which each occurs is similar within a single group of subjects. Therefore, this observational study was designed to test the hypothesis that the V˙O2p (rather than PO) associated with CP, RCP, MLSS, and [HHb]BP would be equivalent and that each may be used to represent the boundary between the heavy and very heavy exercise domains.
Twelve healthy young men (mean ± SD values: age, 25 ± 2 yr; body mass, 86 ± 16 kg; height, 179 ± 7 cm) volunteered and gave a written informed consent to participate in the study. All procedures were approved by the Department of Neurological and Movement Sciences’ ethical committee for research on human subjects. Subjects were nonsmokers who were free of any musculoskeletal, respiratory, cardiovascular, and metabolic conditions and who were not taking any medications that might influence cardiorespiratory or metabolic responses to exercise.
All participants completed the following cycle ergometer tests within a maximum of 3 wk: i) a preliminary maximal ramp incremental (RI) exercise test for maximal V˙O2p and peak PO (POpeak) determination, ii) four to five exhaustive tests (time-to-exhaustion trials) and two to three 30-min constant-power trials at a fixed cadence for the determination of CP, PO at MLSS, and V˙O2p associated with CP and MLSS, and iii) an exit RI test from which the V˙O2p and PO associated with RCP and [HHb]BP were determined. All tests were conducted in an environmentally controlled laboratory for a minimum of eight occasions, each at a similar time of the day, 2–3 h after a standardized meal (composed of 500 mL of water and 2–3 g·kg−1 body mass of low glycemic index CHO). Participants were instructed to abstain from vigorous physical activity in the 24 h preceding each test and to avoid caffeine consumption on the day of testing.
All exercise tests were preceded by 4 min of baseline 20-W cycling at a self-selected pedal cadence (range, 70–100 rpm). The freely chosen cadence of each subject was recorded during the preliminary RI test, and this cadence was maintained during all subsequent tests using visual feedback and verbal encouragement from the experimenters. Failure to maintain the indicated cadence to within 5 rpm (for longer than 5 s) during testing despite strong verbal encouragement was considered as the criterion for exhaustion.
Each participant performed two RI tests to volitional exhaustion, as follows: one before experimental testing (preliminary test) and one at the end of experimental testing (exit test; to ensure that there was no training effect of the experimental protocol). The RI tests consisted of 20-W cycling for 4 min followed by an increase of 25 W·min−1 in PO (5 W every 12 s) for determination of peak V˙O2p (V˙O2peak), gas exchange threshold (GET), RCP, HRmax, and POpeak.
For the determination of CP, each participant performed four to five constant-power trials to the limit of intolerance, which were designed to generate a distribution of time-to-exhaustion (texhaustion) trials between approximately 1 and 20 min in duration (as recommended by Morton (24)). The first three constant-power trials were performed at 80%, 95%, and 115% of POpeak (as determined from the preliminary RI test) in a random order. Thereafter, a fourth and a fifth trial were performed at a PO designed to generate an even distribution of exhaustion times within the target range (i.e., approximately 1–20 min). From these trials, a PO–texhaustion relation was obtained for each subject.
On successive appointments, participants performed two to three 30-min constant-power tests for determination of the V˙O2p at CP and for the determination of PO and V˙O2p at MLSS. The first test was completed at CP. [La−] was measured at rest and at the fifth, 10th, 15th, 20th, 25th, and 30th min during exercise. The intensity of the successive test(s) was dependent on the change in [La−] between the 10th and 30th min of the previous test, as follows: if [La−] increased by >1.00 mM, the successive test was performed at a PO of CP −10 W; if [La−] increased by <1.00 mM, the successive test was performed at a PO of CP +10 W. Thereafter, the PO was increased/reduced by 10 W until the highest PO compatible with a stable [La−] (i.e., increase of <1.00 mM between the 10th and 30th min) was identified. An example of the entire exercise protocol (excluding the preliminary RI) can be seen in Figure 1 (see caption for details).
Equipment and Measurements
All exercise tests were performed on an electromagnetically braked cycle ergometer (Sport Excalibur; Lode, Groningen, Netherlands). Breath-by-breath pulmonary gas exchange and ventilation were continuously measured using a metabolic cart (Quark B2; COSMED, Rome, Italy) as previously described (12). The gas analyzers were calibrated before each experiment using a gas mixture of known concentration, and the turbine flowmeter was calibrated using a 3-L syringe (Hans Rudolph, Inc.). HR was collected using radiotelemetry (SP0180 Polar Transmitter; Polar Electro, Inc., Kempele, Finland) and calculated over the duration of each breath.
During all testing, muscle oxygenation and deoxygenation ([HHb]) were evaluated using a quantitative NIRS system (Oxiplex TSTM; ISS, Champaign, IL). After shaving, cleaning, and drying of the skin area, the NIRS probe was longitudinally positioned on the belly of the vastus lateralis muscle approximately 15 cm above the patella and attached to the skin with a bi-adhesive tape. The probe was secured with elastic bandages around the thigh. The apparatus was calibrated on each testing day after a warm-up of at least 30 min as per manufacturer recommendations. Data were stored online at an output frequency of 25 Hz but were reduced to 1-s bins for all subsequent analyses within the present study.
During all constant-load tests, blood lactate ([La−] (mM)) was assessed at selected intervals using an electroenzymatic method (Biosen C-line; EKF Diagnostics, Barleben, Germany) on arterialized capillary blood samples (20 μL) taken from the heated earlobe. The analyzer was calibrated with a 12-mM standard before and at regular intervals during analyses.
Breath-by-breath V˙O2p data were edited individually, as follows: aberrant data that lay 3 SD from the local mean (22) were removed, and trials were linearly interpolated on a second-by-second basis, time-aligned such that time “zero” represented the onset of exercise (i.e., onset of constant-load or RI exercise), and averaged into 5- and 30-s time bins.
Both the GET and RCP were independently determined by three blinded expert reviewers. The average of the three values was used for analysis as long as all estimates were within 200 mL·min−1. In instances where one of the reviewers’ estimates was not within 200 mL·min−1, an average of the two in closest agreement was used. GET was determined by visual inspection as the V˙O2p at which CO2 output (V˙CO2p) began to increase out of proportion in relation to V˙O2p, with a systematic rise in the minute ventilation (V˙E)-to-V˙O2p relation and end-tidal PO2 whereas the ventilatory equivalent of V˙CO2p (V˙E/V˙CO2p) and end-tidal PCO2 is stable (2). RCP was determined as the point where end-tidal PCO2 began to fall after a period of isocapnic buffering (37). This point was confirmed by examining V˙E/V˙CO2p plotted against V˙O2p and by identifying the second breakpoint in the V˙E-to- V˙O2p relation.
V˙O2peak was defined as the highest 20-s V˙O2p computed from a rolling average, and POpeak was defined as the PO achieved at the termination of the RI test. The achievement of V˙O2max was further confirmed by examining the V˙O2p responses during several of the time-to-exhaustion trials.
The [HHb]BP was identified by fitting the individual values of [HHb] corresponding to the incremental portion of the exercise as a function of time. A piecewise “double-linear” model was used to characterize the increase in [HHb] as follows (36):
where f is the double-linear function, x is time and y is [HHb], BP is the time coordinate corresponding to the interception of the two regression lines (i.e., the [HHb]BP), i1 and i2 are the intercepts of the first and second linear function, respectively, and s1 and s2 are the slopes. Model parameter estimates for each individual were determined by linear least-square regression analysis. Thereafter, to determine the V˙O2p and HR at which the [HHb]BP occurred, V˙O2p and HR data from the RI test were left-shifted by the individual MRT (for details, see Fontana et al. (15)); V˙O2p and HR at [HHb]BP were calculated as 10-s averages.
CP was determined by fitting a three-parameter hyperbolic model (24) to each subject’s PO–texhaustion relation using nonlinear least squares regression analysis, as follows:
where t is time to exhaustion (s), W′ is the anaerobic work capacity in joules, CP is the critical power in watts, and Pmax is the maximal “instantaneous” power. A weighted least squares procedure was used so that weights (wi) of each data point were proportional to the square of yi (i.e., approximately ti2) for the ith data point to account for the increase in variance accompanying increasing exercise times to exhaustion. The “goodness of fit” for the hyperbolic model was determined by computing the 95% confidence interval for CP. To improve the confidence in the CP parameter estimate, model convergence was established, with the Pmax parameter first allowed to vary. Subsequently, the model was iterated again with a fixed value for this parameter.
V˙O2p, HR, and ventilatory responses from the constant-power tests were averaged into 30-s time bins so that responses across time could be examined. One-sample Z-tests were used to identify the time point at which the change in V˙O2p between 1-min intervals (starting at 6 min) and the last minute of exercise (i.e., the 30th min) was no longer different from “zero” (i.e., the time at which V˙O2p reached a “steady state”). Thereafter, the V˙O2p and HR corresponding to CP and MLSS for each subject were calculated as a 1-min mean at the time point when steady state was reached. All data editing, processing, and modeling were performed using OriginLab version 8.5 (OriginLab, Northampton, MA).
Data are presented as means ± SD throughout. One-way repeated-measures ANOVA was used to determine statistical significance for the dependent variables. Tukey post hoc analyses were used when significant differences were found for the main effects of the dependent variables. Bland–Altman plots were used to assess the limits of agreement between the V˙O2p at CP, MLSS, RCP, and [HHb]BP, and one-sample Z-tests were used to determine whether the average difference between values (i.e., the bias) was significantly different from zero. Two-tailed pairwise t-tests were used to compare differences between the values obtained from the preliminary and exit RI tests. All statistical analyses were performed using SigmaPlot version 11.0, (Systat Software Inc., San Jose, CA). Statistical significance was accepted at an alpha level less than 0.05.
No differences were observed for any of the variables between the preliminary and exit RI test; therefore, a possible training effect related to the testing protocol was excluded.
The V˙O2peak achieved in the exit RI test (4.13 ± 0.52 L·min−1) was not different (P > 0.05) from the peak V˙O2p identified during the shortest time-to-exhaustion trials (4.00 ± 0.60 L·min−1), confirming that V˙O2peak achieved during the RI test was representative of V˙O2max. The group mean values for V˙O2max, POpeak, HRmax, and GET from the RI test were 4.13 ± 0.52 L·min−1 (49.3 ± 8.7 mL·kg−1·min−1), 366 ± 48 W, 186 ± 12 bpm (96% ± 6% of age-predicted value), and 2.54 ± 0.36 L·min−1, respectively. The V˙O2p, PO, and HR values associated with RCP and [HHb]BP are reported in Table 1.
Time-to-exhaustion and constant-power trials
The range of relative PO used in the time-to-exhaustion trials was approximately 60%–115% POpeak, resulting in texhaustion ranging from approximately 1–24 min. The group mean values of the CP and W′ parameters derived from the three-parameter hyperbolic model were 226 ± 45 W and 31.1 ± 10.9 kJ, respectively. The 95% confidence interval for CP was 15 ± 6 W. During constant-power trials at CP, all subjects displayed a delayed steady-state V˙O2p, which occurred at a maximum of approximately 13 min after exercise onset (difference between 13th (and thereafter, i.e., 14th, 15th, etc.) and 30th min was not different from “zero” (P > 0.05)). Three of the twelve subjects satisfied the criteria for MLSS (i.e., [La−]b increase of <1.00 mM between the 10th and 30th min) during the constant-intensity trials performed at the estimated CP; MLSS occurred at a PO 10 W above CP in two subjects, 10 W below CP in five subjects (for example, see subject in Fig. 1), 20 W above CP in one subject, and 20 W below CP in one subject, resulting in a mean difference between the PO at CP and MLSS equal to 2 ± 12 W. At the PO corresponding to MLSS, a plateau in V˙O2p was observed in all subjects by the 13th min of exercise. The group mean value of [La−]b at MLSS was 6.34 ± 1.41 mM.
Comparison of CP, RCP, MLSS, and [HHb]BP
The V˙O2p, PO, and HR values associated with CP, RCP, MLSS, and [HHb]BP are displayed in Table 1. There were no significant differences between the V˙O2p and HR values associated with each of the indices of threshold intensity (P > 0.05). However, the PO at RCP and [HHb]BP was greater than the PO at MLSS and CP (P < 0.05).
Figure 2 shows Bland–Altman plots depicting the agreement between individual V˙O2p (L·min−1) values at CP and MLSS (top panel), between CP and both RCP and [HHb]BP (left panels), and between MLSS and both RCP and [HHb]BP (right panels). The mean difference (bias) between CP and MLSS, RCP, and [HHb]BP was not different from “zero” (P > 0.05), with narrow 95% limits of agreement (range, ±0.55 to ±0.63 L·min−1). The mean bias between MLSS and RCP was also not different from “zero” (P > 0.05); however, the bias between MLSS and [HHb]BP (0.13 L·min−1) was greater than zero (P < 0.05).
Figure 3 displays a summary of the group mean V˙O2p response during constant-power trials at MLSS and CP and selected variables from which RCP and [HHb]BP were determined, plotted as a function of % V˙O2max.
The present study tested the hypothesis that the CP, MLSS, RCP, and [HHb]BP occur at the same metabolic rate (i.e., V˙O2p). The main finding was that the V˙O2p values associated with CP, MLSS, RCP, and [HHb]BP were not different, suggesting that each functional index of exercise intensity could provide a method of identifying the boundary between heavy and very heavy exercise domains. This is the first study to directly demonstrate a commonality between these “thresholds” in a single group of subjects, substantiating the notion of a “critical metabolic rate” (1,35) as the highest metabolic rate at which exercise is well tolerated for long durations. Results demonstrate that there is a relation between the metabolic/physiological responses and the V˙O2p values associated with each of these thresholds, suggesting that they may share a common underlying mechanistic link.
To our knowledge, only one other study has attempted to directly compare CP, MLSS, and RCP (13), and it did so on the basis of PO. Dekerle et al. (13) reported that CP and RCP occurred at a greater PO compared with that of MLSS, concluding that these “intensities” are distinct indices of aerobic function. However, it has been shown that in many cases, PO can be disassociated from metabolic rate (i.e., V˙O2p), which may affect the interpretation of these data. For example, depending on the rate of increase during RI exercise, the PO at RCP will differ despite occurring at the same V˙O2p (33). In addition, Barker et al. (1) demonstrated that different combinations of pedaling cadences yield different PO at CP but do not change the V˙O2p associated with CP. In the present study, when PO is used for comparison between “thresholds,” the conclusion would be that RCP, but not CP, occurs at a greater intensity than MLSS.
However, when CP, MLSS, and RCP are described in terms of V˙O2p (rather than PO), it is apparent that “metabolic rate” is coincident among indexes. Many studies have consistently reported group mean values between approximately 75% and 80% V˙O2max for MLSS (3,13,31) and for [HHb]BP or RCP or both (3,13,15,25,36), indirectly suggesting a possible coincidence between indices. On the contrary, the range of values for CP in the literature is broader (approximately 75%–85% V˙O2max) and its correspondence with MLSS is equivocal. For example, studies have reported both a continued increase in [La−]b (13,18,19,23,26,31,35) and an elevated but stable [La−]b during prolonged exercise at CP (1,29,30). Interestingly, those studies not observing a steady state in [La−]b during constant-power exercise at CP also reported a mean CP equal to approximately 85% V˙O2max whereas those that did reported a mean CP of approximately 79% V˙O2max (which is similar to that of the present study, 80% V˙O2max). Given that there are several methodological approaches that can be used to estimate CP and that these approaches can influence CP estimation (e.g., mathematical model (8,16), duration of predictive trials (6), etc.), it is not surprising that accuracy issues could impair this index’s ability to detect a very narrow level of muscle metabolic activation beyond which “physiological steady state” cannot be achieved. The present study cannot discriminate whether the similar V˙O2p associated to CP, MLSS, RCP, and [HHb]BP are mechanistically or coincidentally linked; yet given the high degree of variability and the technical challenges associated with estimation of each of these indices of threshold intensity, the demonstration of a robust association of V˙O2p among all four intensity-based “thresholds” suggests that they may be related and may manifest as a result of similar underlying mechanisms.
Recently, the point at which the rate of increase in [HHb] is reduced during RI exercise (i.e., [HHb]BP) has been associated with both RCP (15,25) and MLSS (3). The results of the present study confirm that the V˙O2p at [HHb]BP is not different from that of RCP. Although the bias was significantly different from “zero” compared with the MLSS, it should be noted that the absolute value of the bias was very small (130 mL·min−1) and practically equivalent to the minimum detectable change (in our laboratory between 100 and 170 mL·min−1 at a V˙O2p of 2.1–3.5 L·min−1) expected of breath-by-breath V˙O2p measurement for steady-state exercise (21)). In addition, this is the first study to associate CP with the [HHb]BP. These data suggest that there is a link between the [HHb]BP and the metabolic boundary demarcating heavy from very heavy exercise. The coincidence may be related to an arterial acidosis expected at this metabolic intensity, as both interstitial lactate concentration and reductions in pH have been considered to contribute to reductions in vascular tone (10,27). The increased arterial [H+], which is associated (in part) by an increased [La−]b, could contribute to an increase in local microvascular vasodilation, causing an increase in muscle perfusion and O2 availability, reducing the requirement for local O2 extraction (although no observable increase in total hemoglobin at this intensity partially contraindicates this mechanism). Alternatively, the “plateau” observed in [HHb] may reflect an increase in the recruitment of Type II glycolytic fibers (relative to Type I oxidative fibers) (14), and indeed, a progressive recruitment of higher-order motor units replacing those that drop out because of fatigue during RI exercise has been proposed in humans (34) and demonstrated in rats exercising above versus those exercising below critical speed (11). An increased rate of glycolytic adenosin triphosphate (ATP) resynthesis in Type I oxidative fibers and consequent reduction in the rate of oxidative ATP resynthesis could also reduce the rate of increase in O2 utilization relative to the rate of O2 delivery. Additional studies are necessary before a mechanistic link between [HHb]BP and CP, RCP, and MLSS can be elucidated.
Identification of exercise intensity domains has important implications/applications for research interventions; however, identification of these indices of aerobic function within an individual is cumbersome because numerous exercise tests are traditionally required for accurate identification of the heavy–very heavy domains. To avoid this issue, many studies have arbitrarily chosen “delta 50” (Δ50 or 50% of the difference in V˙O2p between GET and V˙O2max) to represent “heavy-intensity” exercise. Interestingly, in the present study, Δ50 corresponded to a V˙O2p of 3.33 ± 0.42 L·min−1 (81% ± 10% V˙O2max), which was not different from any of the “thresholds” examined. These findings suggest that within a given sample of individuals, selection of an intensity corresponding to Δ50 would likely elicit V˙O2p responses from both the heavy and very heavy intensity domains, and therefore, depending on the goals of a prospective study, results could be influenced by individual differences in metabolic and gas exchange responses.
The current study has demonstrated that the concepts of CP, MLSS, RCP, and [HHb]BP may be unified by determining the V˙O2p (rather than the PO) associated with each functional index of exercise intensity, substantiating the existence of a “metabolic boundary” partitioning heavy from very heavy exercise domains. These data suggest that the CP, MLSS, RCP, and [HHb]BP constructs may be physiologically equivalent and, providing optimal design and appropriate determination, each could theoretically represent the highest V˙O2p at which [La]b (and V˙O2p) can be stabilized and thus the “boundary” of sustainable versus unsustainable constant-power exercise. This is of valuable practical importance because the interchangeability of each index may provide exercise physiologists, sports scientists, and clinicians with several options for determining the limits of tolerable endurance exercise depending upon the test population, the available resources, and the desired intensity target for exercise prescription.
Support was provided to Daniel A. Keir in the form of an International Mobility (CooperInt) grant from the University of Verona and a postgraduate doctoral scholarship from the Natural Sciences and Engineering Research Council of Canada.
The authors declare no conflicts of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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