Metabolic threshold testing on the water
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Performance Testing on the Water: Lactate and Ventilatory Thresholds in Canoe Sprint
The Short Version
Two former professional canoeists completed a six-step incremental test on the water, followed by a ramp test, with the PaddlePulse recording mechanical power throughout. Every threshold concept the protocol allows was then applied to the data: four methods for LT1, eleven for LT2, plus three criteria each for VT1 and VT2. All percentages refer to each athlete’s individual power at V̇O2max.
- The lactate thresholds. Athlete 01 LT1 120 ± 14 W (54%) and LT2 164 ± 11 W (74%), Athlete 02 LT1 73 ± 2 W (49%) and LT2 106 ± 8 W (72%), each one a weighted consensus across every method that applied.
- The ventilatory thresholds sat above the lactate thresholds in both athletes. VT1 133 and 80 W, VT2 196 and 117 W, both corrected for the athlete’s own oxygen uptake kinetics, a correction that pulls VT1 down by as much as 14 W and VT2 by as much as 16 W.
- Calculated rather than measured. Fed with sprint lactate, gas exchange and body composition, the crossing-point model returns an MLSS of 171 and 125 W, landing within 2.6% of Athlete 01’s measured second lactate threshold.
- A flaw in the protocol shows up, and it traces back to the critical power testing. Only one of the six steps fell below the first lactate threshold, because the whole step scheme had been built on a critical power that was too high. The error carried over from the mechanical side of performance testing to the metabolic side.
Values athlete by athlete in Table 2, the complete picture in Table 6, the methods themselves in the appendix.
How This Article Is Built
First the test protocol and the participants, then the question of what a lactate threshold actually marks, and the curve modelling. After that the methods and how they are combined into a weighted consensus. Only then come the results: first the lactate thresholds, then the ventilatory ones and finally the crossing-point model. At the end come the limitations, the appendix and the sources.
Only here for the numbers? Skip the theory and jump straight to the lactate results, to the ventilatory thresholds, to the calculated crossing-point model or directly to every value at a glance.
Why This Article?
The earlier articles in this series dealt with the external side of load: measuring mechanical power in the boat, the power-duration profile built from it, and critical power as the anchor for training prescription. Critical power is a purely mechanical parameter, the asymptote of a hyperbola fitted to maximal efforts of different durations, and it needs neither a blood sample nor a gas exchange measurement (Monod & Scherrer, 1965; Poole et al., 2016). That is also where it stops: a boundary defined in mechanical terms says nothing about the metabolic state an athlete is actually in at that boundary.
This article adds the metabolic side. Lactate and gas exchange were recorded on the water, and every threshold concept the protocol supports was applied to the resulting curves. Methods that need a finer step resolution, much longer steps or a separate series of constant-load trials were left out. What comes back is deliberately not one number but a 37 W spread inside the same athlete on the same test day. Pick a single value out of that range and call it the anaerobic threshold, and the question is whether you measured it or simply chose it.
The Data
The test protocol
Every result reported here comes from on-water testing in the boat. The sequence is shown in Figure 1.

Figure 1. Structure of the test session. Six steps of 240 s with 120 s breaks for blood sampling (red arrows), the dashed step is optional. After 10 min of recovery the ramp test follows, increasing every 60 s until exhaustion.
Why the steps last 240 s. Step duration is a compromise between two demands pulling in opposite directions. Oxygen uptake needs roughly two minutes to settle at a new intensity, but stretch six steps out much further and the top ones can no longer be completed cleanly. Four minutes is therefore the lower methodological limit. The derivation from the time constant, a worked example and the sources are in the appendix. The 120 s break is long enough for a clean capillary blood sample but not for lactate to clear. What the incremental test captures per step is therefore not an isolated steady state but a cumulative metabolic response.
Anthropometry and body composition
Table 1 Anthropometric data and body composition
| Variable | Athlete 01 | Athlete 02 |
|---|---|---|
| Sex, age | male, 29 yr | female, 24 yr |
| Body mass | 89.9 kg | 79.7 kg |
| Height | 1.92 m | 1.86 m |
| Fat-free mass (FFM) | 75.0 kg (83.4%) | 57.8 kg (72.5%) |
| Body fat | 14.9 kg (16.6%) | 21.9 kg (27.5%) |
| Total body water (TBW) | 54.9 l (61.1%) | 42.3 l (53.1%) |
| Skeletal muscle mass (SMM) | 35.2 kg | 24.9 kg |
What blood lactate concentration actually represents
Where lactate is made, and where it is measured. Lactate is formed from pyruvate in the working muscle, and it is formed continuously. Lactate dehydrogenase holds the two in an equilibrium that sits far over on the lactate side, so lactate production climbs in step with glycolytic flux (Heck et al., 2022, p. 38; Poole et al., 2021). Once formed, lactate leaves the fibre through the monocarboxylate transporters. Those carriers are saturable, following Michaelis-Menten kinetics, so their transport rate cannot keep scaling up indefinitely (Heck et al., 2022, p. 243). From the fibre the lactate spreads out into the body’s watery compartments, the lactate distribution space. Blood is only one part of that space, and it is at the same time the delivery route by which heart muscle, liver and working muscle take the lactate back up. A sample from the earlobe therefore never shows production on its own (Beneke, 2003).
Which leads to the one sentence every lactate interpretation rests on: a measured blood lactate concentration is a balance, not a measure of production. It is always what is left over from production, transport and clearance together, so it says nothing directly about how high the energy turnover is (Heck et al., 2022, p. 39). And because it is a concentration, it depends on the volume the lactate is diluted into. Total body water differs between our two participants by roughly eight percentage points of body mass, which means that the same absolute lactate production would show up as a higher measured concentration in Athlete 02. Every concept built around a fixed target concentration ignores that.
How much muscle is working changes the number. Beneke et al. (2001) measured the MLSS of the same six rowers on a rowing and on a cycling ergometer, that is, the highest intensity at which blood lactate still holds steady across a constant-load trial. Power output and relative intensity came out the same, and yet the BLC was 2.7 while rowing and 4.5 mmol·l-1 while cycling. One and the same physiological state can therefore turn up at very different lactate concentrations, depending on how much muscle is involved. Mader and Heck (1986) put this down to dilution: the lactate distribution space has an upper size, and the less muscle a movement recruits, the larger the passive remainder into which lactate diffuses down its concentration gradient (Heck et al., 2022, p. 74 ff.). What matters is not so much the type of movement as how much active muscle it brings into play. Untrained subjects reach 7.8 mmol·l-1 on an arm crank ergometer against 4.7 on a cycle ergometer, whereas trained canoeists reach 5.4 against 5.9, because their arms, shoulders and back are barely outmatched by their legs (Heck et al., 2022, p. 75, after data from Gertz, 1991).
What a Physiological Threshold Marks
Three processes need to be kept apart, and everyday language keeps rolling them into one. The distinction decides which methods actually describe the same process and may therefore be pooled into a single value, and Figure 3 already shows how far apart the common concepts land. First, though, the basic curve shape that everything else refers back to.

Figure 2. Schematic blood lactate curve over intensity. The domain boundaries drawn in are conventions placed inside a continuous transition. After Jamnick et al. (2020).
The first rise above resting lactate
Lactate is not something the body only makes under load. At rest the BLC already sits at roughly 0.4 to 1.8 mmol·l-1, and muscle is not the only tissue producing it (Heck et al., 2022, p. 38). Production and clearance run alongside each other at all times. Under aerobic conditions lactate is not a waste product but a fuel that shuttles between lactate-producing and lactate-consuming tissues, the lactate shuttle (Brooks, 2018).
At low intensities clearance rises faster than production. The measured BLC can therefore dip below the resting value before the steadily rising glycolytic rate pushes it back up. That minimum is not a measurement error, and several of the concepts below are built on it. The intensity at which production first measurably outpaces clearance is where the rise begins: LT1. Whether the dip shows up at all is another matter: in a large review of ergometer tests the resting value was usually already the lowest, and a value below resting lactate appeared in only about one case in ten (Heck et al., 2022, p. 249 f.). Catching that minimum means setting the opening step low enough, a point we come back to in the results.
The highest steady state
Above LT1 blood lactate still settles into a steady state, just at a higher level. There is, however, an intensity beyond which production permanently exceeds maximal clearance and the concentration climbs until exhaustion: the maximal lactate steady state (MLSS). It is a genuine physiological state, but by definition it can only be pinned down with several constant-load trials of 20 to 30 min separated by long recovery, never from a single incremental test (Billat et al., 2003; Beneke, 2003). And even this reference standard is not defined uniformly: alongside the standard procedure, Heck et al. (2022, p. 227 f.) list nine further research groups, each with its own MLSS criterion. The gold standard is itself a convention.
What an incremental test delivers instead are surrogate criteria: geometrically defined points on the lactate-power curve, assumed to mark the same state the MLSS marks. Every LT2 method belongs in that category. Eleven common constructions arriving at clearly different answers is the direct consequence of that indirect definition, and how far apart they sit is shown in Figure 3. Heck et al. (2022, p. 235) conclude that, judged biochemically and in terms of regulation, only the maximal lactate steady state and the crossing point survive as lactate threshold concepts.
The ventilatory response
The ventilatory thresholds do not measure lactate at all. What they pick up is the respiratory answer to the protons (H+ ions) that glycolysis releases: buffering those protons through the bicarbonate system sets free extra CO2, that CO2 has to be blown off, and it shows up as a disproportionate rise in CO2 output relative to oxygen uptake (Wasserman et al., 1973; Beaver et al., 1986). They are indirect evidence of the same process, not a second measurement of the same variable. In Figure 3 they are therefore listed as concepts in their own right and not merged with the lactate concepts.
Thresholds are transitions, not sharp boundaries
All three are physiologically transitions, and at every level at once: recruitment shifts gradually towards the more glycolytic fibre types, the fuel mix changes continuously, buffering does not switch on abruptly. Blood lactate, for its part, only ever reflects the gap between production and clearance, so it cannot produce a sharp kink in the first place. The word threshold promises a sharpness the underlying curve does not have (Faude et al., 2009; Jamnick et al., 2020; Poole et al., 2021), as the shape in Figure 2 shows. What the methods really settle is therefore a convention about where inside that transition to draw the line.
Jamnick et al. (2020) count at least 30 published lactate threshold methods and, drawing on the review by Faude et al. (2009), put the spread they produce within one and the same person at around 30%. Jamnick et al. (2018) ran 14 methods on the same measured curve. With four-minute steps, exactly our step duration, the group means ran from 202 W for the log-log method to 291 W for the fixed 4 mmol·l-1 criterion, against a measured MLSS averaging 265 W. Put plainly: the same curve yields thresholds more than a third apart, and the only thing that changed was which method was applied to it. Nor is the value fixed within a single athlete, because prior training load, fatigue and carbohydrate availability all shift the curve (Impey et al., 2018). Poole et al. (2021) put what a threshold actually tells you into perspective: it marks the intensity from which lactate starts to accumulate in arterial blood, because glycolytic flux rises with load. It is a landmark you can observe, not a cause of fatigue.
For training practice that has one concrete consequence: two athletes handed the same percentage prescription can end up in different physiological states, and a domain boundary is better treated as a band a few watts wide than as a line. Just how far the methods can spread is shown in Figure 3.

Figure 3. Distribution of eleven threshold methods over relative intensity, 42 tests in 21 trained cyclists. The spread of any one method regularly swallows the medians of its neighbours. Figure by Jem Arnold, threshold methods after Jamnick et al. (2020).
Where critical power sits relative to the lactate thresholds
Critical power is a fourth transition, defined differently again: the asymptote of the power-duration relationship (Figure 4). In practice CP, MLSS and LT2 are often treated as interchangeable. As an approximation that holds, as a definition it does not. Critical power as a rule sits above the MLSS, on average by about 7%, with individual values between 1 and 16% (Jones et al., 2019), and 278 against 239 W in Dekerle et al. (2003). Jamnick et al. (2020) regard critical power as the best-supported method for this domain boundary and place the 30-min MLSS roughly 4% below it. Poole et al. (2021) keep the two apart conceptually: the lactate threshold marks the onset of arterial lactate accumulation, critical power the ceiling for a sustained non-oxidative contribution to energy supply. How little a high correlation says about actual agreement is shown by Lillo-Beviá et al. (2022): between functional threshold power from a 20-min test and the measured MLSS, r > 0.90, and the systematic error was still 12 ± 7 W.

Figure 4. Power-duration relationship with the intensity domains. Below critical power the effort can be held in a steady state, above it the finite work capacity W' is spent down. The two domain boundaries are the same transitions this article determines via lactate: the shift from moderate to heavy corresponds to the first, the shift from heavy to severe to the second lactate threshold.
That is the case for reporting a consensus here rather than a single number. Methods that carry the same label do not necessarily capture the same process, and those that do are tied to it with varying strength. An unweighted mean across all of them would be a number without a defined physiological referent. The sections that follow build the value up the other way round: first the model fitted to the curve, then the methods applied to it, and finally their weighted combination into one value each for LT1 and LT2.
Modelling the Lactate-Power Curve
Almost every threshold concept works not on the measured points themselves but on a continuous function fitted through them, because the constructions call for slopes, curvatures and secants that six discrete points simply do not have. The choice of model function is therefore a methodological decision that helps determine the threshold value, and in practice it often goes unreported. Two models are run in parallel here.
The third-order polynomial
BLC(P) = a3·P3 + a2·P2 + a1·P + a0
A cubic polynomial captures the flat start, the inflection point and the steep rise in one smooth function, and it is the established standard model (Heck et al., 2022; Roecker & Dickhuth, 2001). It is tied down at the lower end by entering the measured resting lactate as a data point at 0 W. With four free parameters, a coefficient of determination close to 1.000 is no proof of quality.
The exponential model
BLC(P) = c1 + c2 · ec3·P
Criteria built on a defined slope or curvature need a curve that rises strictly monotonically and stays convex, and a polynomial can break that locally. Those criteria use the exponential model instead, whose functional form can be derived from the differential equation of lactate kinetics (Hille & Geiger, 1993, cited after Heck et al., 2022, p. 224).
The Threshold Methods Applied
For the first lactate threshold the protocol supports four methods: one that reads the shape of the curve in a double-logarithmic plot, one that works off oxygen uptake, and two that build on an individually measured baseline.
For the second there are eleven methods, in three groups: secant and tangent constructions that go purely on the shape of the curve, methods that add a fixed increment to an individually measured starting point, and one target concentration that is the same for everybody. That order is also the basis of the weighting, because it reflects how much of a method comes out of the athlete’s own curve. Construction, criticism and base weights are given in the appendix in Table A1 and A2, and where each one sits in the wider field is shown in Figure 3.
Every method on the athlete's own curve
The next two figures pull together everything the article has so far treated separately: the measured lactate values, both model functions and every threshold method as a vertical line on one and the same curve. The two weighted consensus values are drawn bold, the ones thrown out at the plausibility or consistency step are faint. How wide the resulting band is can be read straight off both images.

Figure 5. Blood lactate curve over power, Athlete 01. Vertical lines are the individual concepts, bold the weighted consensus values, faint the rejected ones. The flat branch of the curve rests on a single measured point, because the lowest step sat almost exactly at his resting value.

Figure 6. The same for Athlete 02. Her elevated resting lactate lifts the whole curve upwards.
Three things stand out in both figures, and they carry the rest of this article. First, the LT2 methods cluster on the steep branch and still spread across a range wider than any sensible training zone. Second, the LT1 methods fan out further on the flat branch, because there are fewer measured points there and the fitted curve has correspondingly more freedom. Third, the two curves sit at different heights even though both athletes completed the same protocol. What these figures show is not a point but a band, and that is exactly why no single value is reported below.
From a Field of Concepts to a Consensus Value
The consensus threshold reported here is not an arithmetic mean. It is built in four steps:
- Availability. A concept that returns no result counts as failed and is not replaced by a stand-in value.
- Plausibility corridor. A candidate has to lie between 35 and 75% (LT1) or 60 and 100% (LT2) of the individual reference power, expressed relatively, because a fixed watt window would be far stricter on a weaker athlete than on a stronger one.
- Consistency check. Candidates that sit far from the median drop out. The tolerance is either 2.5 times the robust median absolute deviation or 8% of the median, whichever is larger.
- Weighting. Base weight (column "weight" in Table A1 and A2) multiplied by a quality factor built from model fit and data support at exactly the power where the threshold falls. A concept can therefore lose weight on a thinly supported curve without being downgraded in principle.
The reference power itself is not taken from the point of exhaustion in the ramp but calculated from oxygen uptake. The appendix sets out exactly how.
How objective is the weighting? Model fit and data support are calculated reproducibly. The base weights are not, at least not to the same degree: they rest on an expert judgement, and a subjective element cannot be ruled out. They are held in the script as named constants and can be swapped out without changing the structure of the procedure.
Results of the Lactate Analysis
Table 2 is the results table of this article. It lists every calculated threshold for both athletes in one shared list, ordered by power, which makes it visible how the lactate and ventilatory thresholds actually interleave. The two weighted consensus values are shaded, the ventilatory thresholds blue.
Table 2 All calculated threshold concepts from the on-water test, ascending by power
| Concept | Athlete 01 (W) | mmol·l-1 | Athlete 02 (W) | mmol·l-1 |
|---|---|---|---|---|
| LT1 lactate minimum (Pessenhofer) | 87 | 1.68 | 31* | 2.63 |
| LT1 min. lactate equivalent (Berg) | 108 | 1.77 | 74 | 3.11 |
| LT1 weighted consensus | 120 | 1.94 | 73 | 3.09 |
| LT1 log-log (Beaver) | 125 | 2.04 | 73 | 3.10 |
| LT1 first rise +0.4 (Davis, mod.) | 127 | 2.08 | 70 | 3.03 |
| VT1 kinetics-corrected | 133 | — | 80 | — |
| LT2 second rise, IATm (Baldari & Guidetti) | 145 | 2.67 | 93 | 3.83 |
| VT1 ramp, uncorrected | 146 | — | 85 | — |
| LT2 max. curvature (Hille & Geiger) | 154 | 3.11 | 94 | 3.85 |
| LT2 BLCmin + 1.5 (Simon) | 155 | 3.18 | 99 | 4.13 |
| LT2 LT1 + 1.5 (Dickhuth) | 157 | 3.27 | 107 | 4.61 |
| LT2 tangent intersection (Keul) | 164 | 3.70 | 104 | 4.44 |
| LT2 weighted consensus | 164 | 3.74 | 106 | 4.52 |
| LT2 Dmax (Cheng) | 165 | 3.75 | 107 | 4.57 |
| LT2 fixed concentration 4 mmol·l-1 | 168 | 4.00 | 97 | 4.00 |
| LT2 tangent slope 1.00 (Simon) | 171 | 4.19 | 110 | 4.83 |
| LT2 Dmax,mod (Bishop / Jamnick) | 176 | 4.58 | 114 | 5.06 |
| LT2 tangent slope 1.26 (Keul) | 182 | 5.13 | 122 | 5.69 |
| VT2 kinetics-corrected | 196 | — | 117 | — |
| VT2 ramp, uncorrected | 212 | — | 125 | — |
*Rejected at the plausibility step for falling below 35% of the reference power. The angle bisector after Bunc produced no interpretable solution. Red shading marks the lactate consensus values, blue the kinetics-corrected ventilatory thresholds and grey-blue the uncorrected ones.
The consensus values come out at 120 ± 14 W for LT1 (CV 11.5%, all four concepts) and 164 ± 11 W for LT2 (CV 6.5%, ten of eleven) in Athlete 01, and at 73 ± 2 W (CV 2.2%, three of four) and 106 ± 8 W (CV 7.9%, ten of eleven) in Athlete 02. The aerobic-anaerobic transition therefore spans 44 W in one athlete and 33 W in the other. The resulting corridors run from 78 to 166 W and 133 to 222 W in Athlete 01, and from 52 to 112 W and 90 to 150 W in Athlete 02.
The opening step was set too high
The lowest step was set too high, because the entire step scheme had been derived from a critical power that turned out to be badly overestimated.
What we found. Athlete 01 paddled steps from 97 to 220 W against an LT1 of 120 W, Athlete 02 from 56 to 150 W against an LT1 of 73 W. In both cases only one of the six steps fell below the first lactate threshold, so no dip in blood lactate appeared. In Athlete 01 the lowest step sits almost exactly at his resting level, which leaves the flat branch of the curve resting on a single measured point. In Athlete 02 the resting value itself is unusually high at 2.74 mmol·l-1, and the lowest step lands right on it. Both can be read straight off Figure 5 and 6. An incremental test without a dip is not unusual in itself (Heck et al., 2022, p. 249 f.). This is therefore no gross protocol error, but it does mean that the five concepts needing a solid baseline are working from thinner data here. The script accordingly halves the weights of the affected concepts, and in Athlete 02 the lactate minimum drops out of the plausibility corridor altogether.
Putting the lactate levels in context. An aerobic threshold at 3.09 mmol·l-1, as in Athlete 02, is unusually high. Athlete 01 sits at 1.94 mmol·l-1 and therefore in the expected range, and an identical session on the kayak ergometer puts her at 2.05 mmol·l-1. The likeliest cause is her elevated baseline: resting lactate lifts the entire curve, which hits the concentration-based criteria hardest (Heck et al., 2022, p. 252).
What about the 3.74 and 4.52 mmol·l-1 at LT2? Two reference points bracket the expected range, and they pull in opposite directions. Upwards pulls the comparatively small muscle mass a kayak stroke recruits. Beneke (2003) describes an inverse relationship between MLSS lactate and the mass of the primarily involved musculature, and across 856 participants mean MLSS values run, depending on the exercise mode, from 2.6 mmol·l-1 on a rowing ergometer to 7.6 mmol·l-1 on an arm crank ergometer (Heck et al., 2022, p. 228). Downwards pulls the only kayak-specific on-water measurement there is, an MLSS of 3.06 ± 0.68 mmol·l-1 in eleven elite kayakers (Pilotto et al., 2019). Our values fall between the two. That a 240 s step is shorter than a constant-load trial and pushes the curve further up fits the picture, but with two participants it cannot be separated out from other influences. Stated conservatively, the point is that numbers like these cannot be read in absolute terms without knowing how much muscle was working, which leaves a target concentration identical for everybody poorly justified in canoe sprint.
The link to critical power. The critical power tests came first, and the step scheme was derived from them afterwards. The load prescriptions came out of the first critical power estimate of 209 W and 144 W, which rested entirely on maximal efforts between 1 s and 6 min. An asymptote fitted to nothing but short efforts comes out systematically too high, because the flat, long-duration branch of the power-duration curve carries no measured points at all. In sprint-oriented athletes such as canoe sprinters that is especially likely, because their short efforts are very strong relative to their endurance capacity. The two values accordingly sit at 94% and 98% of power at V̇O2max, and therefore 27% and 36% above the second lactate threshold determined here. A sustainable limit above the second lactate threshold makes no physiological sense, and because the whole step scheme hung on that number, it started out systematically too high. The error travelled from the mechanical side of performance testing into the metabolic side, not the other way round. The next two articles follow this up in detail.
What this changes in the protocol. The LT1 consensus for Athlete 02 should be read as a lower bound. Future tests will therefore add a markedly lower opening step, so that the flat branch of the curve carries measured points again.
The Ventilatory Thresholds
The basic principle is the same as for the lactate thresholds: again the task is to locate a breakpoint in a curve. Two differences matter. First, what is analysed is a continuously recorded signal from the ramp test rather than one measured value per step. Second, several criteria read the same physiological event off different signals. The ventilation side supplies the ventilatory equivalent V̇E/V̇O2, the cumulative excess CO2 and ventilation V̇E itself, the gas exchange side the ratio of V̇CO2 to V̇O2 and the end-tidal CO2 partial pressure PetCO2. Two criteria drawn from the same signal family are not two independent pieces of evidence, and the consensus weighting takes that into account. Six criteria are evaluated, three for VT1 and three for VT2, with a seventh shown for illustration only. How each is constructed and weighted is given in the appendix in Table A3.
Correcting the ramp for oxygen uptake kinetics
Our ramp test steps up every 60 s, at a mean rate of 22.6 and 11.0 W·min-1 respectively. Oxygen uptake never reaches a steady state during a ramp. It trails the load by a constant time offset, and that offset is the athlete’s individual time constant τ (Whipp & Wasserman, 1972). A gas exchange event is therefore read off at too high a power and has to be corrected downwards by ΔP = (S · τ) / 60. Derivation, formula and a worked example are in the appendix.
Table 3 Effect of the kinetics correction
| Participant | VT1 uncorr. | VT1 corr. | VT2 uncorr. | VT2 corr. |
|---|---|---|---|---|
| Athlete 01 (τ = 36.8 s, S = 22.6 W·min-1) | 146 W | 133 W (−13.9) | 212 W | 196 W (−16.4) |
| Athlete 02 (τ = 25.0 s, S = 11.0 W·min-1) | 85 W | 80 W (−4.6) | 125 W | 117 W (−8.4) |
In Athlete 01 the correction at VT1 comes to almost ten percent. Leaving it out would put his domain boundary nearly 14 W too high. The difference between the two participants follows directly from time constant and ramp rate, and is therefore itself an individual finding. Figure 7 and 8 show the breakpoints in every signal analysed.

Figure 7. Ventilatory analysis of the ramp test, Athlete 01. For each signal, the breakpoint together with the uncorrected and the kinetics-corrected threshold as separate lines.

Figure 8. The same for Athlete 02, with a markedly smaller correction.
Ventilatory and Lactate Thresholds Compared
Table 4 Ratio of the kinetics-corrected ventilatory to the lactate thresholds
| Participant | VT1 / LT1 | VT2 / LT2 |
|---|---|---|
| Athlete 01 | 1.10 | 1.19 |
| Athlete 02 | 1.10 | 1.11 |
In both of our measurements the ventilatory thresholds sit systematically above the corresponding lactate thresholds. At the first threshold the ratio is identical in both athletes at 1.10, at the second it is not. The literature points the same way: in Dekerle et al. (2003) the second ventilatory threshold sat at 286 W, clearly above the measured MLSS of 239 W. Jamnick et al. (2020) therefore advise against using the respiratory compensation point as a stand-in for MLSS or critical power unless the ramp is very long, and their reasoning is exactly the problem the previous section deals with: a wattage read off a ramp does not correspond to the same oxygen uptake as that wattage under constant load. How tightly the ventilatory response and lactate accumulation are coupled also depends on buffering capacity and respiratory control (Cerezuela-Espejo et al., 2018). For this article the practical consequence is that the two families of methods are reported separately rather than pooled.
Calculating a Threshold Instead of Measuring It
Every threshold shown so far was measured. There is another route. The crossing-point model describes the lactate production rate and the maximal oxidative elimination rate as two functions of power (Mader & Heck, 1986; Mader, 2003), and both thresholds fall out of those same two curves. LT2 is the intersection itself, the point at which production and maximal elimination are equal. Above it, lactate keeps climbing under constant load, which is by definition the MLSS. LT1, in this model, is the point of maximal pyruvate deficit: below it, glycolysis delivers less pyruvate than the oxidative machinery could use, and the shortfall is covered by fat oxidation. Where that shortfall is largest in absolute terms, fat turnover is highest too, and that is the FATmax point, which can also be measured spirometrically. The model therefore explains the same trough that the incremental test sees as the lactate minimum. Both are shown across the full power axis in Figure 9 and 10.
Every input is measured: the maximal lactate production rate from a 15 s sprint, V̇O2max and the slope of oxygen uptake from the on-water test, plus body composition. The lactate distribution volume was derived individually from measured total body water, using the factor of about 0.735 that Mader and Heck (1986) derived on energetic grounds. A few canoe-specific adjustments were made to the original model. They are not spelled out here but held back for the article series devoted to the model.
The next two figures show what the model looks like for our two athletes. Plotted are the lactate production rate, the maximal oxidative elimination rate and the oxidative reserve, that is, the share of energy demand glycolysis does not have to cover. Above the point where the two rates cross, lactate starts to accumulate. The two marked points are set against the measured thresholds in Table 5 below.
The inputs differ considerably between the two participants: the maximal lactate production rate from the 15 s sprint is 0.4479 against 0.2068 mmol·l-1·s-1, the lactate distribution space derived from TBW 40.4 against 31.1 l, and the muscle mass taken to be active, here 60% of the SMM from Table 1, 21.1 against 14.9 kg. Substrate rates come out of the same model: at the FATmax point 48.8 against 46.2 g·h-1 of fat, and at the calculated MLSS 284 against 230 g·h-1 of carbohydrate.

Figure 9. Crossing-point model for Athlete 01. The blue line is the measured V̇O2-power relationship with the step values, the red dashed curve the lactate production rate, the teal dashed one the maximal oxidative elimination rate and the purple one the oxidative reserve. Where the two rates cross is the calculated MLSS at 171 W, and the maximum of the reserve marks FATmax at 107 W.

Figure 10. The same for Athlete 02, with FATmax at 81 W and a calculated MLSS of 125 W. Her markedly lower maximal lactate production rate makes the two rate curves cross earlier and at a shallower angle.
Why the substrate rates come out as they do. At the crossing point the model forces production and maximal elimination to be equal: the oxidative reserve is zero and demand is met almost entirely by carbohydrate, so the rate simply follows oxygen uptake, 3.85 against 3.12 l·min-1, giving 284 against 230 g·h-1. That gap is smaller than the 37% difference in power because Athlete 02 has the higher baseline demand in the boat, 946 against 769 ml·min-1, at an almost identical delta efficiency. Below the MLSS fat takes over more and more of the supply, and there the two effects nearly cancel out: at FATmax he has around 15% more oxygen uptake, she the higher fat fraction (63 against 58%), because her maximal lactate production rate is less than half of his and keeps glycolysis further below the elimination rate at that point.
Table 5 Crossing-point model compared with the measured thresholds
The comparison is made not against the weighted consensus values but against the two concepts the model is calibrated on: log-log for LT1 and Dmax,mod for LT2. In Jamnick et al. (2018), Dmax,mod from the 4 min test came closest of all tested methods to the measured MLSS, and log-log serves there as the reference for the first threshold.
| Participant | FATmax | MLSS | Deviation from LT1 | Deviation from LT2 |
|---|---|---|---|---|
| Athlete 01 | 107 W | 171 W | −13.9% | −2.6% |
| Athlete 02 | 81 W | 125 W | +10.4% | +9.7% |
In Athlete 01 the calculated MLSS lands within 2.6% of the measured second lactate threshold. In Athlete 02 it sits about ten percent above it, and FATmax is off in the same direction. Whether that is down to the model parameters or to a distortion in her measured thresholds cannot be settled with two participants. A full account of the model is reserved for a series of its own.
Every Value at a Glance
Table 6 Summary of all values from the on-water test
Percentages refer to each athlete's individual power at V̇O2max.
| Variable | Athlete 01 | Athlete 02 |
|---|---|---|
| LT1 weighted consensus | 120 W (54%) | 73 W (49%) |
| FATmax (calculated) | 107 W (48%) | 81 W (55%) |
| VT1 kinetics-corrected | 133 W (60%) | 80 W (54%) |
| LT2 weighted consensus | 164 W (74%) | 106 W (72%) |
| MLSS (calculated) | 171 W (77%) | 125 W (85%) |
| VT2 kinetics-corrected | 196 W (88%) | 117 W (79%) |
| Critical power (simple fit, tests 01/02) | 209 W (94%) | 144 W (98%) |
| Power at V̇O2max | 222 W (100%) | 148 W (100%) |
| V̇O2max | 4770 ml·min-1 (53.1 ml·kg-1·min-1) | 3510 ml·min-1 (44.0 ml·kg-1·min-1) |
One observation is worth pulling out, because it points the same way in both data sets. In Athlete 01 the mean of VT1 and VT2 is 164.5 W and therefore sits right on his LT2 consensus of 164 W, with the calculated MLSS of 171 W close by. In Athlete 02 the same calculation gives 98.5 W against an LT2 of 106 W. That the second lactate threshold falls roughly between the two ventilatory thresholds fits the ordering visible in Table 4. With two participants and two measurements, though, this is not a finding but an observation that could just as easily be coincidence. It would need checking in a larger sample before anyone turned it into a rule of thumb.
A note on the critical power values in this table. They come from a simple fit of the three-parameter model to tests 01 and 02 and are reported here unchanged on purpose, because the entire step scheme hung on them. They are, however, clearly too high. The next article shows how critical power can be estimated more plausibly from predominantly short efforts, and what the alternatives are for canoe sprint. There the CP values come down to a more realistic 178 and 132 W.
Limitations
- Sample size. Two participants, one incremental and one ramp test each, no repeat measurement. Nothing can be said about day-to-day reliability.
- Opening step. The LT1 consensus for Athlete 02 should be read as a lower bound, and five of the fifteen concepts rest on a stretch of the curve that was only partly captured.
- Step duration. 240 s is the methodological lower limit, and longer steps would have been hard to sustain in a six-step protocol.
- Absolute lactate levels. They cannot be read in absolute terms without knowing how much muscle was involved, and they do not carry across sports.
- Normalised shape criteria. Four concepts only reach a power axis through a normalisation convention, which is why they are weighted low.
- Base weights. Set on expert judgement, with a subjective element, and replaceable in the analysis script.
- No MLSS reference. Every LT2 value here is a surrogate for the MLSS, and none of them was validated against that criterion.
What Comes Next
Every value in this article needs blood samples, a gas exchange measurement or a metabolic model. In day-to-day training none of that is usually to hand. The power measured in the boat is.
The next article therefore asks what kind of profile can be built from power data alone: critical power, the anaerobic work capacity W' and the fatigue term of the power-duration relationship, including the question of why the 209 and 144 W fitted from efforts between 1 s and 6 min do not hold up. The final article brings both routes together into a canoe-specific intensity scale.
Appendix
What follows is the material that did not fit into the main text: why the steps last as long as they do, how the individual reference power is derived, how the ramp is corrected for oxygen uptake kinetics, and, at the end, a reference section covering every threshold method used, with its construction, weighting and criticism.
Why the steps last 240 s
Kinetics argues for long steps. A measured value can only be read as a steady state if the system has actually reached one. Oxygen uptake approaches the demand of a new load exponentially, and the time constant τ describes how quickly: after one time constant roughly 63% of the step is covered, after four times that roughly 98% (Whipp & Wasserman, 1972; Whipp et al., 1982). τ is individual, and an athlete with a small τ is back in equilibrium sooner after each increase.
Worked example: how long does a step have to be?
Settling time (98%) = 4 · τ = 4 · 31 s = 124 s
240 s step → 116 s of plateau | 120 s → no plateau at all
Calculated with the mean of both athletes, τ = 31 s (individually 36.8 and 25.0 s). With steps that are too short, the value read off comes out systematically too low, and because the time constants differ, it comes out too low by different amounts in different athletes.
Fatigue argues against long steps. Six steps of 240 s already mean 24 min of work, and the 5 to 10 min per step that pure lactate diagnostics calls for (Mader et al., 1976, cited after Heck et al., 2022, p. 211) would have made the upper steps impossible to complete cleanly. Four minutes is therefore the lower methodological limit and at the same time the workable compromise. That longer steps push lactate values upwards, and with them every concentration-based criterion, is well documented (Heck et al., 2022, p. 366 f.; Beneke, 2003).
The individual reference power
All percentages and the plausibility corridor refer to the power at V̇O2max. The point of exhaustion in the ramp depends on day-to-day form and motivation, which makes it unsuitable as a reference. It is calculated instead from the weighted linear relationship between steady-state oxygen uptake and step power.
Worked example: the reference power of Athlete 01
V̇O2,SS(P) = 17.99 · P + 769 [ml·min-1, R2 = 0.991]
P @ V̇O2max = (4770 − 769) / 17.99 = 222 W
For Athlete 02, with 17.37 · P + 946 and 3510 ml·min-1, the reference power comes to 148 W, which is practically her highest step. The slopes correspond to a delta efficiency of 15.8 and 16.3%.
Correcting the ramp for oxygen uptake kinetics
What our “ramp” really was. In the literature a ramp test means a load that rises almost second by second. On the water that is not feasible, because power in the boat cannot be dictated by an ergometer brake. The athlete has to hit it herself. Our protocol therefore steps up every 60 s and is, strictly speaking, a fast incremental test. That does not make it unusable, as long as the calculations work with the mean ramp rate: 22.6 W·min-1 for Athlete 01 and 11.0 W·min-1 for Athlete 02. Comparisons with the 20 to 30 W·min-1 common in cycling should be drawn cautiously, because in kayaking the same absolute rate is a considerably larger relative jump in intensity. On top of that, the test was designed first and foremost to elicit the highest possible V̇O2max. The ventilatory thresholds come out of the same data set, but that is not what it was built for.
Why a correction is needed. A continuously rising load drives energy demand up faster than oxygen uptake can follow. In a first-order system, meaning one whose response to a step change is exponential and captured by a single time constant, the metabolic response settles into trailing the load by a constant time offset, and that offset is exactly τ (Whipp & Wasserman, 1972; Whipp et al., 1982). A gas exchange event at ramp time t was therefore set off by an earlier, lower power, and the threshold is read off at too high a wattage:
ΔP = (S · MRT) / 60 [S in W·min-1, MRT in s]
Both the correction itself and the permissible kinetics ratio are capped. The breath-by-breath data are deliberately not averaged beforehand, because averaging would systematically distort the estimated time constant (Lamarra et al., 1987).
Worked example: correcting VT1 in Athlete 01
ΔP = (22.6 W·min-1 · 36.8 s) / 60 = 13.9 W
VT1,corrected = 146 W − 13.9 W = 133 W
VT1 is corrected with τ because it rests mainly on the V-slope. VT2 is scaled on top of that by the individual ratio τ(V̇CO2)/τ(V̇O2), here 1.18 and 1.83, because it rests on ventilation, ventilation follows CO2, and CO2 kinetics are slower thanks to the bicarbonate stores.
The individual threshold methods
The three tables that follow are meant as a reference. For each method they give the criterion in the curve or in the ramp signal, the base weight assigned to it and an assessment of where it stands.
Table A1 Concepts for determining the first lactate threshold
Classification and criticism after Heck et al. (2022, ch. 9).
| Concept | Criterion in the curve | Weight | Assessment |
|---|---|---|---|
| Log-log Beaver et al. (1985) |
intersection of two regression lines in a double-logarithmic plot | very high |
|
| Minimum of the lactate equivalent Berg et al. (1980) |
vertex of the parabola through the ratio of lactate to V̇O2 | high |
|
| First rise of 0.4 mmol·l-1 after Davis & Gass (1979), modified |
individual baseline concentration plus a fixed increment | medium |
|
| Lactate minimum Pessenhofer et al. (1981) |
lowest point of the modelled curve | low |
|
Table A2 Concepts for determining the second lactate threshold
Classification and criticism after Heck et al. (2022, ch. 9).
| Concept | Criterion in the curve | Weight | Assessment |
|---|---|---|---|
| Modified Dmax Bishop et al. (1998), variant after Jamnick et al. (2018) |
secant from the log-log point to the end point, largest perpendicular distance | very high |
|
| BLCmin + 1.5 mmol·l-1 Simon (1986) |
lactate minimum plus a fixed increment | high |
|
| LT1 + 1.5 mmol·l-1 Dickhuth et al. (1988) |
concentration at the lactate equivalent minimum plus a fixed increment | high |
|
| Dmax Cheng et al. (1992) |
secant from the first load value to the maximal lactate value | medium |
|
| Tangent intersection Keul et al. (1981) |
intersection of the tangents to the flat and the steep branch | medium |
|
| Second rise Baldari & Guidetti (2000) |
first step with a second jump of at least 0.5 mmol·l-1 | low |
|
| Maximal curvature Hille & Geiger (1993) |
point of maximal curvature of the normalised curve | low |
|
| Tangent slope 1.00 Simon et al. (1981) |
point of a defined curve slope | low |
|
| Tangent slope 1.26 Keul et al. (1979) |
as above, with a different slope value | low |
|
| Angle bisector Bunc et al. (1982) |
intersection of the angle bisector of the normalised curve | low |
|
| Fixed concentration 4 mmol·l-1 Mader et al. (1976), justified by Heck et al. (1985) |
power at a concentration identical for everyone | very low |
|
Table A3 Criteria for determining the ventilatory thresholds
| Criterion | Signal in the ramp | Weight | Assessment |
|---|---|---|---|
| VT1 V-slope Beaver et al. (1986) |
breakpoint of V̇CO2 against V̇O2, gas exchange family | very high |
|
| VT1 minimum V̇E/V̇O2 Wasserman et al. (1973) |
minimum of the ventilatory equivalent for O2, ventilation family | medium |
|
| VT1 minimum excess V̇CO2 Roecker et al. (2000) |
minimum of the cumulative CO2 excess, ventilation family | medium |
|
| VT2 V̇E against V̇CO2 Wasserman et al. (1973) and Jamnick et al. (2020) |
second breakpoint of ventilation over CO2 output, ventilation family | very high |
|
| VT2 PetCO2 decline Westhoff et al. (2013) |
maximum and decline of end-tidal CO2 partial pressure, gas exchange family | high |
|
| VT2 V̇E against time Wonisch et al. (2017) |
second breakpoint of ventilation over time, ventilation family | low |
|
| VT2 RER ≥ 1.00 | fixed gas exchange ratio, level criterion | excluded |
|
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A note on the citations. For a few of the threshold concepts calculated here, the primary paper is not held in the project bibliography. Those concepts are named by their common designation and cited through the summarising account in Heck et al. (2022, ch. 9). The primary sources listed there are carried over into the reference list.