Exercise Intensity Thresholds

Keir, Daniel A.; Fontana, Federico Y.; Robertson, Taylor C.; Murias, Juan M.; Paterson, Donald H.; Kowalchuk, John M.; Pogliaghi, Silvia

doi:10.1249/mss.0000000000000613

Cited by 159 publications

(119 citation statements)

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“…Thus, Keir et al (2015) conclude that CP and MLSS occurred at the same power output (and oxygen uptake), overlooking the protocol-dependence of CP and several other studies in the literature. Subsequent studies by Mattioni Maturana et al (2016Maturana et al ( , 2017 found the obvious, when using a 2-parameter hyperbolic model for CP determination.…”

mentioning

confidence: 63%

“…Moreover, this difference is independent of status training as verified by Greco et al (2011). Surprisingly, even so, Keir et al (2015) modelled CP using trials between 1 and 20 min, as well as the 3-parameter model proposed by Morton (1996), which it is known to produce the lowest CP derivation, as demonstrated by Bull et al (2000). Although the authors assume the likely constraint regarding methodological approaches of CP determination, they declare that it is not possible to discriminate if the similarities were mechanistic or coincidental.…”

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confidence: 95%

“…However, I wish to raise some concerns regarding this study, especially considering 2 other studies from the same research group (Keir et al 2015;Mattioni Maturana et al 2017). In my opinion, these studies might cause some confusion with the reader.…”

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confidence: 97%

“…The answer is: it depends! In general terms, the aforementioned studies (Keir et al 2015;Mattioni Maturana et al 2016, 2017, which aimed to compare CP and MLSS, have used different criteria to set CP, providing divergent conclusions.…”

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confidence: 99%

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Discussion of “Can measures of critical power precisely estimate the maximal metabolic steady-state?” – Is it still necessary to compare critical power to maximal lactate steady state?

Lucas

2018

Appl. Physiol. Nutr. Metab.

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confidence: 63%

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confidence: 95%

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confidence: 97%

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confidence: 99%

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Discussion of “Can measures of critical power precisely estimate the maximal metabolic steady-state?” – Is it still necessary to compare critical power to maximal lactate steady state?

Lucas

2018

Appl. Physiol. Nutr. Metab.

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“…de Lucas also correctly points out a discrepancy between the results of Keir et al (2015) andMattioni Maturana et al (2016). That is, the 3-parameter hyperbolically derived CP was shown to approximate (mean bias = −2 W, p > 0.05) and overestimate (mean bias = 19 W, p < 0.05) the MLSS in 2 different sample groups, respectively.…”

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confidence: 79%

Reply to “Discussion of ‘Can measures of critical power precisely estimate the maximal metabolic steady-state?’ – Is it still necessary to compare critical power to maximal lactate steady state?” – When is it appropriate to compare critical power to maximal lactate steady-state?

Keir

Maturana

Murias

2018

Appl. Physiol. Nutr. Metab.

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In his editorial, de Lucas (2018) indicates that the coherence between the intensities corresponding to maximal lactate steadystate (MLSS) and critical power (CP) is dependent on the methods and model used to determine CP. While there is no question that different mathematical models applied to power-time series datasets of varying time limits can produce different CP values, we completely disagree that this refutes an equivalence between these 2 constructs. CP is not a variable that is dependent on power output and time to exhaustion; rather, it is a parameter that contributes to determining how long one can sustain a given power output! The CP concept is predicated on the hyperbolic relationship that exists between exercise intensity and tolerable duration at that constant intensity (Monod and Scherrer 1965). From a mathematical standpoint, such a relationship implies that exercise performed constantly at the asymptotic intensity should be tolerated indefinitely. From a physiological perspective, we know that this intensity cannot be sustained "indefinitely" because other factors (e.g., substrate depletion, muscle fatigue, hyperthermia, motivation, etc.) inevitably intervene to determine tolerable duration. The discord between the mathematical and physiological constructs that predict respectively "infinite" versus "finite" exercise tolerance at CP has contributed to its notoriously ambiguous definition as "the highest intensity that can be sustained for a prolonged time". However, in our view, acceptance as true of the CP output from a mathematical model applied to a power-time series dataset (without verification) is the main obfuscator of what CP truly represents.In his letter, de Lucas, like many others, neglects to acknowledge the appropriate precedence that links the mathematical CP model to distinct underlying physiology. Poole et al. (1988) were among the first to identify CP as the highest intensity above which respiratory and metabolic measures (which included blood lactate) may no longer achieve steady-state. Since this seminal study, CP has been verified to demarcate an intensity above which oxygen uptake, blood and muscle lactate and hydrogen ion concentration, intramuscular phosphocreatine, and inorganic phosphate may no longer be stabilized (e.g., Jones et al. 2008;Black et al. 2017). Collectively, these studies expanded the colloquial definition of CP to "the highest intensity that can be sustained for a prolonged time solely by oxidative energy provision". An important caveat of this expanded definition is that exercise at CP does not draw upon anaerobic metabolism and therefore progressive depletions in phosphocreatine and progressive accumulations of lactate in muscle and blood are not evident with time. Presumably, this minimizes metabolic and acid-base disturbance and reduces (or delays) the initiation of fatigue processes -prolonging exercise tolerance. Therefore, the physiological response expected at CP encompasses the concept of MLSS; any differences observed between these 2 interdepe...

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An integrated view on the oxygenation responses to incremental exercise at the brain, the locomotor and respiratory muscles

et al. 2016

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In the past two decades oxygenation responses to incremental ramp exercise, measured non-invasively by means of near-infrared spectroscopy at different locations in the body, have advanced the insights on the underpinning mechanisms of the whole-body pulmonary oxygen uptake ([Formula: see text]) response. In healthy subjects the complex oxygenation responses at the level of locomotor and respiratory muscles, and brain were simplified and quantified by the detection of breakpoints as a deviation in the ongoing response pattern as work rate increases. These breakpoints were located in a narrow intensity range between 75 and 90 % of the maximal [Formula: see text] and were closely related to traditionally determined thresholds in pulmonary gas exchange (respiratory compensation point), blood lactate measurements (maximal lactate steady state), and critical power. Therefore, it has been assumed that these breakpoints in the oxygenation patterns at different sites in the body might be equivalent and could, therefore, be used interchangeably. In the present review the typical oxygenation responses (at locomotor and respiratory muscle level, and cerebral level) are described and a possible framework is provided showing the physiological events that might link the breakpoints at different body sites with the thresholds determined from pulmonary gas exchange and blood lactate measurements. However, despite a possible physiological association, several arguments prevent the current practical application of these breakpoints measured at a single site as markers of exercise intensity making it highly questionable whether measurements of the oxygenation response at one single site can be used as a reflection of whole-body responses to different exercise intensities.

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Exercise Intensity Thresholds

Cited by 159 publications

References 31 publications

Discussion of “Can measures of critical power precisely estimate the maximal metabolic steady-state?” – Is it still necessary to compare critical power to maximal lactate steady state?

Discussion of “Can measures of critical power precisely estimate the maximal metabolic steady-state?” – Is it still necessary to compare critical power to maximal lactate steady state?

Reply to “Discussion of ‘Can measures of critical power precisely estimate the maximal metabolic steady-state?’ – Is it still necessary to compare critical power to maximal lactate steady state?” – When is it appropriate to compare critical power to maximal lactate steady-state?

An integrated view on the oxygenation responses to incremental exercise at the brain, the locomotor and respiratory muscles

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