Malaysian Journal of Sport Science and Recreation Vol. 6 No.

1, 63-79, 2010

Critical Power Revisited: An Alternate

Interpretation of Physiology Based
on Observation

Bartholomew Kay
University of Auckland,
Dept Sport and Exercise Science
b.kay@auckland.ac.nz

Abstract
This paper is about modelling endurance time during constant power output exercise,
with specific emphasis on cycling. The concept is however, transferable to other modes
of exercise as will be discussed. The modelling technique known as the 2-parameter
critical power (CP) model will be modified to elucidate a novel perspective on the
underlying physiology of performance limitation at the metabolic level. This paper
does not attempt to explain exercise induced muscle fatigue, as this is a multifaceted
phenomenon with both central and peripheral causes (Westerblad & Allen, 2003; Hunter,
Duchateau et al., 2004; St Clair Gibson & Noakes, 2004; Abbiss & Laursen, 2005;
Lambert, St Clair Gibson et al., 2005; Nordstrom, Gorman et al., 2007). Rather, this
paper argues that because maximal ‘instantaneous’ power output is finite, the asymptote
of the power output vs. endurance time hyperbola determined using the 2-parameter CP
technique should be corrected so that the hyperbola intersects time (Y) axis = zero at
the value of maximum ‘instantaneous’ power output as measured. This correction to the
CP technique involving an adjustment to the asymptote of the power output vs. endurance
time hyperbolic function is described, and supported with reference to the likely
underlying physiology, and basic logic. The most salient effect of correcting the time
asymptote is a vast improvement to the predictive ability of the work done vs. endurance
time regression for endurance times under 180s. By way of support for the procedure
indicated, this paper also offers up a perspective on metabolism indicating that: (a)
metabolic inertia is the factor which causes the power function to have a non-zero time
asymptote (from a purely metabolic standpoint), and hence the muscle has a non-
infinite maximal instantaneous power output; (b) that this correction correctly erodes
the parameter typically described as ‘anaerobic work capacity’ (the Y-intercept of the
2-parameter CP model) to value = zero; and that (c) it appears all so called ‘oxygen
independent’ metabolic components (i.e. glycogenolysis, creatine phosphate (PCr))
are functionally coupled to oxygen consumption and have maximum flux rates subject

ISSN 1823-3198
© 2010 Faculty of Sports Science and Recreation, Universiti Teknologi MARA (UiTM), Malaysia.

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Malaysian Journal of Sport Science and Recreation

to the same metabolic inertia. It is concluded that these components are therefore not
oxygen independent, and should rather be conceptualised as a form of capacitance
which is directly activated by exercise in a relative-intensity dependent fashion. The
maximal activation of both glycogenolysis and PCr however, are reliant directly on
VO2: hence, the non-linear relationship between work done and endurance capacity
when the latter is < ~180s (i.e. glycogenolysis and PCr maximal flux rates are both
subject to the same metabolic inertia that VO2 is subject to).

Introduction
The concept of CP has been with us for some time (Monod & Scherrer, 1965;
Moritani, Nagata et al., 1981; Jenkins & Quigley, 1991; Hill, 1993; Hill & Smith,
1994; Vautier, Vandewalle et al., 1995; Morton, 1996; Hill, 2004; Dekerle, Brickley
et al., 2006). Indeed, CP models have been proposed for different exercise
modalities including step wise, constant power, and intermittent power (Morton,
1994; Morton, 1997; Morton, Green et al., 1997; Morton & Billat, 2004). The
simplest form of CP estimation involves subjects exercising to volitional exhaustion
at between 3 to 6 different fixed power outputs in the case of cycling (speed in
running). The power outputs are set at levels designed to elicit volitional exhaustion
in ~3 to ~10-minutes. The endurance time at each work rate is then plotted as a
hyperbolic function (see Figure 1, below). When work done at each work rate is
plotted against endurance time, a linear relationship is derived taking the form
‘work done’ = [value A] x ‘endurance time’ + [value B]. Where value A = CP
(W), and value B = Y-intercept (J).
The concept of a linear 2-parameter CP model has been criticised because
the true CP out beyond ~20-minutes of endurance is often overestimated by the
CP regression technique using exhaustive exercise bouts between ~3 and ~10-
minutes in duration (Housh, Housh et al., 1989; Jenkins & Quigley, 1990;
McLellan & Cheung, 1992). A further consequence of the overestimation of
CP is the ‘underestimation of the Y-intercept’. Thus, a 3-parameter model has
been suggested (Gaesser, Carnevale et al., 1995; Morton, 1996). The 3-
parameter model takes the form of a correction to CP, the Y-Intercept, and the
time asymptote of the hyperbolic function, such that the power function cuts Y
= zero at the individual maximum power output (see Figure 1, below). This final
correction alone (the asymptote correction) appears indicated for endurance
times < ~180s, as the original hyperbolic function suggests that maximum
instantaneous power output should be ‘infinity’, which clearly, it is not. Figure 1
shows the original 2-parameter power function as determined by regression
and the same function with the temporal correction resulting in a finite (and
realistic) predicted maximum power output. The data is for a hypothetical
individual with CP = 250W, and Y-intercept = 5000J. I have arbitrarily decided
that this hypothetical individual has a maximum ‘instantaneous’ power output

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 Critical Power Revisited

300

Power function predicted from critical

250 power regression y=250x+5000. it
predicts that infinite load is maximal
(i.e. asymptote is at zero seconds).
The power curve should intersect
Y=0 at the value of maximum power
200 output.

150 Power function with asymptote

Endurance time (s)

corrected according to measured*

maximum power output (583W).
This asymptotic correction leads to a
15s correction to the y values for the
100 curve i.e. the asymptote is -15s. * I
decided this arbitrarily

50

Maximum power
output
-50
Critical power

-100
0 100 200 300 400 500 600 700 900 900 1000
Power (W)

Figure 1: Hyperbolic function (solid curve) describing power output versus endurance
time at that power output (as predicted from linear regression of time to fatigue vs. work
done in that time between ~3 and ~30-minutes exercise duration [y = 250x + 5000]). As
can be seen, the function predicts that the maximum power output is infinity, which is
clearly not correct. The dashed curve shows the same power function with its time
asymptote corrected so that the function intersects y = 0 at maximum instantaneous
power output. In this hypothetical case, I have arbitrarily decided that this individual’s
maximum power output is 583W. This nets an asymptotic correction of minus15s.

of 583W. This has been done in order to show how the concept applies. The
actual values are not important, as the procedure is the same for any given
individual irrespective of what the values are.
The result of the correction to the time asymptote can be seen when the
work limit is regressed against the endurance time (see Figure 2, below). The
linear relationship becomes curvilinear near X = 0, Y = 0; and the Y-intercept is
correctly resolved to zero without greatly affecting the rest of the relationship.
The value for the Y-intercept must always be zero, despite what many others
have asserted about the variable and non-zero value for this parameter according
to existing 2-parameter, and 3-parameter models. I argue that the Y-intercept
value for the power output versus time to exhaustion regression must always be

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Malaysian Journal of Sport Science and Recreation

100000

75000
Work Limit (J)

50000

Critical power regression

y=250x+5000. Yields linear critical
power function

25000

Critical power corrected via shifted

asymptote. Yields curvilinear critical
power function

0
0 60 120 200 241 300

Endurance time (s)

Figure 2: Linear regression (black line) of hypothetical individual with critical power =
250W, Y-intercept = 5000J. Also shown is a corrected critical power curve (grey curve):
the time asymptote of the power function is corrected to a non zero value which causes
the power function (see Figure 1 above) to cross Y = 0 at maximum instantaneous power
output. In this case, the individual’s maximum instantaneous power is 583W. This
correction results in a -15s change to the time asymptote (see Figure 1). The work limit
is then derived from the shifted power function, and the result is the grey curve shown.

zero, as you cannot do any work in a zero time frame. Power = work / time, and
work = force x distance: work is measured in cycling in watts (which are
synonymous with kilogramme meters per second). Anything divided by zero is
undefined.
The 3rd interdependent parameters maximum instantaneous power output
(P-max), and the asymptotic correction factor ‘k’ (s) were used by Morton (Morton,
1996) to re-fit regression equations to historical data (McLellan & Cheung, 1992)
which those authors originally fitted using the 2-parameter model. The new
regressions (Morton, 1996) are characterised by slightly lower CP, and hence

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 Critical Power Revisited

higher Y-intercept than the 2-parameter model. The predictions of the 3-parameter
model therefore fit better to endurance limits out beyond the ~20-minute mark.
However, while improving endurance time prediction out beyond 20-minutes, the
3-parameter model suggests that the Y-intercept is even higher than predicted by
the 2-parameter model. This means the 3-parameter model violates the above
argument moreso, than does the original 2-parameter model. Therefore, an alternate
interpretation appears warranted.
The purpose of this paper is not to reconsider the full and complex corrections
made by Morton (Morton 1996) for endurance limits beyond 20-minutes, but
rather to use a correction to the time asymptote only to elucidate my argument
concerning the relationships between ‘aerobic rate’, and ‘anaerobic work
capacity’, as described by others. Morton’s 3-parameter corrections remain the
authoritative communication regarding the corrections needed to more accurately
predict endurance out beyond ~20-minutes. However, Morton’s (Morton, 1996)
3-paprameter model is unable to resolve the limitations to correct prediction or
interpretation imposed by fitting any model where the Y-intercept is allowed to
have any value (Chatagnon & Busso, 2006; Dekerle, Brickley et al., 2006). This
paper therefore proposes to improve the predictive ability of CP modelling in the
0-180s endurance limit time frame by adjusting the time asymptote without any
other correction, and also to dispel the apparent misconception that humans have
an immediately available oxygen independent energy pathway (as suggested by
the 2-parameter and the 3-parameter models).
The Y-intercept parameter is almost universally described as analogous to
‘anaerobic work capacity’. Conceptually, authors (Monod & Scherrer, 1965;
Moritani, Nagata et al., 1981; Vautier, Vandewalle et al., 1995; Morton, 1996;
Morton & Hodgson, 1996) propose that an ‘oxygen independent’ or ‘anaerobic
capacity’ equal to the Y-intercept (Joules) exists. Figure 3, below shows the
same data in Figure 2 above, re-plotted with the resolution increased by a factor
of five (i.e. we can now see the relationship between the original and corrected
work vs. endurance prediction for endurance times between 0 and 60s). The
following calculations should show why the corrected line is likely to better
predict actual 1-60 s endurance times and power outputs associated: In addition
to the impossibility of doing any work in a zero time frame, (despite the linear
model suggesting this should be possible), the predicted linear work limit also
suggests the hypothetical individual should be able to complete 5,250 J of work
in 1 second. This equates to 5,250 W power output. No athlete alive can come
anywhere near producing this work, despite the fact that the model predicts it.
Obviously, the above is quite unrealistic (as compared to the corrected
prediction which projects a 1s endurance power output of 563 W. I intend to
use this corrected prediction throughout the rest of this paper in light of recent
research concerning the underlying physiology of exercise to argue: (a) that
metabolic inertia is the factor determining the correct work vs. endurance

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Malaysian Journal of Sport Science and Recreation

20000

15000
Work Limit (J)

10000

Critical power regression y=250x+5000.

Yields linear critical power function

5000

Critical power corrected via shifted

asymptote. Yields curvilinear critical power
function

0
0 10 20 30 40 50 60
Endurance time (s)

Figure 3: The Linear (Solid) and Asymptote Corrected (Dashed) Critical Power Functions
at Higher Resolution (See Figure 2).

relationship (b) that the components of integrated metabolism are functionally

coupled, and all rely entirely upon the rate of oxidative phosphorylation, and
therefore (c) that there is likely no oxygen independent metabolic pathway in
practice.

Metabolic Inertia
It is clear that the rate of oxidative metabolism can’t be up-regulated
instantaneously. This is so, as oxidative metabolism has inertia which must be
overcome (Grassi, Poole et al., 1996; Tschakovsky & Hughson, 1999; Grassi,
Hogan et al., 2000; Parolin, Spriet et al., 2000; Grassi, 2001; Roberts, Loxham et
al., 2002; Greenhaff, Campbell-O’Sullivan et al., 2004; Roberts, 2005; Roberts,
Loxham et al., 2005; Gurd, Peters et al., 2008). The inertia has been ascribed at
least in part to the role of convective and diffusive oxygen delivery limitations

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 Critical Power Revisited

(Wagner, Roca et al., 1990; Grassi, 2000; Grassi, Hogan et al., 2000; Scheufler,
2004; Amann & Calbet 2007), however others prefer to attribute metabolic inertia
to a role played by the carnitine pool (McGarry & Brown, 1997; Roberts, Loxham
et al., 2002; Roberts, 2005; Roberts, Loxham et al., 2005) and others prefer a
more holistic, integrated approach (Tschakovsky & Hughson, 1999; Richardson,
2003; Scheufler, 2004; Grassi, 2006). In short, there is little evidence that muscle
cells suffer from a functional hypoxia during even exhaustive exercise taken
under normobaric normoxic conditions (Connett, Honig et al., 1990; Salathe &
Chen, 1993; Richardson, 1998; Ordway & Garry, 2004; Scheufler, 2004; Teboh-
Ewungkem & Salathe, 2006); hence models proposing that factors other than
hypoxia are causal in metabolic inertia appear more attractive.
That said, the upshot of oxidative metabolic inertia is that any increase in
exercise intensity will necessarily lead to the activation of metabolic components
(such as glycogenolysis) which have far more rapid on-kinetics (Shulman &
Rothman, 2001; Shulman, 2005), i.e. less inertia. Readers may consider the above
statement in terms of what occurs when a resting or exercising subject suddenly
increases the exercise intensity (i.e. power output), such would be the case during
a ‘ramp’ or ‘step’ incremental protocol (i.e. moving from one ‘steady state’ to
another). However, a review of work undertaken by Shulman and Rothman
(Shulman & Rothman, 2001; Shulman, 2005) shows that each and every muscle
contraction involves a massive step increase in ATP cost, followed by a sudden
precipitous drop in ATP cost (all within 40 ms) then a relatively lengthy refractory
period at a cycling cadence of 60 revolutions per minute (~960 ms). Shulman and
Rothman (Shulman & Rothman, 2001; Shulman, 2005) also show why
glycogenolysis is therefore activated during steady state exercise, even at low
intensities. The reason for glycogenolytic flux is apparently oxidative metabolic
inertia.

Glycogenolysis and Oxygen Independence

Shulman and Rothman’s review (Shulman & Rothman, 2001; Shulman, 2005)
concerns research, where 31P NMR scanning was used to follow the time course
of glycogenolysis across muscle contractions with millisecond resolution. This
was undertaken in human muscle contracting at a ‘steady-state’, and at a low
relative muscle VO2 values. Their review reveals that ATP cost increases by
orders of magnitude in the 0-40 ms time scale at the outset of each contraction
(even mild ones). Following this, the ATP cost drops precipitously again and
remains somewhat below the rate of production from oxidative phosphorylation
for the next ~960 ms (i.e. the refractive period if the cadence is 60 contractions
per minute). When the ATP draw and ATP synthesis are plotted together versus
time, at steady state; the integration of both lines will net the same area: i.e. the
concentration of ATP is stable, which is what is observed at all but supra maximal

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Malaysian Journal of Sport Science and Recreation

exercise intensities (Chance, Leigh et al., 1985; Wallimann, Zurbriggen et al.,

1985; Wallimann, Wyss et al., 1992; Conley, Ordway et al., 2000; Jeneson,
Westerhoff et al., 2000). This interpretation suggests that VO2 is functionally
coupled to the rate of glycogenolysis and vice versa (see Figure 4 below).

120
ATP cost (% resting ATP) and VO2 (% maximum)
matching ATP requirement over time

100 .....................................................................................................................................................................

80 .....................................................................................................................................................................

60 .....................................................................................................................................................................

40 .....................................................................................................................................................................

20 .....................................................................................................................................................................

0
0 480 960 1440

Time (ms)

Figure 4: Conceptual model of muscle ATP draw (pulsatile line) and ATP production
(steady line) at steady state and at ~15% VO2 max (60 RPM). The area under both lines
is the same, however functionally glycogenolysis provides ATP during each pulse,
and oxidative phosphorylation provides energy to reform glycogen (from blood
glucose) between contractions. The PCr system shuttles energy between the
mitochondria and the ‘I-bands’ of muscle fibres where the glycogen is stored. Oxidative
phosphorylation cannot fuel muscle contractions alone, as the inertia of the oxidative
system prevents it. Oxidative inertia lasts for ~180s, the ATP requirement increases by
orders of magnitude in the millisecond time scale.

Functional Coupling (Holism) in Metabolism

With the millisecond temporal resolution offered by 31P NMR scanning techniques
(Shulman & Rothman, 2001; Shulman, 2005), it is apparent that the flux rate
through glycogenolysis is many times that ascribed to it using older methods such
as rapid snap-freezing. Snap frozen muscle biopsies have nowhere near the
resolution and hence the signal is not detected (being complete and resolved by
~40 ms). Shulman and Rothman (Shulman & Rothman, 2001; Shulman, 2005) go

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 Critical Power Revisited

on to suggest that if temporally coincident oxidative processes were not operating,

the glycogen in a muscle cell would be completely exhausted at ~20% VO2 max
within 25 contractions at the most (upper limit of agreement). Several points are
salient here; (a) fatigue occurs before glycogen is exhausted, i.e. at a critical but
non-zero concentration, and (b) exercise intensities above 20% would drain the
cell of glycogen more rapidly than the 25 contractions suggested. All in all, this
means the effective oxygen independent work capacity is basically none. It seems
the reason for oxidative metabolism in working muscle cells is almost entirely to
sub-serve glycogenolytic flux, which is required in order to provide ATP in the
millisecond time scale for even mild muscular contractions. Glycogenolysis should
therefore be conceptualised as a form of capacitance to oxidative metabolism,
and not as a discrete and independent alternative to oxidative metabolism (see
Figure 5, below for a conceptual model).

Phosphocreatine and Oxygen Independence

The phosphocreatine system (PCr) is often referred to as another oxygen
independent pathway. However, the integrated functioning of the PCr system
has been elucidated (Wallimann, Zurbriggen et al., 1985; Wallimann, Schnyder et
al., 1989; Wallimann, Wyss et al., 1992; Wallimann, Dolder et al., 1998); and the
system functions as a spatial energy transfer system between the mitochondria
and the muscle machinery / ion pumps. Given that PCr replenishment (temporally
coincident with PCr hydrolysis) is also entirely oxygen dependent; so too is the
PCr system (Meyer, 1988; Wallimann, Dolder et al., 1998; Saks, Kongas et al.,
2000; Roman, Meyer et al., 2002; Haseler, Kindig et al., 2004; Smith, Montain et
al., 2004; Glancy, Barstow et al., 2008). Therefore the same effective zero oxygen
independent capacity should be applied to PCr, and it also should be conceptualised
as a capacitance (Meyer, 1988) to oxidative metabolism (see Figure 5, below for
conceptual model).

Oxygen Independent Metabolism?

The above arguments propose a model of integrated, holistic metabolic functioning;
which suggests that the components typically described as oxygen independent,
are in fact not oxygen independent. The actual capacities of these ’oxygen
independent energy systems’ when subjected to anoxia, is to all intents and
purposes, zero. The historical misinterpretation is apparently because the rate at
which muscle biopsies can be ‘snap’ frozen is far too slow to detect the massive
flux signals of these systems. Their estimated flux rates are therefore typically
massively underestimated. Such systems in fact have flux rates orders of
magnitude higher than historically proposed, and as such would be almost
immediately drained when oxygen is absent. In muscle cells at the point of volitional

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Malaysian Journal of Sport Science and Recreation

exhaustion under normobaric and normoxic conditions, oxygen is present and

available (Downs, 2003). Previous generations of researchers have imagined an
‘anaerobic’ or an ‘oxygen independent’ component of metabolism, most likely
activated because of some oxygen delivery or extraction limitation. This ‘oxygen
independent’ exercise capacity has been said to equal the Y-intercept of the 2-
parameter CP model. If this model were correct, the athlete should be able to
produce slightly more than the Y-intercept worth of work in slightly more than
zero seconds (this should be possible because the linear model proposes that this
‘anaerobic work capacity’ is independent of oxygen). As can be seen from the
above commentary, this projected work cannot be produced and thus the concept
is fundamentally flawed. The new model suggested here (the time asymptote
correction) correctly erodes the value of the Y-intercept to zero (you cannot do
any work in zero time, as the distance parameter of the work equation [w = f x d]
dictates that all work takes time: i.e. how does one move a resistance a set
distance without taking some time to move it)?
Indeed, the conceptual model of metabolism being proposed here can be
considered as analogous to a simple electrical circuit (see Figure 5, below). This
concept is not novel (Meyer, 1988), however I have developed the model of
Meyer (Meyer, 1988) by adding a capacitor which is analogous to glycogenolysis,
on the basis of its flux rate and oxygen dependence. I have also described the
components slightly differently to account for the pulsatile nature of ATP draw in
an isolated muscle cell. This conceptual model shows that both [PCr] and

VM RM V OO
M
+ +

ICY
120
ATP cost (% resting ATP) and VO2 (% maximum)

C11
matching ATP requirement over time

100

C 22 80

60

40

20

0
0 480 960 1440
Time (ms)

- -

Figure 5: Control of metabolism shown as an analogue circuit. The voltage VO is

analogous to the delta G value for ATP (J.Mol-1), The current ICy is a pulsatile draw
analogous to ATP draw at the muscle (see figure 4, above), C1 represents the capacitance
due to PCr, C2 represents the capacitance due to glycogen, RM is the resistance to flow
imposed by the muscle’s inherent properties (and is analogous to metabolic inertia),
and VM is analogous to the variable mitochondrial dipole imposed by the proton motive
force (red-ox potential). It is analogous to VO2. This diagram is developed from the one
proposed by Meyer (1988).

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 Critical Power Revisited

[glycogen] are capacitors connected to the oxidative circuit. The volatage VM is

imposed by the variable dipole across the inner mitochondrial membrane, i.e. the
red-ox potential and proton motive force. As can be seen, the pulsatile draw at
ICY is sub-served by the two capacitors; such that the voltages VM and in particular
VO remain very stable. It should also be clear that if oxidative metabolism were
abolished (i.e. VM = 0), then the capacitors are quickly discharged (in practice,
basically immediately).

Summary
In summary, (a) metabolic inertia determines that the power function time asymptote
should be corrected such that the power function intersects time = 0 at maximum
instantaneous power output. Doing so provides a vastly improved profile of
predicted work vs. endurance limits. (b) The underlying physiology supporting
this procedure indicates that glycogenolysis is entirely dependent on oxidative
phosphorylation to provide for temporally coincident glycogen re-synthesis, and
so too is PCr. In practical terms (as predicted/modelled by the asymptote-corrected
power function), the maximum flux rate of glycogenolysis (i.e. proportional use
of the hypothetical absolute maximum, the linear prediction) is apparently limited
by oxidative inertia (as can be seen in the corrected prediction line shown in
Figure 3). Although glycogenolysis can be rapidly up-regulated, the system is not
independent of oxygen, and does not constitute a functional alternative to oxidative
metabolism, but rather forms functionally coupled and absolutely indispensible
part of integrated metabolism, by way of an oxygen dependent capacitance. This
is so, as the capacity of the system in isolation to oxygen (i.e. no counterbalancing
re-synthesis) is so near zero. Finally (c) there is therefore no apparently oxygen
independent or anaerobic metabolic pathway in humans.

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