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Twitch potentiation and fatigue in skeletal muscle are two conditions in which force production is affected by the stimulation history. Twitch potentiation is the increase in the twitch active force observed after a tetanic contraction or during and following low-frequency stimulation. There is evidence that the mechanism responsible for potentiation is phosphorylation of the regulatory light chains of myosin, a Ca2+-dependent process. Fatigue is the force decrease observed after a period of repeated muscle stimulation. Fatigue has also been associated with a Ca2+-related mechanism: decreased peak Ca2+ concentration in the myoplasm is observed during fatigue. This decrease is probably due to an inhibition of Ca2+ release from the sarcoplasmic reticulum. Although potentiation and fatigue have opposing effects on force production in skeletal muscle, these two presumed mechanisms can coexist. When peak myoplasmic Ca2+ concentration is depressed, but myosin light chains are relatively phosphorylated, the force response can be attenuated, not different, or enhanced, relative to previous values. In circumstances where there is interaction between potentiation and fatigue, care must be taken in interpreting the contractile responses.
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499
Braz J Med Biol Res 33(5) 2000
Coexistence of potentiation and fatigue
Brazilian Journal of Medical and Biological Research (2000) 33: 499-508
ISSN 0100-879X
Coexistence of potentiation and
fatigue in skeletal muscle
1
Laboratório de Fisiologia,
Centro de Ciências da Saúde,
Universidade do Vale do Rio dos Sinos, São Leopoldo, RS, Brasil
2
Human Performance Laboratory, Department of Medical Science,
Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada
D.E. Rassier
1
and
B.R. MacIntosh
2
Abstract
Twitch potentiation and fatigue in skeletal muscle are two conditions
in which force production is affected by the stimulation history.
Twitch potentiation is the increase in the twitch active force observed
after a tetanic contraction or during and following low-frequency
stimulation. There is evidence that the mechanism responsible for
potentiation is phosphorylation of the regulatory light chains of myo-
sin, a Ca
2+
-dependent process. Fatigue is the force decrease observed
after a period of repeated muscle stimulation. Fatigue has also been
associated with a Ca
2+
-related mechanism: decreased peak Ca
2+
con-
centration in the myoplasm is observed during fatigue. This decrease
is probably due to an inhibition of Ca
2+
release from the sarcoplasmic
reticulum. Although potentiation and fatigue have opposing effects on
force production in skeletal muscle, these two presumed mechanisms
can coexist. When peak myoplasmic Ca
2+
concentration is depressed,
but myosin light chains are relatively phosphorylated, the force re-
sponse can be attenuated, not different, or enhanced, relative to
previous values. In circumstances where there is interaction between
potentiation and fatigue, care must be taken in interpreting the con-
tractile responses.
Correspondence
D. Rassier
Laboratório de Fisiologia
Centro de Ciências da Saúde
UNISINOS
Avenida Unisinos, 950
93022-000 São Leopoldo, RS
Brasil
E-mail: drassier@zaz.com.br
Received October 25, 1999
Accepted February 14, 2000
Key words
Posttetanic potentiation
Staircase
High-frequency fatigue
Low-frequency fatigue
Ca
2+
sensitivity
RLC phosphorylation
Myosin light chains
Introduction
The contractile response of a muscle de-
pends to a great extent on the history of its
activation. A brief period of repetitive stim-
ulation results in enhanced contractile re-
sponse (potentiation) while continued stim-
ulation results in impaired or attenuated con-
tractile response (fatigue). Considering that
potentiation and fatigue both result from prior
activation, it seems reasonable to assume
that these two processes are initiated when
contractile activity is started, and that they
coexist during and for some time after repeti-
tive stimulation, as suggested by Krarup (1).
This coexistence of potentiation and fatigue
would make it difficult to quantify either
process independently.
The purpose of this review is to present
evidence that the underlying cellular mechan-
isms for potentiation and fatigue can and do
coexist. We will briefly review the known
mechanisms of potentiation and fatigue, then
consider the probable consequences of their
interaction. Following this, we will review
the evidence that potentiation and fatigue do
coexist. It is our hope that this review will
raise awareness among scientists dealing with
500
Braz J Med Biol Res 33(5) 2000
D.E. Rassier and B.R. MacIntosh
contractile responses of muscles that the
underlying mechanisms of potentiation and
fatigue can coexist, and that care must be
taken in interpreting the contractile responses
under such circumstances.
Definitions
There are several terms used in this re-
view which should be defined. Staircase is
the progressive increase in twitch active force
during repetitive low-frequency stimulation.
Posttetanic potentiation is the enhancement
of twitch active force following a tetanic
contraction. Activity-dependent potentiation
is a term we use to refer collectively to an
enhanced contractile response which can be
attributed to prior activity. It has been dem-
onstrated that this enhancement is evident
not only with twitch contractions, but with
incompletely fused tetanic contractions as
well (MacIntosh BR and Willis JC, unpub-
lished results).
Fatigue refers to the depression of con-
tractile response which can be attributed to
prior activity, and is generally evident as
less active force than otherwise expected.
Fatigue can be further subdivided into low-
frequency fatigue and high-frequency fatigue.
Low-frequency fatigue is evident when prior
activity results in depression of active force
at frequencies which elicit submaximal force
while the maximal force (or force at the
frequency which elicited maximal force prior
to the fatiguing exercise) is unaltered. High-
frequency fatigue is evident when prior ac-
tivity results in depression of maximal force
(or force at the frequency which elicited
maximal force prior to the fatiguing exer-
cise) without depression of force at frequen-
cies which elicit submaximal force.
The expression coexistence of potentia-
tion and fatigue is used in this review to
refer to the situation where the underlying
causes of activity-dependent potentiation and
fatigue are simultaneously present. The re-
sult of this coexistence of potentiation and
fatigue may be enhanced contraction ampli-
tude, depressed contraction amplitude, or no
apparent change from the control situation.
To understand how coexistence of potentia-
tion and fatigue can occur, it is necessary to
be aware of the presumed mechanisms of
potentiation and fatigue.
Mechanisms of potentiation
There is considerable evidence that ac-
tivity-dependent potentiation results from
phosphorylation of the regulatory light chains
of myosin (RLC). Several studies have dem-
onstrated a correlation between the magni-
tude of potentiation and the magnitude of
phosphorylation of RLC (2-5). In addition,
skinned fiber experiments have shown that
the force of contraction at a given submaxi-
mal Ca
2+
concentration is increased, while
maximal force is not altered (6,7). Taken
together, these two observations provide
strong support for the theory that RLC phos-
phorylation is responsible for activity-de-
pendent potentiation.
Phosphorylation of the RLC occurs when
myosin light chain kinase (MLCK) is acti-
vated (8,9). Activation of MLCK occurs when
Ca
2+
concentration rises and the Ca
2+
-cal-
modulin complex binds to MLCK (9). There-
fore, when a muscle is activated, Ca
2+
con-
centration rises resulting in the activation of
MLCK and increased RLC phosphorylation.
Presumably the increased RLC phosphory-
lation causes increased sensitivity of the con-
tractile proteins to Ca
2+
, thereby enhancing
the submaximal contractile response. The
enzyme myosin light chain phosphatase is
responsible for removing the phosphate group
from the RLC. This enzyme proceeds at a
relatively slow rate, approaching control lev-
els of phosporylation after 4-5 min in mam-
malian muscle at 37
o
C.
It has been demonstrated that the en-
hanced submaximal force during high levels
of RLC phosphorylation results from an in-
creased rate of attachment of cross-bridges
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Braz J Med Biol Res 33(5) 2000
Coexistence of potentiation and fatigue
or a greater rate of transition from weak-
binding to strong-binding which results in a
greater number of force-generating cross-
bridges during a contraction. Evidence sup-
porting this conclusion includes the follow-
ing: muscle stiffness increases in proportion
to the increase in active force; myosin ATPase
activity increases in proportion to the in-
crease in active force, and the rate of relax-
ation does not decrease (10). The propor-
tional increase in stiffness indicates that the
enhanced force is associated with an in-
creased number of attached cross-bridges,
and the proportional increase in ATPase ac-
tivity suggests that the time-dependent cross-
bridge turnover is not affected by RLC phos-
phorylation. The steady state number of cross-
bridges engaged is proportional to the sum
of the rate of attachment and the rate of
detachment of cross-bridges. The evidence
presented above suggests that the increase in
attached cross-bridges results from an in-
crease in the rate of attachment. Evidence
that the rate of detachment is not affected
includes no increase in relaxation time (11)
as well as no change in the economy of force
production (12).
The collective evidence presented above
confirms that force enhancement associated
with RLC phosphorylation results from an
increase in the rate of attachment of cross-
bridges, with no change in the rate of detach-
ment and this change in cross-bridge kinet-
ics results in an increased Ca
2+
sensitivity.
Much of the evidence for this mechanism is
based on skinned fiber experiments. Our
knowledge of the mechanisms of activity-
dependent potentiation cannot rule out the
possibility of a contribution by other factors.
In fact it has recently been demonstrated that
staircase can occur without corresponding
RLC phosphorylation (13). In spite of this,
for the purposes of this review, increased
Ca
2+
sensitivity in association with RLC phos-
phorylation will be considered to be the
primary mechanism of activity-dependent
potentiation.
Mechanisms of fatigue
Care must be taken when discussing the
potential mechanisms of peripheral muscle
fatigue. The pattern of stimulation which
induces the fatigue may be an important
determinant of the mechanism. Considering
that there are several steps in the sequence of
activation of a muscle, failure at any of these
could be the mechanism of fatigue. Ulti-
mately, however, depression of active force,
as a consequence of prior activity, results
from either decreased peak (or average)
myoplasmic free Ca
2+
concentration (14-16),
or decreased sensitivity to Ca
2+
(17). The
decreased sensitivity to Ca
2+
may be due to a
decreased Ca
2+
/troponin affinity, or due to a
decreased force produced by each cross-
bridge during contractions. For the purposes
of this review, these two factors will be
considered together, and will be referred to
as Ca
2+
sensitivity.
For many years, indirect evidence has
suggested that failure of excitation-contrac-
tion coupling is the primary mechanism of
fatigue, particularly low-frequency fatigue.
Eberstein and Sandow (18) reported that
force depression during fatigue could be
overcome by treatment with caffeine. This
has been confirmed by others (11). Further-
more, dantrolene, which inhibits Ca
2+
re-
lease in skeletal muscle, mimics several as-
pects of the contractile response of skeletal
muscle fatigue (19,20).
Recently, it has been reported that there
is a reduced peak free Ca
2+
concentration in
the myoplasm (16,21,22) in fatigued muscle.
In addition, it has been suggested (17,23,24)
that several factors associated with fatigue
could result in decreased Ca
2+
sensitivity (as
illustrated in Figure 1A). These factors in-
clude mainly decreased pH and increased
inorganic phosphate concentration. Skinned
fiber experiments conducted at room tem-
perature (or colder) have been done to con-
firm this effect (25-27). However, the im-
pact of acidosis on the contractile response
502
Braz J Med Biol Res 33(5) 2000
D.E. Rassier and B.R. MacIntosh
of skinned mammalian muscle fibers is less
at 30
o
C than at 10
o
C (28). Also, it has re-
cently been demonstrated that the effect of
acidosis on the contractile response of intact
single mammalian muscle fibers is much
less at 32
o
C than at room temperature (29).
These observations place some doubt on the
role of changes in Ca
2+
sensitivity in fatigue
at physiological temperature.
In cases in which there is clear evidence
of high-frequency fatigue, the likely mech-
anism is depressed conduction of the action
potential along the sarcolemma and/or into
the transverse tubules (17). Caution must be
exercised, however, to be certain that appar-
ent high-frequency fatigue is not a result of
coexistence of general fatigue and activity-
dependent potentiation. General fatigue
would depress active force at all frequencies
of stimulation, whereas activity-dependent
potentiation would enhance the force only at
low frequencies. The net result of their coex-
istence would be little or no change in active
force at low frequencies and depression of
active force at high frequencies. This possi-
bility is described further below.
Interactions of potentiation and
fatigue
A steady-state contractile response can
be conveniently related to the force-pCa
2+
relationship (Figure 1). Three lines are drawn
in Figure 1A to illustrate potential factors
which may enhance or depress the steady-
state contractile response. The center heavy
line represents a control condition. Force
can be increased or decreased by changing
the myoplasmic free Ca
2+
concentration. The
line which is on the left represents increased
sensitivity and the line on the right repre-
sents decreased sensitivity to Ca
2+
. Increased
Ca
2+
sensitivity will result in greater force at
any given Ca
2+
concentration (except at satu-
rating levels of Ca
2+
), while decreased Ca
2+
sensitivity has the opposite effect. Maximal
active force is not affected in either case.
Interactions of potentiation and fatigue
can be illustrated using the relationship shown
in Figure 1. Let us assume that potentiation
results from enhanced calcium sensitivity,
and fatigue results primarily from depressed
Ca
2+
release per activating pulse. A further
assumption is needed to relate the force-
frequency relationship with the force-pCa
2+
relationship. It is assumed that as frequency
of stimulation increases for a given brief
period of repetitive stimulation, the average
free Ca
2+
concentration increases. This as-
sumption is consistent with published re-
ports of the free Ca
2+
-frequency relationship
for mammalian muscle (30). With these as-
sumptions, it can be seen that combinations
of fatigue and potentiation will result in a
shift to the left in the force-pCa
2+
relation-
ship, and any given stimulation will result in
a lower peak (or average) free Ca
2+
concen-
tration. This is illustrated in Figure 1B. If the
Relative force
1.0
0.8
0.6
0.4
0.2
0
7.0 6.5 6.0 5.5 5.0 4.5
pCa
2+
Relative force
1.0
0.8
0.6
0.4
0.2
0
7.0 6.5 6.0 5.5 5.0 4.5
pCa
2+
Relative force
1.0
0.8
0.6
0.4
0.2
0
7.0 6.5 6.0 5.5 5.0 4.5
pCa
2+
Figure 1 - Hypothetical force-cal-
cium relationships which demon-
strate various combinations of
potentiation and fatigue. A, The
thick line in this figure represents
the control condition, where Ca
2+
sensitivity is neither increased
nor decreased. The thinner lines
on either side represent en-
hanced (to the left) or decreased
(to the right) sensitivity of the
contractile proteins to Ca
2+
. B,
This figure shows the transition
from a control situation (a) to an
enhanced condition (b) which
could represent myosin light
chain phosphorylation. When fa-
tigue is superimposed on poten-
tiation, the force of contraction
could be at c, which is indicated
to be mobile. That is, the position
of c could represent the same
active force as a, or something
above or below that. The point at
b could also represent high-fre-
quency stimulation (depressed
relative to what it would be). C,
Illustrates the transition from a
control situation (a) to an en-
hanced condition (b), and the
combined effects of fatigue due
to decreased Ca
2+
concentration
(c), and decreased Ca
2+
sensitivi-
ty, superimposed on myosin light
chain phosphorylation.
A
B
C
b
c
a
b
c
a
503
Braz J Med Biol Res 33(5) 2000
Coexistence of potentiation and fatigue
control condition results in a free Ca
2+
con-
centration and active force corresponding
with point a, a shift to the left would give
active force indicated by b at the same Ca
2+
concentration, but point c at a lower Ca
2+
concentration.
Coexistence of fatigue and potentiation
could be detected by measurement of the
force-pCa
2+
relationship. For a given sub-
maximal stimulation, the combined effects
of potentiation and fatigue could result in an
increase, no change or a decrease in active
force, depending on the relative change in
the two parameters (increased sensitivity and
decreased Ca
2+
concentration). This situa-
tion would be further complicated if fatigue
was partly due to a decrease in Ca
2+
sensitiv-
ity, as is clearly the case at room temperature
in vitro. It would no longer be sufficient to
measure the force-pCa
2+
relationship to iden-
tify coexistence of fatigue and potentiation.
The net effect of the corresponding increased
Ca
2+
sensitivity associated with potentiation
and the decreased sensitivity associated with
fatigue could cancel each other out (see Fig-
ure 1C). This difficulty may explain why
assessment of coexistence of potentiation
and fatigue has not been studied in this way.
How then, do we know when potentia-
tion and fatigue coexist? There are several
phenomena that can be observed which indi-
cate coexistence of fatigue and potentiation.
However, there are also situations where
potentiation or fatigue appear to be exclu-
sively evident, but the opposing factor may
be present, decreasing the apparent magni-
tude of the other. The primary observations
which present evidence for coexistence of
fatigue and potentiation include the follow-
ing: depressed high-frequency response while
the twitch is enhanced; a time-dependent
decrease in twitch amplitude following re-
peated activation to active force levels be-
low control; discrepancies in the relation-
ship between potentiation and RLC phos-
phorylation, and altered time-course of the
twitch (slowing of contraction and relax-
ation times) while the twitch active force is
enhanced.
Evidence for coexistence of
potentiation and fatigue
Discrepancies in frequency response
One way of observing the coexistence of
potentiation and fatigue is looking at the
discrepancies in the force response during
different frequencies of stimulation. In cir-
cumstances where high-frequency force is
depressed by fatigue, yet RLC are phospho-
rylated (see Figure 1B), there could be an
enhanced twitch with depressed high-fre-
quency contractile response (b in Figure 1B).
Rankin et al. (31) measured the twitch
and tetanic (100 Hz) contractile response of
individual motor units of soleus and exten-
sor digitorum longus muscles following 6
min of intermittent (1 Hz) tetanic contrac-
tions (40 Hz for 330 ms). In a substantial
proportion of the motor units of extensor
digitorum longus muscles the twitch response
was enhanced relative to the prefatigue twitch
while the tetanic contraction was depressed.
This is a clear example of coexistence of
potentiation and fatigue. Only 15% of the
soleus motor units presented this pattern of
response.
Another example of coexistence of po-
tentiation and fatigue is presented by Jami et
al. (32) who investigated force enhancement
and a delayed force decrease in different
motor units of the cat peroneus tertius muscle
in association with the Burke fatigue proto-
col (successive trains of 13 pulses at 40 Hz,
each train lasting 330 ms and being repeated
every 1 s). Immediately following the Burke
protocol, twitch force was enhanced while
response to 40-Hz and 200-Hz stimulation
was enhanced, depressed or unchanged.
However, after a period of recovery de-
pression of active force for twitch and te-
tanic contractions was evident. This obser-
vation reveals another important aspect of
504
Braz J Med Biol Res 33(5) 2000
D.E. Rassier and B.R. MacIntosh
the interaction of fatigue and potentiation.
These two properties of muscle have differ-
ent time-courses of recovery. Activity-de-
pendent potentiation dissipates within min-
utes (5,11), whereas fatigue, particularly low-
frequency fatigue, persists for hours (33).
The two studies cited above, both of
which were done at physiological tempera-
tures, show the specific cases in which coex-
istence of potentiation and fatigue is appar-
ent. At room temperature (or colder) the
interactions of potentiation and fatigue are
less clear, for two reasons: 1) a given level of
RLC phosphorylation results in less poten-
tiation, and 2) there is evidence that fatigue
can result from decreased Ca
2+
sensitivity. In
spite of these complications, similar obser-
vations have been reported at temperatures
colder than room temperature.
Vergara et al. (34) used single fibers from
the frog semitendinosus muscle to study the
coexistence of potentiation and fatigue at
15
o
C. The authors employed 200-ms stimuli
(20 Hz) to evoke near maximal mechanical
responses, and twitches to measure postte-
tanic potentiation (PTP) before and after the
fiber was stimulated tetanically at 20 Hz for
5-200 s (fatiguing contraction). Tetanic con-
tractions maintained for 50 s or longer pro-
duced substantial fatigue, evidenced by the
decline in the 200-ms 20-Hz contraction ob-
served after the tetanus and through a period
of ~90 min. The twitch response was en-
hanced after the tetanic contraction, and af-
ter 10-40 min, the twitch active force de-
clined. PTP was greater after the long teta-
nus when fatigue was present than it was
after a short tetanus.
The results of Vergara et al. (34) were
supported in later studies from the same
group (35,36). An important aspect of these
observations is that these studies show lev-
els of potentiation that were much smaller
than those found in the studies performed by
Rankin et al. (31) and Jami et al. (32). In
general, reports of activity-dependent poten-
tiation studied at room temperature or colder
demonstrate considerably less potentiation
than when muscle is studied at 35-37
o
C (37).
In fact, Moore et al. (38) observed that there
is less RLC phosphorylation despite a greater
relative staircase potentiation at 35
o
C than at
30
o
and 25
o
C in fast muscles from the mouse
stimulated at 5 Hz for 20 s. Since potentia-
tion is related to an increased Ca
2+
sensitivi-
ty, it is probably being partially masked by a
decrease in Ca
2+
sensitivity caused by fa-
tigue at cooler temperatures.
Together, the studies cited above have
presented evidence for coexistence of poten-
tiation and fatigue. In all of these studies, the
muscle was not able to produce maximal
(control) force during moderate to high-fre-
quency stimulation, but the force during low-
frequency (twitch) stimulation was enhanced
for several minutes after the fatiguing stimu-
lation. Coexistence of fatigue and potentia-
tion would be less evident when maximal
force is not decreased as a result of fatigue,
but force response at low-frequency stimula-
tion is decreased (low-frequency fatigue). In
this case, potentiation could be masked, since
twitch force enhancement and depression
would be present at the same time. Under
these circumstances, it would be necessary
to follow twitch active force for some time to
see if twitch active force decreases to below
the control level during a period of relative
inactivity.
Altered relationship between RLC
phosphorylation and potentiation
In all cases presented above, we have
considered the consequences of a period of
stimulation on enhancing and diminishing
the subsequent active force. Another form of
coexistence of potentiation and fatigue ex-
ists when a muscle which has been fatigued
is subsequently activated in a manner which
elicits potentiation.
MacIntosh and colleagues (11,39-41)
have done a series of experiments looking at
the effects of low-frequency fatigue on the
505
Braz J Med Biol Res 33(5) 2000
Coexistence of potentiation and fatigue
subsequent enhancement of active force dur-
ing 10-Hz stimulation or after a tetanic con-
traction in the whole gastrocnemius muscle
of the rat. These experiments confirmed that
fatigued muscle can undergo staircase and
PTP, and that activity-dependent potentia-
tion is proportional to RLC phosphorylation.
However, the relationship between RLC
phosphorylation and potentiation is altered
in fatigue (see Figure 2) and this alteration is
different for staircase (39) compared to PTP
(40). The relative increase in active force
during staircase (10 Hz for 10 s) and PTP
(500 ms or 2 s at 200 Hz) was similar in
fatigued and rested muscle, but the increase
in RLC phosphorylation was considerably
less during staircase in fatigued than rested
muscle. This was not the case for PTP. This
difference between staircase and PTP is rep-
resented in Figure 2 by the greater apparent
slope of the staircase response in fatigued
muscle.
Staircase in the fatigued muscle resulted
in greater enhancement of twitch active force
for a given change in RLC phosphorylation.
This is similar to results of Palmer and Moore
(42) who observed greater potentiation for a
given change in RLC phosphorylation in
muscle treated with dantrolene, a drug which
inhibits Ca
2+
release. This observation can
possibly be explained by the greater relative
enhancement of force which would be ex-
pected for a given shift (to the left) in the
force-pCa
2+
relationship at low Ca
2+
concen-
trations (see Figure 1). However, this is not
the only possible explanation for this dis-
crepancy in the relationship between RLC
phosphorylation and potentiation in fatigued
muscle. This mechanism cannot explain why
PTP is different from staircase in fatigued
muscle. This difference suggests that at least
in fatigued muscle the mechanism for en-
hancement may be different for staircase and
PTP. This conclusion is consistent with the
observation that staircase can occur in the
absence of RLC phosphorylation at low lev-
els of Ca
2+
release (13). One explanation for
this discrepancy is that there could be an-
other mechanism contributing to staircase
under these circumstances.
Time-dependent twitch characteristics
Twitch contractions can be characterized
by measures of the time-course: contraction
time (C
t
), and half-relaxation time (½R
t
).
Fatigue is known to increase both C
t
and ½R
t
(43). Therefore, detection of these changes
during activity-dependent potentiation may
be evidence of coexistence of fatigue and
potentiation.
It is known that activity-dependent po-
tentiation can occur without an increase in C
t
or ½R
t
(11,44), yet there are several reports
of prolongation of C
t
and/or ½R
t
during PTP
(31,32,34,36,45). In general, studies which
have observed a prolongation of C
t
with PTP
have utilized fairly long tetanic contractions
(usually several seconds) to elicit PTP. Many
authors have argued that the prolongation of
the twitch is a characteristic which limits the
impact of fatigue on the active force (32,36).
Prolongation of C
t
and ½R
t
can result in
enhanced summation and a decrease in the
fusion frequency. This prolongation of the
twitch is independent of RLC phosphoryla-
tion, and may represent an independent (ad-
ditional) mechanism of activity-dependent
potentiation.
Developed tension (% of preactivity twitch)
200
150
100
50
020406080
RLC phosphorylation (%)
Control - PTP
Fatigue - PTP
Control - Staircase
Fatigue - Staircase
Figure 2 - Potentiation and myo-
sin light chain phosphorylation
of the rat gastrocnemius muscle
for staircase (39) and posttetanic
potentiation (PTP) (40). The re-
sults for control and fatigued
muscles refer to the situation in
which potentiation was elicited
before or after the fatigue proto-
col, respectively. In both stud-
ies, fatigue was induced by stim-
ulation at 10 Hz for 5 min, fol-
lowed by 20 min of test contrac-
tions at 0.1 Hz. In both cases,
the line representing the rela-
tionship between potentiation
and light chain phosphorylation
is shifted to the left by fatigue.
Note that the slope of the line
representing staircase in the fa-
tigued muscle is steeper than
the other lines. This may repre-
sent an additional mechanism of
potentiation during staircase in
fatigued muscle.
506
Braz J Med Biol Res 33(5) 2000
D.E. Rassier and B.R. MacIntosh
Caution must be exercised when dealing
with measurements of active force of a twitch
contraction when C
t
and/or ½R
t
is/are pro-
longed. There is very good reason to believe
that there is coexistence of factors which
enhance and diminish the active force. This
makes it impossible to accurately quantify
either potentiation or fatigue.
Physiological consequences
The twitch contraction is the smallest
contractile event which can be evaluated in
an intact skeletal muscle preparation. Meas-
urement of the active force and time-course
of the twitch can be very revealing with
respect to the contractile state of the muscle.
However, voluntary activation of a muscle
results in incompletely fused tetanic con-
traction. It is appropriate to consider the
impact of coexistence of fatigue and poten-
tiation on such contractions. However, very
little research has been done which consid-
ers activity-dependent potentiation for in-
completely fused tetanic contractions.
MacIntosh BR and Willis JC (unpublished
results) have demonstrated that activity-de-
pendent potentiation is evident during re-
peated brief incompletely fused tetanic con-
tractions at stimulation frequencies up to 70
Hz. Therefore there is reason to believe that
intermittent voluntary activation of a muscle
would result in activity-dependent potentia-
tion.
Assuming that the force-frequency curve
can be interpreted in terms of the force-Ca
2+
relationship, it seems reasonable to antici-
pate that activity-dependent potentiation
would result in greater isometric force for a
given pattern of (submaximal) stimulation,
and that fatigue would result in less isomet-
ric force for a given pattern of stimulation. In
order to obtain a target force for repeated
contractions, voluntary recruitment of motor
units would have to be modulated in such a
way that enhancement and reduction were
accounted for. This is an aspect of the study
of activity-dependent potentiation which has
been largely ignored, but which may provide
a fruitful avenue of research in the future.
During repetitive stimulation there are
two opposing processes happening at the
same time inside the muscle cells: one that
enhances muscle performance and one that
decreases muscle performance. This phe-
nomenon results in a coexistence of activity-
dependent potentiation and fatigue, for which
the underlying mechanisms are not yet to-
tally understood. In this review, it was as-
sumed that low Ca
2+
concentration caused
fatigue and increased RLC phosphorylation
was the mechanism of activity-dependent
potentiation. Clearly these two opposing
mechanisms can coexist.
Most investigators have not taken into
account the possible coexistence of poten-
tiation and fatigue. Ignoring this coexistence
may cause problems in the interpretation of
studies done with skeletal muscle. Specifi-
cally, when using results of force measure-
ments made during or just after repetitive
muscle stimulation, fatiguing factors may be
present yet not observable due to potentia-
tion. In order to better understand these phe-
nomena, it seems appropriate to evaluate
force transients over a long period of time, to
be sure that the potentiating factor(s) do not
influence active force when fatigue is as-
sessed.
One of the objectives of this paper was to
raise awareness of the coexistence of poten-
tiation and fatigue. From the studies cited in
this review, it seems clear that this coexist-
ence occurs and is an important component
to be taken into account when investigators
analyze force production during and follow-
ing repetitive muscle stimulation.
507
Braz J Med Biol Res 33(5) 2000
Coexistence of potentiation and fatigue
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Measurements of the intracellular free concentration of Ca2+ ([Ca2+]i) were performed during fatiguing stimulation of intact, single muscle fibers, which were dissected from a mouse foot muscle and loaded with fura-2. Fatigue, which was produced by repeated 100-Hz tetani, generally occurred in three phases. Initially, tension declined rapidly to approximately 90% of the original tension (0.9 Po) and during this period the tetanic [Ca2+]i increased significantly (phase 1). Then followed a lengthy period of almost stable tension production and tetanic [Ca2+]i (phase 2). Finally, both the tetanic [Ca2+]i and tension fell relatively fast (phase 3). The resting [Ca2+]i rose continuously throughout the stimulation period. A 10-s rest period during phase 3 resulted in a significant increase of both tetanic [Ca2+]i and tension, whereas a 10-s pause during phase 2 did not have any marked effect. Application of caffeine under control conditions and early during phase 2 resulted in a substantial increase of the tetanic [Ca2+]i but no marked tension increase, whereas caffeine applied at the end of fatiguing stimulation (tension depressed to approximately 0.3 Po) gave a marked increase of both tetanic [Ca2+]i and tension. The tetanic [Ca2+]i for a given tension was generally higher during fatiguing stimulation than under control conditions. Fatigue developed more rapidly in fibers exposed to cyanide. In these fibers there was no increase of tetanic [Ca2+]i during phase 1 and the increase of the resting [Ca2+]i during fatiguing stimulation was markedly larger. The present results indicate that fatigue produced by repeated tetani is caused by a combination of reduced maximum tension-generating capacity, reduced myofibrillar Ca2+ sensitivity, and reduced Ca2+ release from the sarcoplasmic reticulum. The depression of maximum tension-generating capacity develops early during fatiguing stimulation and it is of greatest importance for the force decline at early stages of fatigue. As fatigue gets more severe, reduced Ca2+ sensitivity and reduced Ca2+ release become quantitatively more important for the tension decline.
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Prolonged activation of skeletal muscle leads to a decline of force production known as fatigue. In this review we outline the ionic and metabolic changes that occur in muscle during prolonged activity and focus on how these changes might lead to reduced force. We discuss two distinct types of fatigue: fatigue due to continuous high-frequency stimulation and fatigue due to repeated tetanic stimulation. The causes of force decline are considered under three categories: 1) reduced Ca2+ release from the sarcoplasmic reticulum, 2) reduced myofibrillar Ca2+ sensitivity, and 3) reduced maximum Ca(2+)-activated tension. Reduced Ca2+ release can be due to impaired action potential propagation in the T tubules, and this is a principal cause of the tension decline with continuous tetanic stimulation. Another type of failing Ca2+ release, which is homogeneous across the fibers, is prominent with repeated tetanic stimulation; the underlying mechanisms of this reduction are not fully understood, although several possibilities emerge. Changes in intracellular metabolites, particularly increased concentration of Pi and reduced pH, lead to reduced Ca2+ sensitivity and reduced maximum tension, which make an important contribution to the force decline, especially with repeated tetanic stimulation.
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At 15 degrees C, direct stimulation of frog single muscle fibers at a frequency of 20 Hz produced a tetanic tension that remained constant for 20 s and then declined. The decline was reversed during 1-s interruptions of the stimulus train in the first 50 s of stimulation, but not with longer stimulation. Posttetanic potentiation (PTP), characterized by prolonged twitch relaxation and contraction times and elevation of twitch height, remained for 10-40 min after a 10-s tetanus and for at least 90 min after a 50- to 150-s tetanus. Posttetanic fatigue appeared only after at least 50s of tetanic stimulation. Fatigue was manifested invariably by a reduction in the height of a 200-ms tetanic contraction and usually by a reduction in twitch height after PTP. Fatigued fibers recovered normal contractile responses in 40-160 min. Hypertonic solutions, which blocked contraction in response to tetanic stimulation, prevented posttetanic fatigue but not PTP. The observations suggest that fatigue is caused by a failure in excitation-contraction coupling, probably in relation to consumption of metabolic substrates. Even 10-s tetani which do not produce fatigue can affect muscle contractile function for up to 40 min.
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Fatigue and recovery from fatigue were related to metabolism in single fibers of the frog semitendinosus muscle. The fibers were held at a sarcomere length of 2.3 microm in oxygenated Ringer solution at 15 degrees C and were stimulated for up to 150 s by a schedule of 10-s, 20-Hz tetanic trains that were interrupted by 1-s rest periods, after which they were rapidly frozen for biochemical analysis. Two kinds of fatigue were produced in relation to stimulus duration. A rapidly reversed fatigue occurred with stimulation for under 40 s and was evidenced by a decline in tetanic tension that could be overcome by 1 s of rest. A prolonged fatigue was caused by stimulation for 100-150 s. It was evidenced during stimulation by a fall in tetanic tension that could not be overcome by 1 s of rest, and after stimulation by a reduction, lasting for up to 82 min, in the peak tension of a 200-ms test tetanus. Fiber phosphocreatine (PCr) fell logarithmically in relation to stimulus duration, from a mean of 121 +/- 8 nmol/mg protein (SEM, n = 12) to 10% of this value after 150 s of stimulation. PCr returned to normal levels after 90-120 min of rest. Stimulation for 150 s did not significantly affect fiber glycogen and reduced fiber ATP by at most 15%. It is suggested that the prolonged fatigue caused by 100-150 s of tetanic stimulation was caused by long-lasting failure of excitation-contraction coupling, as it was not accompanied by depletion of energy stores in the form of ATP. One possibility is that H+ accumulated in fatigued fibers so as to interfere with the action of Ca2+ in the coupling process.
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Phosphorylation of the 18,500 dalton light chain of myosin and conversion of phosphorylase to were examined in relation to isometric tension development. Following a l sec tetanic contraction, light chain phosphate content increased from a pre-tetanic value of 0.10 to 0.75 mol phosphate/mol at 7 sec; phosphorylase activity (ratio of activity ) increased from 0.03 to 0.42 at 4 sec and decreased to control values within 20 sec. Light chain phosphate content, however, declined much more slowly and correlated to post-tetanic potentiation of peak twitch tension. Our results suggest light chain phosphorylation is not obligatory for contraction but may play a role in post-tetanic potentiation.
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1. After severe muscular contraction in man recovery of force is largely complete in a few minutes, but is not wholly so for many hours. The long-lasting element of fatigue is found to occur primarily for low frequencies of stimulation (e.g. 20/sec), and is much less pronounced, or absent, at high frequencies (80/sec). The twitch force is an unreliable measure of the state of fatigue. 2. The long-lasting element of fatigue is not due to depletion of high-energy phosphate nor is it due to failure of electrical activity as recorded from surface electrodes. It is probably the result of an impairment of the process of excitation-contraction coupling. Its practical importance for man could be significant as an explanation of the subjective feelings of weakness following exercise.
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A long-lasting impairment of muscular force generation follows fatiguing exercise (fatigue of long duration), the physiological basis of which is not well understood. To investigate the role of reduced calcium release in long-lasting fatigue, we examined the effects of dantrolene sodium, which selectively decreases calcium release from the sarcoplasmic reticulum. The drug impaired muscle function in a pattern identical to that of long-lasting fatigue. The results are consistent with either independent effects of dantrolene and exercise at the same site in the excitation-contraction coupling chain, or independent actions at separate serial sites.
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1. Single muscle fibres were dissected from the toe muscles of Xenopus laevis and microinjected with Fura-2 to measure myoplasmic calcium concentration ([Ca2+]i). Injected fibres were illuminated at 340 and 380 nm and the ratio of the resulting fluorescence at 505 nm (the Fura-2 ratio) was taken as a measure of [Ca2+]i. Fibres were fatigued at 21 degrees C by repeated tetani until developed tension had fallen to 50% of control. 2. Tetanic tension declined monotonically during fatiguing stimulation, whereas the tetanic Fura-2 ratio first increased and then declined. At the 10th tetanus, tension was 87% of control whereas the Fura-2 ratio was 106% of control. At the end of fatiguing stimulation, where tension was around 50% of control, the tetanic Fura-2 ratio was reduced to 71%. The rate of decline of both tension and the Fura-2 ratio after a tetanus slowed during fatigue. During recovery, the tension and the tetanic Fura-2 ratio recovered in parallel. 3. The resting Fura-2 ratio increased throughout fatigue reaching 237% of control when tension had declined to 50%. There was a rapid phase of recovery, complete within 1 min, by which time the resting Fura-2 ratio was 198% of control. Subsequent recovery was slower and took 20-30 min to reach a stable level which was 121% of control. 4. The resting Fura-2 ratio towards the end of fatiguing stimulation was greater than the tetanic Fura-2 ratio in the early part of recovery although there was no detectable increase of resting tension during fatiguing stimulation. This observation suggests that the Ca2+ sensitivity of the contractile proteins was reduced at the end of fatiguing stimulation. 5. Plots of the tetanic tension against tetanic Fura-2 ratios throughout fatiguing stimulation and recovery also suggested that Ca2+ sensitivity was reduced during fatiguing stimulation when compared to recovery. 6. The increases in resting [Ca2+]i caused by raised [K+]o (from 2.5 to 10 mM) and/or by application of 15% CO2 were much less than those produced by fatiguing stimulation. Much of the elevated [Ca2+]i in fatigue could be reversed by application of dantrolene (25 microM). 7. The results suggest that both reduced tetanic [Ca2+]i and reduced Ca2+ sensitivity contribute to the decline of tension during fatigue.(ABSTRACT TRUNCATED AT 400 WORDS)