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1 Department of Kinesiology, University of Texas Arlington, Arlington, TX 76019-19259, USA 2 Division of Exercise Physiology, West Virginia University School of Medicine, Morgantown, West Virginia, 26506-9227, USADepartments of 3 Anatomy & Physiology4 Kinesiology, Kansas State University, Manhattan, Kansas 66506-5802, USA
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Abstract |
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) differs within muscles composed primarily of type II fibres with contrasting oxidative capacity has not been determined. We tested the hypothesis that, following contractions, the recovery of 
would be slower in the white (WG; low oxidative capacity) versus the mixed gastrocnemius (MG; comparatively high oxidative capacity). Radiolabelled microsphere and phosphorescence quenching techniques were used to measure muscle blood flow (
, hence O2 delivery, 
) and 
during contractions (1 Hz twitch) at low (LO, 2.5 V) and high intensities (HI, 4.5 V) in rat (n
= 15) MG and WG muscle and during subsequent recovery. Following the LO protocol, end-contraction 
was lower in WG (11.6 ± 0.5 mmHg) than in MG (16.2 ± 0.6 mmHg; P < 0.05) while, contrary to our hypothesis, the initial rate of change in 
during recovery (
/dt; MG 0.11 ± 0.01 mmHg s–1 and WG 0.06 ± 0.03 mmHg s–1) and mean response time (MRT; MG 110.3 ± 5.1 s and WG 113.5 ± 8.4 s, P > 0.05) were not different. In contrast, end-contraction baseline 
was not different following the HI protocol (MG 10.3 ± 0.6 mmHg and WG 9.2 ± 0.6 mmHg; P > 0.05) but, in agreement with our hypothesis, 
/dt was slower (MG 0.07 ± 0.01 mmHg s–1 and WG 0.03 ± 0.003 mmHg s–1; P < 0.05) and MRT longer (WG 180.8 ± 4.5 s and MG 115.4 ± 6.7 s; P < 0.05) in WG versus MG following the HI protocol. These data suggest that following high-intensity, though submaximal, muscle contractions, 
recovers much faster in the more oxidative mixed gastrocnemius than in the less oxidative white gastrocnemius.
(Received 8 March 2007;
accepted after revision 16 April 2007; first published online 20 April 2007)
Corresponding author P. McDonough: Department of Kinesiology, University of Texas Arlington, 112 Physical Education Building, 801 Greek Row Drive, Arlington, TX 76019-19259, USA. Email: mcdonough{at}uta.edu
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Introduction |
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) insofar as this regulates microvascular partial pressure of O2 (
; McDonough et al. 2001). Specifically, 
is determined by the 
/O2 utilization (
) ratio and, being a measure of the volume-weighted average 
within the microcirculation, constitutes an approximation of the mean driving pressure for O2 diffusion from the microvascular blood into the myocyte.
The rate at which 
recovers following contractions has been shown to be dependent upon muscle fibre type, end-contraction 
(a measure of contractile intensity) and oxygen delivery (
; McDonough et al. 2004a,b). These studies, by judicious selection of specific muscles, have investigated the differences between slow-twitch and fast-twitch musculature and have taken care to match oxidative capacity across fibre types (see McDonough et al. 2004b). Thus, at present it has not been resolved whether any relationship exists between 
recovery rate and oxidative capacity within a given fibre type (i.e. type I or type II). Of interest, it has been noted that soleus muscle from rats in severe heart failure exhibits both a decreased oxidative capacity and slowed 
recovery (McDonough et al. 2004a). However, whether this effect resulted from the decreased soleus oxidative capacity per se or from some of the other myriad sequelae of heart failure could not be deduced from those studies.
In addition, the effect of contractile intensity on the recovery of 
is presently unclear. There is evidence that, following muscular contractions, various markers of the recovery process are prolonged when work intensity is raised. These include 
(Cunningham et al. 2000; Özyener et al. 2001; Witte et al. 2005), PCr (Arnold et al. 1984) and pH (Arnold et al. 1984), each of which may be impacted directly by altered 
(Haseler et al. 1999). One mechanism that ties these findings together relates to the muscle fibre recruitment profile. Specifically, more type II fibres, some of which may have a lower oxidative capacity than type I fibres, are recruited as work intensity rises (Gollnick et al. 1974). These type II fibres evince a lower contracting 
(McDonough et al. 2005) and also recover their resting 
levels more slowly compared with type I fibres of similar oxidative capacity (McDonough et al. 2004a). Thus, it would be expected that higher intensity contractions that recruit more type II fibres would reduce contracting 
to a greater extent than lower intensity contractions and that this lower 
would recover more slowly. However, contrary to what is noted above, Kindig et al. (2005a) found no difference in the time course of intracellular 
) recovery of Xenopus laevis muscle fibres following contraction protocols of varying duty cycle corresponding to different metabolic rates (200 and 400 ms). Thus, the effects of contractile intensity and oxidative capacity upon the recovery of 
remain ambiguous.
In an attempt to resolve these issues, we examined the recovery of 
in two fast-twitch (type II) muscle portions, the moderately high oxidative capacity mixed gastrocnemius (MG) and the relatively low oxidative capacity white gastrocnemius (WG), following low- and high-intensity contractions. These particular muscles were chosen so as to minimize the effect of differences in fibre type and 
per se upon 
and its kinetics (Behnke et al. 2003; McDonough et al. 2004b). We hypothesized that 
recovery would be prolonged in WG compared with MG and that this effect would be most pronounced at the highest contraction intensity.
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Methods |
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Surgical preparation
All rats (n
= 15) were anaesthetized prior to experimentation with pentobarbitone sodium (40 mg/kg I.P. to effect). In order to ensure that an adequate anaesthetic plane was maintained, reflexes (ocular and pedal) were tested throughout the experiment. If reflex tests proved positive, pentobarbitone was administered in a supplemental dosage (5–10 mg kg–1
I.P. to effect) as needed. The carotid and tail (caudal) arteries were catheterized with polyethylene tubing (PE-10 connected to PE-50). This allowed for the infusion of the phosphorescent probe [palladium meso-tetra(4-carboxyphenyl)porphine dendrimer (R2); 15 mg kg–1; Oxygen Enterprises, Ltd, Philadelphia, PA, USA], measurement of arterial blood pressure (Digi-Medical BPA model 200, Louisville, KY, USA) and withdrawal of arterial blood for blood gas measurement (Nova Stat Profile M, Waltham, MA, USA). In addition, the catheters allowed us to measure muscle blood flow (
) using the radiolabelled microsphere technique (Laughlin et al. 1982; Musch & Terrell, 1992).
The muscles chosen for the present experiment were chosen based on previous research regarding muscle fibre type composition, as well as our own analysis of oxidative enzyme activities (Delp & Duan, 1996; McDonough et al. 2005). The MG is a powerful muscle of plantar flexion and, as such, has an almost universal fast-twitch fibre composition (3% type I, 6% type IIa, 34% type IId/x and 57% type IIb), with a citrate synthase activity of 17.9 µmol min–1 g–1 (in our rats; McDonough et al. 2005). The WG is a plantar flexor of low oxidative capacity (citrate synthase activity 11.0 µmol min–1 g–1) and has a fibre type composition that is purely fast-twitch in nature (8% type IId/x, 92% type IIb; Delp & Duan, 1996; McDonough et al. 2005). Thus, these muscles are perfectly suited to the aims of the present study. Each muscle was exposed for 
measurements as previously detailed (McDonough et al. 2005). The tibial nerve was isolated and a stimulating electrode was attached. The ground electrode was attached distally, near the Achilles tendon. Care was taken to minimize the extent of the surgery in all cases. The exposed tissue was superfused with a Krebs–Henseleit bicarbonate-buffered solution (38°C, equilibrated with 5% CO2, N2 balance) and body temperature was maintained at 
38°C via the use of a heating pad.
Contraction protocols
Prior to beginning the experimental protocol, the R2 probe was infused (via the arterial catheter). The rat was then moved to a purpose-built ergometer and secured as detailed previously (McDonough et al. 2005). The phosphorimeter light guide was positioned (within 1–3 mm) above the belly of the muscle of interest. Approximately 15 min later, the MG or WG was stimulated at 1 Hz for 3 min (2 ms pulse duration) using a Grass S88 stimulator (Quincy, MA, USA) moderate- and heavy-intensity exercise. These contraction intensities were chosen on the basis of an incremental contraction test (stimulation intensity increased by 1 V min–1) and correspond to approximately 30 and 65%, respectively, of the stimulation voltage that produced a minimal 
(P. McDonough, B. J. Behnke, T. I. Musch & D. C. Poole, unpublished observations). These stimulation voltages were chosen simply to span a relatively large intensity range and could be taken to resemble, in certain respects, low- and moderately heavy-intensity exercise. All animals were killed with an overdose of pentobarbitone sodium (> 80 mg kg–1
I.A.) following the conclusion of the experimental protocol.
Muscle blood flow and oxygen consumption
Muscle blood flow (
) and oxygen consumption (
) were measured or estimated in the following manner. The 
was determined using the radiolabelled microsphere technique (Musch & Terrell, 1992) and was measured just prior to the cessation of the 3 min contractions and recovery protocols in the two muscles and expressed as millilitres of blood per minute per 100 g tissue (ml min–1 100 g–1). Three different radiolabelled, 15 µm diameter microspheres (46Sc, 85Sr and 141Ce; New England Nuclear, Boston, MA, USA) were agitated via sonication, and 2.5 x 105 microspheres were injected into the ascending aorta at the specified time point. Tissue radiation counts were performed using a 
scintillation counter (Packard Auto Gamma Spectrometer, Cobra model 5003). The correct placement of the carotid catheter in the aorta was verified postexperiment, while adequate mixing of microspheres was verified via inspection of kidney blood flows, with a difference < 15% between right and left kidney considered acceptable.
Muscle 
was estimated as previously described (Behnke et al. 2002; McDonough et al. 2005). Arterial O2 content (
) was measured directly (carotid arterial blood), and effluent venous O2 content (
) was estimated from 
(because 
is our closest approximation of mixed venous 
; McDonough et al. 2001) using the rat O2 dissociation curve (constructed using an n of 2.6, the measured [Hb], P50 of 38 mmHg and an O2 carrying capacity of 1.34 ml O2 (g Hb)–1 (Altman & Dittmer, 1974). The 
was then calculated via the principle of mass balance using the Fick equation [i.e. 
)].
Principle and measurement of phosphorescence quenching
The principles of phosphorescence quenching have been detailed previously (Poole et al. 1995; McDonough et al. 2001; Behnke et al. 2003). Basically, the Stern–Volmer relationship (Rumsey et al. 1988) describes the nature of the quantitative relationship between probe phosphorescence and 
:
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| (1) |
, gives:
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| (2) |
of zero and kQ the quenching constant of the probe (mmHg s–1). For the R2 probe, t0 is 601 µs and kQ 409 mmHg s–1. Thus, under the physiological conditions studied, the lifetime of the phosphorescence decay is wholly dependant upon the prevailing PO2 (i.e. PmvO2).
A Frequency Domain Phosphorimeter (PMOD 1000; Oxygen Enterprises, Ltd, Philadelphia, PA, USA) was employed, with the light guide focused on a circular area of exposed muscle of 2 mm diameter. The PMOD 1000 modulates the excitation frequencies between 100 Hz and 20 kHz, which can measure 
values from 0 to 240 mmHg. The 
was measured continuously, with data reported at 2 s intervals throughout. Importantly, R2 is restricted to the intravascular space within the muscle, which allows measurement of microvascular O2 tension (
) in a volume (500 µm deep) comprised principally of capillary and venular blood (Poole et al. 2004).
Curve fitting and statistical analysis
For the 
data, curve fitting was accomplished using KaleidaGraph software (version 3.5; Synergy Software, Reading, PA) and was performed on each data set using a one-component model:
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| (3) |
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| (4) |
In addition, data were also fitted to a three-component model, since some preliminary data have demonstrated increased complexity of the off-kinetic response (P. McDonough, B. J. Behnke, D. J. Padilla, T. I. Musch & D. C. Poole, unpublished observations):
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| (5) |
(t) is the 
at any time t, 
is the 
at the immediate offset from contractions, 
1, 2 and 3 are the amplitudes, TD1, TD2 and TD3 are the independent time delays, and 
1, 2 and 3 are the time constants for the phase 1, phase 2 and phase 3 
components, respectively. Phase 1 is the immediate off-transient component, while phases 2 and 3 are the additional components of the recovery response which are both slow to evolve and delayed in their appearance. Goodness of fit was determined by three criteria: (1) the coefficient of determination (i.e. r2); (2) the sum of the squared residuals; and (3) visual inspection and analysis of the residual fit to a linear model. Mean response time (MRT) was calculated using the formula of MacDonald et al. (1997):
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| (6) |
1 and 2, TD1 and TD2 and 1 and 2 are as defined above. If a two-component model provided the best fit, the MRT equation reduced to the following:
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| (7) |
Likewise, if a one-component model provided the best fit, it reduced to:
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| (8) |
In addition, the time to 63% of the final response (T63: a model-independent mean response time) was calculated. Lastly, the relative rate of change in 
/dt) was defined as the initial 
for the off-transient from contractions (McDonough et al. 2004b).
Values of 
at end-contraction and during steady-state recovery (e.g. baseline and ) as well as modelling-dependent (e.g. TD, and MRT) and -independent results (T63) were analysed using standard analysis of variance techniques between muscles (MG and WG). When a significant F value was demonstrated by the ANOVA, a Student–Newman–Keuls (SNK) post hoc test was performed to determine differences among mean values. Pearson product–moment correlations were performed upon selected variables. Statistical significance was accepted at P < 0.05.
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Results |
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In general, while the recovery of 
followed a pattern similar to that noted previously (McDonough et al. 2001, McDonough et al. 2004a,b), some responses were slightly more complex (i.e. a three- versus two-component response; Fig. 1).
This did not present a problem with data interpretation since model-dependent (i.e. MRT) and -independent (measures i.e. T63) of the overall time course of recovery were not different (Table 1).
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was higher in MG compared with WG (Table 1). However, none of the other recovery parameters (see Table 1) were different between MG and WG following the LO protocol.
HI protocol.
At end-contractions, 
was not different in MG compared with WG (Table 1). In addition, the initial 
, time delay and time constant were not significantly different in MG compared with WG (Table 1). However, the initial 
/dt was significantly slower in WG compared with MG (Table 1 and Figs 1 and 2).
In addition, the phase 2 time delay was greater and 
/dt was significantly slower in WG compared with MG (Table 1). Finally, the MRT and T63 were both significantly longer in WG compared with MG following the HI protocol (Table 1, Fig. 3).
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was significantly lower in MG, but not in WG when comparing LO versus HI protocols (Table 1). In addition, the time delay was significantly shorter following HI (in fact, it was virtually non-existent) in MG, but not in WG (Table 1). Finally, the 
/dt (Fig. 2 and Table 1), T63 and MRT were slowed significantly in WG (but not in MG) when comparing LO and HI protocols (Fig. 3 and Table 1). Muscle blood flow and oxygen consumption
LO protocol.
Muscle blood flow (
; in ml min–1 100 g)–1 was significantly higher in WG compared with MG at end-recovery (Table 2
; P < 0.05). Estimated muscle oxygen consumption (
; in ml O2 min–1 100 g–1) followed a similar pattern; however, 
was higher in WG compared with MG at both end-exercise and end-recovery following the LO protocol (Table 2).
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was significantly higher in WG compared with MG at end-recovery (Table 2). However, 
was only elevated in WG compared with MG at end-recovery (Table 2). |
Discussion |
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in fast-twitch muscle is much quicker in the more highly oxidative MG compared with the low-oxidative WG, but only at the highest of the two stimulation intensities examined. This raises the intriguing question of whether the slower recovery of PCr in low-oxidative type II muscles (Kushmerick et al. 1992; Paganini et al. 1997) might result, at least in part, from the lowered 
and the constraint this places on blood–muscle O2 flux. The slowed 
recovery from high-intensity contractions did not appear to result from a lower absolute 
in WG versus MG since, at the end of contractions, 
was not different between muscles and, at the end of the recovery period, 
was, in fact, higher in WG compared with the MG. Since muscle metabolic rate (
) was also higher in WG during recovery, these findings suggest strongly that, at the level of the recovering myocytes, 
recovered more slowly in WG and that 
was inadequate to maintain 
at levels commensurate with that in the MG.
Impact of contraction intensity upon the recovery of 
As stated above, the recovery of 
diverges in an intensity-dependent fashion in fast-twitch hindlimb muscle (present study; Table 1). Kindig et al. (2005a) noted that the time course of intracellular 
recovery was unaffected by an increase in metabolic rate induced by doubling the contraction duty cycle. These data are consistent with those of the present investigation (Table 1) if the amphibian muscle fibres examined corresponded to the more oxidative MG muscle examined in the present study and/or the elevation in metabolic rate was not sufficient to induce slowed recovery dynamics. When these same investigators (Kindig et al. 2005c) examined the association between fatigability and 
recovery in fast-fatiguing and fatigue-resistant muscle fibres (loosely analogous to the WG and MG used in the present study), they noted an inverse relationship between the time course of 
recovery and time to fatigue. These findings suggest that an increase in the relative intensity of contractions leads to a prolongation of recovery, especially in muscle fibres that are easily fatigued (Kindig et al. 2005c) or of low oxidative capacity (present study; Table 1).
Relationship between oxidative capacity and recovery of 
The prolonged recovery of 
found following the HI protocol in the low-oxidative capacity WG (citrate synthase activity 60% that of MG) agrees well with the results of Paganini and colleagues, who showed that PCr recovery was inversely proportional to oxidative capacity (Paganini et al. 1997). Furthermore, Kindig et al. (2005c) noted that the mean response time of 
recovery was inversely related to time to fatigue (which, in their hands, is an indication of fibre oxidative capacity). In addition, Kindig et al. (2005b) noted that 
recovery was appreciably more rapid following contractions during which creatine kinase (CK) was inhibited by iodoacetamide, which suggests that fibres which rely more heavily upon the CK system (i.e. fast-twitch fatigable motor units) exhibit a prolongation of 
recovery. Their findings demonstrate a strong intensity-dependent relationship between oxidative capacity and 
recovery. In addition, Thompson et al. (1995a,b) noted a significant prolongation of PCr recovery half-time with a reduction in mitochondrial capacity in rat hindlimb musculature. These investigations, in combination with the present findings, demonstrate that oxidative capacity can clearly impact the rate at which markers of the cellular energetic state (
) recover following contractions. In the present study, it appears that the speed of recovery of 
co-varies with oxidative capacity in muscles which are more likely to experience a large change in cellular energetic state during contractions, but only when contraction intensity (and thus the alteration of cellular energy state) is sufficiently high. Since the recovery of 
and, probably, 
, are intimately linked (Idstrom et al. 1985; Rossiter et al. 2002; Kindig et al. 2005c), these findings suggest a scenario whereby the prolongation of energetic recovery in health and disease can be attributable, at least in part, to the recruitment of fibres of low oxidative capacity during intense muscular work. The present investigation indicates that the 
ratio, since it determines the 
, might be an important ‘upstream player’ in this scenario (see conclusions).
Impact of heterogeneities in oxygen delivery upon recovery of 
Previously, we have noted that differences in 
and vascular control were the most likely reasons for the different speeds of 
recovery noted between slow- and fast-twitch muscle of similar oxidative capacity (McDonough et al. 2004b). However, given that bulk flow and 
in the present study were not different between muscles at end-contractions and were, in fact, higher in the WG at end-recovery (Table 2), these variables cannot account for the present results. Of interest, Gute et al. (1996) found that capillary-to-fibre ratio, capillary numerical density and capillary surface area density were all reduced in the white versus mixed gastrocnemius. In addition, McAllister (2003) demonstrated that endothelium-dependent vasodilatation was lower in the hindlimb muscles with a low oxidative capacity when compared with those of a high oxidative capacity, while Hirai et al. (1994) reported that the reduction in the exercise blood flow response produced during nitric oxide synthase (NOS) blockade with the agent NG-nitro-L-arginine methyl ester (L-NAME) was blunted in those muscles containing a low versus a high percentage of oxidative fibres. Thus, while bulk blood flow and 
were not different between the contracting white and mixed gastrocnemius, it is likely that different patterns of microcirculatory haemodynamics found between and within different types of muscles or muscle fibres affected the O2 flux from the capillary to the contracting myocyte and may have contributed to the differences in 
found in the present investigation. The greater absolute blood–myocyte O2 flux (
) indicates that there was a substantially higher energetic cost of recovery in WG than in MG following HI-intensity contractions.
Impact of intracellular acidosis upon recovery of 
We have previously discounted the impact of intracellular pH (pHi) alterations upon the recovery of 
because the contraction protocols were designed to be of moderate intensity (i.e. no change in systemic pH). However, since 
recovery following the HI protocol was slowed in WG (compared with both MG and the LO protocol WG response), this allows for the possibility that alterations in pHi may have impacted 
recovery following the more intense contractions. Indeed, PCr recovery is slowed as a direct function of pHi and its effect upon the CK equilibrium (i.e. PCr + ADP + H+
Cr + ATP) following severe versus mild exercise (Arnold et al. 1984; Iotti et al. 1993). Paganini et al. (1997) noted that pHi was significantly reduced in low-oxidative versus high-oxidative capacity muscle following near maximal contractions, which is consistent with the notion that 
recovery may be dependent upon pHi. Indeed, we (P. McDonough, B. J. Behnke, D. J. Padilla, T. I. Musch & D. C. Poole, unpublished observations) have recently observed that 
kinetics during recovery are markedly speeded in creatine-depleted muscle, which typically exhibits a higher oxidative capacity (Moerland & Kushmerick, 1994) as well as less pronounced changes in pHi during high-intensity contractions (Meyer et al. 1986). Thus, it seems plausible that, compared with MG, pHi was lower at end-contractions and during recovery in WG and that this low pHi probably contributed to the slowed 
recovery following the HI protocol.
Conclusions
For contractions of sufficient intensity, muscle comprised of low-oxidative, type II fibres exhibits a prolonged recovery of 
such that, at a given time during recovery, the pressure driving blood–myocyte O2 flux is reduced. Based upon the present findings, the slowing of recovery 
kinetics that has been noted following intense exercise might be the consequence of a reduced blood–myocyte O2 flux caused by a lowered 
specifically within or adjacent to low-oxidative fibres, i.e. where a greater degree of flow heterogeneity (or disproportionality to 
) exists. Moreover, such a lowered 
would be expected to reduce intracellular 
and impair PCr recovery through a direct effect on the CK equilibrium and mitochondrial function. Thus, it is proposed that slowed metabolic recovery in fast-twitch muscle fibres might result from a reduced capillary-to-myocyte 
gradient and a relative reduction in mitochondrial O2 availability, both of which will impair PCr restoration, hence metabolic recovery. The reduced 
found in the present study places an important site of control for slowed metabolic recovery upstream of the muscle myocyte because it results ultimately from a reduced 
ratio that is driven by a suboptimal 
. In total, these findings are consistent with the reduced oxidative capacity and poor fatigue resistance in the fast-twitch WG and may help to illuminate the causes of fatigue during repetitive activities, particularly in physiological and pathophysiological conditions that reduce work capacity and necessitate recruitment of a greater fast-twitch/low-oxidative capacity fibre-type population.
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for medial and white gastrocnemius portions (mixed gastrocnemius (MG) and white gastrocnemius (WG), respectively) during the off-transient from the high (HI)-contraction protocol 
during recovery following LO and HI protocols
/dt) in the mixed gastrocnemius (MG) and white gastrocnemius (WG) during recovery from LO and HI protocols 
/dt is a measure of the rate of recovery which is independent of the amplitude of the response and, as such, indicates the true ‘speed’ of the response. Note the exceptionally slow 
/dt in WG following the HI protocol. * Significant difference from MG; 
significant difference between LO and HI protocol (all P < 0.05).
/dt recovery in the mixed gastrocnemius (MG) and white gastrocnemius (WG) during recovery from LO and HI protocols