Many everyday activities involve various forms of muscular activity with a static component and at a level less than the maximal voluntary isometric contraction (MVC). Repeated activation of muscle induces processes resulting in decreased performance (fatigue) as well as enhanced performance (postactivation potentiation, also known as activity-dependent potentiation). Fatigue is defined as a response that is less than the expected contractile responses for a given stimulation (2), while potentiation corresponds to the increase of electrically evoked twitch force following a “conditioning” activity: after brief MVCs (22) or submaximal levels of activation (7) or as a result of repeated low frequency stimulation (18). The potentiation phenomenon thus can occur after one or several conditioning contractions at maximal or submaximal levels. Finally, both fatigue and potentiation change characteristics of skeletal muscle. Measured force output during repetitive contractile activity reflects the net balance of the opposing effects of fatigue and potentiation (24,25). Low-frequency fatigue, a long-lasting type of fatigue, is thought to be the result of an impairment of the process of excitation-contraction coupling (6) leading to a reduced Ca2+ release from the sarcoplasmic reticulum per action potential (16,33). Potentiation of force by previous activation is caused by increased rates of phosphorylation of the myosin light chains (e.g. 20), leading to an increased in proteins sensitivity to Ca2+. Therefore, it might be expected that potentiation can counteract the effects of the reduced Ca2+ release due to fatigue.
Despite suggestions that potentiation and fatigue coexist (7,25), only one study documented this interaction during submaximal voluntary exercise (at 30% MVC during 60 minutes), but with 4 interruptions of 3 minutes each (7). This study showed that muscle potentiation had a role in overcoming low-frequency fatigue that appeared during the submaximal voluntary exercise. This observation in healthy active subjects should be further investigated with evaluation of muscle contractile properties at regular time intervals interposed in the rest intervals between intermittent submaximal voluntary contractions. An experimental protocol that produces an initial potentiation in twitch torque followed by depression (fatigue) is a series of repetitive contractions (7,15). The rationale for the use of intermittent protocols seems not to be the work-to-rest ratio, but the absolute duration of the contractions and the rest intervals themselves. Short duration contractions would not allow fatigue to build up during contractions, while still promoting potentiation (25). Moreover, the rest interval would allow muscle recovery, enhancing the prevalence of potentiation over fatigue. Such ideas are consistent with findings of French and colleagues (8), who demonstrated that using a protocol consisting of 3 sets of 3 MVCs for 3 seconds was more effective than a similar protocol that held MVCs for 5 seconds. Thus, a short period of contractile activity results in myosin regulatory light chain phosphorylation that will be maintained during intermittent periods of relaxation but poised for potentiation of subsequent contractions.
Among the many components that contribute to neuromuscular performance is also the training status of the subjects. To date, the competitive effects of potentiation and fatigue throughout a repeated submaximal isometric exercise have never been evaluated in subjects with different physical training status (endurance-trained [END] vs. power-trained [POW]). In small mammals, the extent of twitch potentiation is much more pronounced in muscles with a predominance of fast twitch fibers (19). Human muscles with shorter twitch contraction times and a higher proportion of fast fibers exhibit greater postactivation potentiation (13,14). Longitudinal past studies have thoroughly documented the histochemical differences between END and POW athletes, and END athletes typically have a higher percentage of slow twitch muscle fibers in the vastus lateralis (VL) compared with weightlifters, wrestlers or volleyball players (11,28). On this basis, we can assume that END athletes show less potentiation than POW subjects (22), and POW athletes are more sensitive to neuromuscular fatigue compared with END athletes (10, 23, 29). The enhanced fatigue resistance of END athletes' muscles would allow the potentiating effect to prevail over the fatigue effect during repeated submaximal contractions. Little attention, however, has been given to the influence of training history on the interaction of fatigue and potentiation responses during submaximal repeated isometric contractions.
Therefore, the aim of this study was to assess the effect of training history on the interaction between potentiation and fatigue during intermittent submaximal contractions in 2 groups of subjects having different long-term training adaptations (END vs. POW athletes). We hypothesized that potentiation would appear in the two groups during the first minutes of the exercise; and END would be better to offset increases in neuromuscular fatigue when compared with POW in potentiated condition.
Experimental Approach to the Problem
To investigate the effect of training history on the time course of potentiation and fatigue during repeated submaximal isometric contractions of knee extensors, we have determined 2 groups of subjects having different long-term training adaptations (END vs. POW). We have monitored the relative contribution of fatigue and postactivation potentiation by measuring EMG activity and twitch contractile characteristics (neurostimulation procedure) of knee extensors each 10 seconds over an intermittent submaximal exercise (50% MVC, duty cycle of 5 seconds of contraction and 5 seconds of rest). Maximal knee extension torque, activation level (twitch interpolation technique) and twitch contractile characteristics were measured before and after the experimental protocol. Independent variables were time and group (POW and END). Values obtained for the different testing session were used as dependent variables.
Two groups of subjects volunteered to participate in this study: a group of 8 endurance-trained men (END: distance runners and triathletes, with a mean time spent in training to 7 h·wk−1 during the 6 months preceding the experiments, age 26.9 ± 3.4 years) and a group of 7 power-trained men (POW: 4 professional rugby players who were competing within the French Top 14 senior rugby league and 3 weightlifters with experience in national competitions, age 23.7 ± 3.1 years). The sample size was chosen as sufficient to detect significant differences between the means, for each dependent measure, with α = 0.05 and statistical power = 0.9. In POW group, rugby players were engaged in a structured weight-training program (bench press, squat movements) and weightlifters performed Olympic lifts, squats, and heavy periodized training. The 2 groups had the same average age, but body mass was significantly higher in the POW group (Table 1, p < 0.05). All subjects had been training regularly for more than 5 years and participated in competitions at the national or international level. All were informed of the experimental protocol and the conditions of study participation (no physical effort the day before and the day of the tests, no caffeine or alcohol consumption 4 hours before the tests), but they were not aware of the aims and hypotheses of the study. Each subject gave their written informed consent before beginning the tests. The study procedures complied with the Declaration of Helsinki on human experimentation and were approved by the local Ethics Committee.
The subjects reported to the laboratory 24 hours prior to the experimental day. This visit was used as an initial accommodation and testing session in which they became accustomed to neurostimulation and practiced the protocol. During this first session, subjects performed a standardized warm-up (3) (5 minutes at 2 watts.kg−1 of body mass on an electromagnetic-braked ergocycle [Ergoselect 100 P, Ergoline, Germany] with a pedaling frequency ranging between 60 and 80 rev·min−1) followed by several standardized vertical jump tests (2 squat jumps, SJ, and 2 counter movement jumps, CMJ, with a 90° knee angle and with 1 minute of rest between jumps) to evaluate lower limb explosiveness according to Bosco and Komi (4). The twitch maximal rates of torque development (MRFD) and relaxation (MRFR) were evaluated from neurostimulation evaluation (see below) 5 minutes after the vertical jumps. The height obtained while jumping, MRFD, and MRFR (Table 1) were taken as indices of explosiveness and made it possible to confirm the initial selection of subjects in each group on the basis of their training background. POW had significantly higher vertical jump performances than END (SJ, p < 0.01; CMJ, p < 0.05, t-test), as well as greater MRFD and MRFR values (p < 0.05 and p < 0.01, respectively).
Before the experimental protocol on the experimental day, the subjects performed the same 5-minute standardized warm-up that during the first session. The experimental protocol comprised the following: (a) a first sequence of neuromuscular tests (pre-tests) including 2 knee extensor MVCs assessment (the highest was used for calculation of the submaximal target force) with 2 paired stimuli (doublets) delivered over the isometric plateau (surimposed doublet) and 2 seconds after each MVC (potentiated doublet), 10 minutes of rest, 3 single stimulations at rest separated by 5 seconds on the femoral nerve; (b) a 10-minute repeated submaximal exercise at 50% of MVC of the right knee extensors with a duty cycle of 5 seconds of contraction and 5 seconds of rest; and (c) a second sequence of neuromuscular tests including 3 single stimulations at rest separated by 5 seconds and 2 knee extensors MVCs with 1 surimposed doublet and 1 potentiated doublet (post-tests). During the submaximal exercise (step 2), single electrically evoked twitch was delivered every 5 seconds (alternatively at rest and at the end of the submaximal contraction). Electrically evoked twitches indicated to them the onset and the offset of the submaximal voluntary contractions and the subjects used visual force feedback displayed on a screen to control the force level for 5 seconds. Each MVC was 5 seconds in duration with a 60-second rest period between each trial. Strong verbal encouragement was given to the subjects throughout the 10-minute exercise time and during each MVC.
Muscle contractile properties and excitability of the knee extensors (VL and RF) were studied by measuring the mechanical and electrophysiological responses induced by electrical stimulation of the femoral nerve. The percutaneous stimulation was carried out using a stimulator with constant current (model Digitimer DS7 AH, Welwyn Garden City, Hertfordshire, England) delivering 1 rectangular voltage pulse (400 volts) of 0.2 ms duration. The interval of the stimuli in the doublet was 10 ms. The femoral nerve was stimulated using a monopolar cathode pressed by an experimenter into the inguinal crease. The site of stimulation was marked on the skin so that it could be repeated after the sustained contraction and between the testing sessions. The anode consisted of an adhesive rectangular electrode of 50 cm2 (Médicompex S.A., Ecublens, Switzerland) located in the gluteal fold opposite the cathode. The optimal intensity of stimulation (i.e., that which recruited all knee extensor motor units) was considered to be reached when an increase in the stimulation intensity (10-mA increments) did not induce a further increase in the amplitude of the twitch torque and the peak-to-peak amplitude of the VL M-wave. During the second testing session, the stimulation intensity applied to the femoral nerve was set at 10% above the optimal intensity in order to prevent a drop in twitch force following problems of repositioning the stimulation cathode during the test (19). The stimulation intensity ranged between 80 and 130 mA, depending on the subject.
Mechanical responses from the electrical stimulation and MVC of the knee extensors were recorded using an isometric ergometer that comprised a stiff chair connected to a load-cell transducer (DEC 60, Captels, France). The strongest leg (right leg in all instances) was stabilized by several semi-rigid Velcro bands just above the malleolus. Extraneous movement of the upper body was limited by 2 crossover shoulder harnesses and a belt across the abdomen. The chest was maintained firmly against the back of the seat by an adjustable Velcro strap. The back formed a 90° angle with the seat. The knee angle was set at 80° (0° = full extension). From the mechanical response obtained at rest (single twitch), the twitch peak torque (Pt), the time to peak torque (TPT), the half relaxation time (HRT), MRFD and MRFR were measured. Evoked twitches (simple) at rest each 10 s during exercise were used to draw the time course of potentiation and fatigue occurrence based on Pt changes over time. Pre- and post-exercise, maximal voluntary activation (VA) was estimated according to the formula: voluntary activation (VA %) = (1 - [superimposed doublet amplitude/potentiated doublet amplitude]) × 100.
Surface EMG activity was recorded via a dedicated acquisition system (MP30, Biopac Systems, Santa Barbara, CA). The EMG signals were amplified (1000×), band pass filtered (30-500 Hz), and sampled at 2000 Hz. After the skin was prepared (shaved, cleaned with 70° alcohol) to decrease cutaneous impedance below 5 kΩ, 3 pairs of surface electrodes with 9-mm diameters (Ag/AgCl, Contrôle Graphique Medical, Brie-Comte-Robert, France) were placed over the belly of the vastus lateralis (VL) and rectus femoris (RF) muscles. The interelectrode distance was maintained constant at 20 mm. The reference electrode was placed on the kneecap of the opposite lower limb. The EMG signal amplitude was quantified by the calculation of the root mean square (RMS) over a 1-second period during the MVC plateau during pre- and post-tests, and over a 3-second median period during the repeated submaximal exercise, for VL and RF. From the EMG recordings obtained at rest (single twitch), the peak-to-peak M-wave amplitude (mV), duration (s), and area (mV·ms) were measured for both VL and RF. RMS EMG values were then normalized to the M-wave area for the VL and RF muscles so as to obtain the RMS/M ratio.
Data are presented as means of each group ± standard deviation (SD) unless specified. During the exercise, the values of the various measured parameters (RMS/M, M-wave area, Pt, and TPT) were averaged on 3 successive contractions (30-second duration) and then expressed as a function of the first contraction. We systematically checked the adjustment of the variables to the normal law (Kolmogorov-Smirnov test) as well as the homogeneity of the variances. When necessary, a nonparametric test was used. Variables to determine the explosiveness of subjects (SJ, CMJ, MRFD, and MRFR), as well as body mass, height, and age were analyzed using a t-test. Pt, TPT, HRT, MRFD, MRFR, VA, MVC, RMS/M, and M-wave (amplitude, duration and area) for VL and RF were analyzed using a 2-way analysis of variance: a group factor (END vs. POW) and a time factor with repeated measurements. When a group, time, or interaction effect was established, Newman-Keuls post-hoc tests were carried out to locate the effects. Statistical significance was set to p ≤ 0.05. To assess for within-day reliability of the dependent variables, intraclass correlations coefficients (ICCs) were calculated between the 3 Pt measures and the 2 MVC trials; ICC ranged from 0.932 to 0.988.
Prefatigue Testing Sequence
Maximal voluntary contraction, twitch contractile properties and associated M-waves delivered on relaxed muscle for both groups are presented in Table 2. MVC of the knee extensors differed significantly between groups (p < 0.001) but not when MVC was normalized to the body mass of the subject (p = 0.3). POW presented significantly higher Pt values than END (43.4 ± 9.5 N·m vs. 30 ± 5.9 N·m, p < 0.001). MRFD and MRFR were significantly higher in POW than END (p < 0.05 and p < 0.01, respectively). No difference between groups was observed in M-wave parameters (amplitude, duration and area), VA, the RMS/M ratio for VL and RF, TPT and HRT. The ICC was 0.932 between the 2 MVC trials and 0.998 between the 3 Pt measures.
As indicated in Figure 1, Pt time courses were different between END and POW (F = 20.3, p < 0.001, statistical power = 0.99). At 1 minute of exercise, Pt was similar (+53% and +52% for POW and END, respectively; p < 0.001) but differed afterwards: Pt in END still increased at 1.5 minutes (+56%) and remained high until the end of exercise, whereas Pt in POW decreased significantly from 5.5 minutes (−30% at the end of exercise, p < 0.001). TPT values changed differently between groups (F = 4.5, p < 0.001, statistical power = 0.99, Figure 2A). In END, TPT decreased significantly throughout exercise (p < 0.001) while in POW, TPT was significantly below the baseline value only between 1 minute and 4 minutes (p < 0.01). The M-wave area of VL and RF presented no differences during exercise and between groups (Figure 2B, C).
There was no significant group × time interaction for the respective evolution of the VL and RF RMS/M ratios. The VL RMS/M ratio was significantly higher than the baseline value from 7 minutes of exercise for the pooled subjects (p < 0.05) while the RF RMS/M ratio did not present significant changes during exercise.
Postfatigue Testing Sequence
There was a significant reduction in MVC of the knee extensors after exercise in the 2 groups (F = 31.4, p < 0.001, statistical power = 1.00, Table 2). This loss of force was significantly greater (p < 0.001) in POW (−36.2 ± 8.4%) than in END (−15.3 ± 9.2%). There was no significant effect of exercise or group on VA. However, the VL and RF RMS/M ratios significantly decreased after exercise for the pooled subjects (−20.6 ± 19.6%, p < 0.01 and −17.9 ± 14.5%, p < 0.05, VL and RF, respectively).
Pt values were different after exercise between END and POW (F = 19.1, p < 0.001, statistical power = 0.983). Pt values increased significantly (+28.2 ± 28.4%, p < 0.05) after exercise in END, whereas they decreased significantly in POW (−27.7 ± 18%, p < 0.01). TPT values were also different between groups (p < 0.05). TPT in END was shorter after exercise (−23.7 ± 8.5%, p < 0.001), whereas there was no TPT change in POW. There was no significant effect of exercise or group on HRT values. MRFD and MRFR were modified significantly following exercise (p < 0.01, statistical power = 0.937 and p < 0.001, statistical power = 0.982, respectively). A significant rise in MRFD (+63.3 ± 46.4%, p < 0.01) and MRFR (+32.2 ± 33.4%, p < 0.05) was observed in END. In POW, exercise led to a nonsignificant reduction in MRFD (p = 0.08) and a significant reduction in MRFR (−33.5 ± 20.5%, p < 0.01). There was no significant effect of exercise or group on M-wave amplitude, duration or area for the VL and RF muscles.
The objective of our study was to investigate the hypothesis that potentiation, as measured primarily by increased Pt during the submaximal exercise protocol, would be sufficient to offset the development of fatigue in endurance-trained athletes but not in power-trained athletes. We provided a brief rest period at regular intervals during the 10 minutes of exercise to monitor the time course of potentiation during intermittent submaximal fatiguing contractions in 2 groups of subjects with different training history. Our main finding was that significant potentiation of Pt observed during the first minutes of submaximal exercise persisted during the remaining exercising period and offset successfully fatigue in END but not in POW athletes.
Interestingly, it appears in Figure 1 that our exercise protocol elicited an identical potentiation early in exercise for both groups, with a peak of potentiation after 5 to 10 submaximal contractions at 50% of MVC. The potentiation was revealed by an increased Pt (+52%) and was accompanied by a shortening in TPT (Figure 2A). This finding is in agreement with past studies (13,14,21). The potentiation of force production is mainly explained by the increase in the sensitivity of skeletal muscle fibers to a weak concentration of calcium driven by the phosphorylation of myosin regulatory light chains (17). Several muscular and neural factors can contribute to the increase in Pt in knee-extensor muscles in POW and END athletes. Many studies (15,20,31) have shown that fast-twitch fibers have a higher capacity of potentiation than slow-twitch fibers. In their protocol, Hamada et al. (15) found a peak of potentiation on the second MVC for the 2 studied groups, but with different amplitudes (fast fibers +126.4% vs. slow fibers +38.2%). The major difference between our study and that of Hamada et al. (15) resides mainly in the intensity of exercise: 50% of MVC over 10 minutes (duty cycle 5 seconds/5 seconds) and 16 MVC (duty cycle 5 seconds/3 seconds), respectively. Indeed, when MVC are used to induce potentiation, the extent of motor unit activation is expected to affect the magnitude of potentiation (31). So this magnitude can be reduced if the subject did not need to activate high threshold motor units composed of fast-twitch muscle fibers. In our study, the submaximal intensity (50% of MVC) could have induced less potentiation in POW, and equivalent to that in END, contrary to a maximal exercise due to similar motor unit recruitment. At 50% of MVC, we reasonably expect that both groups might recruit mainly slow twitch fibers in the same extent, and then had obtained equivalent potentiation. However, the fact that potentiation can occur during submaximal exercise with the knee extensor muscles in humans is supported by Gollnick et al. (12) who observed that fast-twitch fibers are used at lower force levels than generally believed, and by the previous work by Rutherford et al. (27), who also observed potentiation early in repetitive exercise performed at 30% and 45% MVC. In this case, elevated potentiation in END early during exercise appears a rather counterintuitive finding. However, endurance training may increase the content of fast myosin light chains in slow-twitch fibers; the later is an adaptation that could possibly increase the capacity of myosin light chains phosphorylation, the likely mechanism of potentiation (17). Strength training may also increase postactivation potentiation by causing greater hypertrophy of fast-twitch fiber than slow-twitch fiber, which would increase the portion of a muscle composed of fast-twitch fibers. Thus, END and POW athletes may have produced similar increased Pt early during exercise by different training adaptations. Vandervoort et al. (31) have shown that the duration of the conditioning contraction influenced differently slow and fast muscles even for short duration of 5-10 seconds. Therefore, after 1 minute, the peak twitch potentiation could already be influenced by fatigue, especially in POW group.
Our study provided evidence of higher fatigue resistance in END than POW. In POW, a marked reduction in Pt was observed as exercise (and fatigue) progressed, accompanied by a progressive increase in the twitch duration (TPT; Figure 2A), which probably limited the effect of fatigue on the twitch torque production (25). This phenomenon is independent of the phosphorylation of myosin light chains and is another mechanism of potentiation. Rassier and MacIntosh (25) also suggested that this mechanism could result from a reduction in the fusion frequency and an increase in twitch summation. Nevertheless, little by little fatigue in POW gained the advantage over potentiation from the point at which Pt passed under the baseline values (Figure 1). The TPT values continued to increase but were probably insufficient to limit contractile fatigue development as suggested by Pt. Similarly, Behm and St. Pierre (1) found a reduction in Pt and a prolongation in TPT in explosive subjects during repeated submaximal exercise, suggesting impaired excitation-contraction coupling that affects the release of calcium by the sarcoplasmic reticulum and/or the kinetics of formation of actomyosin cross-bridges. The results observed in POW can also be explained by variations in myosin configuration induced by phosphorylation of the regulatory light chains, which modulates cross-bridge functioning and decreases the sensitivity of fatigued muscle to calcium. In contrast to the early phase of exercise, where Pt was potentiated, Pt was observed to be depressed regularly throughout exercise in POW. This indicated that as potentiation decreased in POW, fatigue became conspicuous. Conversely, Pt persisted above the rest values throughout exercise in END, suggesting that potentiation countered well fatigue. The prolonged potentiation in this type of population could be due to sustained phosphorylation of a specific class of myosin light chains caused by the repeated submaximal contractions (30). From ~7 minutes of exercise, the increase in the VL RMS/M ratio (Figure 1) associated with no significant changes in the M-wave properties (Figure 2B) during exercise may suggest an increase in motor unit recruitment to maintain the target force. In the present study, the RMS/M ratio increased early above the first value in POW (2 minutes of exercise) and at the very end of exercise in END. This increase likely compensated for the decrease in Pt in POW to maintain the target force. Similarly, West et al. (32) showed that during a contraction to 30% of MVC maintained for 3 minutes, a concomitant increase in the integrated EMG was observed. As the exercise progressed, the ability to sustain 50% of MVC in the face of developing fatigue could have been mediated primarily by additional compensatory recruitment of active fast-twitch motor units in POW. Fast-twitch fibers possess the potential to contribute to greater low-frequency fatigue (24). In END, it is possible that changes in firing rates, an other control strategy involved during the course of low-frequency fatigue as currently observed during repeated submaximal exercise, reduced fatigue (9). Moreover, it is known that END athletes have a relatively high percentage of type I muscle fibers (12,28), which have greater resistance and can cause less decrease in force production. When potentiation is developing through the early contractions of exercise, the motor units could, for the 50% MVC force level, actually decrease their firing rates; that is, there would be a leftward shift of the force frequency relation. This would provide economies related to maintained membrane excitability (VL M-wave in Figure 2B) and excitation-contraction coupling (Pt in Figure 1). A decrease in motor unit firing rates has been observed in the first several seconds of sustained contractions at a constant force, despite no compensatory recruitment of other motor units; potentiation was suggested to have a role in the decreased firing rate (5).
Finally, we may wonder whether END athletes were really fatigued after the proposed exercise. Immediately postexercise MVC showed a significant loss in END as well as in POW The reduction in maximum muscular force production of the knee extensors (MVC post; Table 2) could have been due to central factors associated with a modification in the central command, and/or peripheral factors in relation to muscle contractile properties (26). After the intermittent submaximal fatiguing exercise, VA remained unchanged in both groups. In POW, the strong depression in Pt observed during exercise and postexercise argued more for peripheral factors explaining fatigue. With regard to the excitability of the sarcolemma, the unchanged values in M-wave (Table 2) indicated that the integrity of the sarcoplasmic reticulum was most likely preserved (32). Thus the impaired cross-bridges and the resulting reduced force (26, present study) would be the principal factors explaining peripheral fatigue in POW. Conversely, in END, the twitch parameters (Pt, TPT, MRFD, and MRFR) after exercise indicated a potentiation still quite present and in line with the Pt values above the resting level throughout exercise.
In the present study, 5 to 10 repetitions of 5-second submaximal contraction have induced similar potentiation in 2 different groups of subjects (END vs. POW). This finding suggests that with submaximal contractions, power and endurance athletes were able to benefit from potentiation in the same extent. The intensity of the preconditioning stimuli could serve to the coach to modulate the extent of potentiation for the subsequent exercise. The enhanced fatigue resistance of endurance athletes allows the potentiating effect to prevail longer over the fatigue effect during all the 10-minute exercise. On the contrary, fatigue appeared in power athletes from 5 minutes of this submaximal exercise. The presence of potentiation in human muscle during repeated moderate-intensity contractions may have important influences during submaximal voluntary exercise in either the absence of the presence of fatigue. The prevailing influence of potentiation on fatigue seems to be specific to the training level of the subject. Thus, postactivation potentiation could be of a great benefit to athletes performing activities such as running, cycling, cross-country skiing, and swimming at submaximal intensities. Endurance performance typically consists of submaximal contractions that are repeated for prolonged periods. From the beginning of performance, the contractions themselves would activate the mechanisms responsible for the postactivation potentiation. The latter may have a special role in compensating for the impaired excitation-contraction coupling that occurs with fatigue. The mechanisms by which training increases postactivation potentiation may differ for endurance and power training.
1. Behm, DG and St. Pierre, DM. Effects of fatigue duration and muscle type on voluntary and evoked contractile properties. J Appl Physiol
82: 1654-1661, 1997
2. Bigland-Ritchie, B, Furbush, F, and Woods, JJ. Fatigue of intermittent submaximal voluntary contractions: central and peripheral factors. J Appl Physiol
61: 421-429, 1986.
3. Bishop, D. Warm up II: performance changes following active warm up and how to structure the warm up. Sports Med
33: 483-498, 2003.
4. Bosco, C and Komi, PV. Mechanical characteristics and fiber composition of human leg extensor muscles. Eur J Appl Physiol Occup Physiol
41: 275-284, 1979.
5. Deluca, CJ, Foley, PJ, and Erim, Z. Motor unit control properties in constant-force isometric contractions
. J Neurophysiol
76: 1503-1516, 1996.
6. Edwards, RHT, Hill, DK, Jones, DA, and Merton, PA. Fatigue of long duration in human skeletal muscle after exercise. J Physiol
272: 769-778, 1977.
7. Fowles, JR and Green, HJ. Coexistence of potentiation and low-frequency fatigue during voluntary exercise in human skeletal muscle. Can J Physiol Pharmacol
81: 1092-1100, 2003.
8. French, DN, Kraemer, WJ, and Cooke, CB. Changes in dynamic exercise performance following a sequence of precontitioning isometric muscles actions. J Strength Cond Res
17: 678-685, 2003.
9. Garland, SJ and Gossen, ER. The muscular wisdom hypothesis in human muscle fatigue. Exerc Sport Sci Rev
30: 45-49, 2002.
10. Garrandes, F, Colson, SS, Pensini, M, Seynnes, O, and Legros, P. Neuromuscular fatigue profile in endurance-trained and power-trained athletes. Med Sci Sports Exerc
39: 149-158, 2007.
11. Gollnick, PD. Metabolism of substrates: energy substrate metabolism during exercise and as modified by training
. Fed Proc
44: 353-357, 1985.
12. Gollnick, PD, Karlsson, J, Piehl, K, and Saltin, B. Selective glycogen depletion in skeletal muscle fibers of man following sustained contractions. J Physiol
241: 59-67, 1974.
13. Hamada, T, Sale, DG, and Macdougall, JD. Postactivation potentiation in endurance-trained male athletes. Med Sci Sports Exerc
32: 403-411, 2000.
14. Hamada, T, Sale, DG, Macdougall, JD, and Tarnopolsky, MA. Postactivation potentiation, fiber type, and twitch contraction time in human knee extensor muscles. J Appl Physiol
88: 2131-2137, 2000.
15. Hamada, T, Sale, DG, Macdougall, JD, and Tarnopolsky, MA. Interaction of fibre type, potentiation and fatigue in human knee extensor muscles. Acta Physiol Scand
178: 165-173, 2003.
16. Hill, CA, Thompson, MW, Ruell, PA, Thom, JM, and White, MJ. Sarcoplasmic reticulum function and muscle contractile character following fatiguing exercise in humans. J Physiol
531: 871-878, 2001.
17. Houston, ME and Grange, RW. Torque potentiation and myosin light-chain phosphorylation in human muscle following a fatiguing contraction. Can J Physiol Pharmacol
69: 269-273, 1991.
18. Krarup, C. Enhancement and diminution of mechanical tension evoked by staircase and by tetanus in rat muscle. J Physiol
311: 355-372, 1981.
19. Martin, V, Millet, GY, Martin, A, Deley, G, and Lattier, G. Assessment of low-frequency fatigue with two methods of electrical stimulation. J Appl Physiol
97: 1923-1929, 2004.
20. Moore, RL and Stull, JT. Myosin light chain phosphorylation in fast and slow skeletal muscles in situ. Am J Physiol Cell Physiol
247: C462-471, 1984.
21. O'Leary, DD, Hope, K, and Sale, DG. Posttetanic potentiation of human dorsiflexors. J Appl Physiol
83: 2131-2138, 1997.
22. Pääsuke, M, Saapar, L, Ereline, J, Gapeyeva, H, Requena, B, and Oöpik V. Postactivation potentiation of knee extensor muscles in power- and endurance-trained, and untrained women. Eur J Appl Physiol
101: 577-585, 2007.
23. Paavolainen, L, Hakkinen, K, Nummela, A, and Rusko, H. Neuromuscular characteristics and fatigue in endurance and sprint athletes during a new anaerobic power test. Eur J Appl Physiol Occup Physiol
69: 119-126, 1994.
24. Rankin, LL, Enoka, RM, Volz, KA, and Stuart, DG. Coexistence of twitch potentiation and tetanic force decline in rat hindlimb muscle. J Appl Physiol
65: 2687-2695, 1988.
25. Rassier, DE and Macintosh, BR. Coexistence of potentiation and fatigue in skeletal muscle. Braz J Med Biol Res
33: 499-508, 2000.
26. Rochette, L, Lepers, R, Brugniaux, J, Maffiuletti, NA, and Millet, GY. Modifications neuromusculaires et cardio-respiratoires induites par un exercice cycliste de longue durée. Sci Mot
45: 85-100, 2002.
27. Rutherford, OM, Jones, DA, and Newham, DJ. Clinical and experimental application of the percutaneous twitch superimposition technique for the study of human muscle activation. J Neurol Neurosurg Pyschiatry
49: 1288-1291, 1986.
28. Tesch, PA and Karlsson, J. Muscle fiber types and size in trained and untrained muscles of elite athletes. J Appl Physiol
59: 1716-1720, 1985.
29. Thorstensson, A and Karlsson, J. Fatiguability and fibre composition of human skeletal muscle. Acta Physiol Scand
98: 318-322, 1976.
30. Vandenboom, R and Houston, ME. Phosphorylation of myosin and twitch potentiation in fatigued skeletal muscle. Can J Physiol Pharmacol
74: 1315-1321, 1996.
31. Vandervoort, AA, Quinlan, J, and Mccomas, AJ. Twitch potentiation after voluntary contraction. Exp Neurol
81: 141-152, 1983.
32. West, W, Hicks, A, Mckelvie, R, and O'Brien, J. The relationship between plasma potassium, muscle membrane excitability and force following quadriceps fatigue. Pflugers Arch
432: 43-49, 1996.
33. Westerblad, H, Duty, S, and Allen, DG. Intracellular calcium concentration during low-frequency fatigue in isolated single fibers of mouse skeletal muscle. J Appl Physiol
75: 382-388, 1993.