Postactivation potentiation (PAP) is often defined as an increase in electrically evoked contractile muscle function after brief maximal conditioning muscle contractions. PAP is often assumed to be mainly induced because of enhancements in the activation of the myosin heads through phosphorylation of their regulatory light chains (
), leading to an increased cross-bridge cycle efficiency and muscle rate of force development at submaximal calcium concentrations ( 23,24,31 ). Enhancements in such mechanisms, after conditioning, have been found to be correlated with the behavior of evoked contractions (e.g., twitch rate of torque development [RTD 5,23 TW]) ( ). PAP has gained substantial interest in the past few years mainly because of the significant performance enhancements reported in explosive tasks and the possibility that these could be applied by athletes to improve training efficiency and performance ( 27 ). Out of the contractile variables shown to be affected by PAP, rate of torque development (RTD) seems to be better related to sport performance than peak torque (PT) ( 24,30 ), and its analysis at different time phases of the rising torque curve could provide valuable information ( 14 ), especially if analyzed in a condition that somehow mimics the neural and mechanical characteristics of a movement ( 14 ). However, effects on the RTD could also be related to changes in the force transfer due to tensile shifts in the muscle tendon unit (MTU) (i.e., stiffness) ( 14,26,28 ). The present study aimed to investigate the effects of a 6-second maximal voluntary isometric contraction (MVIC) on RTD and neuromuscular efficiency at different portions of the rising torque curve in maximal voluntary concentric plantar flexions (MV 4,29 CC) while considering possible tensile shifts of the plantar flexor MTU and changes in evoked twitch characteristics. Methods
Experimental Approach to the Problem
The current study involved 2 different testing sessions, both of which included a 6-second MVIC as PAP induction conditioning contraction. In addition, both sessions were conducted as preconditioning and postconditioning repeated measures with baseline time series measurement. In the first session, acute effects of the conditioning were assessed during repeated MV
CC plantar flexions performed at 60°·s −1 throughout a postconditioning period of 15 minutes (900 seconds), at 30, 90, 180, 300, 480, and 900 seconds (0.5, 1.5, 3, 6, and 15 minutes, respectively). A 60°·s −1 angular joint velocity was chosen because investigations at our laboratory have previously detected substantial PAP effects on twitch contractile properties during ongoing muscle shortening at that velocity ( ), and previous investigations have only measured effects on MV 8 CC at very low velocities (30°·s −1) and high velocities (180°·s −1) ( ). No information seems to exist at the moderate velocity range. 6
An additional session was performed to investigate PAP through evoked supramaximal contractions (i.e., twitches). As Baudry and Duchateau (
) suggested, without proper assessment of twitch PAP, “It is difficult to associate these improvements (i.e., voluntary sport related task performance) to PAP.” Twitches were induced at identical time points and covered the entire time range chosen in the voluntary assessment session. 2
The timing and durations of the assessments were chosen per recommendations from previous investigations. That is, reports of maximal twitch PAP immediately after conditioning (
), and delayed maximal PAP (7–10 minutes) in explosive voluntary tasks ( 2,8 ), with agreement that both twitch and voluntary potentiation should be nearly insignificant after 15 minutes. The neuromuscular efficiency was measured as the ratio between the plantar flexors muscle activity and torque development ( 30 ) and aimed for a visualization of possible PAP effects in the absence of visible torque enhancements, as the system may compensate for the contractile enhancements due to PAP by a derecruitment of motor units ( 9,18 ). Furthermore, shifts in the tensile properties could affect or help to explain twitch and voluntary post conditioning behavior. Therefore, we evaluated possible tensile shifts after the conditioning protocol and each repeated MV 22 CC through a rather practical but still a valid method to access overall MTU stiffness ( ). 19 Subjects
Nine physically active university students (3 women and 6 men) participated in the study (mean
± SD age 24.0 ± 2.7 years; height 176.0 ± 10.8 cm; mass 75.6 ± 12.5 kg; BMI 24.2 ± 1.5 kg·m −2). All participants were free from previous injury of the right ankle. None of the participants were under 18 years of age. Participants were informed of the objectives of the study and signed an informed consent form. The participants were further instructed that they would visit the laboratory on several occasions and that they were to continue their personal training regimen but abstain from exercising on the day of the experiment. The study was approved by the regional ethics committee of Stockholm and all procedures adhered to the Declaration of Helsinki. Procedures
Participants warmed up by cycling for 5 minutes on a Monark cycle ergometer (model 828E) with a perceived exertion rating ranging between 11 and 12 on the Borg's scale. After this, the skin over the belly of the soleus (SOL), medial gastrocnemius (MG), lateral gastrocnemius (LG), tibialis anterior (TA), and the area covering the head of the fibula and medial femoral head were shaved and cleaned to minimize impedance and noise during surface electromyography (sEMG) signal recordings. Pairs of circular Ag-AgCl electrodes (Ambu Blue Sensor; Medicotest,Ølstykke, Denmark) of 7-mm diameter were then placed over the bellies of the mentioned muscles with an approximate distance of 2.5 cm between the electrodes. Two additional ground electrodes were placed over the fibula and femoral head.
Subsequently, the participants were placed in an isokinetic dynamometer (Isomed 2000; D&R Ferstl Gmbh, Henau, Germany), in the prone position with arms and hands beside their body. The knee was kept fully extended with the right ankle joint at 90° (e.g., neutral position). After alignment of the ankle joint axis with the rotational center of the dynamometer shaft, the right foot was securely strapped to a custom-made footplate, whereas the rest of the body was properly fixed with the appropriate straps for upper body, hip, and legs. The range of motion testing and gravity correction was then performed according to the isokinetic dynamometer software and manufacturer's guidelines. Such procedures were repeated in both sessions (i.e., supramaximal twitch testing session and maximal voluntary concentric session).
In the first session, MV
CC were performed before and after conditioning MVIC. In this session, the isokinetic dynamometer moved the ankle joint from 20° dorsiflexion to 20° plantar flexion at an angular velocity of 60°·s −1 and automatically repositioned the foot back to 20° dorsiflexion at an angular velocity of 5°·s −1. At the most dorsiflexed position and after instructing the participant to remain relaxed, the passive plantar flexor torque was measured in this position. The isokinetic dynamometer was then set to initiate the ankle rotation of 60°·s −1 when the plantar flexor torque exceeded 105% of the passive plantar flexor torque. Such calculations of and setup of the triggering levels were performed before the main testing protocol during a familiarization session. After a 5-minute rest, the participants were asked to perform 3 explosive MV CC at 60°·s −1 (control trials), followed by a 6-second MVIC conditioning contraction, then another 6 explosive MV CC. MV CC occurred at 30, 90, 180, 300, 480, and 900 seconds after conditioning MVIC. Custom-made software triggered the stimulator directly from Spike2 software (Spike2, version 7.0; CED, Cambridge, England), and custom-made sound files produced using Audacity open source software version 2.0.3 (open source) ensured that MVIC duration and timing for evoked and voluntary concentric contraction were consistent within and between sessions.
Within 2–6 days of the first session, a second session was performed investigating supramaximal-evoked contractions (i.e., twitches) before and after conditioning. In this session, during the rest phase that followed the participants' warm-up, an anode (rectangular 100 × 50-mm carbon rubber electrode; Cefar Medical, Malmö, Sweden) was positioned on the anterior surface of the knee, proximal to the patella, and taped in place. A custom-made stimulation pen was then used to localize the optimal location for stimulating the tibial nerve in the popliteal fossa. To this end, single rectangular pulses (1 ms) were delivered through the stimulator pen by a constant current stimulator (Digitimer, model DS7A; Hertfordshire, United Kingdom). The pen position resulting in the largest plantar flexor twitch amplitude was defined as the optimal stimulation point. A small cathode electrode was placed over this optimal stimulation point and subsequently used as a cathode in the electrical stimulation. Subjects were then familiarized with submaximal electrical stimulus. A gradual increase in the current intensity was performed in steps of 5-milliampere (mA) increments until the compound muscle action potential (i.e., SOL M-wave) and the mechanical twitch reached their maximal values, showing no further increases in torque despite further increases in intensity. Maximal stimulation intensity was then increased by a further 20% to the supramaximal intensity used in the subsequent protocol. After a 5-minute rest, twitch PAP assessments were performed. This involved 3 supramaximal stimulations (control trials), followed by a 6-second MVIC conditioning contraction and 9 subsequent supramaximal stimulations at 5, 30, 60, 90, 120, 180, 300, 480, and 900 seconds after the 6-second contraction. The timing of the electrical stimulation inducing the twitches and timing to initiate the voluntary tasks were preprogramed. The stimulation was therefore always performed at identical time points after the 6-second MVIC.
Data Acquisition and Analysis
In both sessions, sEMG signals were amplified 1,000 times for MG, LG, and TA, and to allow better M-wave assessments, 200 times for SOL (NL 824, Digitimer; United Kingdom), and then filtered with a band-pass filter (30 Hz
−1 kHz with a 50 Hz notch filter) (NL 125, Digitimer). Ankle joint torque, position, and angular velocity of the foot were measured and controlled by the isokinetic dynamometer. Analog torque signals were converted to digital signals and sampled, together with the joint position and sEMG signals, at a sample rate of 5 kHz by a power 1,401 (CED; Cambridge, England) in Spike2 software (Spike2, version 7.0; CED, Cambridge, England). The torque signal was smoothed by a time constant of 0.002 seconds before subsequent analysis.
TW was calculated as the peak of the first derivative of torque development (dF/dt), as previously performed by Baudry and Duchateau ( ) and Gago et al. ( 2 ). RTD from MV 8 CC (RTD CC) was calculated as the slope of the rising portion of the torque-time curve during the 50–100 ms, 100–200 ms, 50–200 ms, and 0–200 ms phases. The onset of torque production was carefully inspected and visually determined because it has been suggested that the use of automated procedures may lead to inaccurate placement of the torque onset cursor ( ). PT from MV 25 CC (PT CC) was defined as the maximum torque value achieved during each concentric plantar flexion.
After each concentric plantar flexion, the foot was passively repositioned to 20° dorsiflexion by the isokinetic dynamometer at an angular velocity of 5°·s
−1. During this phase, passive torque values were obtained in 3° increments from 0 to 18° into dorsiflexion using a Spike2 custom-written script. Torque-angle data were exported to Origin software (Version 9.0; OriginLab, Northampton, MA, USA) and curve fitted using a second-order polynomial function, as previously described by Nordez et al. ( ). Passive stiffness index (SI) was then calculated as the slope of the torque-angle linear relationship according to Nordez et al. ( 19 ). 19
Root-mean-square values were computed from the SOL, MG, and LG sEMG raw signals and normalized by their maximal values obtained in the same time frame used when retrieving MVIC mean torque values (i.e., 3 seconds either side of the MVIC PT). The normalized values for MG, LG, and SOL were then combined and averaged to represent the entire triceps surae muscle activation (EMG
TS), as previously described by Kay and Blazevich ( ). In addition, a ratio between EMG 12 TS and RTD CC was calculated to provide a neuromuscular efficiency index ( ). The ratio was calculated as EMG 9,18 TS values divided by RTD CC values at identical phases of the maximal concentric contraction torque rising curve (i.e., 50–100 ms, 50–200 ms, 100–200 ms, and 0–200 ms). An increase in EMG TS/RTD CC implies a decrease in neuromuscular efficiency. Statistical Analyses
Data were analyzed using IBM SPSS Statistics (Version 22; IBM Corp., Armonk, NY, USA). Data distribution was analyzed using the Shapiro-Wilk test. Intraclass correlation coefficients (ICC
3,1) were used to analyze the consistency of the control trials for all parameters. In addition, typical error as a coefficient of variation (CV), expressed in percent, was calculated between control trials for the main parameters to quantify typical measurement error and thus lowest meaningful effect. ICC 3,1 and CV were calculated using Will Hopkins Spreadsheets for the analysis of validity and reliability ( ). 11
Mean values of torque and duration of the conditioning MVICs conducted in both the twitch and voluntary trials were compared using a paired sample student t test. Separate 1-way repeated measures ANOVAs (with the factor Time) were performed for the dependent variables RTD
TW, PT CC, RTD CC, EMG TS, and EMG TS/RTD CC at 50–100 ms, 50–200 ms, 100–200 ms, and 0–200 ms phases. Wherever a significant main effect was found, an LSD post hoc test was applied, and on sphericity violation, a Greenhouse-Geisser correction was used. Differences were considered as significant at p ≤ 0.05. ICC 3,1 values were considered as having good or excellent consistency with values of 0.6–0.8 and 0.8–1, respectively. All values are reported as mean ± SD. Results
No significant differences were found between conditioning MVIC torque and duration in the twitch session (194.3 ± 55.0 N·m; 6.44 ± 0.3 seconds) or in the MV
CC session (201.0 ± 61.5N·m; 6.36 ± 0.2 seconds) with T values from T = −0.64; p = 0.542 and T = −1.45; p = 0.186 for time and mean torque, respectively. In general, ICC 3,1 indicated excellent consistency between control trials ( N = 3) for all the analyzed parameters (RTD Tw, PT CC, and RTD CC, EMG TS and EMG TS/RTD CC ratio at the different rising torque curve phases as well as SI) with values ranging from 0.86 to 0.99. CV values were, in general, lower than the significant enhancements (values provided individually in the result section). Twitch Rate of Torque Development (RTD
A significant main effect of time was found for RTD
TW ( F 9,72 = 52.007, p = 0.00). Post hoc analysis showed that compared with control values (252.51 ± 69.6 N·m·s −1), the RTD TW was significantly ( p < 0.01) enhanced immediately at 5 seconds (404.39 ± 120.3 N·m·s −1), up to 480 seconds (267.19 ± 71.5 N·m·s −1) after a 6-second MVIC. This corresponds to a significant increase from baseline by 59.7% at 5 seconds and 6.0% at 480 seconds ( Figure 1), with a CV of 1.9%. Figure 1.:
Twitch rate of torque development (RTD
TW) % changes from baseline values in the control trials (Cont.) to different times after the conditioning MVIC. Significant ( p ≤ 0.05) differences in RTD TW between control to specific time points after MVIC are indicated with a #. Peak Concentric Contraction Torque (PTCC)
A significant main effect of time was found for PT
CC ( F 6,48 = 2.458, p = 0.037). Post hoc analysis showed that compared with control values (99.78 ± 27.6 N·m), the PT CC was significantly ( p ≤ 0.05) enhanced at 90 seconds (105.47 ± 32.6 N·m), 180 seconds (105.81 ± 33.6 N·m), and 300 seconds (105.62 ± 33.8 N·m) ( Table 1) after a 6-second MVIC, reflecting 5.7, 6.0, and 5.9% increases from the baseline (graphic representation in Figure 2) at the respective time points. CV was 4.6%. Table 1.:
Voluntary maximal plantar flexion peak torque (PT
CC) and rate of torque development (RTD CC) during different phases of the torque rising curve (50–100, 100–200, 50–200, and 0–200 ms).* Figure 2.:
Raw data representation of a supramaximal twitch before (Cont.) and at 90 seconds after a 6-second conditioning MVIC. Note that potentiation (i.e., difference between control [full line] and after MVIC values [dashed line]) was present both in evoked (left side) and voluntary contractions (right side).
Concentric Contraction Rate of Torque Development (RTD
A significant main effect of time was found in RTD
CC for the 100–200 ms ( F 6.48 = 2.981, p = 0.015), 50–200 ms ( F 3.21 = 4.648, p = 0.014), and 0–200 ms ( F 3.22 = 5.208, p = 0.009) phases of the MV CC ( Table 1). Post hoc testing revealed significant ( p ≤ 0.05) increases in RTD CC at the 100–200 ms, 50–200 ms, and 0–200 ms phase from 90 to 300 seconds after MVIC (raw values in Table 1). These enhancements reflect a 7.3% increase from the baseline in the 100–200 ms phase at 180 seconds after MVIC (CV 8.0%), an 8.1, 6.9, and 6.8% increase in the 50–200 ms phase at 90, 180, and 300 seconds after MVIC, respectively, (CV 5.8%) and a 9.5, 8.6, and 9.4% in the 0–200 ms phase at 90, 180, and 300 seconds after MVIC, respectively (CV 4.6%). A graphical representation of the torque curve before and after conditioning is provided in Figure 2. Combined Triceps Surae Electromyographic (EMG
A significant main effect of time was found for the EMG
TS ( F 6,48 = 3.8, p ≤ 0.05). Post hoc analysis detected a significant EMG TS decrease in the 50–100 ms phase at 180 seconds (116.80 ± 29.35; p = 0.010) and at 480 seconds (109.42 ± 23.57; p = 0.001) when compared with pre-MVIC values (129.52 ± 26.21). These results reflect a muscle activity decrease from the baseline of 9.8 and 15.5%, respectively, after MVIC with a CV of 8.2%. No other significant differences were found ( p ≥ 0.05) ( Figure 3). Figure 3.:
Normalized triceps surae activation (EMG
TS) changes from baseline values in the control trials (Cont.) to different time points after the conditioning MVIC. Significant ( p ≤ 0.05) differences in EMG TS between control and post-MVIC values within different portions of the rising torque curve (50–100 ms [white rectangle], 100–200 ms [black rectangle], 50–200 ms [gray rectangle], and 0–200 ms [striped rectangle]) are indicated with a #. Neuromuscular Efficiency (EMGTS/RTDCC)
A significant main effect of time was found in the EMG
TS/RTD CC ratio ( F 6,48 = 3, p = 0.014 for 50–200 ms and F 6,48 = 4.2, p = 0.002 for 0–200 ms). Post hoc analysis detected a significant EMG TS/RTD CC ratio decrease in the 50–200 ms phase at 90 seconds (0.26 ± 0.08; p = 0.009), 180 seconds (0.27 ± 0.10; p = 0.010), and 480 seconds (0.26 ± 0.09; p = 0.004) as compared to pre-MVIC values (0.30 ± 0.10). These results reflect a decrease from the baseline ranging from 8.8 to 12.4%, after MVIC with a CV of 8.9%. Furthermore, in the 0–200 ms phase the EMG TS/RTD CC ratio decreased significantly from the control values at 90 seconds (0.29 ± 0.09; p = 0.002), 180 seconds (0.29 ± 0.11; p = 0.002), 300 seconds (0.30 ± 0.12; p = 0.026), and 480 seconds (0.30 ± 0.10; p = 0.001) after MVIC. These results reflect an EMG TS/RTD CC ratio decrease (i.e., an increase in neuromuscular efficiency) from the baseline ranging from 8.8 to 12.1% after CC with a CV of 7.8%. No significant changes were found in the 50–100 and 100–200 ms phases ( p ≥ 0.05) ( Figure 4). Figure 4.:
Ratio between normalized triceps surae activation (EMG
TS) and voluntary rate of torque development (RTD CC). Changes from baseline values in the control trials (Cont.) to different time points after the conditioning MVIC are represented. Significant ( p ≤ 0.05) differences in EMG TS/RTD CC ratio between control and post-MVIC values within different portions of the rising torque curve (50–100 ms [white rectangle], 100–200 ms [black rectangle], 50–200 ms [gray rectangle], and 0–200 ms [striped rectangle]) are indicated with a #. Stiffness Index (SI)
No significant changes (
F 3,26 = 2.637, p = 0.067) were found between the control values (0.0854 ± 0.05 N·m −2) and the post-MVIC values ( Figure 5). Figure 5.:
Stiffness index (SI) during different times after MVIC conditioning. No significant (
p > 0.05) changes occurred after the 6-second MVIC conditioning. Discussion
In the present study, PT
CC and RTD CC were significantly enhanced after a 6-second MVIC. Furthermore, in an identical time frame (90–300 seconds after MVIC), RTD TW was also potentiated. RTD CC and neuromuscular efficiency were significantly enhanced in the 50–200 and 0–200 ms phases of the rising torque curve. Interestingly, no significant changes were found in the tensile properties of the plantar flexor MTU.
A recent study performed by Fukutani et al. (
) found that after a 6-second MVIC conditioning, enhancements in the plantar flexors twitch PT were maximal immediately after conditioning and remained above baseline up to 5 minutes (300 seconds) after conditioning. In their study, PT 6 CC was potentiated only if the task was performed at a sufficiently high joint angular velocity (i.e., 180°·s −1 as opposed to 30°·s −1). Our results show that PAP after an identical conditioning protocol enhanced PT CC also at a moderate ankle joint angular velocity (i.e., 60°·s −1). The increases in PT CC observed in our study (5.7–6.0%) were slightly lower than the 7% reported by Fukutani et al. ( ). 6
The duration of PAP effects in the PT
CC performed at 60°·s −1 were longer in our study than previously reported at 180°·s −1 by Fukutani et al. ( ) (5 seconds) and Miyamoto et al. ( 6 ) (60–180 seconds). According to the results of Miyamoto et al. ( 15 ), plantar flexion contractions at 180°·s 15 −1 could by themselves elicit a nonsignificant degree of PAP. At the moderate joint angular velocities (e.g., 60°·s −1) used in the current study, such conditioning effects from the test contractions might be even larger. A plantar flexor MVcc at 60°·s −1 might thus be sufficiently sensitive to benefit from PAP effects while also providing ample contraction duration to induce a degree of PAP that would prolong the duration of the PAP effects.
In the current study, the contractile properties of the twitch showed their peak potentiation immediately after conditioning, whereas the voluntary contraction displayed its peak potentiation somewhat later. A different delay in the maximal PAP effects between twitches and voluntary contractions has been previously noted (
). Such delay has been suggested to be related to a brief period of fatigue occurring immediately after an MVIC ( 1,2,16 ) or due to a saturation of free cystolic calcium concentration occurring immediately after an MVIC ( 16 ). This would limit and delay PAP effects because enhanced myosin regulatory light chains phosphorylation is known to maximize force production only at submaximal calcium concentrations ( 1–3 ). Other mechanisms such as an interference effect from changing voluntary task from the isometric to the dynamic action are also possible, and investigating the mechanisms of the shift in timing between twitches and voluntary contractions is outside the scope of the current study. 3,23
Potentiation amplitude in RTD
TW and RTD CC were lower in our study (7.3 and 9.5% respectively) than previously reported by Baudry and Duchateau ( ) (9 and 24% respectively). However, the duration of the effects during our maximal concentric contractions (90–300 seconds) were longer than the ones reported during maximal isometric contractions (5–120 seconds) by Baudry and Duchateau ( 2 ). The greater PAP duration in concentric compared with isometric voluntary contractions might be related to the fact that PAP effects on RTD are prolonged when contractions are performed undergoing muscle shortening ( 2 ). 8
CC was significantly potentiated in the 100–200, 50–200, and 0–200 ms but not in the 50–100 ms phase. This might suggest that PAP effects on RTD might be more relevant in tasks where force production time exceeds 100 ms. In addition, a significant increase (8.8–12.4%) in the plantar flexors' neuromuscular efficiency (i.e., EMG TS/RTD CC ratio decrease) was also found in the 50–200 and 0–200 ms phase after conditioning ( Figures 3 and 4). In endurance athletes, Morana and Perrey ( ) found that although twitch PT potentiation increased, after each bout of an intermittent knee extension task (at 50% of the MVIC), for up to 2 minutes (120 seconds), the electromyographic amplitude of the vastus lateralis decreased from the 1st to the 3rd minute. As pointed out by Morana and Perrey ( 17 ), these types of results suggest an increase in muscle contraction economy, which could have implications for movement economy. The significant enhancements in neuromuscular efficiency occurring in the absence of torque enhancements (compare RTD 17 CC and EMG TS/RTD CC in the 50–200 and 0–200 ms phases at 480 seconds after MV CC) highlight that PAP effects are not limited to visible enhancements of voluntary force production.
Changes in both RTD
CC and EMG TS/RTD CC ratio in the 50–100 ms phase were only insignificant after the Greenhouse-Geisser correction that was performed because of a sphericity violation. The lack of significant changes in the 50–100 and 100–200 ms might also have resulted from lower reliability at these intervals and suggest that longer time frames should be used. Further research is, therefore, needed to confirm that there was truly no potentiation occurring in the early phase of the voluntary contraction.
RTD enhancements in the initial phase of the voluntary RTD (25–75 ms) have been linked to neural factors (
), thus could reflect neural facilitation mechanisms. However, we believe that such mechanisms are unlikely to be decisive in the overall effects of PAP in RTD, as the RTD 14 CC potentiation effects in the 50–200 and 0–200 ms phases were similar, independently of the inclusion or exclusion of the first 50 ms ( Table 1). Furthermore, Hodgson et al. ( ) reported that although PAP was seen in twitch and isometric RTD after conditioning, no significant changes were found in the H-reflex (normalized to M-wave), which led the authors to conclude that PAP of the RTD was unrelated to optimization of neural excitability ( 10 ). 10
Although tensile properties of the MTU may affect contractile measures, variables such as stiffness are often neglected in PAP-related studies. We initially hypothesized that repeated maximal plantar flexions, after a 6-second MVIC conditioning, could result in sufficient mechanical stress and strain on MTU components to reduce stiffness (
) and negatively affect RTD 13,20 CC and PT CC values ( ). Previous PAP-related studies reported no significant changes in the Achilles tendon stiffness or muscle pennation angle after a 6-second MVIC conditioning ( 4 ). In support of these, the present study found no significant changes in plantar flexor passive SI. Passive SI has been previously shown to be a valid alternative when investigating the overall stiffness of the MTU ( 7,21 ). 19
In conclusion, we observed significant enhancements in PT, RTD, and neuromuscular efficiency during maximal voluntary plantar flexions performed at a functionally relevant velocity. PAP effects on voluntary concentric contraction were significant during a time frame where twitch contractile properties were also potentiated. The lack of changes in SI and RTD
CC in the early phase of the rising torque curve reinforces the idea that the acute effects of the conditioning contraction might be mainly related to mechanisms within the muscle. Practical Applications
Our findings suggest that a 6-second conditioning contraction induced substantial enhancements in peak torque, rate of torque development, and neuromuscular efficiency during repeated maximal voluntary plantar flexions. Such information could be pertinent for long, high, and triple jump athletes aiming to enhance force development during repeated jumps at practice or competition. Furthermore, such information might be relevant when aiming to maximize strength and power development in populations that require training at lower angular speeds such as master and veteran athletes. Furthermore, knowing that performance can also be enhanced at a moderate angular velocity (60°·s
−1) suggests that a strong conditioning contraction might be useful for a variety of velocity resistance training strategies. Using a 6-second conditioning contraction to enhance muscle contractility may be especially practically appealing in a situation where there is an unexpected delay between the athletes preplanned warm-up and the start of the event. Acknowledgments
The authors wish to acknowledge the financial support from the Swedish National Center for Research in Sports (CIF) and also to thank the Portuguese Fundação para a Ciência e Tecnologia (FCT), for the PhD Grant (SFRH/BD/103572/2014).
The authors declare no conflict of interest. The results of this study do not constitute an endorsement by the authors or the National Strength and Conditioning Association.
Research was conducted at the Swedish School of Sport and Health Sciences, GIH, Stockholm, Sweden.
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