University of Groningen Effects of lower extremity power training on gait biomechanics in old adults Beijersbergen, Chantal

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Effects of lower extremity power training on gait biomechanics in old adults Beijersbergen, Chantal

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Chapter 6

Power training-induced

increases in muscle activation

during gait in old adults

Chantal Beijersbergen

Urs Granacher

Martijn Gäbler

Paul DeVita

Tibor Hortobágyi

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88

Abstract

Introduction/Purpose: Aging modifies neuromuscular activation of agonist and antagonist muscles during walking. Power training can evoke adaptations in neuromuscular activation that underlie gains in muscle strength and power but it is unknown if these adaptations transfer to dynamic tasks such as walking. We examined the effects of lower extremity power training on neuromuscular activation during level gait in old adults. Methods: Twelve community dwelling old adults (age ≥ 65 years) completed a 10-week lower extremity power-training program and thirteen old adults completed a 10-week control period. Before and after the interventions, we measured maximal isometric muscle strength and electromyographic (EMG) activation of the right knee flexor, knee extensor, and plantarflexor muscles on a dynamometer and we measured EMG amplitudes, activation onsets and offsets, and activation duration of the knee flexors, knee extensors, and plantarflexors during gait at habitual, fast, and standardized (1.25 ± 0.6 m/s) speeds. Results: Power training-induced increases in EMG amplitude (~41%; 0.47 ≤ d ≤ 1.47; P ≤ 0.05) explained 33% (P = 0.049) of increases in isometric muscle strength (~43%; 0.34 ≤ d ≤ 0.80; p≤0.05). Power training-induced gains in plantarflexor activation during push-off (+11%; d = 0.38; P = 0.045) explained 57% (P = 0.004) of the gains in fast gait velocity (+4%; d = 0.31; P = 0.059). Furthermore, power training increased knee extensor activation (~18%; 0.26 ≤ d ≤ 0.29; P ≤ 0.05) and knee extensor coactivation during the main knee flexor burst (~24%, 0.26 ≤ d ≤ 0.44; P ≤ 0.05) at habitual and fast speed but these adaptations did not correlate with changes in gait velocity. Conclusion: Power training increased neuromuscular activation during isometric contractions and level gait in old adults. The power training-induced neuromuscular adaptations were associated with increases in isometric muscle strength and partly with increases in fast gait velocity.

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Chapter 6

6.1. INTRODUCTION

Walking speed in old age is an important predictor of many adverse outcomes in medical, cognitive, and motor function. For example, old adults over age 65 walking at a habitual speed ≥ 1.0 m/s tend to be healthier and have a higher functional status than those who walk slower [1]. Conversely, old adults who walk at a habitual speed slower than 0.6 m/s have greater risks for impaired mobility, falls, and even early mortality [1,2]. As the number of old adults continues to rise, maintaining walking speed and delaying the onset of mobility disability are clinically and functionally important and have become universal health care priorities.

Beyond the visible hallmarks of aged gait, i.e., slowed walking speed, shorter steps, and increased cadence [3,4], aging also affects the neuromuscular control of gait and old compared with young adults typically walk with greater levels of agonist activation [5] and particularly antagonist coactivation in the lower extremity muscles [5–8]. The increased coactivation is associated with increased metabolic cost [5,7,9] and disproportional coactivation can lower the net force exerted by the agonist muscle as well as inhibit the voluntary activation of the agonist muscle [10,11]. Nevertheless, elderly presumably use the increased coactivation in an effort to compensate for reductions in muscle strength and to increase joint stabilization [11].

Longitudinal decline in maximal voluntary knee extensor activation contributes to muscle weakness prior to the onset of declines in gait velocity [12] and high compared with low functioning old adults have lower maximal voluntary plantarflexor activation [13]. A form of resistance training known as power training incorporates exercises with moderate heavy weights and high movement velocities and this type of training is a cost-efficient method to increase muscle strength and power [14–18] as well as functional performance and gait velocity in old adults (for reviews see [16,19]). There is accumulating evidence that power training-induced to increases in voluntary activation of the agonist muscle contribute to the gains in muscle strength and power (for reviews see [10,20]). The results on antagonist coactivation after resistance training for improving muscle strength and power are inconsistent, as both increased and decreased coactivation are reported (for reviews see [10,16]).

Interestingly, little is known about power training-induced adaptations in neuromuscular activation during more dynamic tasks, such as gait. In a rare example, authors examined the effects of 12 weeks of high-velocity heavy-resistance training (75-80% of 1-repetition maximum) on neuromuscular activation during stair ascent in old woman [21]. Along with increased stair-ascent velocity, the elderly walked with increased agonist activation in one (rectus femoris) of five recorded muscles and antagonist coactivation remained unchanged [21]. These data tentative support the never tested idea that power training can induce changes in neuromuscular activation during walking in old adults.

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power training on neuromuscular activation during walking in healthy old adults. We hypothesized that power training produces correlated improvements in gait velocity and increases in agonist activation or decreased antagonist coactivation.

6.2. METHODS

6.2.1. Experimental design and participants

Data used in the present study are from participants enrolled in the Potsdam Gait Study (POGS) and characterized as community-dwelling old adults aged ≥ 65 without mobility limitations [15,22]. Twelve participants completed 10 weeks of power training with subsequently 10 weeks of detraining. Fourteen participants completed 10 weeks of a control period and three of these participants subsequently completed 10 weeks of power training. Testing was performed at baseline, after 10, and after 20 weeks. We combined the three participants from the control group who subsequently conducted power training with the twelve participants who started with the power training and we used this group of fifteen participants to analyze power-training effects. All participants provided written informed consent before testing and the ethics committee of the University of Potsdam, Germany, approved the study protocol (reference number 40/2014) [23] that was conducted according to the ethical standards of the Helsinki Declaration.

6.2.2. Interventions

The lower extremity power-training program consisted of 30 sessions administered over 10 weeks and was designed to improve lower extremity power [23]. Participants performed leg press, ankle press, knee extension, and knee flexion exercises at 40-60% of the three-repetition maximum and were instructed to lift the weights as rapidly and at high movement velocities during the concentric phase, as described in detail previously [15,22]. Participants were instructed to return to or maintain their habitual levels of activity that was present before enrolling in the study for the control and detraining periods.

6.2.3. Data collection

According to guidelines of the International Society of Electrophysiology and Kinesiology [24], we recorded surface EMG activity in five muscles of the right leg, i.e., vastus lateralis (VL), vastus medialis (VM), biceps femoris (BF), gastrocnemius medialis (GM), and soleus (SL). The skin was shaved, slightly abraded, degreased, and disinfected and electrodes affixed to the skin with the inter-electrode resistance below 5 kΩ. Aligned parallel to the muscle fibers, we placed bipolar surface electrodes (Ambu®,type Blue Sensor P-00-S/50, Ag/AgCl, diameter: 13 mm, center-to-center distance: 25 mm, Ballerup, Denmark) on the muscle belly and a reference electrode was placed on the medial aspect of the tibia. We marked the electrode position with waterproof marker

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on the skin and markers were regularly retraced during training sessions to enable precise electrode application in the post tests. The surface EMG signals were amplified, telemetrically transmitted (TeleMyo 2400 G2, Noraxon, Scottsdale, AZ, USA), converted to analog signals (TeleMyo 2400R G2, Noraxon, AZ, USA) and synchronized with the ground reaction force by analog-to-digital conversion on the same A/D board and sampled at 1 kHz.

We recorded torque and EMG data during maximal voluntary contractions (MVC) of the knee flexors, knee extensors, and plantarflexors on an isokinetic dynamometer (Isomed 2000®, Hemau, Germany) [23]. As a warm-up, participants performed a series of 10 submaximal isokinetic contractions, followed by three 3- to 5-second-long isometric MVC’s separated by 30-s of rest. During knee flexion/ extension testing, participants were in a sitting position with the knee fixed at an angle of 45° in the dynamometer. During plantarflexion testing, participants were in a supine position with the ankle joint in neutral position and the knee extended. We selected the trial with the highest isometric torque value for further analysis.

We recorded surface EMG data while the participant walked on a 6.5 x 1.5-meter level walkway and collected five gait trials at habitual, fast (“walk as fast and safely as you can, but do not run”), and standardized (1.25 ± 0.6m/s) walking speed [23], fifteen gait trials in total. The starting position was a taped line on the floor and participants performed three practices trials to ensure participants stepped on the force platform with their right foot and without altering their gait pattern.

6.2.4. Data analysis

We performed two analyses on the EMG data, whereby one analysis focused on the timing of the agonist and antagonist EMG bursts and the second analysis determined the amplitude of the agonist and antagonist muscle activation. For each gait trial, we time-normalized the EMG-signals to stride durations and then performed a timing analysis. Using the Teager-Kaiser Energy Operator (TKEO) [25,26], we determined the relative onset and offset of the main EMG burst in each of the muscles. We averaged the timing of VL and VM to characterize the main knee extensor burst and averaged the timing of GM and SL to characterize the main plantarflexor burst. Next, we bandpass-filtered the raw-EMG (20-450 Hz) and applied a root-mean-square (RMS) envelope using a 40-ms smoothing window. We averaged the RMS-EMG of VL and VM to characterize knee extensor activity and averaged the RMS-EMG of GM and SL to characterize plantarflexor activity, a method used previously [27]. The onset and offset points from the timing analysis were used as a window in which we determined the peak and mean RMS-EMG amplitudes of the agonist and antagonist muscles. We determined knee flexor coactivation during the main burst of the knee extensors and determined knee extensor coactivation during the main burst of the knee flexors [6]. We also computed gait velocity from kinematic analysis, which we described in detail previously [15,22,23].

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For the MVC trials, we also calculated the RMS-EMG using a 40-ms bin and determined peak RMS-EMG amplitude and mean RMS-EMG amplitude for a 1.0-s-long period centered on the peak RMS-EMG value. We used peak isometric torque as a measure of maximal muscle strength.

6.2.5. Statistical analysis

We report data as means (± SDs). For all gait variables, we used participants’ average of five trials per walking speed condition for the statistical analysis. EMGpeak and EMGmean values strongly correlated during the MVC’s and gait trials (r ≥ 0.8, P < 0.05) which is why we decided to present EMGmean values as a measure of EMG amplitude only. We used the Shapiro-Wilk test to confirm normality of data and analyzed all variables with a paired t-test comparing pre-post values for power training and control. The Wilcoxon Signed Rank Test was used when data was not normally distributed. We were unable to perform a repeated-measured ANOVA because three participants crossed over from the control to the power training intervention and [22].

Within-group effect sizes (d) were calculated using z-scores for Cohen’s d to ascertain if an effect was practically meaningful [28]. According to Cohen, effect sizes can be classified as small (0.00 ≤ d ≤ 0.49), medium (0.50 ≤ d ≤ 0.79), and large (d ≥ 0.80) [28].

We used simple linear regression analysis to predict changes in isometric torque from changes in agonist or antagonist EMG amplitudes. Additionally, we predicted changes in gait velocity from changes in agonist or antagonist EMG amplitudes. We quantified the associations between pairs of variables and between changes in variables as correlation coefficient (r-value), level of significance (P value), and the amount of variance explained (r²-value). Values of R = 0.10 indicate small, R = 0.30 medium, and R = 0.50 large size of correlation [28]. We analyzed the data with SPSS 23.0 (SPSS Inc., Chicago, IL) and set the level of significance at P <.05.

6.3. RESULTS

6.3.1. Participants

We excluded three participants from the power-training group and one from the control group due to poor quality of the EMG signals. Thus, data from twelve participants were included for the analysis of the power training intervention (age 72.1 ± 5.4 yr, BMI 26.2 ± 4.1 kg/m2), and 13 for the control intervention (age 69.7 ± 5.0 yr, BMI 25.1 ± 3.2 kg/m2). An additional three participants dropped out from the detraining period leaving not enough participants remaining to statistically analyze detraining effects (n = 9) which is why we report results of the power training and control interventions only.

6.3.2. Isometric muscle strength and maximal EMG amplitude

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agonist muscle. Power training increased isometric muscle strength of the knee flexors (15 ± 10%, d = 0.34, P = 0.002), knee extensors (22 ± 15%, d = 0.74, P ≤ 0.001), and plantarflexors (93 ± 101%, d = 0.80, P = 0.002) and also EMG amplitudes of the knee flexors (45 ± 39%, d = 1.47, P = 0.004), knee extensors (53 ± 61%, d = 0.50, P = 0.013), and plantarflexors (31 ± 56%, d = 0.47, P = 0.076). No changes occurred during the control period in isometric muscle strength (d ≤ 0.31, p ≥ 0.303) but EMG amplitude of the knee extensors increased by 61 ± 66% (d = 0.50, P = 0.021, Fig. 6.1). We observed no changes in knee flexor or knee extensor coactivation during MVCs after power training or the control period (d ≤ 0.28, p ≥ 0.142, data not shown).

6.3.3. Gait velocity

Power training increased fast gait velocity by 3.5 ± 7.1% (d = 0.31, P = 0.059, Table 6.1) but habitual gait velocity was similar pre-post (+5.4%, d = 0.42, P = 0.079). Habitual and fast gait velocity did not change after the control period (d ≤ 0.11, p ≥ 0.240) and standardized gait velocity was similar pre-post in both the power training and control group.

6.3.4. Muscle activation and coactivation during gait

The results of the EMG analysis were generally similar for walking at habitual and standardized speeds and Table 6.1 shows only the changes in timing of agonist muscle activation at habitual and fast speeds. Power training delayed knee flexor offset at habitual (6.2 ± 8.4%, d = 0.66, P = 0.020) and fast speed (4.6 ± 5.6%, d = 0.58, P = 0.009), resulting in a longer duration of knee flexor activation at fast speed (21 ± 39%, d = 0.48, P = 0.016). Power training also delayed the offset of the knee extensors (3.7 ± 6.7%, d = 0.77, P = 0.040) and plantarflexors (0.7 ± 1.2%, d = 0.45, P = 0.040).

Figure 6.1. Maximal isometric muscle

strength (bottom) and EMG amplitude (top) for power training (n = 12) and control (n = 13) groups. Values are mean and standard deviations and expressed in millivolts (mV) or Newton*meters (Nm) *significant change pre-post (P ≤ 0.05)

40 60 80 100 120 140 160 20 180

Knee flexor Knee extensor Plantarflexor

Maximal isometric strength

(N m) 0 0.02 0.04 0.06 0.08 0.10 0.12 EMG amplitude (mV)

Power training pre Power training post Control pre Control post

*

* *

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Fig. 6.2 shows group average RMS envelopes of the EMG signals recorded at habitual and fast speeds for power training and control groups. Power training increased knee extensor (21 ± 26%, d = 0.26, P = 0.013) and plantarflexor (28 ± 45%, d = 0.65, P = 0.006) activation at habitual speed as well as knee extensor (16 ± 21%, d = 0.29, P = 0.022) and plantarflexor (11 ± 17%, d = 0.38, P = 0.045) activation at fast speed.

Fig. 6.3 shows knee flexor and extensor coactivation during gait. Power training increased knee extensor coactivation during the main knee flexor burst at habitual (28 ± 33%, d = 0.44, P = 0.033) and fast (19 ± 22%, d = 0.26, P = 0.010) speed, while knee flexor coactivation during the main knee extensor was unchanged (d ≤ 0.39, p ≥ 0.271). Knee flexor or extensor coactivation during gait was unchanged after the control period (d ≤ 0.52, p ≥ 0.053, Fig. 6.3).

Table 6.1 Gait velocity and timing analysis of EMG bursts during gait

Power training (n = 12) Control (n = 13)

Pre Post d P Pre Post d P

Habitual speed Gait velocity, m/s 1.28(0.14) 1.34(0.17) 0.42 0.079 1.41(0.19) 1.39(0.29) -0.11 0.240 Knee Flexors Onset 28.0(4.3) 28.3(2.3) 0.08 0.396 27.9(5.2) 27.4(4.6) -0.10 0.393 Offset 52.8(5.3) 55.8(3.4) 0.66 0.020 53.6(3.7) 55.5(5.3) 0.40 0.158 Duration 24.8(7.3) 27.5(3.9) 0.46 0.086 25.7(7.5) 28.0(7.9) 0.30 0.101 Knee extensors Onset 37.1(4.5) 36.4(1.8) -0.23 0.221 37.2(3.3) 36.2(3.8) -0.31 0.311 Offset 67.2(4.2) 68.2(2.7) 0.29 0.223 67.4(3.4) 67.2(3.0) -0.08 0.741 Duration 30.0(4.0) 31.8(3.3) 0.49 0.076 30.2(5.0) 31.0(4.7) 0.17 0.577 Plantarflexors Onset 62.7(4.6) 62.6(2.7) -0.02 0.480 63.6(3.0) 62.6(4.2) -0.26 0.303 Offset 96.7(3.9) 97.6(1.9) 0.28 0.213 98.3(1.2) 98.3(1.2) 0.00 0.994 Duration 34.0(5.3) 35.0(3.9) 0.20 0.194 34.7(3.7) 35.7(4.7) 0.23 0.353 Fast speed Gait velocity, m/s 1.82(0.18) 1.88(0.23) 0.31 0.059 1.91(0.26) 1.89(0.26) -0.07 0.396 Knee flexors Onset 30.5(4.2) 29.9(3.1) -0.16 0.182 30.3(4.3) 28.1(3.5) -0.57 0.138 Offset 55.9(5.0) 58.2(2.8) 0.58 0.009 57.9(3.8) 59.0(3.8) 0.29 0.376 Duration 25.4(7.6) 28.3(4.1) 0.48 0.016 27.6(5.7) 30.9(6.8) 0.54 0.096 Knee extensors Onset 38.0(4.6) 37.9(3.2) -0.04 0.451 39.3(4.3) 37.7(4.5) -0.35 0.286 Offset 68.1(3.6) 70.4(2.1) 0.77 0.040 69.0(4.5) 69.0(3.5) -0.01 0.979 Duration 30.1(7.1) 32.5(4.1) 0.43 0.152 29.8(6.2) 31.3(5.4) 0.26 0.458 Plantarflexors Onset 65.8(3.8) 64.3(4.3) -0.36 0.143 64.3(3.3) 64.7(3.8) 0.10 0.640 Offset 98.6(1.7) 99.3(1.1) 0.45 0.040 99.7(0.5) 99.5(0.6) -0.29 0.474 Duration 32.9(5.1) 35.0(4.9) 0.42 0.091 35.4(3.3) 34.9(3.9) -0.14 0.523

Values are mean (±SD). Onset, start of main EMG burst at the specified time after toe-off (0% = toe- off ) ; Offset, end of main EMG burst at the specified time after onset; Duration, EMG activity duration defined as the difference between offset minus onset . d = within-group effect sizes. Significant P values are denoted in bold.

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95 Chapter 6 Figure 6.2 . Gr oup a verage RMS-EMG ov er a full gait c ycle (0-100%) recorded dur ing w alking a t habitual and fast speeds in po w er training (Left, n = 12) contr ol (Right, n = 13) g roups . Knee flexor activ ation is r epr esented by biceps femor is activ ation; Knee extensor activ ation is r epr esented b y av eraged v astus la teralis and v astus medialis activ ation (VL+VM)/2; Plantarflexor activ ation is r epr esented by a veraged gastr ocnemius medialis

and soleus activ

ation (GM+SL)/2. Dark g ra y ar eas indica te +1 or -1 standard de via tion a t pr etest at habitual speed. Light g ra y ar eas indica te +1 or -1 standard de via tion a t pr etest a t f ast speed. V er tical line a t 40% gait c ycle indica tes high str ik e. Muscle activ ation w as calcula ted dur

ing the main

agonist bur st for knee flexor s (~30-55% gait cycle), knee extensor s (~40-70% gait c

ycle) and plantarflexor

s (~60-100% gait cycle). *significant c hange pr e-post at habitual speed (P ≤ 0.05). †significant c hange pr e-post a t fast speed (P ≤ 0.05). 0 20 40 60 80 100%

Knee flexor RMS-EMG (mV)

Power training 0 20 40 60 80 100%

Knee extensor RMS-EMG (mV)

0 20 40 60 80 100% Plantarflexor RMS-EMG (mV) Swing Stance

***********††††††††††

*†

0 20 40 60 80 100% Control Habitual pre Habitual post Fast pre Fast post 0 20 40 60 80 100% 0 20 40 60 80 100% Swing Stance 0 0.05 0.10 0.15 0.15 0.10 0.05 0 0.15 0.10 0.05 0 0 0.05 0.10 0.15 0.15 0.10 0.05 0 0.15 0.10 0.05 0

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6.3.5. Correlation analyses

Power training-induced changes in isometric muscle strength correlated with overall changes in EMG amplitudes (R = 0.578, P = 0.049, n = 12, Fig. 6.4). We found no correlations between power training-induced changes in gait velocity and timing or magnitude of knee flexor or knee extensor activation or coactivation at habitual or fast speed. Measured at fast speed, power training-induced changes in gait velocity correlated with changes in plantarflexor offset (R = 0.662, P = 0.019, n = 12, Fig. 6.5A) and plantarflexor activation (R = 0.760, P = 0.004, n = 12, Fig 6.5B).

6.4. DISCUSSION

The present study is the first to examine the effects of 10 weeks of power training on lower extremity neuromuscular activation during walking in old adults. In addition to gains in maximal EMG amplitudes and isometric strength, old adults showed elevated knee extensors activation and coactivation during early stance and elevated plantarflexor activation during push-off. Our data suggest that the power training-induced mechanisms

Co ac tiv at ion (m V)

Power training pre Power training post Control pre Control post

Knee flexor Knee extensor 0 0.01 0.02 0.03 0.04 0.05 0.06

Habitual speed Fast speed

*

Knee flexor Knee extensor 0 0.01 0.02 0.03 0.04 0.05 0.06

Figure 6.3. Antagonist coactivation during walking at habitual and fast speed for power training (n = 12) and

control (n = 13) groups. Knee flexor coactivation was measured during the main knee extensor burst (~40-65% of stride); Knee extensor coactivation was measured during the main knee flexor burst (~30-55% of stride). Values are mean and standard deviations and expressed in millivolts (mV). *significant change pre-post (P ≤ 0.05).

Figure 6.4. Association between power training-induced

changes in maximal isometric torque and changes in EMG amplitude. Each data point represents an old adult and the data points were created by averaging knee flexor, knee extensor, and plantarflexor isometric torque or EMG amplitude ((∆ KF + ∆ KE + ∆ PF) / 3). The association is characterized by y = 1.04x + 6.9, R² = 0.33 (P = 0.049). ∆ EMG amplitude (%) -50 0 50 100 150 200 20 40 60 80 100 ∆ Maximal isometric strength (%)

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responsible for gains in isometric muscle strength and gait velocity were mainly due to adaptations in neuromuscular agonist activation. We discuss how power training modifies neuromuscular activation and increases muscle strength and walking performance in old adults.

6.4.1. Isometric muscle strength and maximal EMG amplitude

We previously reported that the present power-training program resulted in improvements in training loads (~51%, 0.56≤ d ≤1.76) and isokinetic muscle power (~30%, 0.35≤ d ≤.71) [22]. Despite that the power training involved dynamic exercise whereby elders moved moderately heavy weights at high movement velocities during the concentric actions, it also led to large gains in maximal force recorded during isometric actions (Fig. 6.1). These data confirm previous findings that power training interventions that involves progressive increments of loading intensity can improve both muscle power and muscle strength in healthy old adults [16,22,29,30].

Short-term increases in maximal isometric and dynamic muscle strength can be largely accounted for by increased motor unit activation of the trained agonist muscles [10]. Extending these findings, we found that the gains in isometric muscle strength (~43%) and EMG amplitudes (~41%) were of similar magnitude (Fig. 6.1) and the gains in EMG amplitudes explained 33% of the variance of the gains in isometric strength (Fig. 6.4). These data support the idea that a possible mechanism through which

-1.5 -1.0 -0.5 0.5 1.0 1.5 2.0 2.5 3.0 3.5 -15 -5 5 15 ∆ Plantarflexor offset (%) A -20 -10 10 20 30 40 50 -15 -5 5 15 ∆ Plantarflexor activation (%)

∆ Fast gait velocity (%) B

Figure 6.5. Associations between power training-induced

changes in fast gait velocity and changes in plantarflexor offset or activation. Panel A: Association between changes in fast gait velocity and changes in plantarflexor offset. The association is characterized by y = 0.11x + 0.3, R² = 0.44 (P = 0.019). Panel B: Association between changes in fast gait velocity and changes in plantarflexor activation. The association is characterized by y = 1.83x + 4.5, R2 _{= 0.57 (P = 0.004).}

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power training increases old adults’ isometric muscle strength is by absolute increases in neuromuscular activation of the trained agonist muscle. Mechanism that underlie the increased neuromuscular activation can involve, but are not limited to, increased neural drive via corticospinal pathways, increased motor neuron and/or muscle fiber excitability, increased number of active motor units, and/or increased conduction velocity [20,31].

6.4.2. Muscle activation and coactivation during gait

Muscle activation and coactivation during gait are generally higher in old compared with young adults [5–8] and increased levels of coactivation in elders are important for joint stabilization. In general, the power training-induced adaptations in activation profiles around the knee were similar at habitual and fast speed (Table 6.1). After training but not the control period, knee flexor activation became longer and the percentage of stride during which knee flexors and extensors were simultaneously active increased. Despite the temporal changes in knee flexor activation, power training did not change the magnitude of knee flexor activation or coactivation. In contrast, after training knee extensor activation and coactivation increased (Fig. 6.2 and 6.3). In line with the concept that increased coactivation is important for joint stability, we interpreted the increased magnitudes of knee extensor activation (~18%) and coactivation (~24%) around heel strike as a mechanism to stiffen the knee joint during heel strike and loading response. We previously reported that the old adults walked with 11% less knee extensor angular impulse and 11% less negative knee power after heel contact after the power training intervention [15], suggesting that the knee extensors were less eccentrically active and the elders were better capable of maintaining an extended knee position during loading response. Noticeable is that power training-induced adaptations in neuromuscular activation of the knee flexors or extensors (i.e., timing or magnitude) only played a minor role for improving gait velocity, as we found no associations between changes in activation profiles and gait velocity.

Power training increased plantarflexor activation during push-off (Fig. 6.2) and delayed activation-offset at fast speed. Indeed, the elders walked 5% faster, delayed their plantarflexor offset by 1%, increased their plantarflexor activation during push-off by 10%, and the gains in plantarflexor offset and activation explained 44-57% of the gains in fast walking speed (Fig 6.5). These data only tentatively support the idea that improved plantarflexor muscle activation acted as an enabler mechanism for an improved fast walking speed after power training in old adults. Paradoxically, we previously showed that the present power training intervention resulted in an 8% decrease in plantarflexor velocity during off [22] and an 11% reduction in ankle peak power during push-off [15]. These discrepant results suggest a disassociation between the different types of measures (i.e., kinematics and kinetics vs. EMG) and future research is needed to clarify the role of each type of measure and their interaction for quantifying training effects on

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gait performance in both clinical and research settings. Furthermore, research should explore the role of additional gait and/or dynamic balance training providing real-time feedback of the propulsive force so that old adults can learn to optimize the use of the newly acquired levels of plantarflexor activation [32]. Other factors that may limit the ability to incorporate the improved plantarflexor activation capacity are the age-related architectural changes in the ankle muscle-tendon complex [33,34].

6.4.4. Relative muscle activation

The magnitudes of power training-induced gains in muscle activation differed between tasks (i.e., MVC vs. gait) and between muscle groups, which is why we presented our EMG data in absolute units. Nevertheless, expressing muscle activation during gait as a percent of maximal EMG amplitude during MVC (%MVC) provides information about the level of maximal available capacity that old adults use during gait. The gains in knee flexor activation where greater during MVC (45%) compared to gait (~1%) and consequently, the elderly walked at lower levels of their maximal knee flexor EMG capacity after the training intervention (42 to 27%MVC at habitual speed and 70 to 46%MVC at fast speed, both P ≤ 0.05). Power training did not change the level of knee extensor activation at habitual and fast speed (32 to 28%MVC and 57 to 44%MVC, both P ≤ 0.05). Additionally, the level of plantarflexor activation during gait was 108%MVC at habitual speed and 180%MVC at fast speed and further analysis showed that power training did not change these levels (P > 0.05). The above-maximal level is probably caused by the difference in joint positions and type of contraction between the MVC and gait tests. Nonetheless, these data suggest that old adults walk with relatively high levels of plantarflexor activation, which is not changed after power training. Overall, the old adults exploited the power-training induced increases in maximal knee extensor and plantarflexor muscle activation.

6.4.5. Limitations and conclusion

One limitation of the current study is that the old adults were without mobility limitations, which may have reduced the effectiveness of the power training to improve neuromuscular activation during gait. Second, although EMG is a useful tool for assessing neuromuscular control, a variety of non-neural factors can influence the signal. For example, the amount of subcutaneous adipose tissue and the consistency of electrode placement at the recording site will influence EMG signal characteristics. Finally, due to inconvenience and time constrains we did not measure EMG activity of any hip extensors (i.e., gluteus maximus) or hip flexors (i.e. rectus femoris) and future studies should determine if power training increases hip muscle activation during gait.

In conclusion, we observed that a 10-week power-training program evoked substantial improvements in agonist muscle activation during isometric actions and during walking in old adults. The power training-induced increases in agonist muscle

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activation may in part mediate the increases in isometric strength and fast gait velocity. The present results support the use of power training for improving neuromuscular activation and functional performance in old adults.

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