Muscle & Nerve

Muscular adaptations and insulin-like growth factor-I (IGF-I) responses to resistance training are stretch-
mediated

McMahon, Gerard MSc1,2, Morse, Christopher I PhD1, Burden, Adrian PhD1, Winwood,

Keith PhD1 and Onambélé, Gladys Leopoldine PhD1

1
Institute for Performance Research, Department of Exercise & Sport Science, Manchester

Metropolitan University, Crewe Green Road, Crewe, CW1 5DU, United Kingdom.

2
Sports Institute Northern Ireland, University of Ulster, Newtownabbey, Belfast, BT37 0QB

Corresponding author: Dr Gladys Onambélé-Pearson. Valentine Building, Room 2-7.

Department of Exercise & Sport Science, Manchester Metropolitan University, Crewe Green

Road, Crewe, CW1 5DU, United Kingdom. Tel +44 (0) 161 247 5594; Fax +44 (0) 161 247 6386;

Email: [Link]@[Link]

Running Title: Length modulates adaptation

List of Abbreviations:

CSA; cross-sectional area

EMG; electromyographical
IGF-I; insulin-like growth factor – 1
PI3K/Akt/mTOR; Phosphatidylinositol 3 Kinase/ Akt (protein kinase B)/ mammalian target of rapamycin
MAFBx; muscle atrophy F-Box
MuRF-1; muscle RING finger 1
FOXO; Forkhead box subgroup O

This article has been accepted for publication and undergone full peer review but has not been
through the copyediting, typesetting, pagination and proofreading process which may lead to
differences between this version and the Version of Record. Please cite this article as an
‘Accepted Article’, doi: 10.1002/mus.23884
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Length modulates adaptation 2

ABSTRACT:

Introduction: Modulation of muscle characteristics was attempted through altering muscle

stretch during resistance training. We hypothesized that stretch would enhance muscle

responses. Methods: Participants trained for 8 weeks, loading the quadriceps in a shortened

(SL-0-50o knee flexion; n=10) or lengthened (LL- 40-90o; n=11) position, followed by 4 weeks

detraining. Controls (CON; n=10) were untrained. Quadriceps strength, Vastus Lateralis

architecture, anatomical cross-sectional area (aCSA), and serum IGF-I (insulin-like growth factor

1) were measured at weeks 0, 8, 10, and 12. Results: Increases in fascicle length (29±4% vs.

14±4%), distal aCSA (53±12% vs. 18±8%), strength (26±6% vs. 7±3%), and IGF-I (31±6% vs.

7±6%) were greater in LL compared to SL (P<0.05). No changes occurred in CON. Detraining

decrements in strength and aCSA were greater in SL than LL (P<0.05). Discussion: Enhanced

muscle in vivo (and somewhat IGF-I) adaptations to resistance training are concurrent with

muscle stretch, which warrants its inclusion within training.

Key Words: detraining; hypertrophy; muscle architecture; range-of-motion; resistance training.

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INTRODUCTION:

Skeletal muscle architectural and morphological characteristics are important due to their

direct influence on functional performance (i.e. strength and power). Therefore, a key to

optimizing human function is to understand the mechanical stimuli that induce alterations to

muscle characteristics/ properties. In relation to muscle architecture, there are reports of

increases in fascicle length following resistance training 1-3. An increase in fascicle length is

thought to be brought about by addition of in-series sarcomeres. Muscle length (or passive

tension/ stretch) and excursion have been shown to be major regulators of serial

sarcomerogenesis in animals 4 and appears to be relatively independent of both muscle

activation level and tension 5. However in humans, conflicting evidence from studies on the

major mechanical stimuli for such adaptation exists. In young adults, muscle contraction type

(eccentric vs. concentric) was investigated as a possible primary candidate for fascicle length

change 6. The authors concluded that other factors (possibly excursion of muscle during

resistance training) were the main mechanical stimuli for changes in fascicle length. In contrast,

in older individuals, Reeves et al.1 found that eccentric contractions (through enhanced training

stimulus and associated greater muscle-tendon strain), were the driving force behind greater

increases in fascicle length, compared to conventional weight training. Therefore, the primary

constituent in resistance training for regulating fascicle length in humans remains ambiguous.

The inextricable link between muscle cross-sectional area (CSA) and strength has been known

for many years. The 2 main mechanical signals that induce muscle hypertrophy (therefore

increasing CSA) appear to be muscle force and/ or stretch. In animal models, muscle stretch (i.e.

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lengthening) combined with force generation seems to have an additive effect on protein

synthesis and muscle size over and above the effects of force generation/ stretch applied

separately 7,8. Furthermore, insulin-like growth factor 1 (IGF-I) mRNA has also been shown to

increase to a much greater extent in response to stretch combined with electrical stimulation,

compared to stimulation or stretch alone in adult skeletal muscle 9.

At the other end of the muscle loading spectrum, the response to diminished loading, i.e.

detraining, is the partial or complete loss of training-induced adaptations in response to an

insufficient loading stimulus. Significant decrements in strength, electromyogram amplitude,

and mean fiber CSA have been reported to occur in as little as 2 weeks of detraining 10, with

similar observations in chronic detraining periods (≥4wks) 11,12. However, in vivo changes to

muscle architecture during a relatively shorter period of time (≤4 weeks – such as that found in

short-term injury, illness or tapering) have not yet previously been described. Significant

increases in fascicle length have been reported in as little as 10 days from the onset of

resistance training 2. Counter-intuitively, Blazevich et al.6 documented an increase in VL fascicle

length during 3 months of detraining following 10 weeks of resistance training. Therefore,

following resistance training, the impact of detraining training appears to follow an

unpredictable/uncharted pattern. In addition to its role in increased muscle mass, IGF-I has

been implicated in preventing expression of the Forkhead box (FOXO) class of transcription

factors and the mRNA increases of muscle atrophy F-Box (MAFbx) and muscle RING finger 1

(MuRF1) seen during muscle atrophy 13. Therefore following detraining, it would be interesting

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to describe the possible link between circulating IGF-I levels and the degree of muscle mass

maintenance.

From the evidence of current literature, the aim of this study was to investigate if performing

resistance training at a longer muscle length (high muscle stretch condition) compared to a

shorter muscle length (low muscle stretch condition) with identical load magnitude, would

differentially modulate specific in vivo muscle responses including size, architecture, and

circulating IGF-I. In addition, we also questioned whether the magnitude of the preceding

training responses would also influence the change in muscle parameters during detraining. It

was hypothesized that a group training at longer (LL) muscle lengths (40-90o excursion) would

undergo a greater amount of skeletal muscle hypertrophy and fascicle lengthening compared to

a group training at 0-50o excursion (SL). Secondly, it was also hypothesized that the LL group

would still have a larger muscle mass following detraining, probably due to greater initial gains

and/or IGF-I mediated effects on protein degradation rate. Strength- and fascicle angle-related

parameters were expected to follow a similar response as those associated with hypertrophy.

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Materials & Methods:

Subjects

Thirty one volunteers were recruited from the local university and gave written informed

consent to participate in the study. All procedures and experimental protocols were approved

by the local Ethics Committee. Exclusion criteria included the presence of any known

musculoskeletal, neurological, inflammatory, or metabolic disorders or injury. Participants took

part in recreational activities such as team sports and had either never taken part in lower limb

resistance training or had not done so within the previous 12 months. Team sports included

rugby union and league, soccer, hockey, and netball. Where several participants had the same

sporting background, they were divided evenly and randomly allocated to a training group. All

participants took part habitually in up to 3-5 hours of non-resistance based activity per week.

Twenty one activity-matched participants were allocated to a training group – SL (shorter

muscle length; 6 men, 4 women; aged 19±2.2 years, 1.76±0.15m, 75.7±13.2Kg) or LL (longer

muscle length; 5 men, 6 women; 21±3.4 years, 1.75±0.14m, 74.9±14.7Kg). Ten participants (6

men and 4 women; 23±2.4 years, 1.76±0.09m, 77.9±13.1Kg) were assigned to the non-training

control group (Con), and continued their normal habitual activity throughout the study period.

Inclusion of both genders would allow a general response to the training regime to be identified

regardless of gender and was possible due to very similar numbers of men and women. A one-

way ANOVA revealed that the population was homogeneous at baseline for all parameters of

interest (P>0.05).

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Study Design

The study design was convenience sampling, with random allocation to 1 of 3 groups. Following

familiarization with testing procedures at least 1 week prior to testing proper, participants were

tested for muscle size, architecture, strength, and serum IGF-I at baseline (week 0). The

measurements were repeated after 8 weeks of resistance training (week 8), following 2 weeks

of detraining (week 10), and after a further 2 weeks of detraining (week 12). Blood sampling

was always at the same time of day, whereas the in vivo tests were completed within 2 hours of

the time-of-day of these tests when carried out at week 0 to minimize any impact of diurnal

variability in muscle function. It should be noted here that all sonographs (and other muscle

parameters) were taken/measured ~3-4 days post-training to avoid osmotic fluid shifts that

may confound architectural or morphological measurements 14.

Muscle Excursion

Total muscle excursion was set at that which occurred during 50o range-of-motion (ROM)

carried out at different portions of the knee angle-muscle length spectrum depending on the

training group (Figure 1). With 0o being full knee extension, SL followed an excursion from 0-50o

of knee flexion (i.e. shorter muscle lengths), and LL followed an excursion between 40-90o

(muscle loaded at a longer length). Therefore the work done, since external loads were also

made comparable, (force (see muscle force modelling below) × distance] was also matched

closely. These joint angles were chosen, as both 50o and 90o have been used frequently to

determine physiological responses to various stimuli and are usually referred to being ‘longer’

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or ‘shorter’ muscle lengths (e.g. 15- 17). In addition, placing the muscle at these discrete angles

also allowed the investigators to compare the effect of muscle length change within a common

ROM for this particular muscle group, i.e. 0-90o.

[ INSERT FIGURE 1 NEAR HERE ]

Muscle Force Modelling

Due to the changing moment arm length of the patella tendon at discrete knee joint angles,

differences in muscle force produced between the groups were accounted for. Thus quadriceps

forces at the patella tendon were calculated as follows:

QuadForce = (QuadMaxTorque + HamCoTorque) / Moment ArmPT Equation [1]

where

HamCoTorque = (Co-ConEMG × FlexMaxTorque) /(Max BFEMG) Equation [2]

Where Co-ConEMG is co-contraction of the antagonist muscle group (using the biceps femoris as

representative of the hamstrings), and Max BFEMG is the maximum antagonist EMG18.

FlexMaxTorque is maximum flexion torque, and Moment ArmPT being the moment arm of the

patellar tendon (values obtained from DEXA scans). Based on previous training data from our

laboratory at end ROM, where a short isometric hold would take place, tendon forces produced

at 90o were on average ~32% greater than those produced at 50o [to quantify the training load

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to apply, the torque of the mass of the external resistance (in Nm) is added to the left hand side

of equation (1) above]. Thus, it was calculated that while SL would exercise at a high-intensity

of 80% 1RM (for a more detailed description see resistance training program section), the LL

group would train at a lower intensity of 55% 1RM to equate the absolute load seen by the

tendon (i.e. at the joint center of rotation) in the 2 groups.

Patella Tendon Moment Arm Measurement

The patella moment arm was estimated from sagittal scans of the right leg of each participant

using a single-energy DEXA (Dual Energy X-Ray Absorptiometry) scan (Hologic QDR, Vertec,

Reading, UK ), with the knee placed at 90o of knee flexion. The patella tendon moment arm was

defined as the perpendicular distance between the tibiofemoral contact point and the mid-

portion of the patella tendon. DEXA imaging has been used to estimate moment arm previously

in other anatomical sites with good reliability 19. The single energy scanning method has also

been compared with MRI [(0.2-Tesla MRI scanner (E-scan, Esaote Biomedica, Genoa, Italy)]

images [taken in the sagittal plane using a spin-echo TI half-Fourier (HF) sequence with a slice

thickness of 8mm, inter-slice gap of 0.6mm, and the parameters time to repetition/echo

time/number of excitations (TR/TE/NEX), 420/18/1; field of view, 160∙160mm; matrix, 256∙256

pixels)] in our lab and provides externally valid measurements. We have measured

systematically the knee moment arms of 4 participants (2 men and 2 women) using both pieces

of equipment. This revealed a non-significant (Wilcoxon signed-rank test: Z-score=-1.826, 2-

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tailed P>0.05) trend for the moment arm values using the DEXA to be 7.5±1.5% (or 3.2±0.6mm)

greater than those obtained using an MRI scan.

Estimation of Co-Contraction from Electromyographical (EMG) Activity

A pair of self-adhesive Ag-AgCl electrodes 15 mm in diameter (Neuroline 720, Ambu, Denmark),

was placed on clean, shaved, and previously abraded skin in a bipolar configuration with an

inter-electrode distance of 20 mm at 50% of femur length in the mid-sagittal plane of the biceps

femoris muscle (BF). The reference electrode (Blue sensor L, Ambu, Denmark) was placed on

the lateral tibial condyle. The raw EMG signal was preamplified (MP100, Biopac Systems Inc.,

USA), amplified (MP100, Biopac Systems Inc., USA), bandpass filtered between 10-500 Hz

(Biopac Systems, USA), and sampled at 2000 Hz. All EMG and torque signals were displayed in

real time in AcqKnowledge software (Biopac systems Inc., USA) via a PC (iMac, Apple Inc., USA).

Two maximal flexion contractions were carried out to obtain the EMG at maximal flexion

torque. The root mean square (RMS) EMG activity was averaged for a 500ms period which

coincided with the plateau of peak torque.

As mentioned above, the EMG of the long head of the biceps femoris muscle was measured to

ascertain the level of antagonist muscle co-contraction during the required isometric knee-

extension performances. Biceps femoris torque during a knee-flexion contraction was

calculated by the biceps femoris EMG activity during knee extension divided by the biceps

femoris peak flexor EMG at 70o knee flexion; the maximal flexor torque is then multiplied by

this value to determine co-contraction torque. The co-contraction torque values are used to

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correct the voluntary knee-extension torques (and hence the forces during the ramped

contractions) using the following formula:

CT = OT + CcT Equation [3]

where CT represents corrected knee-extensor torque, OT is the observed knee-extensor torque,

and CcT is the calculated hamstrings torque during knee extension (i.e. antagonist co-

contraction torque).

Resistance Training Program

Resistance training was performed 3 times per week (2 supervised and one home-based

session) by both SL and LL training groups for 8 weeks, using a combination of free, machine

(Technogym, UK), and body weights. Exercises for knee extensors included bilateral barbell

squat, seated leg press, seated knee extension, Bulgarian split squat, and the Sampson chair.

Throughout the training period, participants performed 3-4 sets of 8-10 reps (depending on

stage of program and exercise) at 80% (SL) or 55% (LL) 1 repetition maximum (1RM), defined by

the maximum load that could be lifted throughout the entire designated ROM (i.e. for LL group,

the maximum amount of weight that could be lifted from 90o-40o in a controlled manner).

1RMs were re-assessed every 2 weeks for each of the exercises and training loads adjusted

accordingly. A generalized warm-up was completed at 70-75% age-predicted maximum heart

rate on a treadmill for 5 minutes, after which a goniometer was attached (using double-sided

sticky tape) to the center of rotation of the knee. As the participant performed squat exercises,

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the goniometer rotated. The investigator/training partner confirmed from the scale that 50o or

90o of knee flexion was reached (depending on the training group) during the eccentric phase

and therefore could hold the load steady over 2 seconds, before beginning the concentric

phase of movement and return to the starting joint angle (i.e. either 0 o or 40 o). As participants

performed the leg press and knee extension exercises, the concentric movement was

performed first followed by a hold, and then the eccentric phase was performed back to the

starting joint-angle, which again was confirmed and timed by the investigator/training partner.

The short isometric hold over 2 seconds was to emphasize the stretch at the end of the

excursion. Therefore, the vast majority of quadriceps time-under-tension in SL was spent at

shorter muscle lengths close to and including 50o, whereas the LL group quadriceps was

predominantly at longer muscle lengths close to and including 90o. (NB. The load was removed

in LL prior to the subject straightening up between 40o -0o degrees at the end of each set). All

exercises involved eccentric and concentric contractions, except for the Sampson chair, which

was isometric loading, with LL holding the position with the knee at 90o and the knee at 50o

angle. Timing of contractions was controlled using a metronome (1 second eccentric, 2 second

isometric hold, 1 second concentric). The subjects completed 2 familiarization sessions at 70%

(SL) and 40% (LL) of 1RM prior to commencing the resistance training program.

Muscle architecture and Muscle Length

Architecture was measured at rest with each participant seated in an upright position on an

isokinetic dynamometer (Cybex, Phoenix Healthcare Products, UK). Following equipment

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calibration, each participant was positioned with a hip angle of 80o (straight back 90o) and knee

at 90o knee flexion (straight leg 0o). All muscle architectural measurements were determined at

rest using real-time ultrasonography (7.5-MHz, 40-mm linear array, B-mode ultrasound probe,

AU5, Esaote Biomedica, Italy) at rest. Images were captured using a digital video recorder

(Tevion, UK). The vastus lateralis fascicle pennation angle (θ) was measured as the angle of

fascicle insertion into the deep aponeurosis 20. Images were obtained perpendicular to the

dermal surface of the VL and orientated along the plane of the muscle fascicles. Images were

taken at 25% (proximal), 50% (central) and 75% (distal) of total femur length (as described

below) and 50% of muscle width at each point (where 50% muscle width is defined as the mid-

point between the fascia separating the VL and Rectus Femoris, and fascia separating the VL

and Biceps Femoris muscles). Fascicle length was defined as the length of the fascicular path

between the deep aponeurosis and superficial aponeurosis of the VL. The majority of fascicles

extended off the acquired image, and the missing portion was estimated by linear

extrapolation. This was achieved by measuring the linear distance from the identifiable end of a

fascicle to the intersection of a line drawn from the fascicle and a line drawn from the

superficial aponeurosis. This method has been shown to produce reliable results previously 6.

All images were analyzed and measured using Image J (Wayne Rasband, National Institute of

Health, USA).

VL muscle lengths were also determined using ultrasound in the mid-sagittal plane. This was

determined as the length from the myotendinous junction of the VL and patellar tendon to the

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point where VL adjoins to the tensor fascia latae and rectus femoris muscle. These points were

marked on the skin and measured with standard anthropometric measuring tape.

Muscle aCSA

VL muscle anatomical cross-sectional area (aCSA) was measured using real-time

ultrasonography at rest. aCSA was measured with the ultrasound probe in the transverse plane

at 3 sites: 25%, 50%, and 75% of total femur length. Femur length was defined as the line

passing from the greater trochanter to the central palpable point of the space between the

femoral and tibial condyles when the knee was flexed at 90o. Echo-absorptive tape was placed

at regular intervals (~3cm) along the muscle width at each site so that when the probe was

placed on the leg, 2 distinct shadows were cast on the ultrasound image. Therefore, each

ultrasound image provided a section of VL within the boundaries set by the 2 shadows and

fascia surrounding the muscle. Individual images were reconstructed using the femur and

superficial markers as reference points, and the total aCSA was measured using image J. The

validity and reliability of this technique has been shown previously 21.

Circulating Insulin-Like Growth Factor -1 (IGF - I) levels

At each of the designated testing intervals (i.e. baseline, weeks 8, 10 and 12) and following an

overnight fasting period (~10 hours for all participants), participants reported to the laboratory.

A 21-gauge 1-inch ultra thin wall needle (Terumo Medical Corporation, New Jersey, USA) was

inserted into the antecubital vein of the forearm. Using a vacutainer assembly and serum

separator tubes (Monovette, Sarstedt, Numbrecht, Germany), 5 mL blood samples were

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collected. After being kept on an ice bed for up to 2-hours (or a minimum of 30 min as per the

ELISA kit manufacturer recommendations), the sample was then centrifuged at 4°C for 10 min

at 4,800 rpm, with the supernatant being removed and stored in Eppendorf tubes at −20° C. for

later analysis. The IGF-I (R&D Systems Europe, UK. Sensitivity of 0.026 ng/mL; intra-assay

variability of 4.0%, manufacturer’s data) was analyzed using standard enzyme-linked immuno-

sorbent assay procedures.

Strength measurement

Maximal isometric knee extension torque was measured with the right knee at 70° knee flexion

(full knee extension = 0°) in all participants. The testing angle of 70o was chosen, as this is often

the optimum angle, or very close to, that reported for maximal isometric strength of knee

extensors22. After a series of warm up trials consisting of 10 isokinetic contractions at 60°⋅s−1 at

50-85% maximal effort, participants were instructed to rapidly exert maximal isometric force

against the dynamometer (Cybex, Phoenix Healthcare, UK) lever arm. Participants were given

both verbal and visual encouragement/feedback throughout their effort. Joint torque data

were displayed on the screen of a MacBook Air computer (Apple Computer, Cupertino, CA,

USA), which was interfaced with an A/D system (Acknowledge, Biopac Systems, Santa Barbara,

CA, USA) with a sampling frequency of 2000 Hz. Isometric contractions were held for ∼2 s at

the plateau with a 60 s rest period between contractions. Peak torque was expressed as the

average of data points over a 200 ms period at the plateau phase (i.e. 100 ms either side of the

instantaneous peak torque). The greatest value of peak torque from 3 extensions was used as

the measure of strength in each participant. Measurements were made on the right leg only

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Length modulates adaptation 16

due to time and ethical constraints, the fact that morphological and architectural measures

were only determined on the right limb, and to reduce the impact of fatigue due to prolonged

testing.

Statistics

Data were analyzed using IBM SPSS v19 (IBM Inc, USA). The Shapiro-Wilk and Levene tests

revealed the data sets to be parametric, and they were therefore analyzed using a mixed-design

repeated measures 3×4 ANOVA. The within-group factor was the phase of training (i.e. week 0,

8, 10 and 12) and the between-group factor was training group (i.e. SL, LL or Con). Post-hoc

contrast analyses with Bonferroni corrections were used to compare data to baseline (‘within’

factor) and to control group (‘between’ factor). All data are presented as mean ± standard error

of the mean (SEM). Statistical significance was set with alpha at ≤ 0.05. The average statistical

power of the measured muscle parameters (CSA, pennation angle, fascicle length, and strength)

was statistically adequate at beta ≥ 0.86.

Results:

Measurements precision:

A pilot study was conducted at the onset of the study on a similar population (i.e. age and

physical characteristics). Repeated measures of VL muscle anatomical CSA, architecture, and

strength on a group of 5 individuals (2 men, 3 women) were collected on 3 separate occasions

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(spanning 7 consecutive days). Within-day coefficients of variation (CV in %) of 1.5%, 1.9%,

3.3%, 2.2%, and 0.8%, and between-day CVs of 2.6%, 2.1%, 3.6%, and 1.8% were found for

aCSA, fascicle length, fascicle pennation angle, DEXA moment arm (within-day only –

measurements all preformed on same day), and strength respectively. Therefore the

repeatability of the measurements was considered acceptable.

Quantification of muscle-tendon complex stretch

In order to measure the extent of lengthening (or passive stretch) at each training joint-angle

compared to full extension, VL muscle length was measured as the distance between the 2

myotendinous junctions of the muscle, and the results are shown in Table 1. At 90o knee

flexion, the VL was significantly (P = 0.03) lengthened compared to full extension, but not at

either 40o or 50o.

[ INSERT TABLE 1 NEAR HERE ]

Architecture

Fascicle Length: There were significant relative increases in VL fascicle lengths as a result of the

training protocol in both groups post training and detraining compared to baseline, at all 3

measurement sites (see Figure 2, P<0.001). Post-training, fascicles increased in length to a

greater extent at all sites in LL compared to SL (∆ 27±3mm; ∆21±3mm; ∆ 24±3mm; vs.

∆18±4mm; ∆9±6mm; ∆ 12±5mm; P = 0.02 proximal, P<0.01 central, and distal, respectively).

This significant main effect of group was retained through the entire detraining period at all

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sites (P<0.01). The control group did not display any significant changes in fascicle length during

the training and detraining periods (averaged over 3 sites ∆ 3±4mm; P>0.05).

Fascicle pennation Angle: Both training groups experienced significant increases in fascicle

pennation angle post-training at proximal (SL: 9.9±0.4o to 10.7±0.4o ∆9±4%, and LL: 9.0±0.4o to

10±0.3o ∆14±7%, P=0.034), central (SL: 16.2±0.5o to 17.2±0.4o∆7±2%, and LL: 15.3±0.4o to

16.2±0.5o ∆6±3%, P=0.041), and distal (SL: 16.5±1.2o to 18.1±1.0o ∆11±4%, and LL: 18.1±0.9o to

19.2±0.8o ∆7±3%, P=0.003) sites. Fascicle pennation angle remained elevated compared to

baseline (P<0.05) at week 10 at all 3 sites, but not at week 12 in both training groups at any

measurement site. There was no difference (P>0.05) between SL and LL groups in fascicle angle

at any stage. The control group displayed no changes in fascicle angle over the 12 week period

(averaged over 3 sites - 15.9±0.5o to 15.7±0.5o ∆ 1±1%, P>0.05).

[INSERT FIGURE 2 NEAR HERE]

Anatomical Cross-Sectional Area (aCSA):

Changes to aCSA are shown in Figure 3. VL aCSA increased significantly (P<0.0001) relative to

baseline following training at all sites in both training groups, which was still evident at the

conclusion of the detraining period in both training groups at proximal, central, and distal sites

(P<0.01) . There was also a trend for LL to exhibit greater relative gains in aCSA compared to SL

at all sites at week 8 (P<0.06), but only significantly so distally. Here there was a main group

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effect (P=0.030); LL exhibited a 53±12% increase compared to SL showing 18±8% increment in

VL aCSA. The superior adaptations were retained distally at both week 10 (LL: 45±13% vs. SL:

11±10%, P=0.043) and week 12 (LL: 32±9% vs. SL: 2±7%, P=0.022). There was no notable VL

aCSA change over the 12 week period for the controls (0±2%, 4±6%, 3±4% proximal, central,

and distal, respectively; P>0.05).

[ INSERT FIGURE 3 NEAR HERE ]

Insulin-Like Growth Factor -1 (IGF - I)

Changes in IGF-I are shown in Figure 4. IGF-I levels increased significantly as a result of training

in the LL group but not the SL group at week 8 (SL, 407 ± 25 ng/mL – 429 ± 30 ng/mL, 7±6%;

P=0.438; LL, 375 ± 18 ng/mL – 489 ± 29 ng/mL, 31±6%; P=0.033), with a significant between-

group effect (P<0.001). The LL group maintained greater IGF-I levels compared to baseline

(P=0.006) and the SL group (P=0.013) at week 10 but had returned to baseline levels by week

12, and no main group effect was evident at the conclusion of detraining (P>0.05). The control

group showed no significant change in the circulating levels of this hormone at any stage of the

study period (P>0.05).

[ INSERT FIGURE 4 NEAR HERE ]

Muscle Strength:

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Length modulates adaptation 20

Both SL and LL groups increased strength at 70o knee flexion as a result of the training protocols

( P<0.001), with LL experiencing a significantly (P=0.015) greater increase from 223±30Nm to

268±28Nm (26±6%) compared to SL 273± 37Nm from pre-training torque of 253±32Nm (7±3%).

The strength improvements in LL were retained to a greater extent throughout the detraining

phase (week 10: P=0.008, week 12: P=0.011) compared to SL, although by week 12 SL had

returned to baseline strength measures, whereas LL still remained elevated relative to week 0

(P<0.05). The control group strength did not significantly alter during the 12 week training and

detraining period (P>0.05).

Discussion:

The aim of this study was to identify the in vivo effects of dynamic resistance training at 2

distinct average muscle-tendon unit lengths (shorter versus longer) and to determine the time-

course of any reversibility during detraining on morphological, architectural, and functional

properties of the VL and IGF-I levels. It was hypothesized that, due to a greater internal

physiological stress (i.e. higher activation and metabolic demands of producing force at longer

muscle lengths compared to shorter muscle lengths even when forces are normalized 15,17) and

stretch on the VL muscle when training at longer muscle lengths compared to shorter muscle

lengths, the LL group would have superior adaptations to SL in terms of size and function. These

results showed that although both the SL and LL groups displayed marked increases in muscle

structural and mechanical characteristics compared to a control group. In general, the effect of

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Length modulates adaptation 21

training at longer muscle lengths showed greater adaptation in many of the measured

parameters, thus partially confirming our hypotheses. In addition, we theorized that

adaptations would be retained by the group training at a longer muscle length (due to the

greater adaptations of the preceding training) during a subsequent period of detraining, and

this was also confirmed in our observations.

In vivo changes to muscle architecture following a length-restricted resistance training protocol,

to the authors’ knowledge have not yet been reported. Therefore we contend that this is the

first study to demonstrate superior increases in VL fascicle length following an extended period

of loading at longer muscle lengths. The relative increases in fascicle length were greater in the

LL group than those of SL post-training at each of the 3 measured sites. Observations from

animal models have demonstrated the importance of stretch in modulation of sarcomere

number 23,24 and is associated with an increase in protein synthesis25. Table 1 shows that by

placing the leg at 90o of knee flexion, the VL muscle was stretched to a greater degree than any

other training knee joint angle. By performing load-bearing exercise with the muscle-tendon

complex in a relatively lengthened position (i.e. 40-90o in the LL group), an enhanced

mechanical stimulus is experienced (i.e. greater stretch), thereby augmenting fascicle length

increase by an increase in the number of in-series sarcomeres to allow each sarcomere to work

at optimal length in line with the length-tension relationship of this unit. It should be pointed

out here that, although fascicle length was measured at 90o of knee flexion and the SL group

did not encounter this joint-angle during training specifically, the SL group would still have

experienced this joint angle during their normal daily routine including sit-to-stand transitions.

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Length modulates adaptation 22

Therefore when measuring fascicle length in the laboratory, the in-series and parallel elastic

components should not be sufficiently ‘stiffer’ in this group to justify the large between-group

changes we describe here.

Excursion range has been suggested to be important for regulating sarcomere number in the

rabbit 4, although our results suggest that an excursion with the muscle in a predominantly

lengthened position is the major regulator of fascicle length in vivo. This is due to the fact that

both groups performed the same degree of excursion of 50o, yet they had different levels of

adaptation. Additionally, in favor of the excursion offset hypothesis, is that muscle forces at the

tendon were also matched during resistance training. Therefore, no additional mechanical

stimulus for fascicle length change (i.e. greater force) was present in the LL group, which is in

agreement with previous work 26.

The relationship between muscle aCSA and strength is well established. The LL group had

greater relative increases in aCSAs at all 3 measured sites along the VL following the training

period, however, they were only statistically so distally. A heterogeneous hypertrophic

response following knee-extensor resistance training has been reported previously in the VL

muscle 27,6. A lack of intramuscular homogeneity in stress in knee extensors may be due to 1 or

a combination of several factors to provide “mechanical stability” 28 (the latter refers here to

the ability to efficiently use the combined properties of muscle strength, architecture,

proprioception, and tendon characteristics to effect movement about a joint 29) force

generation and/ or force transfer 30. It has been shown that muscle experiences both serial and

parallel force distribution, and that, depending on muscle length, it can exhibit a proximal-distal

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difference in force transmission31. The difference in the VL distribution of force due to

alteration in its length may be a possible reason for observed distal hypertrophy in the LL group

compared to SL. The increase in strength following the training period measured by isometric

MVC was greater in the LL group than SL and may be reflective of the changes in aCSA and not

in changes to fascicle angle of pennation (Figure 3). Nevertheless, we acknowledge here that

aCSA may not be as strongly correlated with force compared to pCSA, as aCSA taken at right

angles will therefore not pass through all the fibers of a highly pennate muscle. Nonetheless

Bamman et al. 32 found aCSA to be as effective as pCSA in estimating strength. The changes in

strength reported in our study for the LL group are similar to those reported in other training

studies e.g.33,27,34, but those of the SL group are less (we propose that the seemingly low

training responsiveness of SL is due to a combination of lower training duration, volume, and

chronic muscle activation 15 compared with that encountered in the work of Jones &

Rutherford33). Additionally, we point out that not only was the range of motion similar between

the training groups, but also that the isometric strength test angle was 20o from the end range

of motion of each group (i.e. 50 o and 90o), thereby conferring a high degree of equity to the

assessment of strength. Additionally, in a similar study, we have recently shown that there are

significantly greater increases in isometric MVC of the entire measured torque-angle

relationship (30o-90o knee flexion) in a wide range of motion training group compared to that in

a short range of motion training group34. It is also possible that following length-specific training

that optimal angle of force production could have changed due to varying changes in fascicle

length and as an adaptive process to the functional length of the muscle-tendon unit. However

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Length modulates adaptation 24

to gain an insight into changes in optimal angle, one would also need to study changes in

tendon mechanical properties, and from the current data set that would be difficult to predict.

Here, we outline some of the possibilities that may have given rise to generally greater

hypertrophy following length-specific training. First, it has been shown that VL activation and

oxygen consumption are significantly greater during isometric MVCs at longer (60o and 90o)

muscle lengths compared to shorter (30o) muscle lengths, with the greatest activation and

oxygen consumption at 90o 15,35. In conjunction with these results, 1 of the major findings was

that IGF-I levels in this study were significantly greater in LL post training compared to SL (31%

vs. 7% increment). In vivo increases in IGF-I following resistance training in humans have been

reported previously36, and extensive in vitro research has shown that IGF-I is an important

regulator of muscle mass in vivo, and that experimental manipulation of IGF-I levels can cause a

tremendous increase in muscle mass and protein synthesis 9,37. In vivo data from adult skeletal

muscle has shown that, although electrical stimulation failed to increase levels of growth or

protein synthesis, static stretch of muscle increased IGF-I mRNA 12-fold with a concomitant

increase in fractional (138%) and total (191%) protein synthesis rates. Furthermore, stretch

combined with electrical stimulation increased IGF-I mRNA concentration 40-fold , with

fractional and total protein synthesis rates increasing by 345% and 450% respectively in this

condition 9. This evidence suggests that by training at longer muscle lengths (i.e. LL group),

muscle is activated to a greater degree and experiences greater metabolic and mechanical

stress. In response, there is coordinated activation of probably several signalling cascades,

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Length modulates adaptation 25

which may be mediated, at least in part, by the activity of IGF-I. A combination of these factors

may explain the larger hypertrophic response of the LL group compared to SL.

The temporal response of in vivo changes to architecture during a short period of detraining has

not been reported previously. During a period of 3 months of detraining, fascicle length was

previously shown to increase following removal of the training protocol 6. In our study, the

results show that in both SL and LL groups, fascicle lengths were reduced during the detraining

period, and these reductions were fairly linear in each group. For example, there was a ∆-6%

(14% to 8%) and ∆-5% (29% to 24%) reduction (averaged across the 3 sites) compared to

baseline in the SL and LL groups, respectively at week 10, with almost identical reductions at

week 12 (SL: ∆5%, 8% to 3%, LL: ∆6%, 24% to 18%). These data indicate that, although there

appears to be no difference in the rate of loss of adaptation between groups, the LL group’s

greater initial increases to fascicle length during training resulted in retention of increased

fascicle lengths following 4 weeks detraining.

From the results of the effect of detraining on VL aCSA, there were similar magnitudes of

relative losses in aCSA and fascicle length (parallel and serial sarcomere number) in SL (week

10: ∆-4% and week 12: ∆-5% relative to baseline averaged over 3 sites). However in the LL

group, the magnitude of decrements in aCSA were more pronounced compared to fascicle

length especially in the later stages (week 10: ∆-6% and week 12: ∆-13%), however the LL group

still retained greater overall aCSA values relative to baseline at week 12 (+21 ± 6%) compared to

SL (+11 ± 4%). It has been previously shown that IGF-1 has been implicated in preventing

expression of the FOXO class of transcription factors and the mRNA increases of MAFbx and

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Length modulates adaptation 26

MuRF1 seen during muscle atrophy 13. The LL group continued to have significantly greater IGF-I

levels than SL at both week 8 and week 10. Although not a chronic increase in IGF-I levels, the

LL group’s responses certainly lasted longer than the transient increase in IGF-I observed with

acute bouts of resistance exercise. Therefore, there may have been a protective role played by

IGF-I to allow greater retention of muscle mass in LL. In support of this notion is the observation

that the LL group IGF-I levels at week 12 had returned to baseline levels, and that this period

also coincided with the relatively larger magnitude of aCSA decrement in LL group at the

conclusion of the detraining phase. The larger initial gains of muscle mass may also provide a

rationale for generally greater strength retention in LL at the end of the detraining period,

through the positive correlation between mass and strength. In addition, the VL (and vastus

medialis) muscle has been shown to be activated to a greater extent at longer muscle lengths
15
, therefore if the muscle is activated chronically to a greater extent, the magnitude of neural

drive is likely to be retained, thereby sustaining muscle strength gains during at least the first 4

weeks of detraining.

Conclusion

Previous evidence in young humans 6 demonstrated that eccentric training was not the major

determinant for fascicle length adaptations. However in the current study, greater increases in

fascicle length of the VL were present following longer muscle length training, despite identical

overall degree of excursion and muscle forces at the tendon. We show that, in humans, muscle

length controlled excursion is the major mechanical stimulus for changes in fascicle length;

although the exact mechanisms underpinning such adaptations are complex and have yet to be

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Length modulates adaptation 27

elucidated. A previous study 16 of isometric training at longer and shorter muscle lengths found

no differences between training groups in muscle morphology. Here, we present evidence that

prolonged dynamic resistance training at predominantly longer compared to shorter muscle

lengths resulted in more marked improvements in strength and regional muscle hypertrophy,

and these adaptations may be in part mediated from a greater hormonal response elicited.

Furthermore, with muscle architecture and strength being major influences on the

determinants of functional performance from athletes to the elderly, these results suggest that

length-specific training should be implemented. Additionally, since adaptations are retained

more successfully over 4 weeks of detraining with the muscle lengthened, such training could

also be used to offset deleterious effects of detraining or hypoactivity.

Future work should consider the fact that the hip angle, while standardized for most

exercises, was not strictly controlled during the squats. Arguably, where 4 of 5 exercises

standardized hip angles (hence the impact of 1 exercise with no such control would be

minimal), for a protocol with more ‘squat-like’ exercises, it would be advisable to monitor the

activity of the rectus femoris. Indeed this is the only knee extensor (out of a possible 4) that

crosses the hip joint, and it is possible that its contribution to hip flexion may impact on overall

quadriceps muscle shortening within a resistance training program.

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Length modulates adaptation 28

Acknowledgements:

The authors are ever indebted to the study populations without whom none of this work would

have been possible. The authors are also grateful for the continued support from the Institute

for Performance Research, Manchester Metropolitan University.

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Length modulates adaptation 32

Tables:

Knee Joint angle VL Muscle Length Muscle Length to

(o knee flexion) (cm) Femur Length Ratio

0o (Full extension) 32.8±1.1 0.74 : 1

40o 34.7±0.9 0.78 : 1

50o 35.3±0.9 0.80 : 1

90o 37.0±1.1* 0.83 : 1

Table 1. Resting Vastus Lateralis length at various knee-joint angles. NB. In this population,
the average femur length was 44.6 ± 1.0 cm (n=6). * Significantly different from full extension
(P<0.05).

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Figure Legends:

Figure 1: Diagram of training excursions and testing joint angle.

Figure 2: Relative changes to fascicle length following training (PT) and detraining (DT1 &

DT2) in SL (open squares), LL (black squares), and control (dashed line) groups at: A) proximal,

B) central, and C) distal sites of the VL muscle. * Significant difference compared to baseline

(P<0.05) † Significant difference between groups (P<0.05). (BS= Baseline)

Figure 3: Changes following training (PT) and detraining (DT1 & DT2) to aCSA in SL group

(white bars) and LL group (black bars) at: (A) proximal, (B) central, and (C) distal sites of VL

muscle. † Significant group difference in aCSA (P<0.05).

Figure 4: Changes in IGF-I following training (PT) and detraining (DT1 & DT2) in the SL (black

bars), LL (white bars), and control (grey bars) groups. * Significant difference compared to

baseline (P<0.05) † Significant difference between groups (P<0.05).

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Figure 1: Diagram of training excursions and testing joint angle.

254x190mm (300 x 300 DPI)

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Figure 2: Relative changes to fascicle length following training (PT) and detraining (DT1 & DT2) in SL (open
squares), LL (black squares) and control (dashed line) groups at A) proximal, B) central and C) distal sites
of the VL muscle. * Significant difference compared to baseline (p<0.05) † Significant difference between
groups (p<0.05). (BS= Baseline)
190x254mm (300 x 300 DPI)

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 Muscle & Nerve Page 36 of 37

Figure 3: Changes following training (PT) and detraining (DT1 & DT2) to aCSA in SL group (white bars) and
LL group (black bars) at (A) proximal, (B) central and (C) distal sites of VL muscle. † Significant group
difference in aCSA (p<0.05).
190x254mm (300 x 300 DPI)

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Figure 4: Changes in IGF-I following training (PT) and detraining (DT1 & DT2) in the SL (black bars), LL
(white bars) and control (grey bars) groups. * Significant difference compared to baseline (p<0.05) †
Significant difference between groups (p<0.05).
254x190mm (300 x 300 DPI)

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