Studies using animal models have been unable to determine the mechanical stimuli that most influence muscle architectural adaptation. We examined the influence of contraction mode on muscle architectural change in humans, while also describing the time course of its adaptation through training and detraining. Twenty-one men and women performed slow-speed (30 degrees /s) concentric-only (Con) or eccentric-only (Ecc) isokinetic knee extensor training for 10 wk before completing a 3-mo detraining period. Fascicle length of the vastus lateralis (VL), measured by ultrasonography, increased similarly in both groups after 5 wk (Delta(Con) = +6.3 +/- 3.0%, Delta(Ecc) = +3.1 +/- 1.6%, mean = +4.7 +/- 1.7%; P < 0.05). No further increase was found at 10 wk, although a small increase (mean approximately 2.5%; not significant) was evident after detraining. Fascicle angle increased in both groups at 5 wk (Delta(Con) = +11.1 +/- 4.0%, Delta(Ecc) = +11.9 +/- 5.4%, mean = 11.5 +/- 3.2%; P < 0.05) and 10 wk (Delta(Con) = +13.3 +/- 3.0%, Delta(Ecc) = +21.4 +/- 6.9%, mean = 17.9 +/- 3.7%; P < 0.01) in VL only and remained above baseline after detraining (mean = 13.2%); smaller changes in vastus medialis did not reach significance. The similar increase in fascicle length observed between the training groups mitigates against contraction mode being the predominant stimulus. Our data are also strongly indicative of 1) a close association between VL fascicle length and shifts in the torque-angle relationship through training and detraining and 2) changes in fascicle angle being driven by space constraints in the hypertrophying muscle. Thus muscle architectural adaptations occur rapidly in response to resistance training but are strongly influenced by factors other than contraction mode.
The most important anatomical determinants of in vivo joint moment magnitude have yet to be defined. Relationships between maximal knee extensor moment and quadriceps muscle volume, anatomical (ACSA) and physiological (PCSA) cross-sectional area, muscle architecture and moment arm (MA) were compared. Nineteen untrained men and women performed maximal isokinetic knee extensions under isometric conditions (90 degrees joint angle) and at 30 degrees and 300 degrees s(-1). Magnetic resonance and ultrasound imaging techniques were used to measure vastus lateralis PCSA and fascicle length (FL), quadriceps ACSA, volume and patellar tendon MA. Muscle volume was the best predictor of extensor moment measured isometrically (R(2) = 0.60) and at 30 degrees s(-1)(R (2) = 0.74). PCSA x FL was the best predictor of moment at 300 degrees s(-1) (R(2) = 0.59). MA was not an important predictor. ACSA was the second best predictor at all three speeds and could be recommended as an ideal measure given its relative ease of measurement.
Blazevich AJ, Cannavan D, Waugh CM, Miller SC, Thorlund JB, Aagaard P, Kay AD. Range of motion, neuromechanical, and architectural adaptations to plantar flexor stretch training in humans. 117: 452-462, 2014. First published June 19, 2014 doi:10.1152/japplphysiol.00204.2014.-The neuromuscular adaptations in response to muscle stretch training have not been clearly described. In the present study, changes in muscle (at fascicular and whole muscle levels) and tendon mechanics, muscle activity, and spinal motoneuron excitability were examined during standardized plantar flexor stretches after 3 wk of twice daily stretch training (4 ϫ 30 s). No changes were observed in a nonexercising control group (n ϭ 9), however stretch training elicited a 19.9% increase in dorsiflexion range of motion (ROM) and a 28% increase in passive joint moment at end ROM (n ϭ 12). Only a trend toward a decrease in passive plantar flexor moment during stretch (Ϫ9.9%; P ϭ 0.15) was observed, and no changes in electromyographic amplitudes during ROM or at end ROM were detected. Decreases in H max:Mmax (tibial nerve stimulation) were observed at plantar flexed (gastrocnemius medialis and soleus) and neutral (soleus only) joint angles, but not with the ankle dorsiflexed. Muscle and fascicle strain increased (12 vs. 23%) along with a decrease in muscle stiffness (Ϫ18%) during stretch to a constant target joint angle. Muscle length at end ROM increased (13%) without a change in fascicle length, fascicle rotation, tendon elongation, or tendon stiffness following training. A lack of change in maximum voluntary contraction moment and rate of force development at any joint angle was taken to indicate a lack of change in series compliance of the muscle-tendon unit. Thus, increases in end ROM were underpinned by increases in maximum tolerable passive joint moment (stretch tolerance) and both muscle and fascicle elongation rather than changes in volitional muscle activation or motoneuron pool excitability. J Appl Physiol
This study examined the effects of slow-speed resistance training involving concentric (CON, n = 10) versus eccentric (ECC, n = 11) single-joint muscle contractions on contractile rate of force development (RFD) and neuromuscular activity (EMG), and its maintenance through detraining. Isokinetic knee extension training was performed 3 x week(-1) for 10 weeks. Maximal isometric strength (+11.2%) and RFD (measured from 0-30/50/100/200 ms, respectively; +10.5%-20.5%) increased after 10 weeks (P < 0.01-0.05); however, there was no effect of training mode. Peak EMG amplitude and rate of EMG rise were not significantly altered with training or detraining. Subjects with below-median normalized RFD (RFD/MVC) at 0 weeks significantly increased RFD after 5- and 10-weeks training, which was associated with increased neuromuscular activity. Subjects who maintained their higher RFD after detraining also exhibited higher activity at detraining. Thus, only subjects with a lesser ability to rapidly attain their maximum force before training improved RFD with slow-speed resistance exercise.
Maximum joint range of motion is an important parameter influencing functional performance and musculoskeletal injury risk. Nonetheless, a complete description of the muscle architectural and tendon changes that occur during stretch and the factors influencing maximum range of motion is lacking. We measured muscle-tendon elongation and fascicle lengthening and rotation sonographically during maximal plantar flexor stretches in 21 healthy men. Electromyogram (EMG) recordings were obtained synchronously with ultrasound and joint moment data, and H-reflex measurements were made with the ankle at neutral (0°) and dorsiflexed (50% maximal passive joint moment) positions; the maximum H amplitude (normalized to maximum M-wave amplitude; M(max)) and H-amplitude elicited at a stimulation intensity that evoked 10% M(max) were obtained. Maximal stretch was accomplished through significant muscle (14.9%; 30 mm) and tendon lengthening (8.4%; 22 mm). There were similar relative changes in fascicle length and angle, but planimetric modeling indicated that the contribution of fascicle rotation to muscle lengthening was small (<4 mm). Subjects with a greater range of motion showed less resistance to stretch and a greater passive joint moment at stretch termination than less flexible subjects (i.e., greater stretch tolerance). Also, greater fascicle rotation accompanied muscle elongation (9.7 vs. 5.9%) and there was a greater tendon length at stretch termination in more flexible subjects. Finally, a moderate correlation between the angle of EMG onset and maximum range of motion was obtained (r = 0.60, P < 0.05), despite there being no difference in H-reflex magnitudes between the groups. Thus clear differences in the neuromuscular responses to stretch were observed between "flexible" and "inflexible" subjects.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.