No abstract

Skeletal muscle hypertrophy is typically considered to be a slow process. However, this is partly because the time course for hypertrophy has not been thoroughly examined. The purpose of this study was to use weekly testing to determine a precise time course of skeletal muscle hypertrophy during a resistance training program. Twenty-five healthy, sedentary men performed 8 weeks of high-intensity resistance training. Whole muscle cross-sectional area (CSA) of the dominant thigh was assessed using a peripheral quantitative computed tomography scanner during each week of training (W1-W8). Isometric maximum voluntary contractions (MVC) were also measured each week. After only two training sessions (W1), the mean thigh muscle CSA increased by 5.0 cm(2) (3.46%; p < 0.05) from the pre-testing (P1) and continued to increase with each testing session. It is possible that muscular edema may have influenced the early CSA results. To adjust for this possibility, with edema assumedly at its highest at W1, the next significant increase from W1 was at W3. W4 was the first significant increase of MVC over P1. Therefore, significant skeletal muscle hypertrophy likely occurred around weeks 3-4. Overall, from the pre-testing to W8, there was an increase of 13.9 cm(2) (9.60%). These findings suggested that training-induced skeletal muscle hypertrophy may occur early in a training program.

Skeletal muscle fibers hypertrophy in response to strength training, with type II fibers generally demonstrating the greatest plasticity in regards to cross-sectional area (CSA). However, assessing fiber type-specific CSA in humans requires invasive muscle biopsies. With advancements in the decomposition of surface electromyographic (sEMG) signals recorded using multichannel electrode arrays, the firing properties of individual motor units (MUs) can now be detected noninvasively. Since action potential amplitude (APSIZE) has a documented relationship with muscle fiber size, as well as with its parent MU's recruitment threshold (RT) force, our purpose was to examine if MU APSIZE, as a function of its RT (i.e., the size principle), could potentially be used as a longitudinal indicator of MU-specific hypertrophy. By decomposing the sEMG signals from the vastus lateralis muscle of 10 subjects during maximal voluntary knee extensions, we noninvasively assessed the relationship between MU APSIZE and RT before and immediately after an 8-wk strength training intervention. In addition to significant increases in muscle size and strength (P < 0.02), our data show that training elicited an increase in MU APSIZE of high-threshold MUs. Additionally, a large portion of the variance (83.6%) in the change in each individual's relationship between MU APSIZE and RT was explained by training-induced changes in whole muscle CSA (obtained via ultrasonography). Our findings suggest that the noninvasive, electrophysiological assessment of longitudinal changes to MU APSIZE appears to reflect hypertrophy specific to MUs across the RT continuum.

In this study, we examined the minimum number of constant-torque passive stretches necessary to reduce musculotendinous stiffness. Thirteen healthy individuals (mean age 22 years, s = 3; stature 1.67 m, s = 0.1; mass 66 kg, s = 13 kg) volunteered to participate in the investigation and underwent four 30-s constant-torque passive stretches of the plantar flexor muscles. Musculotendinous stiffness was examined from the angle-torque curves generated prior to the passive stretches, at the beginning of each 30-s stretch, and immediately following the four 30-s passive stretches. The results indicated that musculotendinous stiffness of the plantar flexors was reduced following two 30-s constant-torque passive stretches (P < 0.05) compared with the pre- musculotendinous stiffness assessment. Musculotendinous stiffness remained depressed following the third and fourth stretches, but did not decrease further. These findings suggest that two 30-s bouts of constant-torque passive stretching may be necessary to cause a significant decrease in musculotendinous stiffness of the plantar flexor muscles.

Recent evidence has shown acute static stretching may decrease hamstring-to-quadriceps (H:Q) ratios. However, the effects of static stretching on the functional H:Q ratio, which uses eccentric hamstrings muscle actions, have not been investigated. This study examined the acute effects of hamstrings and quadriceps static stretching on leg extensor and flexor concentric peak torque (PT), leg flexor eccentric PT, and the conventional and functional H:Q ratios. Twenty-two women (mean ± SD age=20.6 ± 1.9 years; body mass=64.6 ± 9.1 kg; height=164.5 ± 6.4 cm) performed three maximal voluntary unilateral isokinetic leg extension, flexion, and eccentric hamstring muscle actions at the angular velocities of 60 and 180°/s before and after a bout of hamstrings, quadriceps, and combined hamstrings and quadriceps static stretching, and a control condition. Two-way repeated measures ANOVAs (time × condition) were used to analyze the leg extension, flexion, and eccentric PT as well as the conventional and functional H:Q ratios. Results indicated that when collapsed across velocity, hamstrings-only stretching decreased the conventional ratios (P<0.05). Quadriceps-only and hamstrings and quadriceps stretching decreased the functional ratios (P<0.05). These findings suggested that stretching may adversely affect the conventional and functional H:Q ratios.