Shigeyuki Suzuki

In this study, we aimed to identify the time course effects of different intensities of static stretch (SST) (maximal intensity without pain vs. high-intensity with moderate pain) on flexibility. This study included 16 healthy students (8 men and 8 women) who performed 1) 5-minute SST at 100%, 2) 110%, and 3) 120% intensity, as well as 4) no stretching (control) in a random sequence on four separate days. Static passive torque (SPT), hamstring electromyography (EMG), and pain intensity were continuously recorded during SST. We assessed markers of stiffness, range of motion (ROM), and maximal dynamic passive torque (DPTmax) before SST and 0, 15, 30, 45, 60, 75, and 90 minutes after SST. Stiffness decreased and ROM and DPTmax increased significantly immediately after SST at the three different intensity levels (p < 0.05). The effects of SST at 120% intensity were stronger and lasted longer than the effects of SST at 110% and 100% intensity (stiffness: -17%, -9%, and -7%, respectively; ROM: 14%, 10%, and 6%, respectively; DPTmax: 15%, 15%, and 9%, respectively). SPT decreased after SST at all intensities (p < 0.05). SST at 120% intensity caused a significantly greater reduction in SPT than SST at 100% intensity (p < 0.05). Pain intensity and EMG activity increased immediately after the onset of SST at 120% intensity (p < 0.05), although these responses were attenuated over time. Stretching intensity significantly correlated with the degree of change in ROM and stiffness (p < 0.05). These results support our hypothesis that stretch-induced flexibility is amplified and prolonged with an increase in stretch intensity beyond the pain threshold. Additional studies with more participants and different demographics are necessary to examine the generalizability of these findings.

In this study, we examined the effects of static and dynamic stretching on range of motion (ROM), passive torque (PT) at pain onset, passive stiffness, and isometric muscle force. We conducted a randomized crossover trial in which 16 healthy young men performed a total of 300 s of active static or dynamic stretching of the right knee flexors on two separate days in random order. To assess the effects of stretching, we measured the ROM, PT at pain onset, passive stiffness during passive knee extension, and maximum voluntary isometric knee flexion force using an isokinetic dynamometer immediately before and after stretching. Both static and dynamic stretching significantly increased the ROM and PT at pain onset (p<0.01) and significantly decreased the passive stiffness and isometric knee flexion force immediately after stretching (p<0.01). However, the magnitude of change did not differ between the two stretching methods for any measurements. Our results suggest that 300 s of either static or dynamic stretching can increase flexibility and decrease isometric muscle force; however, the effects of stretching do not appear to differ between the two stretching methods.

Dynamic stretching (DS) is often performed during warm-up to help avoid hamstring muscle injuries, increase joint flexibility, and optimize performance. We examined the effects of DS of the hamstring muscles on passive knee extension range of motion (ROM), passive torque (PT) at the onset of pain (as a measure of stretch tolerance), and passive stiffness of the muscle-tendon unit over an extended period after stretching. Twenty-four healthy subjects participated, with 12 each in the experimental and control groups. Stretching was performed, and measurements were recorded using an isokinetic dynamometer pre-intervention, and at 0, 15, 30, 45, 60, 75, and 90 min post-intervention. DS consisted of ten 30-s sets of 15 repetitions of extension and relaxation of the hamstrings. ROM increased significantly (range, 7%-10%) immediately after DS, and the increase was sustained over 90 min. PT at the onset of pain also increased immediately by 10% but returned to baseline by 30 min. Passive stiffness decreased significantly (range, 7.9%-16.7%) immediately after DS, and the decrease was sustained over 90 min. Post-DS values were normalized to pre-DS values for the respective outcomes in both groups. ROM was significantly higher (range, 7.4%-10%) and passive stiffness was significantly lower (range, 5.4%-14.9%) in the experimental group relative to the control group at all time points. Normalized PT values at the onset of pain were significantly higher in the experimental group at 0-15 min than in the controls, but the differences were smaller at 30-45 min and not significant thereafter. We conclude that DS increases ROM and decreases passive stiffness in a sustained manner, and increases PT at the onset of pain for a shorter period. Overall, our results indicate that when performed prior to exercise, DS is beneficial for the hamstring muscles in terms of increasing flexibility and reducing stiffness.

Work‐related musculoskeletal disorders (WMSD) are caused by the overuse of muscles in the workplace. Performing repetitive tasks is a primary risk factor for the development of WMSD. Many workers in highly repetitive jobs exhibit muscle pain and decline in handgrip strength, yet the mechanisms underlying these dysfunctions are poorly understood. In our study, rats performed voluntary repetitive reaching and grasping tasks (Task group), while Control group rats did not perform these activities. In the Task group, grip strength and forearm flexor withdrawal threshold declined significantly from week 2 to week 6, compared with these values at week 0 (P < 0.05). Relative muscle weight and muscle fiber cross‐sectional area of flexor digitorum superficialis (FDS) muscles decreased significantly in the Task group, compared with the Control group, at 6 weeks (P < 0.05 and P < 0.01, respectively). Nerve growth factor, glial cell line‐derived neurotrophic factor, and tumor necrosis factor α‐expression in FDS muscles were not significantly different in Control and Task groups at 3 and 6 weeks. At 6 weeks, the Task group had elevated MuRF1 protein levels (P = 0.065) and significant overexpression of the autophagy‐related (Atg) proteins, Beclin1 and Atg5–Atg12, compared with in the Control group (both P < 0.05). These data suggested that long‐term exposure to excessive repetitive motion causes loss of grip strength, muscle pain, and skeletal muscle atrophy. Furthermore, this exposure may enhance protein degradation through both the ubiquitin‐proteasome and autophagy‐lysosome systems, thereby decreasing skeletal muscle mass.

The details of the physical activity in patients with mild to moderate pelvic organ prolapse (Pmoderate pelvic organ prolapse (POP) remain under-studied. The purpose of the present study was to investigate objective physical activity levels and the changes in pelvic floor muscle(PFM) strength, symptoms and quality of life (QOL) between before and after PFM training (PFMT) in patients with POP.

It is generally recognized that synthetic glucocorticoids induce skeletal muscle weakness, and endogenous glucocorticoid levels increase in patients with muscle atrophy. It is reported that heat stress attenuates glucocorticoid-induced muscle atrophy; however, the mechanisms involved are unknown. Therefore, we examined the mechanisms underlying the effects of heat stress against glucocorticoid-induced muscle atrophy using C2C12 myotubes in vitro, focusing on expression of key molecules and signaling pathways involved in regulating protein synthesis and degradation. The synthetic glucocorticoid dexamethasone decreased myotube diameter and protein content, and heat stress prevented the morphological and biochemical glucocorticoid effects. Heat stress also attenuated increases in mRNAs of regulated in development and DNA damage responses 1 (REDD1) and Kruppel-like factor 15 (KLF15). Heat stress recovered the dexamethasone-induced inhibition of PI3K/Akt signaling. These data suggest that changes in anabolic and catabolic signals are involved in heat stress-induced protection against glucocorticoid-induced muscle atrophy. These results have a potentially broad clinical impact because elevated glucocorticoid levels are implicated in a wide range of diseases associated with muscle wasting. J. Cell. Physiol. 232: 650–664, 2017. © 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.

This study compared responses to static stretching between eccentrically damaged and non-damaged muscles. Twelve young men performed 60 maximum knee flexor eccentric contractions of one leg, and received a 300-s continuous passive static stretching at tolerable intensity without pain to both knee flexors at 2 and 4 days after the eccentric exercise. Range of motion (ROM) and passive stiffness during knee extension, passive torque at onset of pain (PT), maximum voluntary isometric (MVC-ISO) and isokinetic concentric contraction torque (MVC-CON), and visual analogue scale (VAS) for muscle soreness were measured before, immediately after, 60 min, 2 and 4 days after exercise as well as before, immediately after, 20 and 60 min after the stretching. Changes in these variables after eccentric exercise and stretching were compared between limbs. The eccentric exercise decreased MVC-ISO, MVC-CON, ROM and PT, and increased passive stiffness and VAS (p < 0.05), suggesting that muscle damage was induced to the knee flexors. ROM and PT increased after stretching for both limbs; however, the magnitude of the increase was greater (p < 0.05) for the damaged than non-damaged limb. Passive stiffness decreased for both limbs similarly (4–7 %) at immediately after stretching (p < 0.05). Significant decreases in MVC-ISO torque (7–11 %) after stretching were observed only for the non-damaged limb (p < 0.05), but MVC-CON torque did not change after stretching for both limbs. VAS decreased for the exercised limb after stretching (p < 0.05). These results suggest that the static stretching at tolerable intensity without pain produced greater positive effects on damaged than non-damaged muscles.

To compare the effects of pelvic floor muscle training (PFMT), with or without biofeedback (BF), for stress urinary incontinence (SUI), focusing on condition-specific quality of life (QOL) outcomes. Women with SUI were randomized to PFMT with BF (BF group, n = 23) or without BF (PFMT group, n = 23) for 12 weeks. As primary outcome measures, subjective symptoms and QOL were assessed by the King’s Health Questionnaire (KHQ) and International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF). A voiding diary, 1-h pad test, and measurement of PFM strength were secondary outcome measures. Changes in the primary and secondary outcomes were assessed before and after 12 weeks’ exercise training. Of the 9 domains of the KHQ, the scores of 5 significantly decreased in the PFMT group, and the scores of 7 significantly decreased in the BF group. All ICIQ-SF items and the total score significantly decreased in both groups after therapy. The number of incontinence episodes significantly decreased in the PFMT group, and tended to decrease in the BF group, but this was not significant (P = 0.054). The leakage volume in the 1-h pad test tended to decrease in both groups, but was not significant. Maximum vaginal squeeze pressure significantly increased in both groups. There were no significant inter-group differences in the changes in any of the parameters assessed. The results indicate that PFMT is effective for treating SUI. There is no apparent add-on effect of BF training in short-term follow-up.

Some evidence indicates that nitric oxide (NO) contributes to inflammation, while other evidence supports the opposite conclusion. To clarify the role of NO in inflammation, we studied carrageenin-induced pleurisy in rats treated with an NO donor (NOC-18), a substrate for NO formation (L-arginine), and/or an NO synthase inhibitor (S-(2-aminoethyl) isothiourea or -nitro-L-arginine). We assessed inflammatory cell migration, nitrite/nitrate values, lipid peroxidation and pro-inflammatory mediators. NOC-18 and L-arginine reduced the migration of inflammatory cells and edema, lowered oxidative stress, and normalized antioxidant enzyme activities. NO synthase inhibitors increased the exudate formation and inflammatory cell number, contributed to oxidative stress, induced an oxidant/antioxidant imbalance by maintaining high , and enhanced the production of pro-inflammatory mediators. L-arginine and NOC-18 reversed the proinflammatory effects of NO synthase inhibitors, perhaps by reducing the expression of adhesion molecules on endothelial cells. Thus, our results indicate that NO is involved in blunting—not enhancing—the inflammatory response.