Torque-angle curve of the knee flexors in athletes with a prior history of hamstring strain.

OBJECTIVES: To investigate the knee flexor torque-angle curve after hamstring strain injury using different muscle action types and angular velocities. DESIGN: Cross-sectional. SETTING: Controlled laboratory. PARTICIPANTS: Thirteen collegiate athletes injured hamstring strain (21.0 ± 0.8 years; 173.9 ± 6.5 cm; 70.1 ± 10.5 kg). MAIN OUTCOME MEASURES: Concentric and eccentric knee flexor torque was measured at 60 & 300°/sec. Peak torque and average torque every 10° were determined from torque-angle curve and injured side was compared with non-injured side. RESULTS: No significant differences were found in the concentric muscle actions. However, the eccentric peak torque was significantly lower on the injured side at 60°/sec (p = 0.048) and at 300°/sec (p = 0.002). The average eccentric torque was significantly lower on the injured side at 60°/sec from 10° to 20° of knee flexion (p = 0.012-0.018) and at 300°/sec from 10° to 60° of knee flexion (p = 0.005-0.049). CONCLUSION: The knee flexor torque-angle curve changes with eccentric muscle action after hamstring injury. Eccentric torque declines were close to full knee extension at 60°/sec and a wide range of knee flexion at 300°/sec. The assessment and rehabilitation of eccentric hamstring strength may be important to consider the effect of the angular velocity after hamstring strain injury.

Dynamic postural control correlates with activities of daily living and quality of life in patients with knee osteoarthritis.

BACKGROUND: Knee osteoarthritis (OA) negatively affects dynamic postural control, which is a basic function that individuals use to perform activities of daily living (ADL). The purpose of this study was to investigate the associations of center of pressure (COP) control during the transition from double-leg to single-leg standing with subjective assessments of ADL and quality of life (QOL) in patients with knee OA. METHODS: Thirty-six patients (29 females) with moderate-to-severe knee OA participated. Dynamic postural control was evaluated during the transition from double-leg to single-leg standing. Each patient stood on a force plate, lifted the less affected limb as fast as possible, and maintained single-leg standing with the more affected limb. The COP movements corresponding to anticipatory postural adjustment (APA) and transitional phases were assessed. The maximum displacement and peak velocity of the COP movements in the medial-lateral direction were calculated. The Knee Injury and Osteoarthritis Outcome Score (KOOS) was used for the subjective assessment of ADL and QOL. Pearson's product correlation analysis was performed to investigate the associations of COP movements in the APA and transitional phases with KOOS-ADL and KOOS-QOL. RESULTS: In the APA phase, the maximum COP displacement was significantly correlated with KOOS-ADL (r = -0.353, P = 0.035) and KOOS-QOL (r = -0.379, P = 0.023). In the transitional phase, the maximum COP displacement and peak COP velocity were significantly correlated with KOOS-ADL (maximum displacement: r = 0.352, P = 0.035; peak velocity: r = 0.438, P = 0.008) and with KOOS-QOL (maximum displacement: r = 0.357, P = 0.032; peak velocity: r = 0.343, P = 0.040). CONCLUSIONS: The present study showed that smaller COP movements in the APA phase and smaller and slower COP movements in the transitional phase correlated with poorer ADL and QOL conditions in patients with knee OA. These findings suggest that poor dynamic postural control is associated with poor ADL and QOL conditions in patients with moderate-to-severe medial knee OA. Conservative treatment for patients with knee OA may need to focus on dynamic postural control during the transition from double-leg to single-leg standing.

Influence of Constant Torque Stretching at Different Stretching Intensities on Flexibility and Mechanical Properties of Plantar Flexors.

ABSTRACT: Oba, K, Samukawa, M, Nakamura, K, Mikami, K, Suzumori, Y, Ishida, Y, Keeler, N, Saitoh, H, Yamanaka, M, and Tohyama, H. Influence of constant torque stretching at different stretching intensities on flexibility and mechanical properties of plantar flexors. J Strength Cond Res 35(3): 709-714, 2021-The purpose of this study was to examine the effects of constant torque stretching (CTS) at different stretching intensities on the maximal range of motion (ROM) and muscle-tendon unit (MTU) stiffness of plantar flexors. Fourteen healthy men performed 4 trials of differing stretch intensities: no stretching (control), 50, 75, and 100%. Stretch intensity was defined as maximum passive resistive torque predetermined at a familiarization trial. Each stretch trial consisted of 5 sets of 60-second CTS at the designated stretch intensity. Both maximal ROM and passive resistive torque were assessed during passive dorsiflexion, and MTU stiffness was calculated using the torque-angle curves measured before and after CTS. There were no significant differences in maximal ROM or MTU stiffness at the baseline condition. After the intervention, significantly greater maximal ROM and significantly lower MTU stiffness were observed in the 100% CTS condition than the control condition, whereas there were no significant differences between the submaximal intensity condition (i.e., 50 or 75% intensity) and the control condition. Therefore, our findings suggest that maximal intensity stretching is the most effective approach for improving both flexibility and MTU stiffness with CTS.

Involvement of lysosomal dysfunction in autophagosome accumulation and early pathologies in adipose tissue of obese mice.

Whether obesity accelerates or suppresses autophagy in adipose tissue is still debatable. To clarify dysregulation of autophagy and its role in pathologies of obese adipose tissue, we focused on lysosomal function, protease maturation and activity, both in vivo and in vitro. First, we showed that autophagosome formation was accelerated, but autophagic clearance was impaired in obese adipose tissue. We also found protein and activity levels of CTSL (cathepsin L) were suppressed in obese adipose tissue, while the activity of CTSB (cathepsin B) was significantly enhanced. Moreover, cellular senescence and inflammasomes were activated in obese adipose tissue. In 3T3L1 adipocytes, downregulation of CTSL deteriorated autophagic clearance, upregulated expression of CTSB, promoted cellular senescence and activated inflammasomes. Upregulation of CTSB promoted additional activation of inflammasomes. Therefore, we suggest lysosomal dysfunction observed in obese adipose tissue leads to lower autophagic clearance, resulting in autophagosome accumulation. Simultaneously, lysosomal abnormalities, including deteriorated CTSL function and compensatory activation of CTSB, caused cellular senescence and inflammasome activation. Our findings strongly suggest lysosomal dysfunction is involved in early pathologies of obese adipose tissue.

Inhibitory effect of p53 on mitochondrial content and function during adipogenesis.

The p53 protein is known as a guardian of the genome and is involved in energy metabolism. Since the metabolic system is uniquely regulated in each tissue, we have anticipated that p53 also would play differential roles in each tissue. In this study, we focused on the functions of p53 in white adipose tissue (adipocytes) and skeletal muscle (myotubes), which are important peripheral tissues involved in energy metabolism. We found that in 3T3-L1 preadipocytes, but not in C2C12 myoblasts, p53 stabilization or overexpression downregulates the expression of Ppargc1a, a master regulator of mitochondrial biogenesis. Next, by using p53-knockdown C2C12 myotubes or 3T3-L1 preadipocytes, we further examined the relationship between p53 and mitochondrial regulation. In C2C12 myoblasts, p53 knockdown did not significantly affect Ppargc1a expression and mtDNA, but did suppress differentiation to myotubes, as previously reported. However, in 3T3-L1 preadipocytes and mouse embryonic fibroblasts, p53 downregulation enhanced both differentiation into adipocytes and mitochondrial DNA content. Furthermore, p53-depleted 3T3-L1 cells showed increase in mitochondrial proteins and enhancement of both Citrate Synthase and Complex IV activities during adipogenesis. These results show that p53 differentially regulates cell differentiation and mitochondrial biogenesis between adipocytes and myotubes, and provide evidence that p53 is an inhibitory factor of mitochondrial regulation in adipocyte lineage.

Autophagosomes accumulate in differentiated and hypertrophic adipocytes in a p53-independent manner.

Autophagy is induced by several kinds of stress, including oxidative, genotoxic, endoplasmic reticulum and nutrient stresses. The tumor suppressor p53, which is a stress sensor, plays a critical role in the regulation of autophagy. Although p53 is required for starvation (nutrient deficient stress)-induced autophagy, it is still not clear whether p53 is also required for the autophagy observed in differentiated and hypertrophic adipocytes, which accumulate excessive amounts of nutrients in the form of triglycerides. In this study, we demonstrated that starvation induces autophagy in p53-proficient adipocytes, but not in p53-deficient adipocytes as previously reported. On the other hand, autophagy was equally observed in both p53-deficient and -proficient differentiated and hypertrophic adipocytes. Similar results were obtained by in vivo analysis using white adipose tissue of high-fat diet-induced obese mice. Moreover, unexpectedly, the autophagy observed in the differentiated and hypertrophic adipocytes involved increased accumulation of autophagosomes and decreased autophagic flux. Thus, we concluded that in differentiated and hypertrophic adipocytes autophagosomes accumulate in a p53-independent manner, and this accumulation is caused by reduced autophagic flux.

Differential responses of white adipose tissue and brown adipose tissue to caloric restriction in rats.

Caloric restriction (CR) slows the aging process and extends longevity, but the exact underlying mechanisms remain debatable. It has recently been suggested that the beneficial action of CR may be mediated in part by adipose tissue remodeling. Mammals have two types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). In this study, proteome analysis using two-dimensional gel electrophoresis combined with MALDI-TOF MS, and subsequent analyses were performed on both WAT and BAT from 9-month-old male rats fed ad libitum or subjected to CR for 6 months. Our findings suggest that CR activates mitochondrial energy metabolism and fatty acid biosynthesis in WAT. It is likely that in CR animals WAT functions as an energy transducer from glucose to energy-dense lipid. In contrast, in BAT CR either had no effect on, or down-regulated, the mitochondrial electron transport chain, but enhanced fatty acid biosynthesis. This suggests that in CR animals BAT may change its function from an energy consuming system to an energy reservoir system. Based on our findings, we conclude that WAT and BAT cooperate to use energy effectively via a differential response of mitochondrial function to CR.

Effects of angiotensin II receptor blockers on renal handling of uric acid in rats.

Elevated serum uric acid level has been associated with increased cardiovascular risk in hypertensive patients. Several angiotensin II receptor blockers exhibit differential effects on regulation of serum uric acid level in humans. We have demonstrated that some angiotensin II receptor blockers trans-stimulate the uptake of uric acid by human URAT1 and others inhibit the transport of uric acid mediated by human URAT1, OAT1, OAT3 and MRP4 in vitro. This study investigated the effects of candesartan, pratosartan and telmisartan on renal handling of uric acid in rats in vivo and in vitro. Candesartan (0.1 mg/kg) significantly decreased the urinary excretion of uric acid and increased the plasma uric acid concentration. The kidney candesartan level after low-dose treatment is close to that required to trans-stimulate uric acid uptake in vitro. Pratosartan exhibited dose-dependent hypouricemic and uricosuric effects, while telmisartan showed no effects on plasma uric acid level. Furthermore, we confirmed the effects of the tested drugs on uric acid transport by rat renal brush border membrane transporter(s) and basolateral Oat1 and Oat3. Effects of angiotensin II receptor blockers in rats may be mainly determined by their intrinsic effects (cis-inhibition and trans-stimulation) on uric acid reabsorption transporter(s) and their pharmacokinetic properties in rats.