Factors affecting chronic low back pain among high school baseball players in Japan: A pilot study.

The prevalence of chronic lower back pain (CLBP) among baseball players is high. CLBP is associated with reduced participation in practice and games. This pilot study examined the factors associated with CLBP among high school baseball players in Fukui, Japan. The participants underwent two health examinations in high school: (1) as first-grade baseball players (baseline) and (2) as second-grade baseball players (follow-up); a total of 59 players who could be followed-up a year later were included in the study. Players were divided into three groups based on whether they had no lower back pain (LBP) (n = 30), improved LBP (n = 17), or CLBP (n = 12) after 1 year of follow-up. Players were evaluated on the physical and cognitive aspects of pain. The Number Rating System, Pain Catastrophizing Scale (PCS), Tampa Scale for Kinesiophobia (TSK), Central Sensitization Inventory (CSI), body characteristics (age, height, weight, body mass index, and skeletal mass index), and a medical history questionnaire regarding spondylolysis and baseball loads were used to evaluate the players. Inventory scores were highest in the CLBP group, which indicated that this group had significant pain that affected their willingness to engage in baseball-related activities. The TSK scores in the CLBP group were worse on follow-up. High school baseball players with CLBP were more likely to have lumbar spondylolysis and kinesiophobia, which are also factors related to pain chronicity. Kinesiophobia and the presence of lumbar spondylolysis should be considered when creating an exercise program for high school baseball players with CLBP.

Effects of combined treatment with blood flow restriction and low-current electrical stimulation on capillary regression in the soleus muscle of diabetic rats.

To clarify the preventive effects of low-current electrical stimulation (ES) under blood flow restriction (Bfr) on diabetes-associated capillary regression in skeletal muscles, we assessed the changes in three-dimensional capillary architecture and angiogenic factors. Twenty-four Goto-Kakizaki rats were randomly divided into four groups: the sedentary diabetes mellitus (DM), Bfr (DM + Bfr), electrical stimulation (DM + ES), and Bfr plus ES (DM + Bfr + ES) groups. Six healthy Wistar rats were used as age-matched controls. Bfr was performed using pressure cuffs (80 mmHg) around the thighs of the rats, and low-current ES was applied to the calf muscles of the rats. The current intensity was set at 30% of the maximal isometric contraction (24-30 mA). The treatments were delivered three times a week for 8 wk. In the DM group, the capillary diameter and volume of the soleus muscle decreased, and, the antiangiogenic factor level increased. Furthermore, DM caused an increase in the hypoxia-inducible factor. Individually, Bfr or ES treatments failed to inhibit the DM-associated capillary regression and increase in antiangiogenic factor. However, combined treatment with Bfr and ES prevented DM-associated capillary regression via inhibition of the increased antiangiogenic factor and enhancement of interleukin-15 expression, mitochondrial biogenesis factors, and a proangiogenic factor. Therefore, DM-associated capillary regression inhibited by the combined treatment may prevent the effects of the increased antiangiogenic factor and enhance the proangiogenic factor.NEW & NOTEWORTHY The combined treatment of blood flow restriction and low intensity electrical stimulation attenuated type 2 diabetes (T2D)-associated capillary regression in the skeletal muscles. The treatment inhibits the T2D-associated increase in antiangiogenic factors via inhibition of intramuscular chronic hypoxia; it can inhibit intramuscular chronic hypoxia by enhancing proangiogenic factors. These results suggest that the combined treatment may be an effective therapeutic intervention for the prevention of T2D-associated capillary regression in the skeletal muscles.

Correlation of medial longitudinal arch morphology with body characteristics and locomotive function in community-dwelling older women: A cross-sectional study.

PURPOSE: This cross-sectional study aimed to investigate the effects of foot arch deformities on physical characteristics, muscular strength, and motor function in older women depending on the presence or absence of pain. METHODS: Overall, 145 community-dwelling women aged 65 to 90 years were included in this study. We measured the foot arch height ratio (AHR, dorsal height/truncated foot length) and classified participants with AHR values above, below, or within 1.5 standard deviations into the high-arched group (HAG), Low-Arched Group (LAG), or normal-arched group (NAG), respectively. We also compared body characteristics (age, height, weight, body mass index (BMI), and skeletal mass index), muscle strength (handgrip strength and intrinsic foot strength (IFS)), and locomotive function (two-step value and gait speed) among the three groups. RESULTS: Locomotive examination and muscle strength showed significant differences among the three groups only in the presence of pain; in the two-step test, HAG, NAG, and LAG values were 0.98 cm/cm, 1.19 cm/cm, and 1.18 cm/cm, respectively. The IFS measured 19.2 N, 24.2 N, 31.0 N, respectively, in the HAG, NAG, and LAG. CONCLUSION: This study suggests that decreased IFS affects the mobility function of high-arched feet in older women. Although there was no significant difference in the evaluation of pain, HAG showed the highest average value, which is considered to contribute to the decreased two-step value. It has been suggested that a high-arched foot in the presence of pain is associated with IFS weakness and may affect the decline of mobility function in older women.

Preventive effects of low-intensity endurance exercise for severe hyperglycemia-induced capillary regression in non-obese type 2 diabetes rat skeletal muscle.

Although endurance exercise is effective for reducing diabetes-related capillary regression, it is difficult to prescribe high-intensity endurance exercise due to the potential worsening of complications in patients with severe hyperglycemia. Therefore, this study aimed to examine whether chronic low-intensity exercise training may prevent severe hyperglycemia-induced capillary regression of skeletal muscle in non-obese type 2 diabetes. Non-diabetic Sprague Dawley rats were assigned to a control (Con) group and an exercise (Ex) group. Likewise, spontaneously diabetic Torii rats were assigned to a diabetic sedentary (DM) group or a diabetic exercise (DMEx) group. Rats in the Ex and DMEx groups were placed on a motor-driven treadmill running at low speed (15 m/min) for 60 min/day, 5 days/week, for 14 weeks. Serum glucose levels were significantly increased in the DM group, but not in the DMEx group. Although the capillary-to-fiber ratio in the plantaris muscle was significantly lower in the DM group compared to the control group, the ratio in the DMEx group was significantly higher compared to the DM group. Moreover, the succinate dehydrogenase activity and expression levels of vascular endothelial growth factor and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) were reduced in the plantaris muscle of the DM group. However, those in the DMEx group were significantly higher than those in the DM group. These results indicate that low-intensity chronic endurance exercise training has the potential to prevent the progression of capillary regression in the skeletal muscles of non-obese type 2 diabetes patients with severe hyperglycemia.

Effects of combined treatment with blood flow restriction and low-current electrical stimulation on muscle hypertrophy in rats.

This study aimed to clarify the effects of a combined treatment comprising blood flow restriction and low-current electrical stimulation on skeletal muscle hypertrophy in rats. Male Wistar rats were divided into control (Cont), blood flow restriction (Bfr), electrical stimulation (Es), or Bfr with Es (Bfr + Es) groups. Pressure cuffs (80 mmHg) were placed around the thighs of Bfr and Bfr + Es rats. Low-current Es was applied to calf muscles in the Es and Bfr + Es rats. In experiment 1, a 1-day treatment regimen (5-min stimulation, followed by 5-min rest) was delivered four times to study the acute effects. In experiment 2, the same treatment regimen was delivered three times/wk for 8 wk. Body weight, muscle mass, changes in maximal isometric contraction, fiber cross-sectional area of the soleus muscle, expression of phosphorylated and total-ERK1/2, phosphorylated-rpS6 Ser235/236, phosphorylated and total Akt, and phosphorylated-rpS6 Ser240/244 were measured. Bfr and Es treatment alone failed to induce muscle hypertrophy and increase the expression of phosphorylated rpS6 Ser240/244. Combined Bfr + Es upregulated muscle mass, increased the fiber cross-sectional area, and increased phosphorylated rpS6 Ser240/244 expression and phosphorylated rpS6 Ser235/236 expression compared with controls. Combined treatment with Bfr and low-current Es can induce muscle hypertrophy via activation of two protein synthesis signaling pathways. This treatment should be introduced for older patients with sarcopenia and others with muscle weakness.NEW & NOTEWORTHY We investigated the acute and chronic effect of low-current electrical stimulation with blood flow restriction on skeletal muscle hypertrophy and the mechanisms controlling the hypertrophic response. Low-current electrical stimulation could not induce skeletal muscle hypertrophy, but a combination treatment did. Blood lactate and growth hormone levels were increased in the early response. Moreover, activation of ERK1/2 and mTOR pathways were observed in both the acute and chronic response, which contribute to muscle hypertrophy.

Effects of combined treatment with blood flow restriction and low-intensity electrical stimulation on diabetes mellitus-associated muscle atrophy in rats.

BACKGROUND: Diabetes mellitus (DM) results in decreased muscle mass and harmful complications. Blood flow restriction (Bfr) and electrical stimulation (ES) increase muscle protein synthesis. We hypothesized that combined Bfr and low-intensity ES may be more effective in preventing diabetes-associated muscle atrophy by inhibiting the downregulation of protein synthesis-related pathways. In this study, the effects of combined Bfr and low-intensity ES on diabetes-associated muscle atrophy were investigated by evaluating advanced glycation end-products (AGEs) and receptor for AGEs (RAGE) in rats. METHODS: Twenty-four Goto-Kakizaki (GK) rats were randomly divided into four treatment groups: sedentary DM, DM + Bfr (pressure cuffs placed around the thigh), DM + ES, and DM + Bfr + ES. Six Wistar rats were used as an age-matched control. Levels of AGEs and the expression of RAGE, extracellular signal-regulated kinase (ERK), and ribosomal protein S6 (rpS6) were determined in plantaris muscles. RESULTS: Diabetes resulted in a loss of muscle mass and upregulation of AGEs and RAGE in the plantaris muscle compared with the control group. Treatment with Bfr and ES alone failed to attenuate diabetes-associated loss of muscle mass, and could not prevent the upregulation of AGEs. However, the combination of Bfr and ES prevented the diabetes-associated decrease in muscle mass and upregulation of AGEs. In addition, the combination treatment prevented diabetes-associated decreases in the expression of phosphorylated rpS6. CONCLUSIONS: Combination treatment with Bfr and ES may prevent diabetes-associated muscle atrophy by upregulating inhibition of AGEs, which leads to the activation of protein synthesis.

Effects of skin stretching without joint movement on skin extensibility of rats.

[Purpose] This study examined the possibility of maintaining skin extensibility by stretching the skin involved in disuse joint contracture. [Subjects and Methods] The study was carried out using 18 male Wistar rats. The rats were randomly allocated to three groups. The control group received no intervention for the right ankle joint, the fixation group received one-week's fixation of the right ankle joint in maximum plantar-flexion with a cast, and the stretching group received continuous stretching of the skin over the Achilles tendon for 30 min once daily for one week with the cast removed during the skin stretching, but the joint was not moved. On the final day, skin extensibility of the skin from the posterior aspect of the ankle joint was determined using a tensile strength tester and a length-tension curve. [Results] Statistical analysis of the data revealed significant differences in the skin extensibility among the three groups. The stretching group showed significantly greater improvement of skin extensibility than the fixation group. [Conclusion] Skin stretching without moving the joint was demonstrated to be useful for maintaining skin extensibility.

Exercise training prevents decrease in luminal capillary diameter of skeletal muscles in rats with type 2 diabetes.

The purpose of this study was to examine whether exercise training can prevent microangiopathy of skeletal muscles in rats with type 2 diabetes and if succinate dehydrogenase (SDH) activity, an indicator of mitochondrial oxidative enzyme activity, is involved in the prevention of microangiopathy. Six-week-old male Goto-Kakizaki (GK) rats and age-matched male Wistar rats (control group (Con)) were used. GK rats were randomly assigned to nonexercise (DB) and exercise (DBEx) groups. The DBEx group was trained on a treadmill 5 times a week for 3 weeks. No significant differences in the capillary-to-fibre ratio or the capillary density were observed between the 3 groups. The luminal capillary diameter of the DB group was significantly lower than that of the Con group, whereas the capillary diameter of the DBEx group was significantly higher than that of the DB group. In addition, SDH activity was significantly higher in the DBEx group than in the Con and DB groups. Microangiopathy of skeletal muscles in type 2 diabetes was correlated with a decrease in the luminal capillary diameter, which was prevented by exercise training. Thus, the mitochondrial oxidative capacity appears to be involved in the overall mechanism by which exercise prevents microangiopathy.