Muscle mass reduction, low muscle strength, and their combination are associated with arterial stiffness in community-dwelling elderly population: the Wakayama Study.

Age-related loss of skeletal muscle mass and function is associated with some predisposing factors that increase the risk of vascular damage. This study aimed to examine whether muscle mass reduction, low muscle strength, and their combination were related to arterial stiffness in community-dwelling elderly population. Study participants consisted of 1046 elderly individuals (aged 72 ± 5 years) without cardiovascular disease, chronic kidney disease, or liver disease. Bioelectrical impedance analysis was performed to estimate appendicular skeletal muscle mass (ASM). A value for ASM was normalized for height (ASM index, kg/m2). Handgrip strength (HGS) was measured using a Smedley grip dynamometer. Brachial-ankle pulse wave velocity (baPWV) was evaluated as an index of arterial stiffness using a simple automatic oscillometric technique. When participants were stratified based on baPWV cut-off values (< 1800 cm/s, 1800 to 1999 cm/s, ≥ 2000 cm/s), ASM index and HGS progressively decreased with an increase in baPWV levels (P for trend < 0.001). In multiple regression analysis, baPWV was significantly associated with ASM index (ß = -0.270, P < 0.001) and HGS (ß = -0.102, P < 0.001) independent of potential confounding factors. The baPWV of the subgroup with low ASM index and low HGS was significantly higher than that of those with only low ASM index or low HGS (P < 0.001). These results suggest that loss of skeletal muscle mass and function is associated with increased arterial stiffness in the elderly population, and the combination of muscle mass reduction and low muscle strength may lead to greater arterial stiffness than each of the individual conditions.

The Effects of Well-Rounded Exercise Program on Systemic Biomarkers Related to Cartilage Metabolism.

Nonsurgical treatment such as exercise is the preferred method for management of knee osteoarthritis (OA). A combination of aerobic, muscle strengthening, and flexibility exercises is recommended for older adults. However, effects of the exercise intervention on cartilage metabolism remain unclear. This study used biomarkers to investigate the effects of well-rounded exercise program on cartilage metabolism in 42 women (mean age: 59 years). Participants started a weekly supervised exercise program and continued for 12 weeks. Before and after the program, we measured physical performance on the Timed Up-and-Go Test, 3-Minute Walk Test, and 30-Second Chair Stand Test. We collected serum and urine samples at the start of the program until 24 weeks and measured the concentrations of 4 biomarkers related to type II collagen metabolism: serum cartilage type II procollagen carboxy propeptide (sPIICP), urine C-terminal telopeptide of collagen type II (uCTX-II), urine cleavage of type II collagen by collagenases (uC2C), and serum cartilage oligomeric matrix protein (sCOMP). Participants were divided into pre-OA and OA groups based on X-ray findings. The pre-OA group showed significant increases and decreases in sPIICP and uCTX-II concentrations with improved physical performance, respectively. sCOMP concentrations significantly increased in both groups. The exercise also improved physical performance with no detrimental effect on type II collagen metabolism in the OA group. Thus, well-rounded exercise may not only improve physical capacity but also have beneficial effects on type II collagen metabolism, especially in people without radiological OA.

Effects of exposure to cigarette smoke at different dose levels on extensor digitorum longus muscle fibres in Wistar-Kyoto and spontaneously hypertensive rats.

1. The fibre type distributions, cross-sectional areas (CSA) and succinate dehydrogenase (SDH) activities in the deep (EDLd) and superficial (EDLs) regions of the extensor digitorum longus (EDL) muscle in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were determined after exposure to cigarette smoke at three different dose levels using a smoking machine. 2. Rats were exposed to cigarette smoke at a rate of 15 puffs/min for 20 min/day with 23 cigarettes (low-dose level), 26 cigarettes (medium-dose level) or 30 cigarettes (high-dose level) for 8 weeks. 3. No changes in fibre type distribution, CSA or SDH activity were observed after exposure to cigarette smoke at the low- and medium-dose levels, irrespective of the muscle region or strain. 4. No change in fibre type distribution was observed after exposure to cigarette smoke at the high-dose level, irrespective of the muscle region or strain. A decreased CSA of type IIA and type IIB fibres in EDLd and increased SDH activity of all types of fibres in EDLd and EDLs were observed in WKY rats after exposure to cigarette smoke at the high-dose level. In addition, a decreased CSA of type IIB fibres in EDLd and type IIA and type IIB fibres in EDLs and increased SDH activity of type IIB fibres in EDLd were observed in SHR after exposure to cigarette smoke at the high-dose level. 5. The smaller CSA and higher SDH activity of fibres in EDL observed in WKY rats and SHR after exposure to cigarette smoke at the high-dose level, but not at the low- and medium-dose levels, are adaptive responses, indicating that heavy cigarette smoke affects the morphological and metabolic properties of fibres in skeletal muscle.

Nicotine-induced inflammatory decreasing effect on passive skin arthus reaction in paraventricular nucleus-lesioned wistar rats.

To evaluate the relationship between nicotine and immunological inflammation, we investigated the effects of nicotine on plasma extravasation of the passive skin Arthus reaction, elicited 4 hr after sensitizing skin with antiserum, and serum corticosterone levels in rats. Pretreatment with a single subcutaneous injection of nicotine (0.4 or 0.8 mg/kg) 30 or 60 min. before antigen challenge attenuated the passive skin Arthus reaction immunological inflammation. Serum corticosterone levels were dose-dependently increased 30 and 60 min. after nicotine administration. Both markers co-varied with a similar dose-response and time course after the nicotine-treatment. In addition, we also examined these nicotine-induced responses after bilateral lesions of the hypothalamic paraventricular nucleus; both the nicotine-induced suppression of immunological inflammation and the increased serum corticosterone levels were attenuated in bilateral paraventricular nucleus-lesioned animals. Moreover, the immunological inflammatory decreasing effects of a single subcutaneous injection of nicotine (0.4 mg/kg) were antagonized by intraperitoneal preinjection with mecamylamine (1.0 mg/kg; blocking the brain nicotinic acetylcholine receptors) as well as by subcutaneous preinjection with mifepristone (30 mg/kg; a glucocorticoid receptor antagonist) but not by intraperitoneal preinjection with hexamethonium (2.0 mg/kg; a peripheral nicotinic acetylcholine receptors antagonist). Finally, intraperitoneal preinjection with cycloheximide (2 mg/kg), a protein synthesis inhibitor, abolished both the inhibitory effect of nicotine (0.4 mg/kg) on the dye leakage and the elevation of blood corticosterone levels. These findings indicate that the nicotine-induced decreasing effect on immunological inflammatory response may be related to serum corticosterone levels elevated by an activation of the paraventricular nucleus through the brain nicotinic acetylcholine receptors.

Responses of exposure to cigarette smoke at three dosage levels on soleus muscle fibers in Wistar-Kyoto and spontaneously hypertensive rats.

Fiber type distributions, cross-sectional areas (CSAs) and succinate dehydrogenase (SDH) activities in the soleus (SOL) muscle in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were determined after exposure to cigarette smoke at three different dosage levels using a smoking machine. The rats were exposed to cigarette smoke at a rate of 15 puffs/min, for 20 min/day with 23 cigarettes (low-dosage), 26 cigarettes (medium-dosage) or 30 cigarettes (high-dosage) for 8 weeks. There were no effects on the body weight, SOL weight, fiber type distribution, CSA or SDH activity of WKY after exposure to cigarette smoke, irrespective of the dosage level. In contrast, the body weights of SHR were lower after exposure to cigarette smoke, irrespective of the dosage level. The SOL weights of SHR were lower after exposure to cigarette smoke at the medium- and high-dosage levels. A lower percentage of type I fibers, a higher percentage of type IIA fibers and a smaller CSA of both type I and type IIA fibers were observed in SHR after exposure to cigarette smoke at the high-dosage level, but not at the low- and medium-dosage levels. These results indicate that heavy cigarette smoke causes changes in the enzyme histochemical properties with a reduced CSA of the SOL in SHR, but not in WKY.

Cardiac functions and taurine's actions at different extracellular calcium concentrations in forced swimming stress-loaded rats.

Modulation of the sinus rate and contractile force by taurine at different extracellular Ca2+ concentrations ([Ca2+]o) was examined using rat right atria loaded with forced swimming stress. Serum concentration of corticosterone profoundly increased in stress-loaded rats as compared with native rats. The taurine level in serum also increased in stress-loaded rats, but was not changed in the different heart tissues and aorta. Heat-shock protein (HSP72) was detectable in cardiac muscles and in the lumen of cardiac blood vessels of stress-loaded rats using a monoclonal antibody. Increasing [Ca2+]o (from 0.9 to 3.6 mM) enhanced the sinus rate and contractile force in a [Ca2+]o-dependent fashion in native rats, but not in stress-loaded rats. Taurine (1-20 mM) caused a negative chronotropic and inotropic effect in a concentration-dependent manner. At 1.8 mM [Ca2+]o, the negative chronotropic effect of taurine (10-20 mM) was attenuated in stress-loaded rats as compared with native rats. These results indicate that swimming stress causes a release of taurine into the serum and reduces the sensitivity to [Ca2+]o. Taurine administration might, in part, exhibit the protective actions on acute stress-induced responses.

Effects of running exercise with increasing loads on tibialis anterior muscle fibres in mice.

Cross-sectional areas and succinate dehydrogenase (SDH) activities of type identified fibres in the deep, middle and superficial regions of the tibialis anterior muscle in mice were examined after 4 weeks of voluntary running exercise with increasing loads. Nineteen-week-old male mice were assigned randomly to either a control or exercise group. The mean cross-sectional areas of all types (IIa, IIx and IIb) of fibres in the superficial region of the muscle were greater in the exercise group than in the control group. The mean SDH activities of type IIx and type IIb fibres in the middle region and of all types (IIa, IIx and IIb) of fibres in the superficial region of the muscle were greater in the exercise group than in the control group. These results suggest that voluntary running exercise with increasing loads causes hypertrophy and/or an increase in the SDH activity of fibres in the specific muscle region where fibres with a high threshold and a low-oxidative enzyme activity are distributed, and these fibres are recruited to adapt to changes in exercise conditions.