Calf circumference was positively correlated with appendicular skeletal muscle mass and skeletal muscle index, and could be used as a surrogate marker of muscle mass for diagnosing sarcopenia. The suggested cut-off values of calf circumference for predicting low muscle mass are <34 cm in men and <33 cm in women.

In this study of Japanese men and women, we determine reference values for sarcopenia and test the hypothesis that sarcopenia is associated with risk factors for cardiovascular disease, independent of waist circumference. A total of 1,488 Japanese men and women aged 18-85 years participated in this study. Appendicular muscle mass (AMM) was measured by dual-energy X-ray absorptiometry. Reference values for classes 1 and 2 sarcopenia (skeletal muscle index: AMM/height2, kg m-2) in each sex were defined as values one and two standard deviations below the sex-specific means of reference values obtained in this study from young adults aged 18-40 years. The reference values for class 1 and class 2 sarcopenia were 7.77 and 6.87 kg m-2 in men and 6.12 and 5.46 kg m-2 in women. In subjects both with class 1 and class 2 sarcopenia, body mass index and % body fat were significantly lower than in normal subjects. Despite whole-blood glycohaemoglobin A1c in men with class 1 sarcopenia was significantly higher than in normal subjects, and brachial-ankle pulse wave velocity in women both with class 1 and class 2 sarcopenia were significantly higher than in normal subjects, using one-way ANCOVA with adjustment for the covariate of waist circumference. Although sarcopenia is associated with thin body mass, it is associated with more glycation of serum proteins in men and with greater arterial stiffness in women, independent of waist circumference.

No abstract

Hand grip strength is a widely used proxy of muscular fitness, a marker of frailty, and predictor of a range of morbidities and all-cause mortality. To investigate the genetic determinants of variation in grip strength, we perform a large-scale genetic discovery analysis in a combined sample of 195,180 individuals and identify 16 loci associated with grip strength (P<5 × 10−8) in combined analyses. A number of these loci contain genes implicated in structure and function of skeletal muscle fibres (ACTG1), neuronal maintenance and signal transduction (PEX14, TGFA, SYT1), or monogenic syndromes with involvement of psychomotor impairment (PEX14, LRPPRC and KANSL1). Mendelian randomization analyses are consistent with a causal effect of higher genetically predicted grip strength on lower fracture risk. In conclusion, our findings provide new biological insight into the mechanistic underpinnings of grip strength and the causal role of muscular strength in age-related morbidities and mortality.

Background: The immune system declines in efficiency with advancing age, making the elderly less resistant to pathogenic microorganisms. Upper respiratory tract infection (URTI) is a common illness. Recent studies have shown that suppression of secretory immunoglobulin A (SIgA) is associated with increased incidence of URTI. Objective: To assess the effect of exercise on salivary SIgA in elderly subjects. Methods: Forty five elderly subjects (18 men, 27 women; mean (SD) age 64.9 (8.4) years) performed both 60 minute resistance and 60 minute moderate endurance training a week for 12 months. Saliva samples were obtained before training, and at four and 12 months during the training period. Salivary SIgA concentrations were measured by enzyme linked immunosorbent assay, and the SIgA secretion rate was calculated. Results: SIgA concentrations before training, and at four and 12 months during training were 24.7 (14.4), 27.2 (14.2), and 33.8 (18.5) µg/ml respectively. SIgA secretion rates were 29.5 (26.0), 33.8 (27.2) and 46.5 (35.1) µg/min respectively. The results indicate that both the concentration and secretion rate of SIgA significantly (p<0.01) increased during 12 months of exercise in these elderly subjects. Conclusion: Regular moderate exercise seems to enhance mucosal immune function in elderly subjects.

Flexibility is one of the components of physical fitness as well as cardiorespiratory fitness and muscular strength and endurance. Flexibility has long been considered a major component in the preventive treatment of musculotendinous strains. The present study investigated a new aspect of flexibility. Using a cross-sectional study design, we tested the hypothesis that a less flexible body would have arterial stiffening. A total of 526 adults, 20 to 39 yr of age (young), 40 to 59 yr of age (middle-aged), and 60 to 83 yr of age (older), participated in this study. Subjects in each age category were divided into either poor- or high-flexibility groups on the basis of a sit-and-reach test. Arterial stiffness was assessed by brachial-ankle pulse wave velocity (baPWV). Two-way ANOVA indicated a significant interaction between age and flexibility in determining baPWV (P < 0.01). In middle-aged and older subjects, baPWV was higher in poor-flexibility than in high-flexibility groups (middle-aged, 1,260 +/- 141 vs. 1,200 +/- 124 cm/s, P < 0.01; and older, 1,485 +/- 224 vs. 1,384 +/- 199 cm/s, P < 0.01). In young subjects, there was no significant difference between the two flexibility groups. A stepwise multiple-regression analysis (n = 316) revealed that among the components of fitness (cardiorespiratory fitness, muscular strength, and flexibility) and age, all components and age were independent correlates of baPWV. These findings suggest that flexibility may be a predictor of arterial stiffening, independent of other components of fitness.

Abstract-Habitual moderate-to-vigorous-intensity physical activity attenuates arterial stiffening. However, it is unclear whether light physical activity also attenuates arterial stiffening. It is also unclear whether light physical activity has the same effects in fit and unfit individuals. This cross-sectional study was performed to determine the relationships between amount of light physical activity determined with a triaxial accelerometer and arterial stiffness. A total of 538 healthy men and women participated in this study. Subjects in each age category were divided into either high-light or low-light physical activity groups based on daily time spent in light physical activity. Arterial stiffness was measured by carotid-femoral pulse wave velocity. Two-way ANOVA indicated a significant interaction between age and time spent in light physical activity in determining carotid-femoral pulse wave velocity (PϽ0.05). In the older group, carotid femoral pulse wave velocity was higher in the low-light physical activity level group than in the high-light physical activity level group (945Ϯ19 versus 882Ϯ16 cm/s; PϽ0.01). The difference remained significant after normalizing carotid-femoral pulse wave velocity for amounts of moderate and vigorous physical activity. The carotid-femoral pulse wave velocity (rϭϪ0.47; PϽ0.01) was correlated with daily time spent in light physical activity in older unfit subjects. No relationship was observed in older fit subjects. These results suggested that longer time spent in light physical activity is associated with attenuation of arterial stiffening, especially in unfit older people. (Hypertension. 2010;56:540-546.)

We studied the effects of aerobic exercise training and detraining in humans on post-exercise vagal reactivation. Ten healthy untrained men trained for 8 weeks using a cycle ergometer [70% of initial maximal oxygen uptake (VO2max) for 1 h, 3-4 days.week-1] and then did not exercise for the next 4 weeks. Post-exercise vagal reactivation was evaluated as the time constant of the beat-by-beat decrease in heart rate during the 30 s (t30) immediately following 4 min exercise at 80% of ventilatory threshold (VT). The VO2max and the oxygen uptake at VT had significantly increased after the 8 weeks training programme (P < 0.0001, P < 0.001, respectively). The t30 had shortened after training, and values after 4 weeks and 8 weeks of training were significantly shorter than the initial t30 (P < 0.05, P < 0.01, respectively). The change in the t30 after 8 weeks of training closely and inversely correlated with the initial t30 (r = -0.965, P < 0.0001). The reduced t30 was prolonged significantly after 2 weeks of detraining, and had returned almost to the baseline level after a further 2 weeks of detraining. These results suggest that aerobic exercise training of moderate intensity accelerates post-exercise vagal reactivation, but that the accelerated function regresses within a few weeks of detraining.