Excessive alcohol intake and liver fibrosis are associated with skeletal muscle mass reduction in elderly men: the Wakayama study.

BACKGROUND: Excessive alcohol intake complicated by liver dysfunction has been presumed to affect skeletal muscles. This study aimed to examine the association between excessive alcohol intake, liver fibrosis, and loss of skeletal muscle mass in elderly men. METHODS: The study participants comprised 799 community-dwelling elderly men (age, 71 ± 3 years) with no history of treatment for liver disease. Bioelectrical impedance analysis was performed to estimate the appendicular skeletal muscle mass (ASM) of each participant. The ASM values were also normalized for height (ASM index). Liver fibrosis was evaluated using the Fib4 index, which was calculated using participant age, AST level, ALT level, and platelet count. Usual alcohol intake was estimated based on the type of alcohol, frequency of drinking, and amount of alcohol consumed per day. RESULTS: Among the excess drinkers (≥ 20 g/day), the ASM index of the subgroup with liver fibrosis (Fib4 index ≥ 2.67) was significantly lower than that of the subgroup with no liver fibrosis (Fib4 index < 2.67). However, no significant difference between the subgroups was found in the non-drinkers and moderate drinkers (< 20 g/day). In multiple regression analysis, the Fib4 index was significantly associated with the ASM index, independent of potential confounding factors. The association between the Fib4 index and ASM index was more pronounced in excess drinkers than in non-drinkers and moderate drinkers. CONCLUSION: These results suggest that liver fibrosis is associated with loss of skeletal muscle mass in elderly men, and excessive alcohol intake combined with liver fibrosis may lead to greater muscle mass reduction than each individual condition.

Effects of cigarette smoking on the association between respiratory muscle strength and skeletal muscle mass in middle-aged and older adults: the Wakayama Study.

PURPOSE: This study aimed to examine whether cumulative smoking exposure affects the association between peak expiratory flow rate (PEFR) and skeletal muscle mass in middle-aged and older adults. METHODS: The study participants comprised 832 community-dwelling individuals aged 50-89 years (mean age: 69 years) without chronic obstructive pulmonary disease. Bioelectrical impedance analysis was performed to estimate the skeletal muscle mass of each participant. PEFR was assessed using an electronic spirometer. Cumulative smoking exposure was expressed in pack years, that is a product of the average number of packs of cigarettes smoked per day and smoking duration in years. RESULTS: The whole-body skeletal muscle mass progressively reduced with decreasing PEFR levels in both males and females. In the multiple regression analysis, PEFR was found to be significantly associated with skeletal muscle mass, independent of the potential confounding factors. When participants were stratified based on the cumulative smoking exposure, the association between low PEFR and reduced skeletal muscle mass persisted in individuals with non-smoking and light-to-moderate smoking exposure (< 30 pack-years). However, this association was not clearly observed in individuals with heavy smoking exposure (≥ 30 pack-years). CONCLUSION: The findings of this study support the notion that PEFR declines with a reduction in systemic skeletal muscle mass due to aging. However, chronic cigarette smoking induces respiratory dysfunction exceeding the expected values by age, and thus a low PEFR level may not be used as a marker of reduced muscle mass in older adults exposed to heavy smoking.

[Association of Cigarette Smoking with Muscle Mass Reduction and Low Muscle Strength in Community-Dwelling Elderly Men].

OBJECTIVES: Recently, attention has been paid to the impact of cigarette smoking on skeletal muscles, as its underlying pathophysiological mechanism has been gradually elucidated. In this study, we aimed to examine whether cigarette smoking is associated with muscle mass reduction and low muscle strength in elderly men. METHODS: The study participants comprised 417 community-dwelling elderly men (aged 73±6 years) without severe glucose intolerance, chronic kidney disease, or liver disease. Bioelectrical impedance analysis was performed to estimate appendicular skeletal muscle mass (ASM), which was normalized for height (ASM index, kg/m2). Handgrip strength (HGS) was measured using a Smedley grip dynamometer. Cumulative smoking exposure level during a lifetime was expressed in pack-years, which is a product of the average number of packs of cigarettes smoked per day and smoking duration in years. RESULTS: When the participants were stratified on the basis of cumulative smoking exposure (<10 pack-years, 10-39 pack-years, ≥40 pack-years), the ASM index and HGS progressively decreased with increasing exposure level (P for trend <0.01). In multiple regression analysis, heavy smoking (defined as ≥40 pack-years) was found to be a significant determinant of the ASM index and HGS, independent of potential confounding factors. Among former smokers, the subgroup that quit smoking for ≥20 years had a significantly higher ASM index and HGS than the subgroup that quit smoking for <10 years. The duration of smoking cessation was significantly associated with the ASM index and HGS, even after adjusting for cumulative smoking exposure. CONCLUSIONS: These findings suggest that cigarette smoking contributes to the loss of muscle mass and function in elderly men and that smoking cessation could reverse the impact of cigarette smoking on skeletal muscles.