Abstract
Purpose
Reduced hand grip strength (HGS) is associated with poorer health in chronic conditions, yet there has been little research examining the association with hand grip strength and obstructive sleep apnea (OSA). Further, these studies have not examined, nor adjusted, for muscle mass. The aim of this study was to determine associations between OSA indices, HGS, muscle mass, and fat mass.
Participants and Methods
A total of 613 participants (age range 41–88, BMI 28.6 ± 4.3) from the population-based Men Androgen Inflammation Lifestyle Environment and Stress Study underwent in-home overnight polysomnography, assessment of dominant and non-dominant HGS, and dual x-ray absorptiometry to determine whole body muscle mass and fat mass. Linear models determined cross-sectional associations of polysomnographic-derived OSA indices with hand grip strength, muscle mass, and fat mass, whilst adjusting for lifestyle information (income, smoking status, diet, self-reported physical activity), blood sample derived testosterone and systemic inflammation (C-reactive protein), cardiometabolic health (cardiovascular disease, hypertension, type 2 diabetes), and depression.
Results
In adjusted models, reduced dominant HGS was associated with lower oxygen nadir (unstandardised β [B] = 0.19, 95% confidence interval [CI] 0.08 to 0.29), greater time spent below 90% oxygen saturation (B = −0.08, 95% CI −0.14 to −0.02), and increased apnea duration (B = −0.3, 95% CI −0.23 to −0.02). By contrast, there were no associations between HGS and both AHI and REM AHI. Fat mass was consistently associated with worsening OSA indices, whereas muscle mass demonstrated no associations with any OSA index.
Conclusion
Our findings suggest impairments in HGS may be related to fat infiltration of muscle, hypoxemia-induced reductions in peripheral neural innervation, or even endothelial dysfunction, which is a common outcome of hypoxemia. Longitudinal data are needed to further examine these hypotheses and establish if reduced grip strength in patients with OSA is associated with long-term adverse health outcomes.
Acknowledgments
GW is a Chief Investigator for the FAMAS study. RA is a Chief Investigator for the NWAHS study.
Author Contributions
All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work.
Robert Adams and Gary Wittert are co-senior authors.
Disclosure
DS has received funding from the Flinders Foundation (Australia) and the CRC for Alertness, Safety, and Productivity (Australia), and reports grants from National Health and Medical Research Council, the Hospital Research Foundation, and the ResMed Foundation, during the conduct of the study; and grants from Flinders Foundation, outside the submitted work. RA, GW, and TG have received funding from the National Health and Medical Research Council (Australia). RA has received non-financial support from Embla Systems and reports grants from the National Health and Medical Research Council, The Hospital Research Foundation, and ResMed Foundation, during the conduct of the study. GW has received research funding from Bayer Schering, Eli Lilly, and Lawley Pharmaceuticals; has received funding from Eli Lilly, Bayer Schering, Sanofi, Novo Nordisk, Astra Zeneca, I-Nova, and Elsevier; has served on the International Advisory Boards for Eli Lilly, and Novo Nordisk. RA, GW, and SA have received funding from the ResMed Foundation (USA) and the Sleep Health Foundation (Australia). RA, SA, YAM, and TG have received funding from the Hospital Research Foundation (Australia). TG has received funding from Arthritis Australia. None declared for AV and CH. The authors report no other potential conflicts of interest for this work.