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Published on: September 20, 2019
Intramuscular lipid concentration increased in localized regions of the lumbar muscles following 60 day bedrest
Enrico De Martino1, Julie Hides2, James M Elliott3
1Aerospace Medicine and Rehabilitation Laboratory, Faculty of Health and Life Sciences, Northumbria University, Newcastle upon Tyne, United Kingdom.
Background Context:
Prolonged bedrest induces accumulation of intramuscular lipid concentration (ILC) in the lumbar musculature; however, spatial distribution of ILC has not been determined. Artificial gravity (AG) mitigates some adaptations induced by 60 day bedrest by creating a head-to-feet force while participants are in a supine position.
Purpose:
To quantify the spatial distribution of accumulation of ILC in the lumbar musculature after 60 day bedrest, and whether this can be mitigated by AG exposure.
Study Design:
Prospective longitudinal study.
Patient Sample:
Twenty-four healthy individuals (8 females) participated in the study: Eight received 30 min continuous AG (cAG); Eight received 6 × 5 min AG (iAG), interspersed with rests; Eight were not exposed to AG (CRTL).
Outcome Measures:
From 3T magnetic resonance imaging (MRI), axial images were selected to assess lumbar multifidus (LM), lumbar erector spinae (LES), quadratus lumborum (QL), and psoas major (PM) muscles from L1/L2 to L5/S1 intervertebral disc levels. Chemical shift-based 2-echo lipid and/or water Dixon sequence was used to measure tissue composition. Each lumbar muscle was segmented into four equal quartiles (from medial to lateral).
Methods:
Participants arrived at the facility for the baseline data collection before undergoing a 60 day strict 6° head-down tilt (HDT) bedrest period. MRI of the lumbopelvic region was conducted at baseline and Day-59 of bedrest. Participants performed all activities, including hygiene, in 6° HDT and were discouraged from moving excessively or unnecessarily.
Results:
At the L4/L5 and L5/S1 intervertebral disc levels, 60-day bedrest induced a greater increase in ILC in medial and lateral regions (∼+4%) of the LM than central regions (∼+2%; p<.05). A smaller increase in ILC was induced in the lateral region of LES (∼+1%) at L1/L2 and L2/L3 than at the centro-medial region (∼+2%; p<.05). There was no difference between CRTL and intervention groups.
Conclusions:
Inhomogeneous spatial distribution of accumulation of ILC was found in the lumbar musculature after 60 day bedrest. These findings might reflect pathophysiological mechanisms related to muscle disuse and contribute to localized lumbar spine dysfunction. Altered spatial distribution of ILC may impair lumbar spine function after prolonged body unloading, which could increase injury risk to vulnerable soft tissues, such as the lumbar intervertebral discs. These novel results may represent a new biomarker of lumbar deconditioning for astronauts, bedridden, sedentary individuals, or those with chronic back pain. Changes are potentially modifiable but not by the AG protocols tested here.
