A study of male and female humans 1 subjected to three bouts of lumbar flexion-extension prior to, and after 10 minutes of static lumbar flexion confirmed prior animal studies that concluded static flexion caused lumbar creep in nearby viscoelastic tissues and alterations and spasms of the associated muscle functions. Researchers proposed micro-damage in the viscoelastic tissues occurred as the muscles attempted to compensate the relative loss of tension, creating spasms in more than half of the subjects while maintaining static flexion poses.
What’s at Stake?
Workers who must endure long periods of static lumbar flexion suffer high rates of lower back pain and degeneration, making static lumbar flexion a common risk factor for developing lower back pain and degeneration. How this occurs is not well understood. Recent studies have used feline models to better understand the processes involved in how static lumbar flexion creates creep and electromyographic spasms of the multifidi in the lumbar viscoelastic tissues under loads. In these studies, the multifidus muscles developed hyperexcitability during the post-static lumbar flexion resting period, particularly between the 6th and 7th hours of rest, and a full muscular hyperexcitability and creep recovery could take as long as 48 hours, which suggests that a transient neuromuscular disorder occurs after 20 minutes of static lumbar flexion. This new study was conducted to determine if healthy humans would experience the same transient disorder after static lumbar flexion.
Study subjects included 24 males and 25 females with an average age of 23.7 years and no history of spinal function disorders. An additional six subjects were included in a control group. Electrodes were applied at the L3-4 level of the erector spinae musculature. Two-dimensional video motion analysis was performed to determine joint angles, and the data was collected prior to calculating lumbar flexion and overall flexion levels.
The subjects were instructed to stand quietly for three seconds then perform a full anterior flexion position over 2-3 seconds and hold the position for 3-4 seconds. The subjects then extended into an upright position over the course of 2-3 seconds and stand in a static position until the end of the recording. The recordings were 16 seconds long, with approximately 12 seconds of trial consideration. The subjects performed the deep flexion trials three times, with a 3—50 second break in between each trial.
Following the first trial sets, each subject was placed in a full lumbar flexion position on a physical therapy mat, with a foam bolster placed beneath their hips to ensure their pelvis was posteriorly placed and their knees were able to flex. This positioning reduced hamstring stretching and focused any tension (or creep) towards the posterior of the lumbar spine. They were asked to hold this position for 10 minutes while an EMG recording monitored any spasms or muscle activity. After this deep flexion period, the subjects were asked to stand up and perform three more flexion trials. The variables and data from all the trials were then extracted and analyzed.
The results of the trial study indicated that there were clinically relevant changes in the flexion-relaxation response after 10 minutes of deep static lumbar flexion. The erector spinae muscles remained active longer and became active earlier prior to anterior flexion and during extension. This was due to moderate creep in the viscoelastic structures of the spine. The muscle activity intensity remained the same after static flexion, and there appeared to be variation in the flexion-relaxation response between the male and female subjects. Static flexion stances appeared quite often to cause visible EMG spasms.
When the subjects initiated anterior flexion, the muscles in their erector spinae slowly increased contraction to counter the increasing gravity effect on the upper trunk and head. Eventually, the passive forces of the strained viscoelastic structures were able to offset the upper body and head mass gravity, making the muscular forces unnecessary and causing them to disperse. The increase in flexion required the subjects to contract their abdominal muscles to counter the posterior viscoelastic tissue forces.
In this study, static lumbar flexion developed lumbar creep in the viscoelastic structures of the subjects. However, this effect was countered by the subjects’ musculature, which initiated or maintained the necessary active force during the periods of decreased viscoelastic tissue capacity. The results of the study confirm a synergy between the neurological system and the body’s ligaments and muscles that helps preserve skeletal stability and control movement. Further, microdamage to the collagen structure that may create spasms in the muscles appear to be related to viscoelastic tissue creep.