Gluteus Max. - Latissimus Dorsi Muscle Sling

Gluteus Max. - Latissimus Dorsi                            Muscle Sling

Together, the latissimus dorsi and opposite gluteus maximus muscles create a force that induces nutation on the gluteal side and counternutation on the latissimus dorsi side. In a right SI lesion, the left GM and right LD will contract and the right GM and left LD will be inhibited.

Snijders [1] developed a biomechanical model of the transfer of loads through the sacroiliac joint and noted that the lumbodorsal fascia is not connected to either the spine or ligaments at the level of L4 to L5. Instead, these free fibers mesh with fibers of the latissimus dorsi and superior division of the contralateral gluteus maximus to provide a coupling action which, Snijders surmised, can assist in sacroiliac joint stability by providing a force relatively perpendicular to the joint surface.

Gracovetsky [2] describes the coupled action of the latissimus dorsi, through the lumbodorsal fascia to the gluteus maximus, as a key component of energy transfer in gait. A lateral bending movement in the spine is converted into axial torque that drives pelvic rotation. Through this mechanism, energy is transmitted between the upper extremities and legs.

Together, these two muscles generate a force that produces a nutation moment on the gluteal side and a counternutation moment on the latissimus dorsi side. Thus, with a right nutation lesion, the counternutation response would inhibit the right gluteus maximus and the left latissimus dorsi and activate the left gluteus maximus and right latissimus dorsi. In this situation, tension in the left gluteus maximus and contralateral latissimus dorsi would decrease tension in the left long dorsal sacroiliac ligament, indicating that they produced nutation on the left [3, 4].

Combining Color Doppler Imaging with oscillation, Wingerden [5] showed that the gluteus maximus, along with the erector spinae and the biceps femoris, produced a significant increase in sacroiliac joint stiffness, along with a lesser, but similar, effect from the contralateral latissimus dorsi. We can assume that these muscles produced a nutation effect on the gluteal side since, during nutation, the joint surfaces approach each other as the interosseous ligament winds tighter and the joint may become more stable.

In an interesting investigation, Mooney et al. [6] did an EMG study on patients with confirmed sacroiliac joint dysfunction. On patients with right painful sacroiliac joints, they found hyper-activity of the right gluteus maximus during left trunk rotation, which would induce nutation at the right sacroiliac joint. As a result, they concluded that one significant finding of their study is that the gluteus maximus is hyper-active in sacroiliac joint dysfunction when stress is applied to the sacroiliac joint during strengthening. They apparently mis-interpreted this hyperactivity as an indication that the gluteus maximus was trying to stabilize the sacroiliac joint dysfunction. They also found the contralateral latissimus dorsi to be concurrently hypoactive. Exercise to both muscles resulted in increased tone to the latissimus dorsi and decreased tone to the gluteus maximus, with a reduction in pain. In other words, they incorrectly indicate that the normal gluteus maximus/latissimus dorsi coordination does not work when the sacroiliac joint is in lesion. At first glance, this finding does not agree with the nutation lesion concept that both the ipsilateral gluteus maximus and contralateral latissimus dorsi are inhibited in sacroiliac joint dysfunctions.

However, with a different interpretation of the results, it appears that what actually happened does fit into the model of the nutation lesion. The compensating pattern of counternutation should have caused anterior pelvic tilt, facet jamming at L4 to S1, and narrowing of the lateral canals. The narrowed canals most likely led to compressive irritation of the inferior gluteal nerve (L5 to S2), causing gluteus maximus hyperactivity. Left trunk rotation increased the right lumbar lordosis [2], further narrowing the lateral canals and increasing pressure on the nerve roots. The opposite latissimus dorsi wasn’t involved because it is fed by the thoracodorsal nerve from C6 to C8. The left latissimus dorsi was hypotonic, as the right gluteus maximus would have been if not for the extra complication of irritation to the nerve roots.

Interestingly, their study showed that exercise to both muscles increased tone to the latissimus dorsi and decreased tone to the gluteus maximus; this is the clue that leads to understanding the apparent incongruity. It appears that the superior division of the gluteus maximus, being a pelvic extensor, when strengthened, eventually created enough posterior rotation of the pelvis that it was able to decrease the acute angulation at the lumbosacral area and decompress the lateral canals. The pressure on the inferior gluteal nerve was removed and normal tone, or even hypotonia (because the ipsilateral sacroiliac joint was in lesion), was restored to the gluteus maximus. Although, post-exercise, left torso rotation increased lordosis, as it did pre-exercise, the lateral canals may have opened enough to allow the lordosis to occur without pressing on the nerve roots. This is good example of a compensation-to-a-compensation pattern. Having a good understanding of the underlying patterns can greatly assist one in finding and fixing the problem.

In normal movement, during right weight bearing, the right internal oblique and left external oblique pull the left rib cage down and forward, while the right latissimus dorsi and left gluteus maximus pull the right shoulder down and backward. Normally, these patterns reverse during left weight bearing. However, with a right sacroiliac nutation lesion, the movement is magnified and becomes chronic as these muscles remain in a state of tension to remove tension from the sprained ligaments on the right side. A counternutation compensation pattern develops in the structure as the spine laterally flexes and rotates to the right. If it ended there, the person would remain twisted to the right and bent forward. However, proprioceptive responses would come into play as the person unconsciously attempts to stand erect. Righting reflexes would cause the upper trunk to counter-rotate to align the shoulders with the pelvis and bring C2 in line with S2. This secondary compensation pattern will, in turn, twist the upper spine to the left, while the lower spine is twisted to the right. The mixing of these two patterns will lead to other adaptations and eventual structural stresses throughout the body. Please see my section on structural overcompensation patterns for more examples.

A good understanding of the interplay between nutation and counternutation, in both normal movement and compensation to injury, will give the observer a superior method of treating the musculoskeletal system as a functioning whole.

1.    Snijders, C.J., Transfer of Lumbosacral Load to Iliac Bones and Legs: Part 2 - Loading of the Sacroiliac Joints when Lifting in a Stooped Position. Clinical Biomechanics, 1993b. 8: p. 295-301.
2.    Gracovetsky, S. Locomotion - Linking the Spinal Engine with the Legs. in Proceedings of the Second Interdisciplinary World Congress on Low Back Pain. 1995. San Diego, CA.
3.    Vleeming, A., et al., The role of the sacroiliac joints in coupling between spine, pelvis, legs and arms., in Movement, Stability, and Low Back Pain, A. Vleeming, et al., Editors. 1997, Churchill Livingstone. p. 53-71.
4.    Vleeming, A., et al., The function of the long dorsal sacroiliac ligament: its implication for understanding low back pain. Spine, 1996. 21(5): p. 556-62.
5.    Wingerden, J.v., et al. Muscular Contribution to Force Closure: Sacroiliac Joint Stabilization In Vivo. in 4th Interdisciplinary World Congress on Low Back & Pelvic Pain. 2001.
6.    Mooney, V., et al., Coupled motion of contra lateral latissimus dorsi and gluteus maximus-its role on sacroiliac stabilization, in Movement, Stability, & Low Back Pain, A. Vleeming, et al., Editors. 1997, Churchill Livingstone. p. 115-122.