Spiral Motion and Mitochondrial Health in the Shoulder

Spiral Motion in the Shoulder

Scapulohumeral Rhythm is a biomechanical term that explains how the shoulder joints move in a rotational cascade. In other words, the humerus, scapula and clavicle all rotate within the soft tissue matrix to produce complex movement. Physiopedia defines scapulohumeral rhythm as the ratio of the glenohumeral movement to the scapulothoracic movement during arm elevation.

Try it yourself right where you are, with your arms resting alongside your body. Now, slowly raise your free arm up (doesn't matter if it's out to the side or in front of you). After about 15 degrees, humeral elevation (that's your long arm bone that connects to your shoulder) starts picking up the shoulderblade (scapula).

As the shoulder continues flexing up over your head, the humerus externally rotates and the scap upwardly rotates in coordination with the collarbone (clavicle), which rotates in tune with the rest of the shoulder tissue.

The scapulohumeral rhythm is a biomechanical term referring to the kinematics of coupled motion. From a continuum point of view, we're talking about joints rotating within their capsules, bones rotating within their connective tissue sheaths, muscles and their itinerant fascia, and all the vessels and nerves and everything else falling into the continuum of motion.

When it is smoothly orchestrated, the spiral motion sleeve keeps the joint spaces congruently rotating and all the delicate matrix structures protected within a rolling/gliding motion. However, the human shoulder has evolved for an increased mobility advantage over the hip, which has evolved for more stability. 

Evolutionarily, the shoulder gave up some stability in order to achieve the mobility, so the upshot is that the shoulder is prone to particular flavors of inflammation. Indeed, the rotator cuff tendon gets it pretty tight, sandwiched as it is between the two bony structures that can act as a mortar and pestle.

The tendon of supraspinatus (one of the four cuff muscles) courses medially to join the connective tissue structure that stabilizes and contributes to glenohumeral rotation. Situated between the roof of the acromion above and the head of the humerus below, that tendon is vulnerable to "friction". 

I'm going to clarify that what I mean by friction is nonscientific, it isn't like sandpaper friction. I use the term friction in the general sense of undue force that goes against the "roll and glide" of healthy joint movement. With poor movement patterns or acute injury, vulnerable joint materials like the supraspinatus tendon are anatomically predisposed to getting banged up in the normal course of physical activity.  

Our movement habits contribute to metabolism by way of the mitochondrial activity that results from training and injury. This study by Thankam et al (2018) investigates how mitochondria (the energy-producing structures in cells) function in tendon tissue after rotator cuff injury (RCI), which is a common shoulder injury for the reasons previously explained.

Study Overview

Specifically, this study looks at how mitochondrial health is affected by low oxygen (hypoxia) during the healing process. Researchers used rats with surgically induced shoulder tendon injuries and cultured swine tendon cells to explore mitochondrial activity and its role in tendon repair. The study aims to better understand how mitochondria influence tendon healing and whether they could be targeted to improve recovery from RCI.

Methods Used

1. Animal Model and Injury Induction

• The researchers created a rotator cuff injury (RCI) in rats by surgically cutting the tendon (called "tenotomy").
• They took tendon tissue samples from injured rats at different healing stages: early (3–5 days), middle (10–12 days), and later stages (22–24 days). They also took tendon samples from the uninjured side of the rats to use as controls. 

2. Cell Culture

In addition to the rat model, the researchers also worked with swine (pig) tendon cells grown in a lab to simulate tendon injury. These cells were exposed to low-oxygen conditions (hypoxia) to see how this affected their mitochondria.

3. Mitochondrial Markers

The researchers measured specific proteins in the tendon tissue to understand mitochondrial function. These proteins include:

• Citrate synthase: A marker for overall mitochondrial activity.
• Complex-1: A key protein involved in energy production in mitochondria.
• BAX and Bcl2: Proteins involved in cell death, which help determine whether cells survive or die. BAX is linked to cell death, and Bcl2 is linked to cell survival.

4. Hypoxia Exposure:

In the lab, tendon cells were exposed to hypoxia (low oxygen), which mimics the conditions in injured tissues. Researchers then measured changes in mitochondrial behavior and cell health.

Key Findings

1. Mitochondrial Activity in Injured Tendons

1. In the injured tendons, mitochondrial activity was higher in the early stages (3–5 days) compared to the control tendons. This suggests that the body was trying to increase energy production to heal the tendon.
2. However, as time went on, mitochondrial activity decreased. In the later stages of healing (22–24 days), the mitochondrial activity was much lower, which could indicate that the tendon was nearing the end of its healing process or that the injury had caused long-term damage.

2. Changes in Proteins Related to Cell Death

• The study found an increase in BAX (a protein linked to cell death) in the early and middle stages of healing, suggesting that more tendon cells were at risk of dying during these stages.
• On the other hand, **Bcl2** (a protein that helps cells survive) was higher in the injured tendons compared to the controls, which might indicate that the body was trying to protect the cells from dying.
• The ratio of BAX to Bcl2 was higher in the early and middle stages of injury, showing an increased risk of cell death in the injured tendons.

3. Effect of Hypoxia on Lab-Grown Tendon Cells

• When the lab-grown tendon cells were exposed to low oxygen (hypoxia), they showed increased mitochondrial activity and changes in mitochondrial shape and number. This suggests that the cells were adjusting their energy production in response to the injury and lack of oxygen.
• These cells also showed higher levels of mitochondrial **superoxide** (a harmful byproduct of energy production), which could lead to oxidative stress and cell damage.

Conclusion

The study highlights that mitochondria play a critical role in tendon healing after rotator cuff injury. When the tendons are injured, mitochondria work harder to produce the energy needed for healing, but this can lead to increased cell stress and risk of cell death, especially under low-oxygen conditions. The results suggest that mitochondrial health is an important factor in tendon healing, and targeting mitochondrial function could potentially help improve recovery from rotator cuff injuries.

In simple terms, the study shows that the mitochondria in tendon cells are very active after an injury, working hard to repair the damage. However, this increased activity can also cause damage to the cells, which may slow down healing. Better understanding and potentially improving mitochondrial function could help tendons heal faster and more effectively.

My Interpretation

Who said that healing doesn't happen in a straight line?

Well, studies show that this is about as accurate as it gets where mitochondria are concerned. My take is that preventing injury is the best plan, and our best shot at preventing injury is to focus on the coupled motion units like Scapulohumeral Rhythm that protects the joints from undue wear and tear. And in the unavoidable situations where we do sustain an injury, for example to the rotator cuff, coming back into gently rotational movement may nurture the chemical processes of healing to get the joint back into rhythm where it can continue charging its chemical batteries. Rupture, repair, rotate, repeat.