One of the most confronting findings for physiotherapists working with tennis players is infraspinatus atrophy. Studies in both male and female professional tennis players show that nearly 60% demonstrate visible or clinical infraspinatus atrophy, despite competing at the highest level without shoulder pain.
So the obvious question is, if so many players have it and remain asymptomatic, why do we still see so many shoulder injuries in tennis?
The answer lies not in the presence of atrophy itself, but in what the infraspinatus is required to do, and when it is asked to do it.

If you want to learn more about this topic, you can watch Fredrik Johansson's lecture here:

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The role of the infraspinatus in tennis

In tennis, the infraspinatus is not primarily a “power” muscle. It’s most critical role is eccentric deceleration. During the serve and overhead strokes:
✓ The shoulder internally rotates at extremely high velocity.
✓ Immediately after ball contact, that motion must be rapidly slowed.
✓ The infraspinatus plays a major role in braking the arm and racket.

Why atrophy doesn’t automatically mean injury

Atrophy is a structural observation, not a diagnosis. In tennis players, infraspinatus atrophy may reflect:
• Long-term exposure to unilateral loading
• Neural or morphological adaptation
• Redistribution of load within the kinetic chain

Many athletes continue to perform pain-free because:
• Their kinetic chain is efficient
• Their total training load is well managed
• Recovery windows are adequate

In these cases, the system compensates successfully.
This is why atrophy alone has poor predictive value for pain or injury.

When Atrophy Becomes a Problem

Infraspinatus atrophy becomes clinically relevant when deceleration demand exceeds available capacity.
This typically occurs during:
• Sudden spikes in serving volume
• Tournament congestion
• Reduced recovery time
• Accumulated fatigue

Atrophy may reduce:
• Eccentric force capacity
• Fatigue resistance
• Load-sharing ability during braking

When this happens, excess stress is transferred to the posterior capsule, the labrum, the long head of biceps and other rotator cuff structures. Symptoms don’t arise because the muscle is smaller, they arise because the system can no longer tolerate the load placed upon it.

Why traditional “Prehab” often misses the mark

Most tennis players already perform:
• External rotation exercises
• Band-based rotator cuff work
• High-rep, low-load routines

Yet infraspinatus atrophy remains prevalent.
Why?
Because most of these exercises are low velocity, emphasise concentric control, do not replicate high-speed eccentric braking and are performed in a non-fatigued state.They do not sufficiently prepare the muscle for what it actually does in tennis.

The bigger picture: kinetic Chain and load

The infraspinatus never works in isolation.
If force transfer from the legs, pelvis and trunk
is inefficient, the shoulder and specifically the decelerators must absorb more load.
This explains why:
• Strong shoulders still get injured.
• Atrophy is tolerated in some players but not others.
• Shoulder pain often appears during high-load phases rather than during training blocks.

Clinical implications for physiotherapists

Instead of asking:
“Why is the infraspinatus atrophied?”
A more useful question is:
“Can this shoulder tolerate repeated high-speed deceleration this week?”

What should be taken into consideration?
• Total serving volume
• Match density
• Fatigue levels
• Recovery opportunities
• Kinetic chain efficiency

Key takeaways 

☑ In tennis, the shoulder doesn’t fail because a muscle looks smaller.
☑ It fails when the demands of the sport exceed what the system can tolerate at that moment in time.
☑ Understanding that difference is what separates exercise prescription from true clinical reasoning.

If you want to learn more about this topic, you can watch Fredrik Johansson's lecture here:

Click here

Source:
From the lecture ‘The Rotator Cuff in Tennis - Is the Abnormal Normal? by Dr. Fredrik Johansson’