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GAS, ISRmt, and the Immune System: A Unified Model of Exercise Stress

New insights from Krüger et al. (2019) in Deutsche Zeitschrift für Sportmedizin show how exercise immunology mirrors classic stress biology. Let's connect the dots 🧠💪


🏋️‍♂️ Exercise = Immune Activation + Recovery Challenge

When you exercise, your immune system gets a workout too:

🧪 Acute bouts cause:

  • A spike in leukocytes, NK cells, and cytokines

  • Mobilization of T & B cells, neutrophils, monocytes

  • Short-term oxidative stress & inflammation

But what happens next depends on dose + recovery


⚖️ All stress responses, including exercise, have 3 possible outcomes:


1️⃣ Baseline recovery – immune system returns to where it was

2️⃣ Hormetic adaptation – immune function improves:

  • Enhanced pathogen defense

  • Increased naive T cells

  • Reduced chronic inflammation

  • Improved vaccine responses in older adults

3️⃣ Maladaptation – from overload or under-recovery:

  • Impaired mucosal immunity (e.g. ↓ SIgA)

  • ↑ Infections (URTI)

  • T-cell exhaustion

  • Inflamm-aging acceleration in older adults

This fits GAS (General Adaptation Syndrome) perfectly:

⚠️ Alarm → Resistance → Exhaustion (if energy runs out or stress stays high)


🔋 What's the key to adaptation?

Metabolic and bioenergetic resources.

No fuel = no immune regeneration.

No recovery = no gains.

Overload = maladaptation.


This is also reflected in:

  • Mitochondrial ISRmt (Integrated Stress Response)

  • Immune remodeling under exercise load

  • Oxidative stress buffering via SOD, HSP72, cytokine shifts (IL-6, IL-10)

 

💡 Bottom line:

🧬 Train smart

🍽️ Fuel well

😴 Recover fully

🔥 Adapt better


📖 Ref: Alack, Pilat & Krüger (2019).Current knowledge and new challenges in exercise immunology. Dtsch Z Sportmed, 70(10), 250–260

 



 
 
 

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