Exercise-induced stress pathways: Crosstalk between AMPK, HSPs, and inflammation

Area of Science:

• Exercise physiology
• Molecular biology
• Cellular stress response

Background:

• Exercise is a physiological stressor disrupting cellular homeostasis.
• Key modulators include heat shock proteins (HSPs), AMP-activated protein kinase (AMPK), and inflammatory pathways.
• These systems are crucial for cellular adaptation and energy balance restoration.

Purpose of the Study:

• To review recent cellular and molecular findings on the crosstalk between HSPs, AMPK, and inflammation during exercise.
• To elucidate the adaptive and potentially maladaptive roles of these pathways.

Main Methods:

• Synthesis of recent findings from cellular and molecular studies.
• Analysis of signaling pathways and molecular chaperones involved in exercise adaptation.

Main Results:

• Exercise activates AMPK to restore energy balance and promote mitochondrial biogenesis.
• HSPs protect protein integrity against various stressors.
• Inflammation, while promoting repair, can be maladaptive if dysregulated.
• HSPs inhibit inflammatory signaling, and AMPK modulates inflammation and HSP expression.

Conclusions:

• There is a complex, dynamic crosstalk between HSPs, AMPK, and inflammatory pathways during exercise.
• This interplay is critical for cellular adaptation to exercise stress.
• Understanding this crosstalk is vital for optimizing exercise-induced adaptations and preventing maladaptive responses.