Different Resistance-Training Regimens Evoked a Similar Increase in Myostatin Inhibitors Expression

Area of Science:

• Exercise Physiology
• Molecular Biology
• Sports Science

Background:

• The myostatin (MSTN) signaling pathway plays a crucial role in regulating muscle mass.
• Understanding how different resistance training modalities affect this pathway is important for optimizing training protocols.
• Gene expression analysis provides insights into the molecular adaptations to exercise.

Purpose of the Study:

• To investigate the impact of distinct resistance-training regimens (strength vs. power) on MSTN signaling pathway gene expression.
• To compare the effects of high-intensity strength training (S) and low-intensity power training (P) on specific gene markers.

Main Methods:

• 29 physically-active males with prior strength training experience were divided into strength (S) and power (P) training groups, plus a control (C).
• Both S and P groups underwent 8 weeks of supervised squat training, 3 times per week.
• Muscle biopsies from the vastus lateralis were analyzed for gene expression of MSTN, ACTIIB, GASP-1, FOXO-3A, FLST, FL-3, and SMAD-7 before and after training.

Main Results:

• No significant changes were observed in MSTN, ACTIIB, GASP-1, or FOXO-3A gene expression following either training protocol.
• Both strength (S) and power (P) training significantly increased the gene expression of MSTN pathway inhibitors: FLST (4.2-fold and 3.7-fold, respectively) and FL-3 (5.6-fold for both).
• SMAD-7 gene expression also showed a similar increase after both S (2.5-fold) and P (2.8-fold) training protocols.

Conclusions:

• Neither strength nor power training altered the expression of key MSTN pathway genes (MSTN, ACTIIB, GASP-1, FOXO-3A).
• Both resistance training regimens effectively activated the expression of inhibitory components within the MSTN signaling pathway, specifically FLST, FL-3, and SMAD-7.
• The findings suggest that different resistance training protocols can similarly modulate the MSTN pathway through the upregulation of its inhibitors.