Habitual high-protein diet does not influence muscle protein synthesis in response to acute resistance exercise in rat
Satoru Ato Nutrition Available online 5 March 2020, 110795
Highlights
• Habitual high protein intake (4 weeks) caused fat mass loss and skeletal muscle mass gain.
• Basal skeletal muscle mTORC1 activity and protein synthesis were not affected by the high protein diet.
• Habitual high protein diet did not affect the response of mTORC1 activation and MPS to acute resistance exercise.
Objectives
Resistance training combined with high-protein diet (HPD) consumption is typically recommended to increase muscle mass, as both acute resistance exercise and dietary protein intake stimulate mechanistic target of rapamycin complex 1 (mTORC1) and muscle protein synthesis (MPS). However, the effect of chronic HPD on MPS response to an acute resistance exercise (RE) remains to be determined.
Research Methods & Procedures
Male Sprague-Dawley rats aged 10 weeks were fed HPD (50 kcal % protein, for 4 weeks) or normal protein diet (NPD) (20 kcal % protein). After the 4-week dietary intervention, the rats were fasted overnight and the right gastrocnemius muscle was subjected to percutaneous electrical stimulation to mimic acute RE, while the left gastrocnemius muscle served as control. The rats were euthanized at 6 h after exercise and the tissues were sampled immediately.
Results
From the results, the HPD group showed significantly lower fat mass and higher skeletal muscle mass than the NPD group without affecting body weight. Resting mTORC1 activity did not differ between groups. In addition, resting MPS was also unchanged after HPD. Acute RE significantly increased mTORC1 activity and MPS in both groups. However, difference in diet did not influence the response of mTORC1 activation to acute RE. Furthermore, HPD did not affect the response of MPS to acute RE.
Conclusion
Our results suggested that although 4 weeks of HPD reduces body fat and increases skeletal muscle mass, it does not affect muscle protein synthesis at basal state, and in response to acute RE.