IGF-1) has been questioned, leading to discovery of alternative mechanosensing–signalling to MPS.
Finally, the molecular regulation of MPS by exercise and its regulation via ‘anabolic’ hormones (e.g. while ‘mixed’ MPS increases similarly with endurance and RE, increases in myofibrillar MPS are specific to RE, prophetic of adaptation (i.e. myofibrillar, sarcoplasmic, mitochondrial) may provide a readout of chronic exercise efficacy in addition to effect size in MPS per se, i.e. Analysing distinct subcellular fractions (e.g. However, low-intensity exercise performed to failure equalises this response. Studies manipulating exercise intensity/workload have shown that increases in MPS are negligible with RE at 20–40% but maximal at 70–90% of one-repetition maximum when workload is matched (according to load × repetition number).
the feeding × exercise combination is ‘more anabolic’ than nutrition alone) even ≥24 h beyond a single exercise bout, casting doubt on the importance of nutrient timing vs. Intriguingly, this ‘muscle-full set-point’ is delayed by resistance exercise (RE) (i.e. Nutrient-driven increases in MPS are of finite duration (∼1.5 h), switching off thereafter despite sustained amino acid availability and intramuscular anabolic signalling. Recent findings in this arena have been progressive. Muscle protein synthesis (MPS) is the driving force behind adaptive responses to exercise and represents a widely adopted proxy for gauging chronic efficacy of acute interventions, (i.e.
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