But endurance exercise caused a MPS response. There's more:
Resistance exercise and the mechanisms of muscle mass regulation in humans: Acute effects on muscle protein turnover and the gaps in our understanding of chronic resistance exercise training adaptation - ScienceDirecttranslation initiation of muscle protein synthesis (mammalian target of rapamycin signaling), and satellite cell mediated myogenesis are highlighted as pathways of special relevance to muscle protein metabolism in response to acute resistance exercise. Furthermore, research focused on quantifying signaling and molecular events that modulate muscle protein synthesis and protein degradation under conditions of chronic resistance training is highlighted as being urgently needed to improve knowledge gaps
Exercise-induced skeletal muscle signaling pathways and human athletic performance | Request PDFit is clear that exercise performance is a complex phenomenon resulting from the integration of multiple physiological, biomechanical and psychological factors. As such, it is naive to think that any single ‘molecular marker’ can predict or explain variability in exercise responses and subsequent performance capacity. Indeed, there is often a mismatch between the changes in cellular „mechanistic‟ variables ( often reported as increases in the phosphorylation status of signaling molecules and/or increases in the expression of genes and proteins involved in mitochondrial biogenesis or muscle protein synthesis ) and whole body functional out comes (changes in training capacity or measures of performance)
I don't want to bore everyone with this anymore. But the fundamental premise of perman's posts is wrong. Unless perman tells us how exactly and in what contexts certain MPS rates translate to ACTUAL training, it is safe to say that he just proposed an idea, not an actual argument. I'm telling you, MPS rates are only useful to exercise physiologists.
If you don't have access to the 3rd paper I linked: Sci-Hub | Exercise-induced skeletal muscle signaling pathways and human athletic performance. Free Radical Biology and Medicine, 98, 131–143 | 10.1016/j.freeradbiomed.2016.02.007
Perhaps perman should reveal his ideas and help these scientists struggling to understand MPS.. Such approaches to unraveling the complexity of exercise-induced signaling events is both exciting and somewhat daunting because it is already apparent that there are many redundant molecular pathways engaged in many key acute and chronic responses to exercise. Indeed, direct evidence linking specific signaling events to defined performance measures or specific health outcomes and understanding how these effects exert their benefits in different populations is elusive and represents a major challenge for future research in this field. Connecting distinct signaling cascades to defined metabolic responses and specific changes in gene expression in skeletal muscle that occur after exercise is likely to be a complex and perhaps, ultimately futile task because the majority of these pathways are not linear, but, rather, they constitute a complex network, with a high degree of crosstalk, feedback regulation, and transient activation. In the final analyses, perhaps the only obligatory response to the numerous and widespread exercise-induced perturbations to cellular homeostasis is the defense of homeostasis itself.