Library.

“During an acute stress response, splanchnic vasoconstriction reduces gastrointestinal perfusion and prioritizes blood flow to the heart, lungs, and skeletal muscle.”

The statement captures the main physiology: acute sympathetic activation constricts the splanchnic circulation, lowering gastrointestinal blood flow and helping preserve perfusion for the heart and active skeletal muscle. The weak point is "lungs": pulmonary flow usually rises because cardiac output rises, not because blood is selectively diverted there. Many references also emphasize preservation of brain perfusion and arterial pressure.

“Skeletal muscle lacks glucose-6-phosphatase and therefore stores glycogen for internal use rather than releasing glucose into the bloodstream.”

This claim accurately reflects a well-established biochemical principle. Multiple authoritative biomedical sources confirm that skeletal muscle lacks functional glucose-6-phosphatase and therefore cannot convert glucose-6-phosphate to free glucose for export into the bloodstream, meaning muscle glycogen serves as a local energy reserve. The only minor caveat is that the causal "therefore" slightly oversimplifies: muscle glycogen retention also reflects other physiological factors, and some sources describe G6Pase distribution as "mainly" liver/kidney rather than stating absolute absence.

“Mitochondrial dysfunction is the primary cause of age-related decline in skeletal muscle.”

The scientific literature does not support singling out mitochondrial dysfunction as "the primary cause" of age-related skeletal muscle decline. While multiple peer-reviewed reviews describe mitochondrial dysfunction as an important contributor and sometimes hypothesize it as an upstream initiator, the broader evidence base consistently characterizes sarcopenia as multifactorial—driven by denervation, neuromuscular junction failure, chronic inflammation, hormonal changes, and anabolic resistance alongside mitochondrial impairment. At least one high-authority source explicitly identifies denervation, not mitochondrial dysfunction, as the dominant driver in very old muscle.