From 3fe881d4652028e3b8e511f995e96c4d28bbd13d Mon Sep 17 00:00:00 2001 From: violettelassit Date: Thu, 18 Sep 2025 19:47:29 +0800 Subject: [PATCH] Add 'Why Post-workout Nutrition Important in Our Routine?' --- Why-Post-workout-Nutrition-Important-in-Our-Routine%3F.md | 1 + 1 file changed, 1 insertion(+) create mode 100644 Why-Post-workout-Nutrition-Important-in-Our-Routine%3F.md diff --git a/Why-Post-workout-Nutrition-Important-in-Our-Routine%3F.md b/Why-Post-workout-Nutrition-Important-in-Our-Routine%3F.md new file mode 100644 index 0000000..6354cff --- /dev/null +++ b/Why-Post-workout-Nutrition-Important-in-Our-Routine%3F.md @@ -0,0 +1 @@ +
The speed of fall of the glycogen was linear in the course of the period of aglycemia. This prompt that if glycogen was unregulated previous to introducing aglycemia then the latency to CAP failure could possibly be prolonged if glycogen was metabolized at the same steady rate. Glycogen may be unregulated by bathing the nerve in supra-physiological concentrations of glucose, thus incubating the nerve in 30 mM glucose for two h will increase the glycogen content by an element of about two compared to baseline ranges, where the nerve is incubated in 10 mM glucose for 2 h (Wender et al., 2000). Exposing the optic nerve to aglycemia after increasing glycogen content material did certainly lead to a rise within the latency to CAP failure. Incubating nerves in increasing concentrations of glucose such that quite a lot of glycogen levels had been attained resulted in a linear relationship whereby the latency to CAP failure was determined by the glycogen content material, i.e., rising glycogen content within the nerve at the onset of aglycemia extended the latency to CAP failure.

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