The Combination of Fasting, Acute Resistance Exercise, and Protein Ingestion Led to Different Responses of Autophagy Markers in Gastrocnemius and Liver Samples

Abstract

The present study verified the responses of proteins related to the autophagy pathway after 10 h of fast with resistance exercise and protein ingestion in skeletal muscle and liver samples. The rats were distributed into five experimental groups: control (CT; sedentary and without gavage after fast), exercise immediately (EXE-imm; after fast, rats were submitted to the resistance protocol and received water by gavage immediately after exercise), exercise after 1 h (EXE-1h; after fast, rats were submitted to the resistance protocol and received water by gavage 1 h after exercise), exercise and supplementation immediately after exercise (EXE/Suppl-imm; after fast, rats were submitted to the resistance protocol and received a mix of casein: whey protein 1:1 (w/w) by gavage immediately after exercise), exercise and supplementation 1 h after exercise (EXE/Suppl-1h; after fast, rats were submitted to the resistance protocol and received a mix of casein: whey protein 1:1 (w/w) by gavage 1 h after exercise). In summary, the current findings show that the combination of fasting, acute resistance exercise, and protein blend ingestion (immediately or 1 h after the exercise stimulus) increased the serum levels of leucine, insulin, and glucose, as well as the autophagy protein contents in skeletal muscle, but decreased other proteins related to the autophagic pathway in the liver. These results deserve further mechanistic investigations since athletes are combining fasting with physical exercise to enhance health and performance outcomes.

Physical Exercise and Liver Autophagy: Potential Roles of IL-6 and Irisin

“…Although hepatic LC3BII/I ratio did not change with RE, there was a lower LC3BII/I ratio with COMB at 12 h postexercise than that immediately and 18 h postexercise. The different responses observed by Pinto et al (59) and Marafon et al (42) with RE could be due to the animal model or the feed-fasting state; however, further investigation is warranted.…”

“…In a study by Pinto et al (59), expression of Sqstm1 was higher after 10 h of fasting combined with RE in liver samples compared with sedentary rats. In contrast, BECN1, p-mTOR/mTOR, and p-ULK1/ULK1 ratios were not different between groups.…”

A single bout of exhaustive treadmill exercise increased AMPK activation associated with enhanced autophagy in mice skeletal muscle

“…For example, a swimming exercise increased expression of autophagy markers Beclin1, LC3II and the ratio of LC3II/LC3I, but not LC3I and p62 in skeletal muscle of mice, 3 while moderate cycling and exhaustive treadmill running exercise did not change expression of LC3II and p62 proteins in skeletal muscle of human and mice 2,4 . In addition, acute resistance exercise did not change the expression of p62 mRNA and Beclin1 and LC3II/LC3I protein 5 …”

“…However, the link between AMPK and autophagy in exercise is still controversial and especially the change of these mechanisms in the recovery phase of exercise. For example, it has been shown that acute exercise activated autophagic activity, 4‐10 however, Liu et al reported no change of phosphorylation of AMPK (pAMPK) after exhaustive treadmill exercise, 13 while Halling et al reported an increase of pAMPK after a treadmill exercise 14 . In addition, it has been suggested that high‐intensity cycling exercise may induce AMPK activation and increase autophagy in human vastus lateralis 15 .…”

Exercise, mTOR Activation, and Potential Impacts on the Liver in Rodents

“…Regarding the liver, exercise training attenuates obesity-induced insulin resistance by the inhibitory regulation of the cardiolipin synthase 1 (CRLS1)/interferon-regulatory factor-2 binding protein 2 (IRF2bp2)-activating transcription factor 3 (ATF3) pathway cascade [ 6 ]. Resistance exercise training results in higher protein expression of sqstm1/p62 (sequestosome 1), a peptide involved in the autophagy process within the liver [ 7 ]. In addition, exercise results in greater mRNA expression of peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1), which is an inducible co-regulator of nuclear receptors involved in a wide variety of biological responses, such as glucose and lipid metabolism, as well as in reducing triacylglycerol levels in the liver and plasmatic glycemia in diet-induced obese rats [ 8 ].…”