אימונים Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in hum

[Mike Bikov]

Am J Physiol Endocrinol Metab. 2013 Jul 1;305(1):E22-32. doi: 10.1152/ajpendo.00091.2013. Epub 2013 Apr 30.

Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in human skeletal muscle.
Apró W, Wang L, Pontén M, Blomstrand E, Sahlin K.

Source
Åstrand Laboratory, Swedish School of Sport and Health Sciences, Stockholm, Sweden. [email protected]

Abstract
The current dogma is that the muscle adaptation to resistance exercise is blunted when combined with endurance exercise. The suggested mechanism (based on rodent experiments) is that activation of adenosine monophosphate-activated protein kinase (AMPK) during endurance exercise impairs muscle growth through inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). The purpose of this study was to investigate potential interference of endurance training on the signaling pathway of resistance training [mTORC1 phosphorylation of ribosomal protein S6 kinase 1 (S6K1)] in human muscle. Ten healthy and moderately trained male subjects performed on two separate occasions either acute high-intensity and high-volume resistance exercise (leg press, R) or R followed by 30 min of cycling (RE). Muscle biopsies were collected before and 1 and 3 h post resistance exercise. Phosphorylation of mTOR (Ser²⁴⁴⁸) increased 2-fold (P < 0.05) and that of S6K1 (Thr³⁸⁹) 14-fold (P < 0.05), with no difference between R and RE. Phosphorylation of eukaryotic elongation factor 2 (eEF2, Thr⁵⁶) was reduced ~70% during recovery in both trials (P < 0.05). An interesting finding was that phosphorylation of AMPK (Thr¹⁷²) and acetyl-CoA carboxylase (ACC, Ser⁷⁹) decreased ~30% and ~50%, respectively, 3 h postexercise (P < 0.05). Proliferator-activated receptor-γ coactivator-1 (PGC-1α) mRNA increased more after RE (6.5-fold) than after R (4-fold) (RE vs. R: P < 0.01) and was the only gene expressed differently between trials. These data show that the signaling of muscle growth through the mTORC1-S6K1 axis after heavy resistance exercise is not inhibited by subsequent endurance exercise. It is also suggested that prior activation of mTORC1 signaling may repress subsequent phosphorylation of AMPK.

PMID: 23632629 [PubMed - indexed for MEDLINE]​

:hungry:

 

[ברק]

מישהו הגיב על המאמר בפורום של לייל:

They're saying the cycling was at 88% of max HR and 70% of max VO2. That doesn't seem possible, not really sure what to make of it.

mTOR dropped quite a bit more in the cardio group (from 1.9 after leg press to 1.4 3 hrs later) vs. the non-cardio group (2.28 to 2.1 over the same interval) but the small sample size meant it wasn't statistically significant.

There's no reference to post workout nutrition (or any nutrition at all), which makes these results basically worthless anyhow. Also, twas done in a fasted state, so it's not unreasonable to conclude that mTOR wasn't able to be properly triggered in either situation when preworkout protein might've resulted in differential effects (or more meaningful lack of difference) in mTOR.

עד שלא יאספו יותר מידע אני אמשיך להפריד בין האימונים או לרוץ בהתחלה.

 

[Mike Bikov]

בילבול מוח כרגיל. מחפשים את המחקר המושלם בהקשר של אימונים שיתייחס לכל הפרמטרים האפשריים. חיים בסרט (לדוגמה על החלק של התזונה).
הוא מוזמן לתרום מיליון דולר לשוודים (איפה שהמחקר בוצע), שיעשו מחקר לטעמו עם כל הפרמטרים האפשריים (בספק אם בכלל מיליון דולר יספיק להכניס X בני אדם לכלוב [מוסד רפואי] ל Y חודשים ולבדוק את כל הפרמטרים הללו).

 

[ברק]

כן אבל הנושא של האוכל כן חשוב כי חלבון הוא הגורם העיקרי שמפעיל את הMTOR ,אני שולח מייל לחוקרים לפחות כדי לדעת אם היתה ארוחה של אחרי האימון. זה מאמר שבאמת תומך בכך שאירובי אחר כך לא מפריע. אבל אני עדיין ארגיש בטוח יותר אם יהיה עוד אחד בתנאים קצת שונים.