Macrolide Antibiotics and Muscle Gain

[89tiger89]

I was wondering if macrolide antibiotics affect muscle gain, because they are said to inhibit protein synthesis. I have heard some conflicting posts on here with regard to whether or not antibiotics can inhibit some muscle growth... As I am taking them (Azithromycin), I was wondering if any one has a more definite answer?

[NO HYPE]

I was wondering if macrolide antibiotics affect muscle gain, because they are said to inhibit protein synthesis. I have heard some conflicting posts on here with regard to whether or not antibiotics can inhibit some muscle growth... As I am taking them (Azithromycin), I was wondering if any one has a more definite answer?

Considering the fact that macrolides inhibit muscle protein synthesis, I would tend to think that they also aquire the ability to diminish gains by some degree however, I do not believe there are any studies that have directly evaluated the use of macroglides in respect to exercise and their impact on overall gains. Nonetheless....


J Physiol. 2009 Apr 1;587(Pt 7):1535-46. Epub 2009 Feb 2.
Drummond MJ, Fry CS, Glynn EL, Dreyer HC, Dhanani S, Timmerman KL, Volpi E, Rasmussen BB.
Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis.

Muscle protein synthesis and mTORC1 signalling are concurrently stimulated following muscle contraction in humans. In an effort to determine whether mTORC1 signalling is essential for regulating muscle protein synthesis in humans, we treated subjects with a potent mTORC1 inhibitor (rapamycin) prior to performing a series of high-intensity muscle contractions. Here we show that rapamycin treatment blocks the early (1-2 h) acute contraction-induced increase (approximately 40%) in human muscle protein synthesis. In addition, several downstream components of the mTORC1 signalling pathway were also blunted or blocked by rapamycin. For instance, S6K1 phosphorylation (Thr421/Ser424) was increased post-exercise 6-fold in the control group while being unchanged with rapamycin treatment. Furthermore, eEF2 phosphorylation (Thr56) was reduced by approximately 25% post-exercise in the control group but phosphorylation following rapamycin treatment was unaltered, indicating that translation elongation was inhibited. Rapamycin administration prior to exercise also reduced the ability of raptor to associate with mTORC1 during post-exercise recovery. Surprisingly, rapamycin treatment prior to resistance exercise completely blocked the contraction-induced increase in the phosphorylation of ERK1/2 (Thr202/Tyr204) and blunted the increase in MNK1 (Thr197/202) phosphorylation. However, the phosphorylation of a known target of MNK1, eIF4E (Ser208), was similar in both groups (P > 0.05) which is consistent with the notion that rapamycin does not directly inhibit MAPK signalling. We conclude that mTORC1 signalling is, in part, playing a key role in regulating the contraction-induced stimulation of muscle protein synthesis in humans, while dual activation of mTORC1 and ERK1/2 stimulation may be required for full stimulation of human skeletal muscle protein synthesis.

[neuron]

While rapamycin is indeed a chemical macrolide, it is not an antibiotic macrolide. Rapamycin has a much different MOA then antibiotic macrolides, which tend to be specific for prokaryotic ribosomes. Rapamycin binds to eukaryotic mTOR and effects immune function.

[NO HYPE]

While rapamycin is indeed a chemical macrolide, it is not an antibiotic macrolide. Rapamycin has a much different MOA then antibiotic macrolides, which tend to be specific for prokaryotic ribosomes. Rapamycin binds to eukaryotic mTOR and effects immune function.

Thanx for the correction. So do you feel that antibiotic macrolides will have a minimal impact on gains?

[neuron]

Thanx for the correction. So do you feel that antibiotic macrolides will have a minimal impact on gains?

I think rapamycin would ultimately effect gains, but not antibiotic macrolides. Similarly, I think being sick would prevent gains much more quickly then being on an antibiotic.

[NO HYPE]

Wurd. Thanks again.

[michael3435]

antibiotic macrolides, which tend to be specific for prokaryotic ribosomes

this.

macrolides are very specific for prokaryotic ribo****l subunits. there should be no effect at all on human cells. this is a major reason why the prokaryotic ribosome is an important drug target.

[89tiger89]

this.

macrolides are very specific for prokaryotic ribo****l subunits. there should be no effect at all on human cells. this is a major reason why the prokaryotic ribosome is an important drug target.

So in effect, macrolide antibiotics only limit the protein synthesis of bacteria in the body and my own protein synthesis will be unaffected?

[michael3435]

So in effect, macrolide antibiotics only limit the protein synthesis of bacteria in the body and my own protein synthesis will be unaffected?

yes

[Al.Capone]

I've been taking Azithromycin for over ten years, so I have the same question.

I wasn't sure whether it targets bacteria only or interferes with protein synthesis period.

My muscle growth is slow, but that may also be put down to my medical condition.

[AphtaLyfe]

Just giving my +1 to what's already been said.

Macrolide antibiotics target a ribo****l subunit not found in eukaryotes. Theoretically they should not directly affect protein synthesis in humans at all.

Even though the MOA of macrolide antibiotics shouldn't interfere with our protein synthesis... There could always be alternative pathways that indirectly suppress protein synthesis.

[TheWaffleIron]

Just giving my +1 to what's already been said.

Macrolide antibiotics target a ribo****l subunit not found in eukaryotes. Theoretically they should not directly affect protein synthesis in humans at all.

Even though the MOA of macrolide antibiotics shouldn't interfere with our protein synthesis... There could always be alternative pathways that indirectly suppress protein synthesis.

Bingo. Macrolide antibiotics reversibly bind to the 50S subunit.

Thread rated five stars. Excellent work by everyone.