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The Influence of Resistance Exercise Intensity and Metabolic Stress on Anabolic Signaling and the Expression of Myogenic Genes in Skeletal Muscle

Abstract

Introduction: We investigated the effect of resistance exercise intensity and exercise-induced metabolic stress on the activation of anabolic signaling and expression of myogenic genes in skeletal muscle. Methods: 10 strength-trained athletes performed high-intensity [HI, 74% of 1 repetition maximum (RM)], middle-intensity (MI, 54% 1RM), or middle-intensity (54% 1RM) no-relaxation exercise (MIR). Kinase phosphorylation level and myogenic gene expression in muscle samples were evaluated before, 45 min, 5h, and 20 h after exercise. Results: The lactate concentration in MI was approximately 2-fold lower than in the 2 other sessions, and it was highest in MIR. The phosphorylation level of extracellular kinase 1/2Thr202/Tyr204 after exercise was related to metabolic stress. Metabolic stress induced a decrease in myostatin mRNA expression, whereas mechano-growth factor mRNA level depended on exercise intensity. Conclusion: This study demonstrates that both intensity and exercise-induced metabolic stress can be manipulated to affect muscle anabolic signaling.

Full-text

Alex’s Notes: I love reading prospective studies and being able to share with the Super Human Nation information hot off the press, but I must admit sometimes manuscripts are a complete pain. In this article, for instance, there is a giant “Accepted Article” background text along the entire left side of every page that is very distracting. For those of you who are able to access the full-text you will see what I mean.

Anyways, a common goal of resistance training is increased muscle hypertrophy and strength. Numerous studies have investigated the effects of exercise intensity on the anabolic signaling cascade, gene expression, and protein synthesis rates, but most of those studies have a major flaw: The training loads differed in intensity, the total number of contractions, and total time under tension. Most conclude that higher intensity work usually corresponding to the 5-8RM range is ideal for both strength and mass, but the above flaws provide a caveat and high-intensity exercise isn’t always ideal. Recently, there has been a growing interest in blood-flow-restricted (BFR) training, which has shown extreme anabolic potential with loads as low as 20-30% 1RM, likely due to the excessive metabolic stress. Yet, these studies compared the BFR training to traditional resistance training matched for intensity and work (20% 1RM) and it has been known for a long time that exercise performed without substantial fatigue does not increase muscle protein synthesis, muscle hypertrophy, or strength.

In addition to the above, no one has looked at the effects of BFR when using a middle-intensity (50% 1RM). Thus, the goal of the study at hand was to evaluate the effects of resistance exercise intensity and metabolic stress on the activation of anabolic signals and gene expression within the exercises muscle. The participants were ten 23 year old amateur athletes (sprinters or middle-distance runners) and physically active men who usually perform 1-2 strength training sessions per week. They all performed three separate resistance training sessions once per week that consisted eight sets of 12 reps on the leg extension machine at a high-intensity (HI; 75% 1RM), middle-intensity (MI; 50% 1RM), and middle-intensity with no-relaxation (MIR; 50% 1RM) with six minutes of rest between each set. HI and MI had three seconds of rest between each repetition, while MIR performed each rep continuously. All groups had equivalent total tension time, number of contractions, and range of motion on the leg extension. The rationale behind the leg extension is because the secretion of anabolic hormones depends on the muscle mass involved, and using this single muscle group allowed for avoidance of exercise-induced blood hormone increases that could influence anabolic signaling.

As we can see, the study was very well controlled for and allowed for differentiation of the effects of different exercise intensities. During MI both mechanical load and metabolic stress were low; during MIR load was low but stress was high; and during HI both load and stress were high. Not surprisingly, lactate increased in all protocols but was highest in MIR, followed by HI then MI. It is clear that lactate production is a result of metabolic stress given that MIR was more than 2-fold greater than MI despite the identical intensity.

One of the components of the mTOR signaling cascade is activated p70S6K, which is directly related to increased muscle mass after exercise. Interestingly, it increased 1.3-fold 22 hours after the MI session, but not after the HI or MIR sessions. This could be connected with the activation of mTOR’s antagonist AMPK, which was found to be elevated after the HI session, likely due to depletion of muscle energy reserves (ATP, phosphocreatine, and glycogen). HI training recruits both slow- and fast-twitch muscle fibers from the beginning, compared to MI and MIR which may only need to recruit slow-twitch fibers given the low intensity. Moreover, total work in HI was approximately 25% higher than in the other protocols, which may lead to more pronounced glycogen depletion. Decreased muscle glycogen at rest leads to increased AMPK levels, which would have offset the increase in p70S6K.

Another anabolic pathway is the ERK1/2 pathway. Activation of ERK1/2 was not difference between HI and MI, which again could be the result of elevated AMPK in the HI group. However, ERK1/2 did increase significantly at 45 minutes and 22 hours after the MIR session, suggesting that its activation depends on the degree of metabolic stress. Actually, other studies have suggested that hypoxia enhances and prolongs ERK1/2 activation.

Then there are satellite cells, which are critical for muscle hypertrophy. No session had significant changes in direct markers of satellite cell activation, but HI did induce MGF expression which ultimately leads to satellite cell activation. This suggests that MGF depends on the training load rather than metabolic stress, and may be stimulated by the breakdown and microtrauma of skeletal muscle. Similarly, myostatin is muscle growth’s worst nightmare and completely blocks the anabolic process. HI reduced myostatin expression by 20-fold, while MIR reduced it by 6-fold, suggesting that substantial metabolic stress is enough to suppress it but that intensity plays an even larger role.

Overall, this was a well-controlled study that showed that in trained skeletal muscle, ERK1/2 activation depends on metabolic stress and not intensity, while MGF depends on intensity and not metabolic stress. The evil myostatin can be suppressed if metabolic stress is great enough, but lifting heavy is more effective.

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