Resistance Training With Excessive Training Load and Insufficient Recovery Alters Skeletal Muscle Mass–Related Protein Expression


The aim of this study was to investigate the effects of a resistance training program with excessive training load and insufficient recovery time between bouts on muscle hypertrophy- and atrophy-related protein expression. Male Wistar rats were randomly assigned to either a trained (TR, N = 9) or a sedentary (SE, N = 9) group. The TR group was subjected to a 12-week resistance training program with excessive training load and insufficient recovery between bouts that was designed to induce plantaris muscle atrophy. After the 12-week experiment, the plantaris muscle was collected to analyze the cross-sectional area (CSA) of the muscle fibers, and MAFbx, MyoD, myogenin, and IGF-I protein expression (Western blot). The CSA was reduced significantly (−17%, p ≤ 0.05) in the TR group compared with the SE group. Reciprocally, there was a significant (p ≤ 0.05) 20% increase in MAFbx protein expression, whereas the MyoD (−27%), myogenin (−29%), and IGF-I (−43%) protein levels decreased significantly (p ≤ 0.05) in the TR group compared with the SE group. In conclusion, our data indicated that muscle atrophy induced by resistance training with excessive training load and insufficient recovery was associated with upregulation of the MAFbx catabolic protein and downregulation of the MyoD, myogenin, and IGF-I anabolic proteins. These findings suggest that quantitative analysis of these proteins can be important and complementary with other biochemical markers to confirm a possible overtraining diagnosis.


Alex’s notes: We know that resistance training leads to microtrauma that stimulates and adaptive recovery response to enhance performance later on. But not everything is so cut and dry. Overtraining or a lack of adequate recovery (when the growth and adaptation happen) can actually lead to muscle loss. The study at hand simply aimed to examine the chronic response of several important anabolic and catabolic regulatory genes from an excessive amount of training with insufficient recovery.

The researchers used a 12-week resistance training program designed to achieve an overload 15% greater than recommended in rats. The intensity and volume were progressive and training was conducted on five consecutive days. After 12 weeks, the overtrained (TR) rats had less bodyweight but similar food intake as the control rats, suggesting muscle loss (since you cannot burn fat without the caloric deficit, and food intake was the same). Further support comes from the reduced cross-sectional area of the worked muscles in the TR rats compared to the control.

Now, the first gene of interest is MAFbx, which was shown to be 20% greater in the TR group. MAFbx – if you recall from a previous study on how whey protein suppresses its expression – plays a key role in regulating muscle catabolism. As the authors point out,

“It is important to note that the common process of muscle regeneration in response to acute resistance training is associated with reduced MAFbx expression (analyses at 8, 12, and 24 hours after exercise) (23,26,28,43); this downregulation in MAFbx expression appeared to be necessary for promoting muscle regeneration (29).”

This increased MAFbx protein expression was also associated with the downregulation of MyoD (-27%) and myogenin (-29%) protein expression as well. It has been demonstrated that increased MyoD and myogenin expression is essential for successful skeletal muscle hypertrophy. Finally, IGF-1 expression was suppressed by a whopping 43%! Unfortunately, IGF-1 unleashes a signaling cascade that counters MAFbx, and if the increased IGF-I levels are capable of suppressing MAFbx expression and preventing muscle atrophy, it seems logical to think that the downregulation of IGF-I is required to increase the MAFbx protein level and promote muscle atrophy, which is exactly what was found!

The bottom line is that the assessed proteins – MAFbx, MyoD, myogenin, & IGF-1 – play a critical role in skeletal muscle anabolism and catabolism. While it is unfortunate that the current study did not measure the other proteins involved with muscle atrophy and hypertrophy (MuRF-1, Akt, mTOR, etc.), any of the stress hormones (cortisol), or any markers of muscle damage (creatine kinase), the results do suggest that these proteins could become a potential future biomarker for assessing overtraining. In fact, perhaps one day they will be involved in therapeutic methods for many neuromuscular diseases.

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