The present study aimed to examine the effect of HICT protocol on muscle growth regulatory serum factors in adolescent male soccer players. The main findings of the present study showed that the resting serum values of MyoG in adolescent male soccer players did not change significantly after eight weeks of HICT, but the resting serum values of MSTN decreased significantly. Also, performing eight weeks of HICT did not significantly affect the acute response of serum MyoG and MSTN adolescent male soccer players to the maximum aerobic test.
By investigating the effect of adaptation on serum MyoG and MSTN’s acute response to the maximum aerobic test, no significant changes were observed in either training or control groups in comparison before and after eight weeks of HICT. Therefore, it can be concluded that eight weeks of HICT did not impact the acute response of serum MyoG and MSTN to the maximum aerobic test.
The current study showed that eight weeks of HICT did not show the difference in the resting serum values of MyoG in boy adolescent soccer players. In contrast to our data, Wilborn et al. investigated the effect of different intensities (60–65% 1RM and 80–85% 1RM) of resistance training on myogenic regulatory factors (MyoG, MRF4, Myf5, MyoD) in 13 young men recreationally active but nonresistance-trained [24]. The results of Wilborn et al. showed a significant increase in the expression of myogenic regulatory factors in both training intensities [24]. This heterogeneity of the results is probably due to differences in variables (Protein and Gene). Our results agreed the results of Costa et al. who showed no change in the expression values of myogenic factors on the seventh day after six days of repetitive bouts of eccentric exercise. But contrary to the results of the present study, there was a significant decrease in the MSTN gene expression on the seventh day [25]. Therefore, because Gene expression does not necessarily lead to protein translation [26], an increase in MyoG/MSTN gene expression does not necessarily lead to an increase in serum values of myogenin protein. For this reason, we examined MyoG and MSTN values based on their half-life in serum. Also, another critical point that can be mentioned is recovery. Xiao et al. and De Souza et al. showed insufficient recovery between training sessions led to anti-anabolic conditions and reduction of MyoG, MyoD, and IGF-I [18, 19]. Also, Schwarz et al. showed that lack of sleep reduced the cellular indicators of muscle repair in male rats [27]. Yang et al. found that lack of sleep reduced protein synthesis [28]. In addition, in a recent review, Vlahoyiannis and colleagues stated that young athletes, especially young athletes of Asian descent with low sleep quality [29].
This study reported eight weeks of HICT decreased the resting serum values of MSTN in boy adolescent soccer players significantly. Similarly, to the present study, MSTN gene and protein expression after 12 weeks of resistance training decreased in young men [30]. A possible explanation for the similarity in findings may be the existence of resistance nature in high-intensity circuit training protocol. De Souza et al. in a study, investigated the effects of concurrent strength and endurance training on genes associated with the MSTN signaling pathway and musculoskeletal responses [19]. The results of this study showed that MSTN and its associated genes, activin, GASP-1, FOXo-3a, FLST-3a, IIB genes remained unchanged after eight weeks of combined training [19]. The reason for the contradictions among these studies is not apparent. These inconsistencies may be partly due to the differences in the protocol type, the intensity and duration of exercise, gender and personal traits of the participants, measurement method, and the timing for sampling. The present study's findings were in accordance with those obtained by Bahram and Pourvaghar and Bagheri et al. [31, 32]. Bahram and Pourvaghar about the effect of 10 weeks of resistance training on serum MSTN values in non-athlete obese adolescent boys showed that resistance training for ten weeks significantly decreased plasma Myostatin values [31]. Also, Bagheri et al. after examining the effect of three categories, upper-trunk, lower-trunk, and combined lower and upper-trunk resistance training protocols for eight weeks on serum values of MSTN and follistatin in healthy middle-aged men, showed a significant decrease in serum values of MSTN in both lower-trunk and combined training protocols (upper trunk and lower trunk) [32]. These findings are following the current study. All these studies indicated that both chronic exercise and single session resistance exercise-induced a reduction in myostatin expression, thus promoting protein synthesis. This exercise-induced downregulation likely forms part of a beneficial hypertrophic adaptive response [33].
We are the first to show the preconditioning effect of HICT on the acute response of serum MyoG and MSTN to a maximum aerobic test. Most studies investigated the acute response of MyoG and MSTN to HICT and aerobic training. Our results showed non-significant changes in the acute serum values of MyoG to the maximum aerobic test after eight weeks of HICT in boy adolescent soccer players. The myokines investigated here play a critical role in muscle growth and metabolism. Coffey et al. showed an acute cycling bout increased mRNA myostatin by 2-fold, MyoD by 3-fold, and MyoG by < 1-fold in endurance-trained subjects [34]. One study has reported increased myostatin expression after an acute resistive session [30]. In addition, an acute bout of resistance training can reduce [35] or not change [36] MyoG values and increase MyoD mRNA expression [34] in young but not elderly. Probably due to the catabolic condition of the body after an exercise bout, in the present study, MyoG values remained unchanged. The effects of acute exercise on myostatin remain unclear, with some studies finding a downregulation of myostatin mRNA expression after different types of exercise [37, 38, 39] but others failing to find such changes [40, 41]. Although MacKenzie et al. found a decrease in MSTN transcriptional activity after resistance exercise, the exercise stimulus activated Notch, a TGF-B inhibitor [41]. The authors concluded that despite the acute increase in myostatin expression, the inhibition of its transcriptional activity might contribute to exercise-induced skeletal muscle hypertrophy [41].
In the present study, the participants were students. One of the limitations of the present study was the lack of control over extracurricular activities outside the club and during school hours (e.g., excessive physical activity during physical education lessons at school) and the values of sleep. On the other side, in addition to holding a briefing session for the subjects and their parents to raise awareness of nutritional requirements, recovery, and research stages before the start of interventions and verbal questions and answers from the subject about nutrition and their sleep before each intervention session, there was the lack of nutritional, sleep and mood and anxiety control of participants. Also, because of our limitations in the number of EIA Kits and could include a maximum of 20 subjects in the study, but we ran the experiment with high quality and accuracy.