Recovery from exercise refers to the period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It is a dynamic period in which many physiological changes occur. A large amount of research has evaluated the effect of training on intramuscular lipid metabolism. However, data are limited regarding intramuscular lipid metabolism during the recovery period. In this study, lipid metabolism-related proteins were examined after a single bout of exercise in a time-dependent way to explore the mechanism of how exercise induces intramuscular lipid metabolism adaptation. Firstly, all rats in the exercise group underwent a five-week training protocol (HIIT, five times/week), and then performed a more intense HIIT session after 72 h of the last-time five-week training. After that, rats were sampled in a time-dependent way, including 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, and 96 h following the acute training session. Our results discovered that five weeks of HIIT increased the content of intramuscular triglyceride (IMTG) and enhanced the lipolytic and lipogenesis-related proteins in skeletal muscle. Furthermore, IMTG content decreased immediately post HIIT and gradually increased to baseline levels 48 h postexercise, continuing to over-recover up to 96 h postexercise. Following acute exercise, lipolytic-related proteins showed an initial increase (6-12 h) before decreasing during recovery. Conversely, lipogenesis-related proteins decreased following exercise (6-12 h), then increased in the recovery period. Based on the changes, we speculate that skeletal muscle is predominated by lipid oxidative at the first 12 h postexercise. After this period, lipid synthesis-related proteins increased, which may be the result of body recovery. Together, these results may provide insight into how the lipid metabolism-related signaling changes after chronic and acute HIIT and how protein levels lipid metabolism correlates to IMTG recovery.
Background: High-intensity Interval Training (HIIT) is a time-efficient form of exercise and has gained popularity in recent years. However, at molecular level, the understanding about the effects of HIIT is not comprehensive, and even less is elucidated about HIIT of different training duration cycles, although different durations always lead to different post-training consequences. Method: In this study, by training SD rats using HIIT protocols lasting for different training duration cycles, we investigated the adaptive response of intramuscular triglyceride abundance and mitochondria enhancement after HIIT training (2, 4, 6, 8, and 10 weeks). We selected 72h after the last session of training as the time point of sacrifice. Results:The suppressed activation of the cAMP-PKA pathway indicates that skeletal muscle was in the recovery phase at this time point. Intramuscular triglyceride abundance was significantly elevated after 2, 4, and 10 weeks of HIIT. However, the lipid metabolism-related proteins inconsistently changed in a chaotic trend (see Table . 1). The expression levels of PGC1-α and COX IV decreased after 2 and 4 weeks of training and began to rise when the training duration reached 6 weeks. Interestingly, the variation tendency of PGC1-α and COX IV is very similar to that of CPT-1B. Conclusion:Given the fact that CPT-1B is responsible for the transfer of free fatty acids into the mitochondria to facilitate muscular lipid oxidation, there is a great possibility that: A) the IMTG accumulation observed within 0-4 weeks [defined as phase 1 here] of HIIT might be primarily attributed to damaged mitochondria oxidation capacity. B) when the training duration reached 6 weeks [defined as phase 2], mitochondria function and biogenesis began to be improved by training stimulus and might result in the disappearance of IMTG increase. We believe the phase 2 is rather similar to the condition of athletes`paradox, which should be a healthy adaptation induced by exercise training. Also, for HIIT Rat Modelling, intervention duration cycles longer than 4 weeks are recommended if similar HIIT frame of this study is used.
Background : High-intensity Interval Training (HIIT) is a time-efficient form of exercise and has gained popularity in recent years. However, at molecular level, the understanding about the effects of HIIT is not comprehensive, and even less is elucidated about HIIT of different training duration cycles, although different durations always lead to different post-training consequences. Method: In this study, by training SD rats using HIIT protocols lasting for different training duration cycles, we investigated the adaptive response of intramuscular triglyceride abundance and mitochondria enhancement after HIIT training (2, 4, 6, 8, and 10 weeks). We selected 72h after the last session of training as the time point of sacrifice. Results: The suppressed activation of the cAMP-PKA pathway indicates that skeletal muscle was in the recovery phase at this time point. Intramuscular triglyceride abundance was significantly elevated after 2, 4, and 10 weeks of HIIT. However, the lipid metabolism-related proteins inconsistently changed in a chaotic trend (see Table. 1). The expression levels of PGC1-α and COX IV decreased after 2 and 4 weeks of training and began to rise when the training duration reached 6 weeks. Interestingly, the variation tendency of PGC1-α and COX IV is very similar to that of CPT-1B. Conclusion: Given the fact that CPT-1B is responsible for the transfer of free fatty acids into the mitochondria to facilitate muscular lipid oxidation, there is a great possibility that: A) the IMTG accumulation observed within 0-4 weeks [defined as phase 1 here] of HIIT might be primarily attributed to damaged mitochondria oxidation capacity. B) when the training duration reached 6 weeks [defined as phase 2], mitochondria function and biogenesis began to be improved by training stimulus and might result in the disappearance of IMTG increase. We believe the phase 2 is rather similar to the condition of athletes` paradox, which should be a healthy adaptation induced by exercise training. Also, for HIIT Rat Modelling, intervention duration cycles longer than 4 weeks are recommended if similar HIIT frame of this study is used.
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