The effects of HIIT/MICT on the inhibition of fat accumulation during training and detraining

doi:10.21203/rs.3.rs-4366450/v1

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Research Article

The effects of HIIT/MICT on the inhibition of fat accumulation during training and detraining

https://doi.org/10.21203/rs.3.rs-4366450/v1

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published 22 Jul, 2024

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Background:

HIIT had at least comparable effect on inhibiting the increase of fat compared with MICT. However, few studies have been conducted to examine their effects of detraining on body fat with high-fat diet rats. This study aimed to compare the effects of 10-week high-intensity interval training (HIIT) and moderate intensity continuous training (MICT) as well as 6-week detraining on body fat in high-fat diet rats.

Methods:

After 8-week high-fat feeding, fifty-four rats were randomly assigned to six groups: 1)CON-T(n = 9): sedentary for 10 weeks (T10); 2)MICT-T(n = 9): 10-week MICT; 3)HIIT-T(n = 9): 10-week HIIT; 4)CON-D(n = 9):sedentary for 16 weeks (T16); 5)MICT-D(n = 9): 10-week MICT and 6-week training cessation; 6)HIIT-D(n = 9): 10-week HIIT and 6-week training cessation. The training cession performed 5 days/week. The subcutaneous (inguinal; SCAT), visceral (periuterine; VAT) adipose tissue and serum lipid profiles were analyzed by histological staining. ATGL expression in VAT was assessed by Western Blot at T10 and T16.

Results:

Ten-week HIIT and MICT inhibited the increase of SCAT, VAT and serum lipid levels compared with CON. After 6-week detraining, HIIT continued to inhibit the increase of adipose tissue mass whereas MICT at least maintained this inhibition induced by the training compared with CON. The inhibition primarily resulted from the adipocyte hypertrophy prevention. HIIT showed the most significant expression of ATGL after training and detraining.

Conclusions:

HIIT which had a comparable effect to MICT in preventing fat mass increase during training showed superior sustainability to MICT after detraining.

HIIT

MICT

detraining

adipose tissue

Obesity/overweight is closely related to many chronic diseases including type 2 diabetes, fatty liver and cardiovascular diseases[1, 2]. Moderate intensity continuous training (MICT) which predominantly utilizes the fat as the main metabolic substrate is a non-pharmacological way for controlling weight[3]. However, training cessation may lead to the fat rebound influencing individual’s choice of training modalities[4]. A recent meta-analysis reported that there was an increase in fat mass resulting from the enlarged adipocyte diameters after moderate continuous training cessation[5]. According to the compensatory effect, fat consumed during training period may be resynthesized when the people with obesity stop training[6, 7]. It was reported that MICT enhanced the activity of adipose triglyceride lipase (ATGL), the lipolytic activity decreased significantly after detraining for two weeks[8, 9].

Recent studies have proven that high intensity interval training (HIIT) with lower time commitment had at least comparable effect with MICT on fat loss, especially more evident in reducing the visceral adipose tissue (VAT)[10]. But whether the physiological adaptions on fat reduction are different between the interruption of HIIT and MICT is not well known. Given the improvements in fat reduction, it is hypothesized that HIIT may outperform MICT in combating fat accumulation after training cessation[11, 12]. Although HIIT may be less efficient in fat expenditure than MICT and utilizes more glycogen during exercise, most of studies suggest it enhances post-exercise oxygen consumption (EPOC) and resting metabolic rate in obese and overweight individuals[13, 14]. It has been noted that the substantial glycogen consumed during high-intensity interval exercise needs to be replaced by burning more fat through ‘liver-adipose tissue axis’ after exercise [15, 16]. Furthermore, HIIT could enhance the higher activity and longer duration of lipase including hormone sensitive lipase (HSL) in VAT[17].

Based on these findings, the fat which was not served as the primary substrate during HIIT suggest that adipose tissue may not require excessive recovery post training cessation. Moreover, previous studies have indicated that HIIT performed a better maintenance in VO_2max and anorectic effect for the overweight individuals post detraining[11]. It was possible that the beneficial effects also exist in the adipose tissue. It was hypothesized that the enhanced post-exercise lipolysis induced by the long-term HIIT may imply a lower risk of fat rebound. Therefore, to compare the different maintenance between MICT and HIIT after training cessation, high-fat diet rats were randomly divided for the training and interruption of training intervention to investigate their effect on the fat in adipose tissue and serum lipid profiles. The current study aims to provide insights into physiological adaptation changes post-training cessation and offers guidance on training modalities for sustained weight management.

1.1 Study design

Fifty-four female Sprague Dawley rats (7-week-old/174.24 ± 7.95g) were fed at single standard cages separately. The rats were under controlled temperature (22 ± 2℃) and humidity (50 ± 5%) conditions with a 12 h light/dark cycle. After 8-week high fat diet(60% standard chow, 18% protein powder, 16%sugar, 5%fat and 1% sodium cholate) the animals were randomly divided into the following groups: 1)CON-T(n = 9):sedentary for 10 weeks (T10); 2)MICT-T(n = 9): 10-week MICT; 3)HIIT-T(n = 9): 10-week HIIT; 4)CON-D(n = 9):sedentary for 16 weeks (T16); 5)MICT-D(n = 9): 10-week MICT and 6-week training cessation; 6)HIIT-D(n = 9): 10-week HIIT and 6-week training cessation. All the rats continued to be on the high-fat diet throughout the study. The body weight, the food intake and voluntary running wheels were measured at every end of week.

1.2 Exercise protocol

After 7 days of adaptive training (10min/day, 5m/min), the rats in the training groups were then subjected to the incremental exercise test (IET) to determine their running speed. The rodents were subjected to a 15° uphill treadmill at the initial speed of 9m/min, after which it increased by 2m/min for 2min until exhaustion (inability to complete the test despite the physical pokes). The running speed preceding the exhaustion velocity was defined as the high-intensity running speed (85%~100%VO_2peak). Each training session for HIIT comprised alternating 1-min intervals of high-intensity running speed and 2-min intervals of medium running speed cycles. Based on the relationship between running speed and VO_2peak, the medium running speed for HIIT and the intensity for MICT were set as 50%~70%VO_2peak. The duration of HIIT sessions was adjusted to achieve an equal running distance as that of MICT (50%~70%VO_2peak, 45min). The rats in both HIIT and MICT were underwent training sessions for 10 weeks, 5 days/week. After the final session of the 2nd, 4th, 6th, 8th and 10th weeks, IET was repeated to adjust running intensity. (see Fig. 1). Exercise intensity for subsequent weeks was modified based on the speed measured at these time points.

1.3 Sample collection

After 48 h of rest, the rats were sacrificed after anaesthesia (intraperitoneal pentobarbital sodium, Solarbio, China). Blood samples were collected immediately following each sacrifice at T10 and T16. Approximately 10 ml of blood was drawn from the apex of heart and transferred to centrifuge tubes. The blood samples were then centrifuged at 3500 r/min for 20 minutes following a 30-min resting period. The serum was extracted from the supernatant of the processed blood samples and stored at -80°C until analysis. The subcutaneous (inguinal; SCAT), visceral (periuterine; VAT) adipose tissue were excised and weighed. Half of the aforementioned fat pads were fixed in 4% paraformaldehyde for hematoxylin and eosin(H&E) staining. The rest of periuterine fat pads were frozen at -80°C for Western blot analysis.

1.4 Histological assessment of adipose tissue

The adipocyte numbers and size (areas) were measured by H&E staining. In short, adipose tissue was embedded in paraffin after fixation. Then, the embedded tissue was sectioned into 6 ~ 8µm sections, dewaxed, rehydrated, stained with haematoxylin, washed with water and subjected to alcohol dehydration and finally stained with eosin. Following dehydration and sealing, the prepared microscope slides were examined under an optical microscope. Each group consisted of 9 samples and 3 fields with clear and intact cell membranes were chosen for each sample. The distance between each visual field was at least 200µm. Image J 1.8.0 was used to measure and then analyzed the adipocyte numbers and diameters.

1.5 Measurement of serum lipid profiles

All blood samples were analyzed for total cholesterol(TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) using established assay kits (Jiancheng Bio, Chian).

1.6 Western Blot for ATGL in VAT

Cryopreserved VAT was homogenized with RIPA buffer (Solaribo), protease and phosphatatase inhibitor. Then, the homogenate was centrifuged (4℃, 12000rpm, 20min) and the protein layer was extracted and boiled (98℃, 5min). The extracted protein samples were electrophoresed on a 12% gel and then transferred into the polyvinylidene difluoride membranes(Millipore). Primary antibody(anti-ATGL, Cell Signaling) was used to detect ATGL. The second antibody (Solarbio, China) was employed for luminescence detection. GAPDH was used as the loading control.

1.7 Statistical analyses

Data were expressed as mean\(\pm\)SD. The repeated-measure ANOVA was used to analyze the changes in weight during the training and detraining period. The effect of food intake, voluntary running wheels, the mass of adipose tissue, the adipocyte numbers and areas, the gray value of oil red O staining and the protein expression were compared using the 3\(\times\)2 two-way ANOVA. The 2 represents time (T10 and T16), and the 3 represents group(CON/MICT/ HIIT). If the interaction effect or main effect was significantly different, post-hoc comparison was conducted using the least significant differences (LSD) method. P < 0.05 was considered statistically significant difference.

1. Body weight, food intake and number of voluntary wheel rotations.

Figure 1a and 1b shows the changes in body weight in the 10-week training intervention and 6-week detraining periods respectively. The average body weight of rats in each group were similar after the high-fat diet feeding. After 10-week training, the body weight in all three groups were significantly higher (F=7.430, P<0.05) compared to baseline due to the high-fat diet. Both training groups inhinited the increase in body weight. At the end of 10^th week, the average body weights in the MICT-T(354.39±18.79) and HIIT-T(350.74±23.07) groups were significantly 8% and 9% (p>0.05) lower, respectively than in the CON-T group(382.30±35.34). After 6-week detrainig, both HIIT and MICT maintained the effect of fat reduction(interaction effect: time×group, P>0.05). Table 1 illustrates that there was no main (time, groups) and interaction effect (time×group, P>0.05) in the average daily food intake and number of voluntary wheel rotations.

2. Fat mass in SCAT and VAT.

HIIT and MICT induced more inhibition of fat accumulation compared with CON in the mass(g) of SCAT (HIIT-T: 3.67±0.95 vs. CON-T: 6.29±2.10, MICT-T: 3.71±1.13, vs. CON-T, p<0.05) and VAT (HIIT-T: 7.10±1.74 vs. CON-T: 10.05±2.62, MICT-T: 7.19±2.1 vs. CON-T) at T10 with no significant difference between two training types). When the training was interrupted, Figure 2a and 2b indicated that HIIT continued to suppress the increase of mass in VAT and SCAT (HIIT× time vs. CON× time, p<0.05). The figures also showed that MICT maintained the inhibition of fat accumulation in SCAT (MICT×time vs. CON×time, p>0.05) and continued to inhibit the increase of fat in VAT (MICT×time vs. CON×time, p<0.05). Moreover, the fat increase in HIIT was lesser than MICT (HIIT×time vs. MICT×time, p<0.05) in both adipose tissues.

2.1 Comparison of the adipocyte areas and numbers in SCAT and VAT

Figure 2c, d, e and f display that HIIT and MICT significantly inhibit the increase in adipocyte areas (×10⁴ μm²) after a 10-week intervention (p<0.05) in SCAT (HIIT-T: 5.96±1.16 vs. CON-T: 7.25±0.98, MICT-T: 6.22±1.11, vs. CON-T, p<0.05) and VAT (HIIT-T: 6.16±1.22 vs. CON-T: 12.23±1.93, MICT-T: 10.39±1.88, vs. CON-T, p<0.05). After detraining, HIIT and MICT continued to inhibit the adipocyte hypertrophy (HIIT/MICT×time vs. CON×time, p<0.05). Additionally, HIIT proved to be more effective to inhibit the adipocyte size enlargement than MICT (HIIT×time vs. MICT×time, p<0.05). The results of the two-way ANOVA indicated no significant difference in the main and interaction effect (P>0.05) in adipocyte numbers (Figure 2g, h). The increase of fat mass is in theory explained by the inhibition of increase in adipocyte size and/or adipocyte number[13]. In the present study, the inhibition of hypertrophy was the main reason for HIIT and MICT refraining the fat accumulation in SCAT and VAT during the training and detraining periods.

**Insert Figure 1 near here**

2.2 The expression of ATGL in VAT

The expression of ATGL in HIIT was significantly higher (p<0.05) than MICT and CON after 6-week training and maintained it after detraining (Figure 3).

3. Serum lipid profiles

The TG and LDL-C in both HIIT-T and MICT-T groups were lower than those in the CON-T group post training (p<0.05). Both HIIT and MICT maintained the inhibition of the increase in TG and LDL-C after detraining compared with CON, with no significant difference between the two training types. (HIIT/MICT×time vs. CON×time, p>0.05). There was no interaction and main effect in TC and HDL-C (P>0.05)(Table 2).

**Insert Table 2 near here**

This study compared the effect of the same running distance of HIIT and MICT on fat reduction after 10 weeks and continued to investigated their maintenance after 6-week training cessation. Our results confirmed that while both HIIT and MICT perform comparable effect on inhibiting the increase of VAT, SCAT and serum lipid profiles including TG and LDL-C, HIIT exhibited a superior effect on continuing to inhibit the increase of VAT and SCAT during training cessation in high-fat diet rats. Consistent with our hypothesis, the adaptions inhibiting fat enlargement induced by training continued to maintain when the training ended[18, 19]. Higher intensity training is more advantageous in maintaining the inhibition of fat accumulation[20] than MICT due to the higher activity of lipolysis. These findings provide a practical guidance for retraining following the interruption of physical activity.

Effect of 10-week training

In our study, 10-week HIIT and MICT had comparable effect on weight control in high-fat diet rats with the former saving almost half of time than the latter which has also been shown in other studies[21–23]. For individuals who are obesity/overweight, high-intensity interval exercise is a time-efficient strategy for inhibiting the increase of VAT mass than MICT, resulting from decreased postprandial insulin levels and increased fat oxidation after exercise as suggested by a recent meta-analysis[24, 25]. However, due to the genetic polymorphisms, sensitivity to obesity varies despite the high-fat diet. There may be inter-individual variability in fat loss caused by training and interruption of regular physical activity, which hasn’t been rule out in this study[26, 27].

Central obesity is characterized by excess abdominal fat. Visceral adipose tissue is a key risk factor for type Ⅱ diabetes and cardiovascular disease[20]. In our study, both HIIT and MICT significantly inhibited the increase of VAT mass during the 10-week training intervention. The primary source of triglycerides in adipocytes is the intake of free fatty acids (FFA) and the lipoprotein lipase (LPL) is a key protein to hydrolyze the TG into FFA in the capillaries of skeletal muscle or adipose tissue and then been transported into the cytoplasm[28]. ATGL is the main enzyme involved in the initial step of fat mobilization hydrolyzing TG into diglycerides and FFA. Only HIIT upregulated the expression of ATGL after the ten-week training period. In line with our result, the existing literature suggests that chronic HIIT can be more effectively increase the activity of ATGL in white adipose tissue than MICT[8, 29].

In the present study, current data didn’t clearly elucidate the fat reduction of relatively shorter HIIT. Previous researches have confirmed that during the process of vigorous intensity training, fatty acid mobilization from adipose tissue may be suppressed. The reason for the similar influence on fat reduction may be that HIIT consumes more fat after exercise, called exercise-post oxygen consumption (EPOC)[30, 31]. Studies have shown that the lipolytic activity in HIIT still maintained higher after 3h and 24h of exercise than the rest[16, 29]. Therefore, observing the changes in fat after training suspension also aims to examine the EPOC following a very long period of training on fat hydrolysis.

Chronic high-fat diet resulted in increased body weight. The obesity/overweight occurs when the energy intake exceeds the energy expenditure[32]. Regular exercise and caloric restriction are effective strategies for fat reduction[33, 34]. Long-term and acute HIIT were associated with lower appetite than MICT and maintained this effect after the suspension of training but neither training type affected the total food intake[35, 36]. Moreover, our results (Table 1) showed that the weight control may not be solely attributed to the unchanged caloric intake and non-exercise physical activity.

Effect of 6-week detraining

Individuals who are obese/overweight may discontinue training due to time constraints or negative affective valence, potentially reversing the benefits of exercise[11, 37]. Studies examining the effect of HIIT after detraining remain limited, with few focusing on the fat rebound. However, these studies have indicated that HIIT may have a greater or similar effect on maintaining the body weight compared with long-term sedentary[11, 36, 38, 39]. In our study, both exercise groups maintained the inhibition of weight gain after detraining. As the inactivity duration prolongs, it becomes increasingly challenging for high-fat diet rats to overcome the metabolic adaptations formed in the exercise period[7].

In the present study, both training types didn’t alter the food intake and voluntary physical activity after training cessation which was in line with the Ahmadizad et al.[36] Though the HIIT decreased appetite, it didn’t change total energy intake after detraining. The unchanged food intake and voluntary physical activity may indicate the establishment of a new energy balance[7]. Weight control maintenance in our study couldn’t be explained by nutritional changes, it is possible that the effect of training on inhibiting the growth of body fat can still be maintained after training suspension.

The mass of adipose tissue reduced by the exercise in adulthood is more associated with the inhibition of hypertrophy rather than the inhibition of hyperplasia when performing moderate intensity aerobic training[13, 40]. In our study, the adipocyte number wasn’t the main reasons for inhibiting the increase of fat mass. However, the findings about the changes of adipocyte numbers after training cessation were inconsistent and the adipocyte numbers may increase to the pre-training level after detraining[13, 41]. Sertie et al.[42] found that a shorter detraining duration (4 week) after 8-week aerobic continuous training (1 h/day, 5 days/week, 8 weeks) increased the expression of PPARγ with the increased adipocyte numbers for standard diet rats. High-fat diet undertaking also lead to an increase in PPARγ expression[43] and we observed that the number of adipocytes increased after detraining but without significant difference in training groups. More detraining duration may stimulate the adipocyte proliferation.[44] What’s more, exhaustive exercise caused damaged to cellular DNA which accelerated the process of apoptosis and decreased the mature adipocyte numbers, thus, it may contribute to the reduction of adipose tissue mass and maintained it after training cessation[41, 45].

Regardless of the high-fat or standard diet, the response of the adipocyte diameter to discontinuing activity follows the same pattern to fat accretion.[44] In the present study, both HIIT and MICT inhibited the increase of adipose tissue mass accompanying the inhibition of increase in adipocyte areas after detraining. The inhibition of fat accumulation may disappear induced by the physical inactivity. A study conducted by Yasari et al.[46] found that obesity adult rats that detrained for 6 weeks after 8-week moderate continuous training completely increase the intrabdominal fat deposition resulting from the increase of adipocyte diameter compared with the sedentary rats. A shorter detraining duration (4 week) after 8-week aerobic continuous training (1 h/day, 5 days/week, 8 weeks) induced hypertrophy in both subcutaneous and visceral fat pad compared with the sedentary control in normal undertaking rats[42]. In terms of a series studies, Sertie et al. proved the mass of VAT rebounded after moderate intensity exercise. They observed that the proportion of glucose oxidation into fat and fat synthesis in adipose tissue increased after detraining while the lipolysis didn’t change significantly[41, 42, 47]. Agarwal et al.[48] also showed that discontinuing activity for 2 weeks after 6 weeks of moderate intensity training could not completely eliminate the beneficial effects of regular exercise and training cessation for a longer period of time may lead to a complete reversal of the beneficial effects. In the above studies, MICT with lower exercise intensity and less training time stimulated less lipolysis in VAT.

Higher intensity training may maintain longer duration of beneficial effects obtained in the training. After 12 weeks of moderate intensity continuous training, it can significantly reduce the levels of inflammatory factors such as IL-6 and TNF-α in obese participants, increased antioxidant capacity and promoted fat metabolism. However, this inhibitory effect returned to the level of pre-exercise after 4-week suspension[49]. The authors mentioned that exercise intensity is a detrimental factor influencing the fat reduction and its maintenance[49]. It is speculated that high-intensity training further reduced the level of inflammation than MICT and maintained better effect of the fat reduction obtained by detraining[49, 50]. Plasma nesfatin-1 (anorectic effects) in HIIT was higher and maintained it after 1-week training suspension which may be related to the improvement of insulin sensitivity[36]. Moghadasi et al. also demonstrated that insulin resistance which inhibited the lipolysis levels decreased after the suspension of high-intensity endurance training[51, 52]. High intensity exercise may prevent the dramatic decline in resting metabolic rates after the training hiatus that would result in only modest rebound of body fat mass.[53] Therefore, it is still possible for HIIT to maintain a good weight loss after discontinuing of training, which may be related to the longer duration of post-exercise effect.

What we have already investigated was that sprint interval training with intensity more than 100%V̇O_2max and HIIT reduced more abdominal visceral fat mass accompanied by the release of serum growth hormone and epinephrine[23]. Acute HIIT increased the activity of hormone-sensitive triglyceride lipase (HSL) for at least 12h compared with MICT which may be the one of the reasons for the EPOC and reducing fat[16]. Due to the limitations of experimental conditions, the current studies show that the volume of oxygen consumption after HIIT are greater than that of the MICT with equivalent work-done and the duration of EPOC in HIIT lasting for more than 24h [30, 54, 55]is longer than MICT. Similarly, we can speculate that the reason for HIIT has a better maintenance than MICT after the end of detraining may be that the EPOC level of HIIT is greater than that of MICT after the suspension of training. And the increase of lipolytic enzyme activity for a longer period until the end of detraining may contributes to the EPOC[55]. Visceral adipose tissue is harmful to our health. Interestingly, we observed that the great maintenance (inhibit the increase of VAT and SCAT mass) carried into the period of training cessation, furthermore, the inhibition in HIIT was superior than MICT. We prolonged the detraining duration and further investigated the lipolytic activity and found that the expression of ATGL was still higher than MICT after the 6-week training cessation in VAT. Bae et al.[56] also showed that 6-week moderate intensity treadmill training reduced the visceral fat area of high-fat-diet rats compared with the long-term sedentary after 8 weeks of suspension accompanied by the increased expression of ATGL and other lipid droplet-related signaling proteins decreasing lipolytic rates[57]. Compared with MICT, HIIT has been confirmed the superior influence in VAT reduction and the training cessation preserve the reduction possibly for the higher activity of lipolytic in our study[24].

In our study, HIIT and MICT reduced TG and LDL-C after 10-week training. Neither HIIT nor MICT improved the TC and HDL-C. After detraining, HIIT and MICT maintained the improvement of TG and LDL-C. Few studies have found significant changes in all serum lipid profiles after training and detraining[58, 59]. Higher intensity intermittent exercise leads to more decreased level of LPL and ATGL expression after cessation of training and may therefore reduce the LDL catabolism[59]. Similar to our study, Dinari et al., [19]found that the effect of MICT on improving LDL-C in diabetic rats was maintained after 4-week detraining. Compared with nonlinear resistance training, 12 weeks of high intensity aerobic interval training (3 times/week, running protocols:4×4min, 90%HR_max, interval:3min, 65%HR_max) increased HDL-C for middle-aged obese men and remained no rebound after 4-week detraining which had a stronger anti-coronary heart disease effect and proved that higher intensity had a better lipid-lowering effect[39]. HDL was the most sensitive parameters to aerobic exercise. Most studies show that HIIT may be better in improving HDL compared with MICT after training cessation[59–61]. Kodama et al.[62] showed that there would be significant increase on serum HDL when the exercise duration was more than 120 minutes or the external work-done was at least 900kcal per week. Low volume exercise may be the reason why HIIT and MICT had no effect on HDL in our study. The increased energy demand during exercise and the utilization of triglycerides as fuel leading to a decrease in TG which was maintained after training cessation[59].

Several limitations to this study still need to be acknowledged. First, due to the genetic polymorphism the sensitivity of obesity in high-diet rats in this study was not the same. And they were not analyzed for the subcutaneous and visceral adipose fat and blood lipid profile before the start of exercise which may affect the reliability of our results. Secondly, we didn’t perform the gas metabolism analysis during the training and detraining in this study and whether the better maintenance of HIIT is related to the higher metabolic rates after interruption needs further investigation. Finally, we only investigated the effect of detraining of MICT/HIIT from the organ and tissue level but the mechanism at the molecular level could not be further studied. For instance, the other lipase, activity of fatty acid synthesis and other mechanisms related to the insulin resistance, inflammation and others.

In conclusion, both HIIT and MICT induced a comparable effect on inhibiting the increase of VAT, SCAT and TG and LDL-C compared with the long-term sedentary in high-fat diet rats. After detraining, both HIIT and MICT inhibited the fat accumulation in VAT and SCAT. However, HIIT perform a superior effect on inhibiting the increase of adipose tissue mass due to the inhibition of adipocyte hypertrophy. The higher expression of ATGL in VAT may be the reason for HIIT maintaining the effect of fat loss.

HIIT

High-intensity Interval Training

MICT

Moderate-intensity Continuous Training

V̇O_2max

Maximal Oxygen Uptake

VAT

Visceral adipose tissue

SCAT

Subcutaneous adipose tissue

ATGL

Adipose Triglyceride Lipase

Triglyceride

Total Cholesterol

LDL-C

Low-density Lipoprotein Cholesterol

HDL-C

High-density Lipoprotein Cholesterol.

Ethics approval and consent to participate

This study were approved by the Ethical Committee of Hebei Normal University for the Use of Human and Animal Subjects in Research provided ethical approval of this study.

Consent for publication

Not applicable.

Availability of data and materials

The datasets used in this study are available from the corresponding author upon reasonable request.

Competing interests

The authors declare that they have no competing interests.

Funding

Not applicable.

Authors' contributions

ZHF took part in study design. LY wrote the manuscript. WQQ, LH and ZXG conducted the experiment of inducing obesity, training, detraining and sacrificed. ZLK performed the Western Blot. LH analyzed the data. All the authors also read and approved the final version of this manuscript.

Acknowledgments

Not applicable.

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Table 1 The food intake and number of voluntary wheel rotations at T10 and T16

Training periods(T1-T10)

Detraining periods(T10-T16)

Two-way ANOVA

Main effects

(time)

Main effects

(group)

Interactive effect

CON-T（n=9）

MICT-T（n=9）

HIIT-T（n=9）

CON-D（n=9）

MICT-D（n=9）

HIIT-D（n=9）

Food intake (g/week)

114.91±

7.73

116.61±

11.63

114.46±

5.47

119.73±

16.77

121.90±

15.04

118.71±

10.55

0.244

0.784

2.182

0.146

0.008

0.992

The number of voluntary wheel rotation

2161.39±

596.76

1955.72±

606.55

2173.33±

738.48

1761.11±

502.33

1859.56±

311.05

2101.56±

273.71

1.077

0.356

3.075

0.092

0.957

0.398

Note: CON-T :sedentary for 10 weeks (T10); MICT-T: 10-week MICT; HIIT-T: 10-week HIIT; CON-D: sedentary for 16 weeks; MICT-D: 10-week MICT and 6-week training cessation; HIIT-D: 10-week HIIT and 6-week training cessation.

Table 2 The serum lipid frofiles at T10 and T16

The end of training(T10)

The end of detraining(T16)

Two-way ANOVA

Main effects (time)

Main effect (group)

Interaction effect

CON-T（n=9）

MICT-T（n=9）

HIIT-T（n=9）

CON-D（n=9）

MICT-D（n=9）

HIIT-D（n=9）

TC(mmol/L)

2.25±0.19

2.14±0.30

2.13±0.29

2.40±0.40

2.39±0.89

2.27±0.50

0.259

0.773

1.523

0.224

0.074

0.929

TG(mmol/L)

0.89±0.43

0.60±0.05^*

0.52±0.17^*

0.97±0.42

0.72±0.32^*

0.60±0.33^*

5.946

0.005

1.106

0.299

0.014

0.986

LDL-C(mmol/L)

0.77±0.22

0.51±0.15^*

0.41±0.17^*

0.74±0.18

0.53±0.27^*

0.51±0.11^*

10.754

0.000

0.337

0.564

0.423

0.658

HDL-C(mmol/L)

2.22±0.25

2.32±0.29

2.33±0.30

2.25±0.35

2.25±0.29

2.28±0.41

0.197

0.822

0.071

0.791

0.102

0.904

Note: *: significant difference from the corresponding CON group(p<0.05). CON-T :sedentary for 10 weeks (T10); MICT-T: 10-week MICT; HIIT-T: 10-week HIIT; CON-D: sedentary for 16 weeks; MICT-D: 10-week MICT and 6-week training cessation; HIIT-D: 10-week HIIT and 6-week training cessation

No competing interests reported.

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The effects of HIIT/MICT on the inhibition of fat accumulation during training and detraining

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Abstract

Background:

Methods:

Results:

Conclusions:

Figures

Background

Methods

1.1 Study design

1.2 Exercise protocol

1.3 Sample collection

1.4 Histological assessment of adipose tissue

1.5 Measurement of serum lipid profiles

1.6 Western Blot for ATGL in VAT

1.7 Statistical analyses

Results

Discussion

Effect of 10-week training

Effect of 6-week detraining

Conclusion

Abbreviations

Declarations

References

Tables

Additional Declarations

Status:

Journal Publication

Version 1