Tue, Apr 16, 2024
Volume 15, Issue 2 (Mar-Apr 2021)
mljgoums 2021, 15(2): 42-47 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Dadban Shahamat M, askari A, Arab Koohsar R. Effects of Four Weeks of High-Intensity Intermittent Training and Continuous Walking on Atherogenic Indices of Obese Middle-Aged Men. mljgoums 2021; 15 (2) :42-47
URL: http://mlj.goums.ac.ir/article-1-1278-en.html
URL: http://mlj.goums.ac.ir/article-1-1278-en.html
1- Department of Physical Education, Azadshahr Branch, Islamic Azad University, Azadshahr, Iran , m_dadban@yahoo.com
2- Department of Physical Education, Grogan Branch, Islamic Azad University, Gorgan, Iran
3- Department of Physical Education, Azadshahr Branch, Islamic Azad University, Azadshahr, Iran
2- Department of Physical Education, Grogan Branch, Islamic Azad University, Gorgan, Iran
3- Department of Physical Education, Azadshahr Branch, Islamic Azad University, Azadshahr, Iran
Full-Text [PDF 676 kb]
(531 Downloads)
| Abstract (HTML) (1998 Views)
Full-Text: (891 Views)
INTRODUCTION
Lipids are small hydrophobic molecules that play a critical role in energy storage, signaling pathways and cellular responses (1). However, abnormal lipid levels can contribute to the development of atherosclerosis (2-4). Obesity and overweight are independent risk factors for atherosclerotic cardiovascular disease (2,5). A body mass index (BMI) of more than 25 kg/m2 and 30 kg/m2 indicates overweight and obesity, respectively (2,6-8). People with visceral obesity have evidently impaired plasma lipids, including increased triglycerides, apolipoprotein B and low-density lipoprotein-cholesterol (LDL-C) concentrations and decreased high-density lipoprotein-cholesterol (HDL-C) levels (2,9). Men are at a higher risk of developing obesity since fat mostly accumulates in the pelvic area and lower extremities of women (gynoid fat) but in the abdominal and visceral areas of men (android fat). Accumulated upper body fat increases the risk of stroke, diabetes, hypertension and biliary disease, which is more common in android obesity than in gynoid obesity (10).
Exercise can boost body metabolism, muscle strength, cardiovascular function, metal health and sex appeal, all of which are associated with a high level of confidence (1). Regular exercise prevents various diseases such as hypertension, heart disease, type 2 diabetes and obesity in both men and women (2, 11, 12). Frequent exercise, mostly regular aerobic exercise, such as jogging is one of the best non-pharmacological strategies in the prevention and treatment of cardiovascular disease (2, 11, 13). Exercise causes a drastic increase in post-heparin lipoprotein lipase (LPL), which in turn increases triglyceride clearance and decreases HDL-c clearance from plasma (7). LPL is the most important enzyme in plasma triglyceride catabolism and is thought to be elevated in skeletal muscle, adipose tissue and plasma of individuals with an active lifestyle (14), Such adaptation is usually enhanced by increased fatty acid delivery and oxidation in the skeletal muscle promoted by LPL and adaptation of the carnitine palmitoyl transferase system even under high-intensity interval training (HIIT) (15). Previous studies have shown that metabolic adaptation and oxidation are usually higher following intense exercise compared to endurance training (16, 17). In a study by Sheikh al-Islami et al. (2011) on obese women, both HIIT and moderate endurance training resulted in a significant decrease in visceral fat oxidation (18). Given the well-established positive effects of medium- and long-term exercise on lipid oxidation, this study aims to determine effects of short-term HIIT and light walk on risk factors of obesity and atherosclerosis in overweight middle-aged men.
MATERIALS AND METHODS
Study population consisted of 36 male teachers aged 35-50 years, with mean BMI of 30.7 ± 3.5 kg/m2 who were working in the city of Galikesh, northeastern Iran. Inclusion criteria included willingness to participate and no history of metabolic and orthopedic disorders, medication use, smoking and physical activity in the last six months. The subjects were enrolled via purposeful sampling and were randomly matched and equally divided into two experimental groups and a control group. Before and after the intervention, anthropometric characteristics (height, weight and BMI) and blood pressure of each subject were measured. The subjects participated in a briefing session and signed a consent form. Fasting blood samples (7 ml) were taken from the left brachial vein 12 hours before the first exercise session and 12 hours after the last exercise session to determine lipid profile.
For subjects in the HIIT group, a 20 m distance was marked by three cones that were placed 10 m apart. The subjects ran at maximum speed from the start point (cone 1) to cone 2 (path A), returned and then ran at the opposite direction for 20 m towards cone 3 (route B) and finally back to the start point (route C). The total distance covered was 40 m. This protocol was performed with four repetitions and at 75% maximum heart rate in the first two sessions. The intensity was gradually increased to eight repetitions and 90% maximum heart rate by session 12. A 30-sec rest interval was given between each repetition.
Subjects in the second experimental group performed 30 minutes of continuous walking at 50% maximum heart rate in the first session. The walking intensity increased to 75% maximum heart rate in the 12th session (5). The control group did not perform any exercise activity during the study. Serum concentrations of triglyceride, total cholesterol, HDL-C and LDL-C were measured using Pars Azmoon kits and a photometric device. The level of very low-density lipoprotein (VLDL) was calculated by dividing the total triglyceride by 5.
Obtained data were expressed as mean ± standard deviation. The Shapiro-Wilk test was used to assess normality of data. In addition, one-way ANOVA (Scheffe test) and t-test were used to analyze inter- and intra-group changes, respectively. All statistical analyses were performed in SPSS 18, at significance level of 0.05.
RESULTS
The descriptive characteristics of the subjects are shown in table 1.
Table 1. The characteristics of the subjects in the study groups
Our results showed that the four-week walking exercise significantly decreased serum LDL-C (P=0.001) and triglyceride (P=0.001) levels. In addition, HIIT significantly increased HDL (P=0.004) and significantly reduced LDL-C (P=0.049) levels. No significant change in the cholesterol/HDL ratio was observed (Table 2).
Table 2. The lipid profile of subjects in the study groups
*statistically significant
The results of ANOVA (Scheffe test) showed a significant increase in HDL-c values and a significant decrease in VLDL-C, LDL/HDL, triglyceride, BMI and blood pressure of HIIT group compared to the control group (Table 3).
Table 3. The inter-group changes in the lipid profile variables
*statistically significant
DISCUSSION
Our results showed that the four-week walking exercise significantly decreased serum LDL-C and triglyceride levels. In addition, HIIT increased HDL-C and reduced LDL-C, LDL/HDL, triglyceride, BMI and blood pressure. HDL-C transports cholesterol from peripheral tissues to the liver, which then channels the excess cholesterol for excretion into the bile. It is known that elevated HDL-C levels may play a protective role against coronary artery disease (19, 20). However, our results are inconsistent with finding of Kozehchian (21), Pauli (22) and consistent with Ding (23). The mechanism of HDL-C alterations following exercise is complex; enzymes such as LPL, hepatic lipase and cholesteryl ester transfer protein (CETP) play important roles in altering HDL-C concentration. LPL is the most important regulator of HDL-C concentration through hydrolysis of plasma triglycerides (24). It seems that HIIT may contribute more to the hydrolysis of triglycerides and increased LPL activity than walking; however, the HDL-C elevation immediately after exercise is not related to increased LPL activity but rather to a possible decrease in CETP concentration or activity. Cholesteryl ester transfer protein is responsible for the transport of lipids in HDL-C and other lipoproteins. It has been reported that CETP might decrease after exercise, which slows down HDL catabolism thereby increasing HDL-C concentrations (3). One of the mechanisms that could increase HDL-C catabolism is elevation of blood triglycerides, which results in the formation of triglyceride-rich particles, which are suitable substrates for hepatic lipase. In addition to transporting cholesterol to the liver, HDL-C has been proposed as an antioxidant, anti-inflammatory and anti-thrombotic agent that exerts protective effects on endothelial cell function by inhibiting apoptosis (2, 19). Moreover, LDL-C oxidation is known as a key step for initiation of atherosclerosis and HDL-C inhibits LDL-C oxidation through its antioxidant activity (2).
In our study, both exercise protocols caused a significant decrease in triglyceride level, which is in line with findings of previous studies (25-27). Changes in triglyceride levels can be attributed to the LPL’s response to exercise. It has been established that LPL regulates lipoprotein levels and breakdown of triglyceride-rich lipoproteins. Studies have shown that regular aerobic exercise reduces hepatic lipase, thereby lowering triglyceride production in VLD L-C and LDL-C (3). LDL-C elevation is an independent risk factor for coronary artery disease, while lowering LDL-C to 60 mg/dL reduces the incidence of coronary heart disease by 50% over two years (2). It is well-demonstrated that physical activity increases LDL-C diameter, thereby reducing its oxidation rate and ultimately lowering the risk of cardiovascular disease. In other words, increased LDL-C diameter limits its permeability in arteries, and reduces the risk of atheroma plaques formation (21). It has been suggested that exercise intensity may be correlated with the decrease in LDL-C concentrations (28). In a previous study, six weeks of HIIT increased lipids and carbohydrates metabolism, improved the content of several mitochondrial proteins by 18 to 29% (citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and pyruvate dehydrogenase) and increased fatty acid transporters (FABP pm, FAT/CD36) (6). Two studies reported an increase in oxidative capacity and beta-hydroxyacyl coenzyme A dehydrogenase enzyme after two weeks of HIIT. The molecular mechanisms involved in post-HIIT skeletal muscle adaptation have been investigated to some extent. Exercise intensity is a key factor in increasing PGC1-α, the key enzyme in mitochondrial biogenesis. Gibala (29) and Little et al. (30) reported a significant increase in PGC1-α three hours after HIIT. Although upstream signals that stimulate PGC1-α and mitochondrial biogenesis are not well understood, they might be related to strong changes in phosphorylation potential (ATP/ADPAMP) during physical activity. Simultaneous activation of AMPK (29) and p38/MAPK via increased reactive oxygen species production might enhance PGC1-α and mitochondrial biogenesis (31). In addition, two weeks of HIIT (10 × 1min with one minute rest interval) increased PGC1-α by 25% (29-31). Yasari et al. showed that six weeks of treadmill exercise at 60-70% VO2max could lower stearoyl-CoA desaturase-1 (SCD-1), which can limit biosynthesis of monounsaturated fatty acids, the main constituents of VLDL-C and triglycerides In 2-week-old rats, inhibition of SCD-1 increased lipid oxidation (32). Eight weeks of moderate exercise on treadmill (60% VO2max) also increased the carnitine palmitoyltransferase in the liver and prevented hepatic steatosis in trained rats. Thus, exercise is capable of inducing hepatic fat oxidation (33, 34).
Opposed to HIIT, walking exercise did not cause a significant decrease in BMI and blood pressure. Similar to our findings, Kanan et al. found that HIIT can significantly reduce BMI, LDL-c and diastolic blood pressure in sedentary obese individuals (35). Important physiological factors including cardiac output, total peripheral resistance, blood volume and the autonomic nervous system regulate blood pressure (36). Other factors such as age, sex and circadian rhythm are also effective in blood pressure regulation (37).
Another risk factor for cardiovascular disease is body weight or BMI. Physical activity decreases with age, which can result in weight gain and fat accumulation. Abdominal obesity is one of the most important risk factors for acute myocardial infarction. Studies show that both genetic and environmental factors can contribute to abdominal obesity and body weight. Lifestyle and dietary habits modification can lower the risk of these conditions (5, 7).
CONCLUSION
As an effective alternative to traditional aerobic exercise, HIIT can be utilized to induce favorable physiological, functional and health-related changes. This finding is of great importance from a public health perspective since this type of training can cause more favorable physiological adjustments in a shorter time compared to moderate-intensity inerval training.
ACKNOWLEDGEMENTS
We would like to express our gratitude to all participants and collogues in the city of Galikesh who helped us in this project.
CONFLICT OF INTEREST
The authors declare that there is no conflict of interest.
Lipids are small hydrophobic molecules that play a critical role in energy storage, signaling pathways and cellular responses (1). However, abnormal lipid levels can contribute to the development of atherosclerosis (2-4). Obesity and overweight are independent risk factors for atherosclerotic cardiovascular disease (2,5). A body mass index (BMI) of more than 25 kg/m2 and 30 kg/m2 indicates overweight and obesity, respectively (2,6-8). People with visceral obesity have evidently impaired plasma lipids, including increased triglycerides, apolipoprotein B and low-density lipoprotein-cholesterol (LDL-C) concentrations and decreased high-density lipoprotein-cholesterol (HDL-C) levels (2,9). Men are at a higher risk of developing obesity since fat mostly accumulates in the pelvic area and lower extremities of women (gynoid fat) but in the abdominal and visceral areas of men (android fat). Accumulated upper body fat increases the risk of stroke, diabetes, hypertension and biliary disease, which is more common in android obesity than in gynoid obesity (10).
Exercise can boost body metabolism, muscle strength, cardiovascular function, metal health and sex appeal, all of which are associated with a high level of confidence (1). Regular exercise prevents various diseases such as hypertension, heart disease, type 2 diabetes and obesity in both men and women (2, 11, 12). Frequent exercise, mostly regular aerobic exercise, such as jogging is one of the best non-pharmacological strategies in the prevention and treatment of cardiovascular disease (2, 11, 13). Exercise causes a drastic increase in post-heparin lipoprotein lipase (LPL), which in turn increases triglyceride clearance and decreases HDL-c clearance from plasma (7). LPL is the most important enzyme in plasma triglyceride catabolism and is thought to be elevated in skeletal muscle, adipose tissue and plasma of individuals with an active lifestyle (14), Such adaptation is usually enhanced by increased fatty acid delivery and oxidation in the skeletal muscle promoted by LPL and adaptation of the carnitine palmitoyl transferase system even under high-intensity interval training (HIIT) (15). Previous studies have shown that metabolic adaptation and oxidation are usually higher following intense exercise compared to endurance training (16, 17). In a study by Sheikh al-Islami et al. (2011) on obese women, both HIIT and moderate endurance training resulted in a significant decrease in visceral fat oxidation (18). Given the well-established positive effects of medium- and long-term exercise on lipid oxidation, this study aims to determine effects of short-term HIIT and light walk on risk factors of obesity and atherosclerosis in overweight middle-aged men.
MATERIALS AND METHODS
Study population consisted of 36 male teachers aged 35-50 years, with mean BMI of 30.7 ± 3.5 kg/m2 who were working in the city of Galikesh, northeastern Iran. Inclusion criteria included willingness to participate and no history of metabolic and orthopedic disorders, medication use, smoking and physical activity in the last six months. The subjects were enrolled via purposeful sampling and were randomly matched and equally divided into two experimental groups and a control group. Before and after the intervention, anthropometric characteristics (height, weight and BMI) and blood pressure of each subject were measured. The subjects participated in a briefing session and signed a consent form. Fasting blood samples (7 ml) were taken from the left brachial vein 12 hours before the first exercise session and 12 hours after the last exercise session to determine lipid profile.
For subjects in the HIIT group, a 20 m distance was marked by three cones that were placed 10 m apart. The subjects ran at maximum speed from the start point (cone 1) to cone 2 (path A), returned and then ran at the opposite direction for 20 m towards cone 3 (route B) and finally back to the start point (route C). The total distance covered was 40 m. This protocol was performed with four repetitions and at 75% maximum heart rate in the first two sessions. The intensity was gradually increased to eight repetitions and 90% maximum heart rate by session 12. A 30-sec rest interval was given between each repetition.
Subjects in the second experimental group performed 30 minutes of continuous walking at 50% maximum heart rate in the first session. The walking intensity increased to 75% maximum heart rate in the 12th session (5). The control group did not perform any exercise activity during the study. Serum concentrations of triglyceride, total cholesterol, HDL-C and LDL-C were measured using Pars Azmoon kits and a photometric device. The level of very low-density lipoprotein (VLDL) was calculated by dividing the total triglyceride by 5.
Obtained data were expressed as mean ± standard deviation. The Shapiro-Wilk test was used to assess normality of data. In addition, one-way ANOVA (Scheffe test) and t-test were used to analyze inter- and intra-group changes, respectively. All statistical analyses were performed in SPSS 18, at significance level of 0.05.
RESULTS
The descriptive characteristics of the subjects are shown in table 1.
Table 1. The characteristics of the subjects in the study groups
| Variable | Control group (n=12) | Walking group (n=12) | HIIT group (n=12) |
| Height (cm) | 176.3±7.1 | 171.6±7.7 | 174±3.9 |
| Weight (kg) | 88.4±15.1 | 84.8±9.6 | 82.6±6.8 |
| Age (years) | 42.9±4.3 | 43.3±5.5 | 40.2±4.9 |
| BMI (kg/m2) | 28.22±5 | 29.7±2.2 | 29.5±3.5 |
Our results showed that the four-week walking exercise significantly decreased serum LDL-C (P=0.001) and triglyceride (P=0.001) levels. In addition, HIIT significantly increased HDL (P=0.004) and significantly reduced LDL-C (P=0.049) levels. No significant change in the cholesterol/HDL ratio was observed (Table 2).
Table 2. The lipid profile of subjects in the study groups
| Variable | Group | Pretest | Posttest | Within-group changes | ||||||||
| t | P | |||||||||||
| Cholesterol (mg/dl) |
Walking | 186.3±52.7 | 179.1±35.8 | 0.0917 | 0.376 | |||||||
| HIIT | 210.6±27.8 | 206.5±29.4 | 0.20 | 0.784 | ||||||||
| Control | 182.6±19.5 | 181.5±31 | 0.607 | 0.680 | ||||||||
| Triglyceride (mg/dl) |
Walking | 183.5±76.9 | 144.2±55.3 | 4.172 | 0.001 | |||||||
| HIIT | 107.9±181.5 | 151.6±92.7 | 3.097 | 0.010 | ||||||||
| Control | 180.1±104.7 | 190.6±99.7 | 0.743 | 0.786 | ||||||||
| HDL (mg/dl) |
Walking | 31.2±13.2 | 35.2±12.5 | -1.4 | 0.179 | |||||||
| HIIT | 40.2±9.4 | 45.2±8.6 | -0/85 | 0.004 | ||||||||
| Control | 42.1±16.8 | 38.9±7.6 | 0.557 | 0.284 | ||||||||
| LDL (mg/dl) |
Walking | 103.3±37.2 | 98.8±37.7 | 4.172 | 0.001 | |||||||
| HIIT | 143.3±27.4 | 132.5±30.7 | 2.186 | 0.049 | ||||||||
| Control | 107±17.3 | 101±29.5 | 1.747 | 0.074 | ||||||||
| VLDL (mg/dl) |
Walking | 35.2±13.2 | 31.2±12.5 | -1.12 | 0.282 | |||||||
| HIIT | 40.6±24.7 | 31.3±18 | 0.316 | 0.758 | ||||||||
| Control | 39±22.7 | 38.9±20.3 | 0.662 | 0.314 | ||||||||
| LDL/HDL | Walking | 2.9±1 | 2.9±0.8 | 0.098 | 0.923 | |||||||
| HIIT | 3.4±0.7 | 3±0.7 | 4 | 0.002 | ||||||||
| Control | 2.5±0.84 | 2.6±0.67 | 0.680 | 0.70 | ||||||||
| Blood pressure (mm/hg) |
Walking | 133.4±7.2 | 131.5±7.2 | 1.989 | 0.068 | |||||||
| HIIT | 125.3±12.6 | 121.9±11.5 | 4.154 | 0.002 | ||||||||
| Control | 122.8±8 | 123.1±6.4 | 1.09 | 0.101 | ||||||||
| Cholesterol/ HDL |
Walking | 4.9±1.2 | 4.6±0.77 | 1.037 | 0.319 | |||||||
| HIIT | 5.3±1.13 | 5.2±1.4 | 0.326 | 0.750 | ||||||||
| Control | 4.6±0.9 | 4.7±0.96 | -0.246 | 0.809 | ||||||||
| BMI (kg/m2) |
Walking | 29.5±3.5 | 28.8±2.2 | 1.004 | 0.566 | |||||||
| HIIT | 30.7±2.2 | 27.3±2.3 | 2.55 | 0.027 | ||||||||
| Control | 28.22±5 | 28.52±5.2 | -0.28 | 0.784 | ||||||||
The results of ANOVA (Scheffe test) showed a significant increase in HDL-c values and a significant decrease in VLDL-C, LDL/HDL, triglyceride, BMI and blood pressure of HIIT group compared to the control group (Table 3).
Table 3. The inter-group changes in the lipid profile variables
|
|
|
Mean difference |
|
| Cholesterol | 2 | -24.143 | 0.142 |
| Triglyceride | 2 | 7.382 | *0.024 |
| HDL | 2 | -5.07 | *0.042 |
| LDL | 2 | 4.341 | 0.052 |
| VLDL | 2 | 5.166 | *0.032 |
| LDL/HDL Cholesterol/ HDL |
2 2 |
0.293 1.653 |
*0.041 0.248 |
| BMI | 2 | 7.354 | *0.048 |
| Blood pressure | 2 | 10.08 | *0.016 |
DISCUSSION
Our results showed that the four-week walking exercise significantly decreased serum LDL-C and triglyceride levels. In addition, HIIT increased HDL-C and reduced LDL-C, LDL/HDL, triglyceride, BMI and blood pressure. HDL-C transports cholesterol from peripheral tissues to the liver, which then channels the excess cholesterol for excretion into the bile. It is known that elevated HDL-C levels may play a protective role against coronary artery disease (19, 20). However, our results are inconsistent with finding of Kozehchian (21), Pauli (22) and consistent with Ding (23). The mechanism of HDL-C alterations following exercise is complex; enzymes such as LPL, hepatic lipase and cholesteryl ester transfer protein (CETP) play important roles in altering HDL-C concentration. LPL is the most important regulator of HDL-C concentration through hydrolysis of plasma triglycerides (24). It seems that HIIT may contribute more to the hydrolysis of triglycerides and increased LPL activity than walking; however, the HDL-C elevation immediately after exercise is not related to increased LPL activity but rather to a possible decrease in CETP concentration or activity. Cholesteryl ester transfer protein is responsible for the transport of lipids in HDL-C and other lipoproteins. It has been reported that CETP might decrease after exercise, which slows down HDL catabolism thereby increasing HDL-C concentrations (3). One of the mechanisms that could increase HDL-C catabolism is elevation of blood triglycerides, which results in the formation of triglyceride-rich particles, which are suitable substrates for hepatic lipase. In addition to transporting cholesterol to the liver, HDL-C has been proposed as an antioxidant, anti-inflammatory and anti-thrombotic agent that exerts protective effects on endothelial cell function by inhibiting apoptosis (2, 19). Moreover, LDL-C oxidation is known as a key step for initiation of atherosclerosis and HDL-C inhibits LDL-C oxidation through its antioxidant activity (2).
In our study, both exercise protocols caused a significant decrease in triglyceride level, which is in line with findings of previous studies (25-27). Changes in triglyceride levels can be attributed to the LPL’s response to exercise. It has been established that LPL regulates lipoprotein levels and breakdown of triglyceride-rich lipoproteins. Studies have shown that regular aerobic exercise reduces hepatic lipase, thereby lowering triglyceride production in VLD L-C and LDL-C (3). LDL-C elevation is an independent risk factor for coronary artery disease, while lowering LDL-C to 60 mg/dL reduces the incidence of coronary heart disease by 50% over two years (2). It is well-demonstrated that physical activity increases LDL-C diameter, thereby reducing its oxidation rate and ultimately lowering the risk of cardiovascular disease. In other words, increased LDL-C diameter limits its permeability in arteries, and reduces the risk of atheroma plaques formation (21). It has been suggested that exercise intensity may be correlated with the decrease in LDL-C concentrations (28). In a previous study, six weeks of HIIT increased lipids and carbohydrates metabolism, improved the content of several mitochondrial proteins by 18 to 29% (citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and pyruvate dehydrogenase) and increased fatty acid transporters (FABP pm, FAT/CD36) (6). Two studies reported an increase in oxidative capacity and beta-hydroxyacyl coenzyme A dehydrogenase enzyme after two weeks of HIIT. The molecular mechanisms involved in post-HIIT skeletal muscle adaptation have been investigated to some extent. Exercise intensity is a key factor in increasing PGC1-α, the key enzyme in mitochondrial biogenesis. Gibala (29) and Little et al. (30) reported a significant increase in PGC1-α three hours after HIIT. Although upstream signals that stimulate PGC1-α and mitochondrial biogenesis are not well understood, they might be related to strong changes in phosphorylation potential (ATP/ADPAMP) during physical activity. Simultaneous activation of AMPK (29) and p38/MAPK via increased reactive oxygen species production might enhance PGC1-α and mitochondrial biogenesis (31). In addition, two weeks of HIIT (10 × 1min with one minute rest interval) increased PGC1-α by 25% (29-31). Yasari et al. showed that six weeks of treadmill exercise at 60-70% VO2max could lower stearoyl-CoA desaturase-1 (SCD-1), which can limit biosynthesis of monounsaturated fatty acids, the main constituents of VLDL-C and triglycerides In 2-week-old rats, inhibition of SCD-1 increased lipid oxidation (32). Eight weeks of moderate exercise on treadmill (60% VO2max) also increased the carnitine palmitoyltransferase in the liver and prevented hepatic steatosis in trained rats. Thus, exercise is capable of inducing hepatic fat oxidation (33, 34).
Opposed to HIIT, walking exercise did not cause a significant decrease in BMI and blood pressure. Similar to our findings, Kanan et al. found that HIIT can significantly reduce BMI, LDL-c and diastolic blood pressure in sedentary obese individuals (35). Important physiological factors including cardiac output, total peripheral resistance, blood volume and the autonomic nervous system regulate blood pressure (36). Other factors such as age, sex and circadian rhythm are also effective in blood pressure regulation (37).
Another risk factor for cardiovascular disease is body weight or BMI. Physical activity decreases with age, which can result in weight gain and fat accumulation. Abdominal obesity is one of the most important risk factors for acute myocardial infarction. Studies show that both genetic and environmental factors can contribute to abdominal obesity and body weight. Lifestyle and dietary habits modification can lower the risk of these conditions (5, 7).
CONCLUSION
As an effective alternative to traditional aerobic exercise, HIIT can be utilized to induce favorable physiological, functional and health-related changes. This finding is of great importance from a public health perspective since this type of training can cause more favorable physiological adjustments in a shorter time compared to moderate-intensity inerval training.
ACKNOWLEDGEMENTS
We would like to express our gratitude to all participants and collogues in the city of Galikesh who helped us in this project.
CONFLICT OF INTEREST
The authors declare that there is no conflict of interest.
Research Article: Original Paper |
Subject:
Sport Physiology
Received: 2020/01/11 | Accepted: 2020/05/31 | Published: 2021/02/28 | ePublished: 2021/02/28
Received: 2020/01/11 | Accepted: 2020/05/31 | Published: 2021/02/28 | ePublished: 2021/02/28
References
1. Ikekpea Zu Ej, Oranwa cj, ogbu SI, onyekelu Ck, et al. Lipid profile of people Engaged in Regular Exercise: Department of medical laboratory science, Nigeria. Ann Med Health Sci Res. 2017;7: 36-39. [Google Scholar]
2. Moazami M, Askari A. effect of six- month aerobic exercise on Lipid profile, inflammatory Markers and Risk factors of cardiovascular Disease in obese women. medical laboratory journal. 2018; 12(2): 32-37. [View at Publisher] [DOI:10.29252/mlj.12.2.32] [Google Scholar]
3. Askari A, Askari B, Fallah Z, Kazemi SH. Effect of eight weeks aerobic training on serum lipid and lipoprotein levels in women. Journal of Gorgan University of Medical Sciences. 2012; 14(1): 26-32. [View at Publisher] [Google Scholar]
4. Pedersen LR, Olsen RH, Anholm C, Walzem RL,Fenger M, Eugen-Olsen J, et al. Weight loss issuperior to exercise in improving the atherogeniclipid profile in a sedentary, overweight populationwith stable coronary artery disease: A randomizedtrial. Atherosclerosis. 2016; 246 (31): 221-228. [DOI:10.1016/j.atherosclerosis.2016.01.001] [PubMed] [Google Scholar]
5. Fan H, Li X, Zheng L, Chen X, lan Q, Wu H, et al. Abdominal obesity is strongly associated with Cardiovascular Disease and its Risk Factors in Elderly and very Elderly Community-dwelling Chinese. Sci Rep. 2016; 6: 21521. [DOI] [PubMed] [Google Scholar]
6. Reljic D, Frenk F, Herrmann HJ, Neurath MF, Zopf Y. Effects of very low volume high intensity versus moderate intensity interval training in obese metabolic syndrome patients: a randomized controlled study. Sci Rep. 2021 Feb 2;11(1):2836. [DOI] [PubMed] [Google Scholar]
7. Sari CI, Eikelis N, Head GA, Schlaich M, Meikle P, Lambert G, Lambert E. Android Fat Deposition and Its Association With Cardiovascular Risk Factors in Overweight Young Males. Front Physiol. 2019; 10: 1162. [DOI] [PubMed] [Google Scholar]
8. Kostrzewa-Nowak D, Nowak R, Jastrzębski Z, Zarębska A, Bichowska M, Drobnik-Kozakiewicz I, et al. Effect of 12-week-long aerobic training programme on body composition, aerobic capacity, complete blood count and blood lipid profile among young women. Biochem Med (Zagreb). 2015; 25(1): 103-13. [DOI:10.11613/BM.2015.013] [PubMed] [Google Scholar]
9. Gharipour M, Sadeghi M, Dianatkhah M, Nezafati P, Talaie M, Oveisgharan S, et al. Comparison between European and Itanian cutoff points of triglyceride/high-density lipoprotein cholesterol concentrations in prediction cardiovascular disease outcomes. J Clin Lipidol, 2016; 10(1): 143-149. [DOI:10.1016/j.jacl.2015.10.008] [PubMed] [Google Scholar]
10. Monteiro PA, Chen KY, Lira FS, Cicotti Saraiva1 BT, Antunes BMM, Campos EZ, et al. Concurrent and aerobic exercise training promote similar benefits in body composition and metabolic profiles in obese adolescents. Lipids in Health and Disease. 2015, 14: 153. [DOI] [PubMed] [Google Scholar]
11. Lima LG, Bonardi JTM, Campos GO, Bertani RF, Scher LML, Moriguti JC, Ferriolli E, Lima NKC. Combined aerobic and resistance training: are there additional benefits for older hypertensive adults? Clinics (Sao Paulo). 2017; 72(6): 363-369. [DOI] [PubMed] [Google Scholar]
12. Hojjati Z, Shahsavari S.AcuteEffects of Aerobic and combind Exercise on serum lipid profile in type11 Females: Department of Physical Education, Rasht Browch, I Ran. Iranian journal of Health Sciences, 2015; 3(2): 31-37. [View at Publisher] [Google Scholar]
13. Lira FS, Yamashita AS, Uchida MC, Zanchi NE, Gualano B, Martins E Jr, et al. Low and moderate, rather than high intensity strength exercise induces benefit regarding plasma lipid profile. Diabetol Metab Syndr. 2010; 2: 31. [DOI:10.1186/1758-5996-2-31] [PubMed] [Google Scholar]
14. Chatterjee C, Sparks DL. Hepatic lipase, high density lipoproteins, and hyper triglyceridemia. Am J Pathol. 2011; 178: 1429-1433. [DOI:10.1016/j.ajpath.2010.12.050] [Google Scholar]
15. Lira FS, Carnevali LC Jr, Zanchi NE, Santos RV, Lavoie JM, Seelaender M. Exercise intensity modulation of hepatic lipid metabolism. J Nutr Metab. 2012;2012:809576. [DOI:10.1155/2012/809576] [PubMed] [Google Scholar]
16. Stephen H, Boutcher SH. High-Intensity Intermittent Exercise and Fat Loss. J Obes. 2011; 2011: 868305. [DOI:10.1155/2011/868305] [PubMed] [Google Scholar]
17. Gibala MJ, Little JP, Macdonald MJ, Hawley JA. Physiological adaptations to low-volume, high-intensity interval training in health and disease. J Physiol. 2012; 590(5): 1077-84. [DOI:10.1113/jphysiol.2011.224725] [PubMed] [Google Scholar]
18. Dun Y, Thomas RJ, Smith JR, Medina‑Inojosa JR, Squires RW, Bonikowske AR, et al. High‑intensity interval training improves metabolic syndrome and body composition in outpatient cardiac rehabilitation patients with myocardial infarction. Cardiovasc Diabetol. 2019; 18: 104. [Google Scholar]
19. Oram JF. HDL apolipoproteins and ABCA1: partners in the removal of excess cellular cholesterol. Arterioscler Thromb Vasc Biol. 2003; 23(5): 720-7. [DOI:10.1161/01.ATV.0000054662.44688.9A] [PubMed] [Google Scholar]
20. Lamina S, Okoye GC. Therapeutic effect of a moderate intensity interval training program on the lipid profile in men with hypertension: a randomized controlled trial. Niger J Clin Pract. 2012; 15(1): 42-7. [View at Publisher] [DOI:10.4103/1119-3077.94096] [PubMed] [Google Scholar]
21. Koozehchian MS, Nazem F, Kreider RB, Roberts WJ, Best TM, Rong Y, et al. The role of exercise training on lipoprotein profiles in adolescent males. Lipids Health Dis. 2014 Jun 9;13(1):95. [DOI:10.1186/1476-511X-13-95] [PubMed] [Google Scholar]
22. Paoli A, Pacelli QF, Moro T, Marcolin G, Neri M, Battaglia G, et al. Effects of high-intensity circuit training, low-intensity circuit training and endurance training on blood pressure and lipoproteins in middle-aged overweight men. Lipids Health Dis. 2013; 12: 131. [DOI:10.1186/1476-511X-12-131] [PubMed] [Google Scholar]
23. Ding D, Li X, Qiu J, Li R, Zhang Y, Su D, et al. Serum Lipids, Apolipoproteins, and Mortality among Coronary Artery Disease Patients. Biomed Res Int Epub. 2014; 29: 709. [DOI:10.1155/2014/709756] [PubMed] [Google Scholar]
24. Plowman SA, and Smith DL. Exercise physiology for health, fitness, and performance: Lippincott Williams & Wilkins" 2008.
25. Tsekouras YE, Magkos F, Kellas Y, Basioukas KN, Kavouras SA, Sidossis LS. High-intensity interval aerobic training reduces hepatic very low-density lipoprotein-triglyceride secretion rate in men. Am J Physiol Endocrinol Metab. 2008; 295(4): E851-8. [DOI:10.1152/ajpendo.90545.2008] [PubMed] [Google Scholar]
26. Behzare A, Gaeini A, Mogharnasi M, Taherzadeh J, Seyedahmadi M, Keavanlou F, et al . Comparison of intermittence and continuative exercise methods on hs-CRP and Lipids as predictors of coronary heart disease . JNKUMS. 2012; 3 (4) :35-42 [View at Publisher] [DOI:10.29252/jnkums.3.4.35]
27. Zois CE, Tokmakidis SP, Volaklis KA, Kotsa K, Touvra AM, Douda E, et al. Lipoprotein profile, glycemic control and physical fitness after strength and aerobic training in post-menopausal women with type 2 diabetes. Eur J Appl Physiol. 2009; 106 (6): 901-7. [DOI:10.1007/s00421-009-1104-8] [PubMed] [Google Scholar]
28. Zolfaghary M , Taghian F, Hedayati M. Comparing the effect of green tea extract consumption, aerobic exercise and combination of these two methods on CRP Level in obese women. Razi Journal of Medical Sciences. 2013; 20(110): 8-12. [View at Publisher] [Google Scholar]
29. Gibala M J. Molecular responses to high-intensity interval exercise. Applied Physiology,Nutrition, and Metabolism. 2009; 34 (3): 428-432. [View at Publisher] [DOI:10.1139/H09-046] [PubMed] [Google Scholar]
30. Little JP, Safdar A, Bishop D, Tarnopolsky MA, Gibala MJ. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol. 2011; 300(6): R1303-10. [View at Publisher] [DOI:10.1152/ajpregu.00538.2010] [PubMed] [Google Scholar]
31. Kang C, O'Moore KM, Dickman JR, Ji LL. Exercise activation of muscle peroxisome proliferator-activated receptor-gamma coactivator-1alpha signaling is redox sensitive. Free Radic Biol Med. 2009;47(10):1394-400. [DOI:10.1016/j.freeradbiomed.2009.08.007] [PubMed] [Google Scholar]
32. Yasari S, Prud'homme D, Wang D, Jankowski M, Levy E, Gutkowska J, et al. Exercise training decreases hepatic SCD-1 gene expression and protein content in rats. Mol Cell Biochem. 2010; 335(1-2): 291-9. [DOI:10.1007/s11010-009-0279-y] [PubMed] [Google Scholar]
33. Rector RS, Thyfault JP, Morris RT, Laye MJ, Borengasser SJ, Booth FW, et al. Daily exercise increases hepatic fatty acid oxidation and prevents steatosis in Otsuka Long-Evans Tokushima Fatty rats. Am J Physiol Gastrointest Liver Physiol. 2008; 294(3): G619-26. [DOI:10.1152/ajpgi.00428.2007] [PubMed] [Google Scholar]
34. Rector RS, Thyfault JP, Laye MJ, Morris RT, Borengasser SJ, Uptergrove GM, et al. Cessation of daily exercise dramatically alters precursors of hepatic steatosis in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. J Physiol. 2008; 586(17): 4241-9. [DOI:10.1113/jphysiol.2008.156745] [PubMed] [Google Scholar]
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
Enamad
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.