A Comparison of Continuous, Interval, and Accumulated Workouts with Equalized Exercise Volume: Excess Post-Exercise Oxygen Consumption in Women

doi:10.21203/rs.3.rs-2494234/v1

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A Comparison of Continuous, Interval, and Accumulated Workouts with Equalized Exercise Volume: Excess Post-Exercise Oxygen Consumption in Women

https://doi.org/10.21203/rs.3.rs-2494234/v1

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Background: Despite the various benefits of exercise, women's participation in exercise is low. Therefore, we need to consider ways to maximize the effect of exercise. Excess post-exercise oxygen consumption (EPOC) can maximize energy consumption. We aimed to compare the EPOC during different exercise modalities including continuous exercise (CE), interval exercise (IE), and accumulated exercise (AE) that spent the homogenized energy expenditure during exercise in healthy women.

Methods: Study design: Randomized crossover trial.

Participants: Forty-four participants (age, 36.09 ± 11.73 years) were recruited and randomly allocated to three groups.

Trials: The intensity of each modality was set as follows: CE was performed for 30 min at 60% peak oxygen uptake (VO₂peak). IE was performed once for 2 min at 80% VO₂peak, followed by 3 min at 80% VO₂peak, and 1 min at 40% VO₂peak, for a total of six times over 26 min. AE was performed for 10 min with a 60% VO₂peak and was measured three times a day.

Results: During exercise, carbohydrate oxidation (CHO) and fatty acid oxidation (FAO) were the largest in IE (p < 0.05) and CE (p < 0.001), respectively, and there was no difference in energy expenditure (EE) (p = 0.635) between exercise modalities. On the other hand, CHO, FAO, and EE were the largest in AE (all p < 0.001) during EPOC. As a result, the greatest energy metabolism was shown in AE (all p < 0.001) during exercise and EPOC.

Conclusions: We confirmed that more effective energy metabolism can occur due to the accumulation of EPOC when short-time exercise is repeated several times. In recommending regular exercise, AE can increase compliance with exercise participation through a short exercise time and can help improve health with an exercise modality that maximizes energy consumption through EPOC.

Trial registration: Clinical number (KCT0007298), Institutional Review Board of Konkuk University (7001355-202201-E-160).

excess post-exercise oxygen consumption

homogenized energy expenditure

women

continuous exercise

interval exercise

accumulated exercise

Physical activity and exercise can help reduce the risk of non-communicable lifestyle-related diseases (NCDs), such as cardiovascular disease [1], cancer [2], and type 2 diabetes [3], and improve quality of life [4]. Exercise is one of the representative interventions that can prevent and correct high blood cholesterol, high blood sugar, hypertension, and overweight or obesity, which are all risk factors for NCDs [5, 6]. In particular, as women age, the risk of developing NCDs such as cerebrovascular disease, osteoporosis, and breast cancer increases [7]. Older women also show significantly lower health-related physical fitness characteristics, such as cardiopulmonary endurance, muscle strength, muscular endurance, flexibility, and body composition, than younger women [8]. On the other hand, regular physical activity and exercise can prevent the deterioration of health due to aging [9], and the effect is reported to be more effective in women than men [10]. Exercise also improves the quality of life, increases energy expenditure (EE), and effectively promotes bone health [11]. Accordingly, many public health organizations and countries provide guidelines for physical activity and exercise [6]. In particular, in the 11th edition of the American College of Sports Medicine (ACSM) Guidelines for Exercise Testing and Prescription, published in 2021, all healthy adults aged between 18 and 65 years are encouraged to engage in moderate-intensity aerobic exercise for at least 30 min per day, 5 days a week, or engage in high-intensity aerobic exercise for at least 20 min per day, 3 days a week [12].

However, the prevalence of insufficient physical activity announced by the World Health Organization (WHO) in 2018 tended to decrease from 25.5% in 2001 to 23.4% in 2016 for men and slightly increase from 31.5% in 2001 to 31.7% in 2016 for women. By country, the prevalence of insufficient physical activity was higher in women than men in 137 of 146 countries [13]. Therefore, considering that the lack of physical activity is more prominent in women than in men, it is very urgent to recognize the barriers to exercise participation and solve them so that the rate of women's participation in physical activity can be increased [14]. In this regard, Baillot et al. [15] analyzed the motivations and barriers to exercise. They found that physical barriers such as pain and physical discomfort, psychological barriers such as a lack of self-discipline and motivation, and socio-ecological barriers such as a lack of time were reported to be major impediments to exercise participation. That is, it is very important to suggest an exercise method that can improve exercise compliance and effectively improve body composition and health while considering the barriers to exercise participation [16, 17].

Exercise has traditionally been used as an intervention program to increase daily energy expenditure [18]. Moderate-intensity continuous exercise (CE) is generally suggested to increase physical activity and improve cardiorespiratory capacity [19]. However, because the exercise time is relatively long, it may not be an appropriate exercise modality for those for whom a “lack of time” is a barrier to exercise participation [20]. To overcome the time barrier, high-intensity interval exercise (IE), which performs high-intensity exercises in several stages with recovery, has a shorter exercise time than that of CE [21, 22]. However, IE may be an unsuitable exercise strategy if one has “physical discomfort” or “self-training”, that is, if one’s fitness level is low [23]. Accumulated exercise (AE) is proposed as a way to overcome “physical discomfort” and “self-training” [24]. AE is an exercise strategy that accumulates short, moderate-to-high-intensity exercises throughout the day. It can overcome the “lack of time” exercise barrier by allowing the total daily exercise time to be filled and is recognized as a strategy to improve exercise compliance [25, 26]. However, it is reported that AE dose not show the improvement effect of cardiopulmonary health seen during long-term exercise [26, 27].

To maximize energy consumption, it is necessary to consider not only how to increase the effect by changing the exercise method but also the energy consumption that appears continuously after exercise. In other words, when calculating the total energy consumption of exercise, excess post-exercise oxygen consumption (EPOC) should be considered in addition to EE during exercise [28]. EPOC has been reported to be a very important factor in energy consumption during exercise, especially for weight loss [18, 29]. However, when calculating the total energy consumption by exercise, EPOC, which is the additional energy consumption after exercise, is not adequately considered [30]. Although there are very few prior studies related to the differences in EPOC according to various exercise modalities, a study by Hunter et al. [31] confirmed the differences in EPOC according to CE and IE in 33 healthy women and reported that EPOC by IE was larger than EPOC by CE. A study by Larsen et al. [32] confirmed the difference in EPOC according to CE and IE in seven men with metabolic syndrome and showed significantly largest energy consumption and duration during EPOC in IE than in CE. Additionally, split exercises performed by dividing sessions of moderate-intensity persistent movements reported a significant increase in overall energy consumption by exercise due to the accumulation of EPOC [33]. Jung et al. [34] compared the difference in EPOC according to CE and AE in 34 healthy male and female college students and reported that EPOC was larger in AE than in CE.

Studies have attempted to maximize the EPOC through various modalities of exercise. However, a fragmentary approach was attempted in terms of “CE vs. IE” or “CE vs. AE,” and intervention studies were predominant rather than acute studies. As found in several studies, exercise improves metabolic and cardiovascular disease factors in addition to help maintain and lose weight. Therefore, it is very important to suggest and inform people about the effective types and contents (form, frequency, duration, and intensity) of exercise to create exercise habits for people who lack physical activity. The purpose of this study was to confirm the differences EPOC including energy metabolism and cardiopulmonary function in CE, IE, and AE, with the equalized energy expenditure during exercise, in healthy women. We hypothesized that there would be differences in EPOC for the three different exercise modalities.

Participant

Forty-four healthy women (36.09 ± 11.73 years) from a community that did not exercise regularly participated in this study voluntarily. All participants were informed about the experimental procedure and purpose of the study, and written informed consent and a Physical Activity Readiness Questionnaire Plus (PAR-Q⁺) were subsequently obtained. All study procedures were approved by the Institutional Review Board of Konkuk University (7001355-202201-E-160) in Korea and registered with cris.nih.go.kr (No. KCT0007298). The CONSORT flow chart for the study procedure and participant inclusion and exclusion criteria is shown in Fig. 1, and the physical characteristics of the participants are shown in Table 1.

Table 1

Characteristics of the participants (n = 44)
Variables	Total (Mean ± SD)
Age (years)	36.09 ± 11.73
Body height (cm)	160.46 ± 4.92
Body weight (kg)	54.90 ± 6.06
BMI (kg/m²)	21.33 ± 2.24
Lean body mass (kg)	38.71 ± 3.64
Fat mass (kg)	16.13 ± 4.60
Percent body fat (%)	28.80 ± 6.21
VO₂peak (mL/min/kg)	29.30 ± 4.42
Data are expressed as mean ± SD, SD: standard deviation, BMI: body mass index, VO₂peak: peak oxygen uptake

Study Design

This study was a crossover, randomized controlled trial. All participants were randomly assigned to CE, IE, or AE and had a one-week washout period before the next trial. At the first visit, body composition and a graded exercise test (GXT) for peak oxygen uptake (VO₂peak) confirmation were performed as pretests. The second to fourth measurements were from exercise sessions. After visiting the laboratory, participants wore a heart rate monitor (Polar 800; Polar Electro, Kempele, Finland) and rested until their heart rate stabilized. When the heart rates stabilized, a respiratory gas analyzer (Quark CPET; Cosmed, Rome, Italy) was used, and breathing data were collected for 5 min after sitting in a chair and resting for 5 min. The average respiration data measured during the resting 5 min was used as the end point of the EPOC measurement period after exercise. CE, IE, and AE exercises were performed using a cycle ergometer (Aero bike 75 XLIII; Konami, Tokyo, Japan), and exercise intensity was set using the results of the GXT with reference to previous studies [35, 36] that homogenized EE during exercise. CE was performed the 30-min exercise with 60% VO₂peak intensity; IE was performed once for 2 min at 80% VO₂peak, followed by 3 min at 80% VO₂peak, and 1 min at 40% VO₂peak, for a total of six times over 26 min, and AE was a divided exercise in which 60% VO₂peak 10-min exercise was performed a total of three times at approximately 2-h intervals. After each exercise session, for EPOC measurements, the participants got off the cycle ergometer and sat in a chair to rest until breathing and heart rate were stable. The study design is illustrated in Fig. 2.

Measures

Body composition

Body composition measurements were taken in the morning in a state where fasting for 8 h and strenuous physical activity for 48 h had been prohibited before the test and participants were wearing light clothes. Body composition was measured using an Inbody 770 (Inbody, Seoul, Korea) to determine body weight (kg), body mass index (BMI) (kg/m²), lean mass (kg), body fat mass (kg), and body fat percentage (%). For height (cm), a BMS330 (Inbody, Seoul, Korea) was used.

Graded exercise test

GXT was measured using a cycle ergometer (Aero Bike 75 XLIII; Konami, Tokyo, Japan), a respiratory gas analyzer (Quark CPET; Cosmed, Rome, Italy), and a heart rate monitor (Polar 800; Polar Electro, Kempele, Finland). The participants were seated in a chair, rested so that their heart rates could be stabilized, and then measured. The GXT protocol was performed at a speed of 50 rpm at an intensity of 25 watts/min for the first 2 min, and then the intensity was increased by 12.5 watts/min at an interval of 2 min [36]. During measurement, the ratings of perceived exertion (RPE) were checked using the Borg scale at each step. The criteria for ending the GXT were as follows: 1) When respiration or heart rate did not increase, even when exercise intensity increased. 2) When the respiratory exchange rate (RER) is greater than 1.15. 3) when RPE was higher than 17 on the Borg scale. The measurement was terminated when two of these conditions were satisfied.

Cardiopulmonary function and energy metabolism during trials

Respiratory function was measured minute ventilation (VE), oxygen uptake (VO₂), carbon dioxide excretion (VCO₂), and RER using a respiratory gas analyzer (Quark CPET, Cosmed, Rome, Italy) during exercise and EPOC. Heart rate (HR) was measured using a heart rate monitor (Polar 800; Polar Electro, Kempele, Finland) during exercise and EPOC. The energy metabolism during exercise and EPOC was calculated using VO₂ and VCO₂ obtained from a respiratory gas analyzer and substituted into the following formulas to calculate carbohydrate oxidation (CHO), fatty acid oxidation (FAO), and energy expenditure (EE): CHO(g/min) = 4.210 × VCO₂(mL/min)– 2.962 × VO₂(mL/min), FAO(g/min) = 1.695 × VO₂ (mL/min) – 1.701 × VCO₂ (mL/min), EE (kcal/min) = 4.07 × CHO (g/min) + 9.75 × FAO (g/min) [37–39]

EPOC criteria and O₂ deficit calculation

The end time of each participant’s EPOC was determined based on the average values of measured VE, VO₂, RER, and HR for 5 min in a resting state before exercise. The results of calculating the EPOC measurement time for each exercise modality using the aforementioned termination criteria were as follows: CE was 20.43 ± 8.28 min and IE was 19.46 ± 6.33 min. For AE, it was 13.81 ± 5.52 min during one exercise and 41.44 ± 16.56 min when a total of three exercises were performed. The O₂ deficit was calculated by subtracting the amount of O₂ intake during the time to reach the steady state after obtaining the area based on the O₂ intake when reaching the steady state.

Statistical analysis

Data obtained in this study were analyzed using the SPSS 25.0 (IBM Corporation, Armonk, NY, USA), and the mean and standard deviation (SD) were calculated to present descriptive statistics. The assumptions of normality and equal variance for parametric statistical analysis were verified using the Shapiro-Wilk test for all dependent variables. To verify the difference in cardiopulmonary function and energy metabolism during exercise and EPOC as well as in O₂ deficit during exercise and the O₂ intake during EPOC between trials, a one-way analysis of variance (ANOVA) with repeated factors was conducted. Post hoc analysis was conducted using the Bonferroni correction to verify the significant difference between trials. Pearson’s correlation analysis was performed to verify the correlation between the O₂ deficit during exercise and O₂ intake during EPOC. The level of significance was set at p < 0.05.

Cardiopulmonary function and energy metabolism during exercise

The differences in cardiopulmonary function and energy metabolism during the three exercise trials are shown in Fig. 3. This study showed that EE (kcal) during exercise was not significantly different between CE, IE, and AE [144.86 ± 26.98 vs. 142.13 ± 25.64 vs. 145.17 ± 24.13 (p = 0.635, η² = 0.009) in CE, IE, and AE, respectively]. A significant main effect by trials was observed in HR_sum, RER, CHO and FAO [HR_sum (beat): 3775.03 ± 563.24 vs. 3562.03 ± 495.78 vs. 3653.67 ± 450.29 (p < 0.001, η² = 0.168); RER: 0.93 ± 0.05 vs. 0.98 ± 0.04 vs. 0.94 ± 0.06 (p < 0.001, η² = 0.352); CHO (g): 27.00 ± 7.49 vs. 30.23 ± 7.86 vs. 28.41 ± 7.11 (p < 0.05, η² = 0.092); FAO (g): 3.43 ± 1.98 vs. 2.02 ± 1.24 vs. 3.18 ± 2.05 (p < 0.001, η² = 0.230) in CE, IE, and AE, respectively]. On post hoc analysis, IE was significantly lower than CE in HR_sum and FAO and significantly higher than CE in RER and CHO.

Cardiopulmonary function and energy metabolism during EPOC

The differences in cardiopulmonary function and energy metabolism during EPOC after the three different exercise trials are shown in Fig. 4. A significant main effect by trials was observed in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, RER, CHO, FAO, EE [HR_sum (beat): 1462.78 ± 671.34 vs. 2017.87 ± 651.34 vs. 3788.66 ± 1223.35 (p < 0.001, η² = 0.709); VE_sum (L): 202.62 ± 74.99 vs. 263.51 ± 80.78 vs. 508.86 ± 149.91 (p < 0.001, η² = 0.775); VO₂_sum (mL): 5239.12 ± 1833.14 vs. 6578.96 ± 2347.63 vs. 13259.97 ± 3849.27 (p < 0.001, η² = 0.790); VCO₂_sum (mL): 4720.25 ± 1640.82 vs. 5922.87 ± 1953.23 vs. 12505.99 ± 3567.45 (p < 0.001, η² = 0.822); RER: 0.90 ± 0.05 vs. 0.89 ± 0.05 vs. 0.93 ± 0.05 (p < 0.001, η² = 0.210); CHO (g): 4.30 ± 1.70 vs. 5.43 ± 1.49 vs. 13.89 ± 4.99 (p < 0.001, η² = 0.814); FAO (g): 0.82 ± 0.46 vs. 1.18 ± 0.70 vs. 1.59 ± 0.91 (p < 0.001, η² = 0.255); EE (kcal): 26.17 ± 9.63 vs. 33.07 ± 11.29 vs. 68.47 ± 18.40 (p < 0.001, η² = 0.819) in CE, IE, and AE, respectively]. On post hoc analysis, IE was significantly higher than CE in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, CHO, FAO, and EE. AE was significantly higher than CE in all variables (all p < 0.001) and significantly higher than IE in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, RER, CHO, and EE.

Cardiopulmonary function and energy metabolism during total (exercise plus EPOC)

The differences in cardiopulmonary function and energy metabolism during the three exercise trials and EPOC measurements are shown in Fig. 5. A significant main effect by trials was observed in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, RER, CHO, FAO, and EE [HR_sum (beat): 5298.49 ± 1049.86 vs. 5546.38 ± 991.28 vs. 7039.35 ± 1558.87 (p < 0.001, η² = 0.488); VE_sum (L): 1138.68 ± 187.85 vs. 1183.52 ± 229.44 vs. 1390.23 ± 271.53 (p < 0.001, η² = 0.440); VO₂_sum (mL): 33718.33 ± 5119.70 vs. 34011.29 ± 5774.35 vs. 42333.92 ± 9095.61 (p < 0.001, η² = 0.519); VCO₂_sum (mL): 31233.79 ± 5013.45 vs. 32673.22 ± 5593.07 vs. 39473.25 ± 8182.03 (p < 0.001, η² = 0.524); RER: 0.91 ± 0.04 vs. 0.93 ± 0.03 vs. 0.94 ± 0.05 (p < 0.001, η² = 0.167); CHO (g): 31.73 ± 8.17 vs. 35.58 ± 5.66 vs. 42.17 ± 10.60 (p < 0.001, η² = 0.414); FAO (g): 4.07 ± 1.90 vs. 2.85 ± 1.68 vs. 4.68 ± 2.96 (p < 0.001, η² = 0.206); EE (kcal): 170.65 ± 30.94 vs. 171.24 ± 29.08 vs. 215.15 ± 39.49 (p < 0.001, η² = 0.541) in CE, IE, and AE, respectively]. On post hoc analysis, CE was significantly higher than IE in FAO, and IE was significantly higher than CE in RER and CHO. AE was significantly higher than CE in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, RER, CHO, and EE, and significantly higher than IE in HR_sum, VE_sum, VO₂_sum, VCO₂_sum, CHO, FAO, and EE.

Difference between O₂ deficit and EPOC according to three different exercise modalities

The difference between the O₂ deficit after exercise and VO₂ during EPOC according to the three different exercise modalities is shown in Fig. 6. A significant main effect of trials was observed for O₂ deficit [1050.91 ± 245.37 vs. 1346.53 ± 283.93 vs. 3386.73 ± 868.89 (p < 0.001, η² = 0.893) in CE, IE, and AE, respectively] and VO₂ (mL) during EPOC [5239.12 ± 1833.14 vs. 6578.96 ± 2347.63 vs. 13259.97 ± 3849.27 (p < 0.001, η² = 0.790) in CE, IE, and AE, respectively]. On post hoc analysis, IE was significantly higher than CE in O₂ deficit and EPOC. AE was significantly higher than CE and IE for the O₂ deficit and EPOC.

Correlation between O₂ deficit and EPOC according to the three different exercise modalities

The correlation between the O₂ deficit after exercise and VO₂ during EPOC according to the three different exercise modalities is shown in Fig. 7. There was a significant correlation between the O₂ deficit after exercise and VO₂ during EPOC in all exercise modalities (R = 0.377 for CE, R = 0.308 for IE, and R = 0.558 for AE). In addition, for all exercise modalities, the correlation between the O₂ deficit after exercise and VO₂ during EPOC was R = 0.840.

The purpose of this study was to identify the effects of three exercise modalities, in which EE was homogenized, on cardiorespiratory function and energy metabolism during EPOC and the difference in EPOC according to modality. As per the design, EE during the three exercise sessions did not show a significant difference between the exercise types. This means that the exercise program of this study was properly configured, and there was no difference in exercise volume in CE, IE, and AE, indicating that the measurement was performed correctly. During exercise, CHO was highest in IE, and FAO was highest in CE. However, both cardiorespiratory function and energy metabolism were significantly higher in AE than in CE and IE during EPOC. As a result, during the full session, including exercise and EPOC, AE showed a higher metabolic benefit from EPOC than the other two exercise modalities.

Oxygen demand increases rapidly at the beginning of exercise, but the supplied VO₂ does not meet the oxygen demand, resulting in an oxygen deficit while the supplied oxygen reaches a steady state [40]. During exercise, VO₂ shows an elevated steady state to support the increased energy demand according to exercise intensity. Immediately after exercise, oxygen demand should decrease to a resting state, but EPOC appears as a compensatory action for an oxygen deficit that occurs early in exercise [41, 42] and can be mainly divided into the alactacid and lactacid components during exercise. The alactacid component is related to the resynthesis of phosphocreatine used in muscle during exercise, oxygen storage in muscle and blood, and an increase in heart rate and respiratory rate after exercise. The lactacid component is associated with lactate elimination, elevated body temperature, elevated hormone levels, and elevated heart and respiratory rates after exercise [43]. In general, EPOC shows a quantitative correlation with exercise intensity and is reported to increase linearly as the exercise duration increases at an exercise intensity of more than 50% maximal oxygen uptake (VO₂max) [44]. In particular, it has been reported that exercise intensity affects both the duration and size of EPOC, while exercise time only affects EPOC duration [45].

In this study, the difference in cardiopulmonary function and energy metabolism among the three exercise sessions showed that RER was significantly higher in IE (0.98 ± 0.04 mL/min) than in CE (0.93 ± 0.05 mL/min) and AE (0.94 ± 0.06 mL/min). Accordingly, CHO was significantly higher in IE (30.23 ± 7.86 mL/min) than in CE (27.00 ± 7.49 mL/min) and AE (28.41 ± 7.11 mL/min). The reason IE showed more carbohydrate oxidation than CE and AE seems to be due to its higher-intensity nature, comprising repeated high-intensity exercise and recovery exercise as compared to CE, comprising continuous moderate-intensity exercise sessions, and AE with divided exercise sessions [36]. CE (3.43 ± 1.98 mL/min) showed significantly higher FAO than IE (2.02 ± 1.24 mL/min) and AE (3.18 ± 2.05 mL/min). CE and AE included exercises with the same intensity, but FAO appeared higher in CE. In the case of AE, these results were obtained by dividing the exercise into three separate times, and oxygen deficit occurred three times. This appears to have resulted in the consumption of more CHO and less FAO [34].

Regarding EPOC, the catecholamine response stimulated by exercise affects EPOC during moderate-intensity or high-intensity exercise. In particular, among the catecholamines, the increase in epinephrine and norepinephrine, which affect energy substrate mobilization, is a potential stimulator of mitochondrial respiration after exercise, resulting in lipolysis, and it has been reported to contribute to increased oxidation [46–48]. In addition, high-intensity exercise can cause glycogen depletion, which can increase the size of the EPOC through lactate, hydrogen ion (H⁺) accumulation, and glycogen resynthesis, and the size of the EPOC appears in proportion to the O₂ deficit [49]. In particular, EPOC contributes to fat oxidation by increasing adenosine triphosphate (ATP) and oxygen consumption through glycogen resynthesis after exercise [22, 50, 51]. As high-intensity exercise continues, mitochondrial activity and oxygen consumption increase in muscle cells to generate more ATP [52] however the amount of ATP gradually decreases during exercise and is resynthesized during the recovery period to provide additional energy [53].

In a study comparing the EPOC for CE and IE, Islam et al. [54] compared the EPOC and FAO after CE and IE in eight healthy men. CE included 30 min of running at 65% VO₂max intensity, and IE included 30-sec of running and 4-min of rest at > 100% VO₂max intensity for a total of four times. During EPOC, VO₂ was significantly higher in IE (42.8 ± 3.6 L) than in CE (38.8 ± 3.7 L), and FAO was significantly higher in IE (0.115 ± 0.026 g/min) than in CE (0.047 ± 0.018 g/min). Kristian et al. [55] compared the EPOC of CE and IE for walking exercises with similar oxygen consumption in 10 participants with type 2 diabetes. Exercise intensity was designed as follows: CE included 60 min of exercise at 73% VO₂peak intensity; IE included a total of 60 min of exercise by repeating 54% VO₂peak and 89% VO₂peak intensity every 3 min. As a result, the total EPOC size was larger in IE (8.4 ± 1.3 L) than in CE (3.7 ± 1.4 L), but carbohydrate and lipid oxidation rates were not different between IE (1.54 ± 1.03 and 3.06 ± 0.20 mg/kg/min) and CE (9.24 ± 0.92 and 3.26 ± 0.28 mg/kg/min). Nevertheless, looking at the oxygen consumption in the end of EPOC, there was a significant difference between IE (271 ± 10 mL/min) and CON (252 ± 9 mL/min) but no difference with CE (259 ± 9 mL/min) and CON, confirming that the EPOC period of IE can last longer than that of CE. Greer et al. (56) compared the EPOC in isocaloric CE and IE using a cycle ergometer in 10 healthy men. CE was performed for approximately 43 min at approximately 39% VO₂peak intensity, and IE was performed for approximately 44 min by repeating 30 sec of exercise at 90% VO₂peak and 120 to 180 sec of rest. As a result, energy consumption during EPOC was higher in IE (62 ± 7.2 kcal/30 min) than in CE (50 ± 5.3 kcal/30 min). In this study, when CE and IE were compared during EPOC, IE had significantly greater HR_sum, VE_sum, VO₂_sum, VCO₂_sum, CHO, FAO, and EE during EPOC based on higher exercise intensity and a greater O₂ deficit during exercise than CE. This means that when performing an exercise with homogenized energy consumption, IE has a shorter exercise time than CE but a larger EPOC, that is, energy consumption after exercise, which is consistent with the results of previous studies [54–56].

AE, which divides exercise, causes an O₂ deficit several times and accumulates. It has been reported that accumulated O₂ deficit affects the size of EPOC by inducing the oxidation of more energy substrates to compensate for energy consumption after exercise [57, 58]. In addition, lipolysis (an increase in free fatty acids and glycerol) in adipose tissue during moderate-intensity aerobic exercise is enhanced when repeated workouts of same intensity and duration [59]. Stich et al. [60] confirmed the effect of repeated bouts of aerobic exercise on glycerol and catecholamine concentrations in seven male participants. For exercise, 60 min of exercise and 60 min of rest were repeated twice at an intensity of 50% VO₂max using a bicycle ergometer. The glycerol concentration at the end of the 2nd exercise (1,126 ± 298 µM) was significantly higher than that at the end of the 1st exercise (728 ± 159 µM). In addition, the plasma catecholamine concentration that induces the mobilization of the energy substrate was confirmed in this study. As a result, norepinephrine increased significantly in the first and second exercise sessions (35.417 ± 4.743 pg/mL and 37.425 ± 3.950 pg/mL), but did not increase any more during repetitive exercise. On the other hand, epinephrine was significantly higher during the second exercise (10.502 ± 1.73 pg/mL) than in the first exercise (2.927 ± 2.07 pg/mL).

In a study comparing the EPOC for CE and AE, Goto et al. [61] confirmed the difference in the effects of CE and AE on fat oxidation during EPOC in nine male participants. The exercise sessions were CE performed at 60% VO₂max for 30 min and AE performed at 60% VO₂max for 10 min of exercise and 10 min of rest, for a total of three times using a cycle ergometer. It was reported that the contribution of fat to total energy consumption during EPOC was significantly greater in AE (77.6 ± 2.7%) than in CE (62.1 ± 5.7%). Darling et al. [62] compared EE during EPOC for CE and AE in 20 male participants. The exercise sessions were CE performed at 70% VO₂max for 30 min of walking exercise and AE performed at 70% VO₂max for 10 min of walking exercise, three times and at 3-h intervals. Energy consumption during exercise was higher in the CE (409 ± 67 kcal) group than in the AE (462 ± 67 kcal) group. On the other hand, EE during EPOC was greater in the AE (105 ± 13 kcal) group than in the CE (83 ± 9 kcal) group, and consequently, in total EE by exercise, AE was greater than CE. Additionally, Jung et al. [36] confirmed the difference in EPOC size according to CE, IE, and AE in nine female participants. The exercise session was CE performed at 60% VO₂max for 30 min and IE performed at 80% VO₂max for 2 min, followed by 40% VO₂max for 1 min, and 80% VO₂max for 3 min, repeated six times for a total of 26 min. For AE, 10 min of exercise at 60% VO₂max intensity were repeated three times at 1-h intervals, and a cycle ergometer was used for all exercises. As a result, the EPOC period was longer in IE (42.44 ± 14.06 min) and AE (45.00 ± 14.31 min) than in CE (25.22 ± 15.06 min), and the energy consumption during EPOC was in the following order: AE (88.57 ± 43.03 kcal/min), IE (63.54 ± 21.39 kcal/min), and CE (38.81 ± 23.06 kcal/min).

It has been reported that EPOC size appears to be proportional to the increase in exercise intensity [53]. In other words, during high-intensity exercise, the amount of oxygen required at the beginning of exercise increases rapidly, and the amount of oxygen deficiency increases accordingly, which seems to affect EPOC as a result [43]. Thornton and Potteiger [63] reported that high-intensity exercise results in a larger EPOC than moderate-intensity exercise. AE causes an O₂ deficit to accumulate, thus increasing the size of EPOC [33]. Therefore, in the difference between oxygen deprivation and EPOC according to the three different exercise treatments in this study, IE appeared larger than CE, and AE appeared larger than CE and IE (O₂ deficit: 1,050.91 ± 245.37 mL/min, 1,346.53 ± 283.93 mL/min, 3,386.73 ± 868.89 mL/min; p < 0.001 in CE, IE, and AE respectively, and EPOC: 5,239.12 ± 1,833.12 mL/Rec, 6,578.96 ± 2,347.63 mL/Rec, 1,3259.97 ± 3,849.27 mL/Rec; p < 0.001 in CE, IE, and AE respectively). The correlation between O₂ deficit and EPOC according to the exercise trials also showed a significant correlation with CE, IE, and AE (R = 0.377; p < 0.05, R = 0.308; p < 0.05, R = 0.558; p < 0.001 for CE, IE, and AE, respectively). As a result, it was confirmed that the O₂ deficit caused by high-intensity exercise not only affects the size of the EPOC but also that the accumulation of the O₂ deficit due to AE affects the size of the EPOC.

In this study, AE showed significantly greater cardiopulmonary function and energy metabolism than CE and IE did during EPOC. This means that AE showed a significantly larger EPOC based on more compensation systems because of the accumulation of O₂ deficit by exercise repeated three times. This was confirmed through the correlation between the O₂ deficit due to exercise and EPOC. These results show that even if the exercise is performed in short 10-min increments, as it was in this study, EPOC can be maximized based on a repetitive O₂ deficit to increase oxidation of energy metabolism, which is consistent with the results of previous studies [36, 60–62].

Since 1995, the US Physical Activity Guidelines have recommended that physical activity be accomplished by accumulating short exercise sessions throughout the day [64]. Exercise that accumulates short workouts throughout the day is more attractive and can encourage exercise participation than traditional long-duration workouts; if short exercises can be accumulated for 10 min each, it becomes easier to achieve the recommended 30 min of moderate-intensity exercise as a daily amount of physical activity [65]. As is well known, regular aerobic exercise not only prevents metabolic and cardiovascular diseases but also reduces their risk of death [66, 67]. In addition to regular exercise, there are health benefits that can be obtained by simply replacing sedentary time with shorter periods of activity [67, 68]. Altena et al. [69] reported that accumulated physical activity is effective in lowering triglyceride concentrations after a meal, which is important because a high postprandial triglyceride concentration increases the risk of cardiovascular disease [70]. Murphy et al. [57] reported that AE could contribute to cardiovascular health and the normalization of blood pressure by increasing fat oxidation as well as maximizing EE through EPOC. Taken together, AE and EPOC can contribute to lipid oxidation and energy consumption and are considered an important form of exercise that lowers the barrier to participation in exercise for individuals who want to maintain or lose weight.

On analyzing the EPOC according to the three modalities of exercise in which energy consumption was homogenized during exercise in healthy women, the oxidation of energy metabolism, especially energy consumption, was larger in AE than in CE and IE. Therefore, performing an AE can help with regular exercise participation by increasing exercise compliance. Further studies examining the effects of the CE, IE, and AE on various metabolic and cardiovascular diseases based on long-term exercise interventions are needed.

ACSM

American College of Sports Medicine

Accumulated exercise

ATP

Adenosine triphosphate

BMI

Body mass index

Continuous exercise

CHO

Carbohydrate oxidation

Energy expenditure

EPOC

Excess post-exercise oxygen consumption

FAO

Fatty acid oxidation

GXT

Graded exercise test

Heart rate

Interval exercise

NCDs

Non-communicable diseases

PAR-Q⁺

Physical activity readiness questionnaire plus

RER

Respiratory exchange rate

RPE

Ratings of perceived exertion

Standard deviation

VCO₂

Carbon dioxide excretion

Minute ventilation

VO₂

Oxygen uptake

VO₂max

Maximal oxygen uptake

VO₂peak

Peak oxygen uptake

WHO

World Health Organization

Ethics approval and consent to participate

All study procedures were approved by the Institutional Review Board of Konkuk University (7001355-202201-E-160) in Korea and were conducted in accordance with the Declaration of Helsinki.

Consent for publication

Not applicable

Availability of data and materials

The data analyzed in this study are available upon reasonable request. ([email protected]).

Competing interests

The authors declare that they have no competing interests.

Funding

This study was not supported by any grants.

Authors' contributions

Acknowledgments

This study was supported by Konkuk University in 2022.

Authors’ information

Yerin Sun and Hun-Young Park contributed equally to this work.

Affiliations

Department of Sports Medicine and Science, Graduate school of Konkuk University, Seoul, South Korea

Yerin Sun, Hun-Young Park, Sung-Woo Kim, Jisoo Seo, Jeaho Choi, Jisu Kim, and Kiwon Lim

The Physical activity & Performance Institute, Seoul, South Korea

Hun-Young Park, Won-Sang Jung, Sung-Woo Kim, Jisu kim, and Kiwon Lim

Department of Physical Education, Graduate school of Konkuk University, Seoul, South Korea

Kiwon Lim

Dod HS, Bhardwaj R, Sajja V, Weidner G, Hobbs GR, Konat GW, et al. Effect of Intensive Lifestyle Changes on Endothelial Function and on Inflammatory Markers of Atherosclerosis. Am J Card. 2010 Feb 1;105(3):362-7. https://doi.org/10.1016/j.amjcard.2009.09.0.
Friedenreich CM, Neilson HK, Lynch BM. State of the epidemiological evidence on physical activity and cancer prevention. Eur J Cancer. 2010 Sep 1;46(14):2593-604. https://doi.org/10.1016/j.ejca.2010.07.028.
Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, et al. Exercise and type 2 diabetes: The American College Of Sports Medicine and The American Diabetes Association: Joint position statement executive summary. Diabetes Care. 2010 Dec 1;33(12):2692-6. https://doi.org/10.2337/dc10-1548.
Ekelund U, Steene-Johannessen J, Brown WJ, Fagerland MW, Owen N, Powell KE, et al. Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality? A harmonised meta-analysis of data from more than 1 million men and women. The Lancet. 2016 Sep 24;388(10051):1302-10. https://doi.org/10.1016/S0140-6736(16)30370-1.
Wagner K heinz, Brath H. A global view on the development of non communicable diseases. Prev Med. 2012 May 1;54:S38-41. https://doi.org/10.1016/j.ypmed.2011.11.012.
Anderson E, Durstine JL. Physical activity, exercise, and chronic diseases: A brief review. Sports Medicine and Health Science. 2019 Dec 1;1(1):3-10. https://doi.org/10.1016/j.smhs.2019.08.006.
Dalal PK, Agarwal M. Postmenopausal syndrome. Indian J Psychiatry. 2015 2015 Jul;57(Suppl 2):S222. https://doi.org/10.4103/0019-5545.161483.
Kim Y. The effects of a physical inactivity-related health risk message intervention on changes in risk perceptions and physical activity in middle-aged women. J Women Aging. 2020 Apr 30;32(5):546-62. https://doi.org/10.1080/08952841.2019.1607678.
Seo DY, Hwang BG. Effects of exercise training on the biochemical pathways associated with sarcopenia. Phys Act Nutr. 2020 Sep 30;24(3):32–8. https://doi.org/10.20463/pan.2020.0019
Hankinson AL, Daviglus ML, Bouchard C, Carnethon M, Lewis CE, Schreiner PJ, et al. Maintaining a high physical activity level over 20 years and weight gain. JAMA. 2010 Dec 15;304(23):2603-10. https://doi.org/10.1001/jama.2010.1843.
Dibble KE, Bellizzi KM, Taxel P, Pescatello LS, Siembida EJ, Schifano ED, et al. Physical activity and health-related quality of life among postmenopausal women with breast cancer treated with aromatase inhibitors. Support Care Cancer. 2021 May;29(5):2385-94. https://doi.org/10.1007/s00520-020-05741-1.
Fountaine CJ. Introduction to High-Intensity Interval Training and Chronic Diseases. ACSMs Health Fit J. 2021 Sep;25(5):11-2. https://doi.org/10.1249/FIT.0000000000000707.
Sallis JF, Bull F, Guthold R, Heath GW, Inoue S, Kelly P, et al. Progress in physical activity over the Olympic quadrennium. The Lancet. 2016 Sep 24;388(10051):1325-36. https://doi.org/10.1016/S0140-6736(16)30581-5.
Nahas MV, Goldfine B, Collins MA. Determinants of physical activity in adolescents and young adults : The basis for high school and college physical to promote active lifestyles. Physical Educator. 2003 Winter;60(1):42.
Baillot A, Chenail S, Barros Polita N, Simoneau M, Libourel M, Nazon E, Riesco E, Bond DS, Romain AJ. Physical activity motives, barriers, and preferences in people with obesity: A systematic review. PloS one. 2021 Jun 23;16(6):e0253114. https://doi.org/10.1371/journal.pone.0253114.
Strohacker K, Fazzino D, Breslin WL, Xu X. The use of periodization in exercise prescriptions for inactive adults: A systematic review. Prev Med Rep. 2015 Jan 1;2:385–96. http://dx.doi.org/10.1016/j.pmedr.2015.04.023.
Selk-Ghaffari M, Hassanmirzaei B, Nakhostin-Ansari A, Mahdaviani B, Khonji MS, Aghajani R, et al. Conceptualization and development of a questionnaire to determine physical activity barriers. Phys Act Nutr. 2022 Jun 1;26(2):17–21. https://doi.org/10.20463/pan.2022.0009.
Cunha FA, Midgley AW, McNaughton LR, Farinatti PT. Effect of continuous and intermittent bouts of isocaloric cycling and running exercise on excess postexercise oxygen consumption. J Sci Med Sport. 2016 Feb 1;19(2):187–92. http://dx.doi.org/10.1016/j.jsams.2015.02.004.
Zheng L, Zhang X, Zhu W, Chen X, Wu H, Yan S. Acute effects of moderate-intensity continuous and accumulated exercise on arterial stiffness in healthy young men. Eur J Appl Physiol. 2015 Jan;115(1):177–85. https://doi.org/10.1007/s00421-014-3008-5.
Gaesser GA, Angadi SS. High-intensity interval training for health and fitness: Can less be more? J Appl Physiol. 2011 Dec;111(6):1540–1. https://journals.physiology.org/doi/full/10.1152/japplphysiol.01237.2011.
Bartlett JD, Close GL, Maclaren DPM, Gregson W, Drust B, Morton JP. High-intensity interval running is perceived to be more enjoyable than moderate-intensity continuous exercise: Implications for exercise adherence. J Sports Sci. 2011 Feb 24;29(6):547–53. https://doi.org/10.1080/02640414.2010.545427.
Keating SE, Johnson NA, Mielke GI, Coombes JS. A systematic review and meta-analysis of interval training versus moderate-intensity continuous training on body adiposity. Obes Rev. 2017 May 17;18(8):943–64. https://doi.org/10.1111/obr.12536.
Hardcastle SJ, Ray H, Beale L, Hagger MS. Why sprint interval training is inappropriate for a largely sedentary population. Front Psychol. 2014 Dec 23;5(DEC):2013–5. https://doi.org/10.3389/fpsyg.2014.01505.
Miyashita M, Burns SF, Stensel DJ. An update on accumulating exercise and postprandial lipaemia: Translating theory into practice. J Prev Med Public Health. 2013 Jan;46(SUPPL 1):S3–11. https://doi.org/10.3961/jpmph.2013.46.S.S3.
Chang CR, Russell BM, Dempsey PC, Christie HE, Campbell MD, Francois ME. Accumulating Physical Activity in Short or Brief Bouts for Glycemic Control in Adults With Prediabetes and Diabetes. Can J Diabetes. 2020 Dec;44(8):759–67. https://doi.org/10.1016/j.jcjd.2020.10.013.
Shambrook P, Kingsley M, Taylor N, Gordon B. Accumulated or continuous exercise for glycaemic regulation and control: A systematic review with meta-analysis. BMJ Open Sport Exerc Med. 2018 Dec 17;4(1):1–12. http://dx.doi.org/10.1136/bmjsem-2018-000470.
DeBusk RF, Stenestrand U, Sheehan M, Haskell WL. Training effects of long versus short bouts of exercise in healthy subjects. Am J Cardiol. 1990 Apr 15;65(15):1010–3. https://doi.org/10.1016/0002-9149(90)91005-Q.
Schaun GZ, Alberton CL, Ribeiro DO, Pinto SS. Acute effects of high-intensity interval training and moderate-intensity continuous training sessions on cardiorespiratory parameters in healthy young men. Eur J Appl Physiol. 2017 May 09;117(7):1437–44. ttps://doi.org/10.1007/s00421-017-3636-7.
Santos MA dos, Matzenbacher F, Albarello JC dos S, Halmenschlager GH. Comparison of epoc and recovery energy expenditure between hiit and continuous aerobic exercise training. Rev Bras Med Esporte. 2019 Jan-Feb;25(1):20–3. https://doi.org/10.1590/1517-869220192501181346.
Lyons S, Richardson M, Bishop P, Smith J, Heath H, Giesen J. Excess post-exercise oxygen consumption in untrained men following exercise of equal energy expenditure: comparisons of upper and lower body exercise. Diabetes Obes Metab. 2006 Dec 14;9(6):889–94. https://doi.org/10.1111/j.1463-1326.2006.00679.x.
Hunter GR, Moellering DR, Carter SJ, Gower BA, Bamman MM, Hornbuckle LM, Plaisance EP, Fisher G. Potential Causes of Elevated REE following High-Intensity Exercise. Med Sci Sports Exerc. 2017 Dec;49(12):2414-21. https://doi.org/10.1249/MSS.0000000000001386.
Larsen I, Welde B, Martins C, Tjønna AE. High- and moderate-intensity aerobic exercise and excess post-exercise oxygen consumption in men with metabolic syndrome. Scand J Med Sci Sports. 2014 Jun;24(3):e174–9. https://doi.org/10.1111/sms.12132.
Scott CB. Combustion, respiration and intermittent exercise: A theoretical perspective on oxygen uptake and energy expenditure. Biology. 2014 Mar 28;3(2):255–63. https://doi.org/10.3390/biology3020255.
Jung WS, Hwang H, Kim J, Park HY, Lim K. Effect of accumulated vs continuous exercise on excess post-exercise oxygen consumption. Ethiop J Health Dev. 2020 May 25;34(3).
Cassidy S, Thoma C, Houghton D, Trenell MI. High-intensity interval training: a review of its impact on glucose control and cardiometabolic health. Diabetologia. 2017 Sep 28;60(1):7–23. https://doi.org/10.1007/s00125-016-4106-1.
Jung WS, Hwang H, Kim J, Park HY, Lim K. Comparison of excess post-exercise oxygen consumption of different exercises in normal weight obesity women. J Exerc Nutrition Biochem. 2019 Jun 30;23(2):22–7. https://doi.org/10.20463/jenb.2019.0013.
Simonson DC, Defronzo RA. Indirect calorimetry: methodological and interpretative problems. Am J Physiol - Endocrinol Metab. 1990 Mar 1;258(3):E399-412. https://doi.org/10.1152/ajpendo.1990.258.3.E399.
Jung K, Seo J, Jung WS, Kim J, Park HY, Lim K. Effects of an acute pilates program under hypoxic conditions on vascular endothelial function in pilates participants: A randomized crossover trial. Int J Environ Res Public Health. 2020 Apr 9;17(7):2584. https://doi.org/10.3390/ijerph17072584.
Péronnet F, Massicotte D. Table of nonprotein respiratory quotient an update. Can J Sport Sci. 1991 Mar 1;16(1):23–9.
Medbo JI, Mohn AC, Tabata I, Bahr R, Vaage O, Sejersted OM. Anaerobic capacity determined by maximal accumulated O2 deficit. J Appl Physiol. 1988 Jan 1;64(1):50-60. https://doi.org/10.1152/jappl.1988.64.1.50.
Burt DG, Lamb K, Nicholas C, Twist C. Effects of exercise-induced muscle damage on resting metabolic rate, sub-maximal running and post-exercise oxygen consumption. Eur J Sport Sci. 2013 Apr 8;14(4):337–44. https://doi.org/10.1080/17461391.2013.783628.
Mendonca G v., Vaz JR, Pezarat-Correia P, Fernhall B. Effects of Walking with Blood Flow Restriction on Excess Post-exercise Oxygen Consumption. Int J Sports Med. 2015 Mar;36(3):e11-8. https://doi.org/10.1055/s-0034-1395508.
Børsheim E, Bahr R. Effect of Exercise Intensity, Duration and Mode on Post-Exercise Oxygen Consumption. Sports Med. 2013 Dec;33(14):1037-60. https://doi.org/10.2165/00007256-200333140-00002.
Mann TN, Webster C, Lamberts RP, Lambert MI. Effect of exercise intensity on post-exercise oxygen consumption and heart rate recovery. Eur J Appl Physiol. 2014 Sep 1;114(9):1809–20. https://doi.org/10.1007/s00421-014-2907-9.
Sedlock DA, Fissinger JA, Melby CL. Effect of exercise intensity and duration on postexercise energy expenditure. Med Sci Sports Exerc. 1989 Dec 1;21(6):662–6. https://doi.org/10.1249/00005768-198912000-00006.
Imamura H, Shibuya S, Uchida K, Teshima K, et al. Effect of moderate exercise on excess post-exercise oxygen consumption and catecholamines in young women. J Sports Med Phys Fitness. 2004 Mar;44(1):23-9.
Nariman AM, Lene S, Jens B. Post‐exercise adipose tissue and skeletal muscle lipid metabolism in humans: the effects of exercise intensity. J Physiol. 2000 May 01;524(3):919–28. https://doi.org/10.1111/j.1469-7793.2000.00919.x.
Zouhal H, Jacob C, Delamarche P, Gratas-Delamarche A. Catecholamines and the Effects of Exercise, Training and Gender. Sports Med. 2008 May;38(5):401-23. https://doi.org/10.2165/00007256-200838050-00004.
Moniz SC, Islam H, Hazell TJ. Mechanistic and methodological perspectives on the impact of intense interval training on post-exercise metabolism. Scand J Med Sci Sports. 2020 Mar 12;30(4):638–51. https://doi.org/10.1111/sms.13610.
Casey A, Constantin-Teodosiu D, Howell S, Hultman E, Greenhaff PL. Metabolic response of type I and II muscle fibers during repeated bouts of maximal exercise in humans. Am J Physiol – Endocrinol Metab. 1996 Jul 1;271(1):E38-43. https://doi.org/10.1152/ajpendo.1996.271.1.E38.
Kimber NE, Heigenhauser GJF, Spriet LL, Dyck DJ. Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans. J Physiol. 2003 May 1;548(3):919-27. https://doi.org/10.1111/j.1469-7793.2003.00919.x.
Gibala MJ, Little JP, van Essen M, Wilkin GP, Burgomaster KA, Safdar A, et al. Short-term sprint interval versus traditional endurance training: Similar initial adaptations in human skeletal muscle and exercise performance. J Physiol. 2006 Sep 6;575(3):901–11. https://doi.org/10.1113/jphysiol.2006.112094.
Laforgia J, Withers RT, Gore CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006 Nov 24;24(12):1247–64. https://doi.org/10.1080/02640410600552064.
Islam H, Townsend LK, Hazell TJ. Excess Postexercise Oxygen Consumption and Fat Utilization Following Submaximal Continuous and Supramaximal Interval Running. Res Q Exerc Sport. 2018 Oct 16;89(4):450–6. https://doi.org/10.1080/02701367.2018.1513633.
Karstoft K, Wallis GA, Pedersen BK, Solomon TP. The effects of interval- vs. continuous exercise on excess post-exercise oxygen consumption and substrate oxidation rates in subjects with type 2 diabetes. Metabolism. 2016 Sep;65(9):1316–25. https://doi.org/10.1016/j.metabol.2016.05.017.
Greer BK, Sirithienthad P, Moffatt RJ, Marcello RT, Panton LB. EPOC comparison between isocaloric bouts of steady-state aerobic, intermittent aerobic, and resistance training. Res Q Exerc Sport. 2015 Feb 12;86(2):190–5. https://doi.org/10.1080/02701367.2014.999190.
Murphy MH, Blair SN, Murtagh EM. Accumulated versus continuous exercise for health benefit. Sports Med. 2009 Jan;39(1):29–43. https://doi.org/10.2165/00007256-200939010-00003.
Scott CB. The effect of time-under-tension and weight lifting cadence on aerobic, anaerobic, and recovery energy expenditures: 3 submaximal sets. Appl Physiol Nutr Metab. 2012 Mar 8;37(2):252–6. https://doi.org/10.1139/h11-158.
Kurobe K, Nakao S, Nishiwaki M, Matsumoto N. Combined effect of coffee ingestion and repeated bouts of low-intensity exercise on fat oxidation. Clin Physiol Funct Imaging. 2017 Feb 22;37(2):148–54. https://doi.org/10.1111/cpf.12279.
Stich V, de Glisezinski I, Berlan M, Bulow J, Galitzky J, Harant I, et al. Adipose tissue lipolysis is increased during a repeated bout of aerobic exercise. J Appl Physiol. 2000 Apr 1;88(4):1277-83. https://doi.org/10.1152/jappl.2000.88.4.1277.
Goto K, Tanaka K, Ishii N, Uchida S, Takamatsu K. A single versus multiple bouts of moderate-intensity exercise for fat metabolism. Clin Physiol Funct Imaging. 2011 Apr 7;31(3):215–20. https://doi.org/10.1111/j.1475-097X.2010.01003.x.
Darling JL, Linderman JK, Laubach LL. ENERGY EXPENDITURE OF CONTINUOUS AND INTERMITTENT EXERCISE IN COLLEGE-AGED MALES. J Exerc Physiol online. 2005 Aug;8(4):1–8.
Thornton MK, Potteiger JA. Effects of resistance exercise bouts of different intensities but equal work on EPOC. Med Sci Sports Exerc. 2002 Apr 1;34(4):715-22. https://doi.org/10.1097/00005768-200204000-00024.
Pate RR, Pratt M, Blair SN, et al. Physical Activity and Public Health: A Recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA. 1995 Feb 1;273(5):402-7. https://doi.org/10.1001/jama.1995.03520290054029.
Miyashita M, Burns SF, Stensel DJ. Exercise and postprandial lipemia: effect of continuous compared with intermittent activity patterns. Am J Clin Nutr. 2006 Jan 1;83(1):24-9. https://doi.org/10.1093/ajcn/83.1.24.
Franklin BA, Billecke S. Putting the Benefits and Risks of Aerobic Exercise in Perspective. Curr Sports Med Rep. 2012 Jul-Aug;11(4):201-8. https://doi.org/10.1249/JSR.0b013e31825dabd4.
Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee IM, et al. Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory, Musculoskeletal, and Neuromotor Fitness in Apparently Healthy Adults: Guidance for Prescribing Exercise. Med Sci Sports Exerc. 2011 Jul;43(7):1334–59. https://doi.org/10.1249/MSS.0b013e318213fefb.
Andersen RE, Wadden TA, Bartlett SJ, Zemel B, Verde TJ, Franckowiak SC. Effects of Lifestyle Activity vs Structured Aerobic Exercise in Obese Women: A Randomized Trial. JAMA. 1999 Jan 27;281(4):335-40. https://doi.org/10-1001/pubs.JAMA-ISSN-0098-7484-281-4-joc80705.
Altena TS, Michaelson JL, Ball SD, Thomas TR. Single sessions of intermittent and continuous exercise and postprandial lipemia. Med Sci Sports Exerc. 2004 Aug;36(8):1364–71. https://doi.org/ 10.1249/01.MSS.0000135793.43808.6C.
Geluk CA, Halkes CJM, de Jaegere PPT, Plokker TWM, Cabezas MC. Daytime triglyceridemia in normocholesterolemic patients with premature atherosclerosis and in their first-degree relatives. Metabolism. 2004 Jan;53(1):49–53. https://doi.org/10.1016/j.metabol.2003.08.008.

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A Comparison of Continuous, Interval, and Accumulated Workouts with Equalized Exercise Volume: Excess Post-Exercise Oxygen Consumption in Women

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