Rates of both obesity and obesity-related diseases have been rising in most developed countries (6). Physical activity (PA) is often recommended as a strategy for obesity prevention. The International Association for the Study of Obesity has adopted a consensus statement stating that a PA level (PAL) of 1.7, or moderate-intensity PA for 45 to 60 min·d−1, is recommended to prevent weight and fat gain in adults (25). However, a recent systematic review and another report indicated that weight changes cannot be fully explained by lower PA (37) or decreases in PA over time (36). Westerterp and Speakman (36), interestingly, reported that PAL in adults evaluated by the doubly labeled water method has not decreased since the 1980s. Therefore, it is possible that other factors related to PA, but independent of PAL, may influence weight and fat gain in adults.
Several previous studies have indicated that lower fat oxidation capacity predicts weight and fat gain over a year or more (4,5,27,40). Dietary record data indicate that fat consumption changes dramatically from day to day (38), and that the percentage of fat consumed changes from meal to meal. For both carbohydrate (CHO) and protein, it has been shown that oxidation is strongly regulated by the relative intake of these nutrients compared with fat. Thus, even if energy is balanced, positive fat balance tends to be induced during switching from a high-carbohydrate (HC) meal to a high-fat (HF) meal (31). Thus, modern eating habits tend to result in a positive fat balance. In addition, some studies have noted that a positive fat balance could be a positive energy balance (EB) (23), as it is possible that a negative CHO balance results in a subsequent appetitive drive (7,22). Thus, dulling metabolic adaptation during a switch from a carbohydrate to a fat diet may be a determinant of fat accumulation. Therefore, with modern eating habits, particularly during simply switching from an HC meal to an HF meal, it appears to be important to use ingested fat as efficiently as possible (higher fat oxidation capacity) over the course of the day to prevent a positive fat balance and, ultimately, weight or fat gain.
Previous studies have reported that higher PAL induces greater fat utilization when switching from an HC to an HF meal (3,10,26,30). These studies showed results consistent with the International Association for the Study of Obesity consensus statement. However, it has not been investigated whether PA patterns influence fat utilization during switching from an HC to an HF meal independent of PAL. In general, moderate-intensity PA, and in particular, prolonged moderate-intensity exercise lasting for 10 min or more, is widely believed to be one of the easiest ways to use PA to increase energy expenditure (EE) while burning a large proportion of energy from fat. In fact, most previous studies have investigated the effects of continuity of exercise with a duration over 10 min (18). However, increased accumulated intermittent PA and intense nonlocomotive PA are effective alternatives to prolonged PA, and both increase EE and fat utilization. Troiano et al. (33) suggested that moderate to vigorous PA (MVPA) carried out for 10 or more minutes accounted for only one third of total time spent on MVPA as measured using an accelerometer. Interestingly, it was shown that the amount or frequency of intermittent PA (“breaks in sedentary”) may play a role in obesity-related outcomes (12), independent of total time spent on MVPA or sedentary behavior. Thus, although intermittent PA carried out for less than 10 min may be an important factor for PAL and obesity-related outcomes independent of MVPA, there is no evidence on whether intermittent PA influences fat utilization or subsequent weight or fat gain.
Therefore, the aim of the present study was to determine whether continuous and intermittent PA differentially influence fat utilization over the course of a whole day. We measured both continuous and intermittent PA using a human calorimeter over 1 d with an HF meal.
The study protocol was approved by the Ethical Committee of the National Institute of Health and Nutrition (NIHN) in Japan. Ten Japanese nonobese healthy young men participated and gave written informed consent for this study. However, only nine participants were used in the current analysis, because one was regarded to have dyslipidemia; the blood triacylglycerol (TG) and LDL cholesterol (LDL-C) levels of the excluded participant were above 150 and 140 mg·dL−1, respectively, under fasted conditions on day 2 in both trials. Participants were nonsmokers, nonshift worker adults, and had no chronic diseases affecting metabolism or PA such as diabetes, metabolic disease, or digestive disease. They did not use any medicines or supplements. In addition, when participants were recruited, men who performed specific exercises on a regular basis that would prevent them from wearing an accelerometer (e.g., swimming) were excluded.
After completing medical history screening including food allergies, anthropometric measurements and a habitual PA questionnaire (International Physical Activity Questionnaire (IPAQ)) were completed, and maximum oxygen uptake was measured in the morning under fasted conditions. Body fat mass and fat-free mass were measured using dual-energy x-ray absorptiometry (Hologic QDR-4500; Hologic, Inc., Bedford, MA). Participants completed two trials, with an interval of 10 d to 3 wk. Each participant wore a triaxial accelerometer (Active style Pro HJA-350IT; Omron Healthcare, Kyoto, Japan) during all measurement periods after trial commencement (about 1 month).
This was a randomized study using a crossover design. Each participant performed two PA trials (continuous and intermittent exercise), each involving a 39-h session (two nights and three days) in a respiratory chamber (Fig. 1). During the day while participants stayed in the room, intentional vigorous PA such as exercise was restricted. Participants consumed all meals provided until 1330 h and drank water freely. Participants arrived at the NIHN in the evening at 1730 h, were weighed lightly clad, put on the accelerometer, were fitted with an electrode for measuring heart rate, and entered the calorimeter at 1850 h. They consumed the HC meal at 1930 h and were permitted to sleep at 2300 h. The HF experiments commenced at 0800 h on day 2 after an equilibration period and finished at 1005 h on day 3. While in the calorimeter, participants adhered to an identical fixed schedule of eating meals, exercising, and sleeping. Minimum sleeping metabolic rate was recorded overnight and calculated as minimum EE over 3 h on each of the two consecutive nights. Other metabolic parameters while sleeping were analyzed from 2305 to 0700 h on each of the two consecutive nights. Participants temporarily left the chamber from 0715 until 0730 h on the two consecutive mornings to provide a blood sample.
For 2 d before entering the chamber, participants consumed a provided HC weight maintenance diet (15% of kilocalories from protein, 15% from fat, and 70% from carbohydrate). Energy requirements were calculated individually as estimated by basal metabolic rate (BMR) × habitual PAL. BMR was estimated from age, sex, height, and body weight using Ganpule equation (8), derived from Japanese adults at the NIHN. Habitual PAL was estimated using IPAQ criteria, and 1.7 or 1.9 was applied, on the basis of a report on the relationship between the IPAQ criteria and PAL evaluated by the doubly labeled water method for Japanese adults (13). Energy intake (EI) of the participants was either 2000, 2500, or 3000 kcal·d−1 depending on their estimated energy requirements. In addition, participants were asked to spend some time as similar as possible during the 2 d before entering the chamber for each trial.
Participants consumed the HF meals (15% of kilocalories from protein, 50% from fat, 35% from carbohydrate) starting from breakfast on day 2. They consumed the same meal four times (breakfast, lunch, dinner, and breakfast) to avoid interactions of differences in food with time. Energy requirements in the chamber were calculated individually as estimated BMR × 1.6 (PAL of 1.6). The EI of a total of three meals (breakfast, lunch, and dinner) for each participant was either 2200, 2400, 2600, or 2800 kcal·d−1 depending on their estimated energy requirements. Fatty acid profiles of all meals consumed in the chamber were held constant with equal proportions of saturated, monounsaturated, and polyunsaturated fatty acids (1.4/1.0/0.5). All diets were commercial products (processed foods) with known nutritional status and were provided by a dietitian.
The participants performed a total of 85 min of exercise using a static cycling ergometer (Aerobike 75XL ii; Combi Wellness Corporation, Tokyo, Japan) at workload of 5.5 METs determined for each individual. In the continuous PA trial, participants started exercise at 1350 h and finished at 1550 h. They performed a 10-min warming up, 45 min of exercise followed by a 10-min break, then 40 more min of exercise, and a 15-min cooling down. In the intermittent PA trial, the participants started exercise at 1000 h and finished at 1905 h. They performed 5 min of exercise every 30 min for a total of 17 bouts. They performed an identical 10-min warming up and 15-min cooling down at the same time as in the continuous PA trial. The workload for warming up and cooling down was 20 W.
The workload of 5.5 METs was calculated by regression of the 20, 60, and 90 W points while measuring maximum oxygen uptake. Maximum oxygen uptake was measured by increasing the load every 3 min until exhaustion. Expired gas was sampled into Douglas bags, and V˙O2 was obtained from oxygen and carbon dioxide concentrations measured using a mass spectrometer for respiration (ARCO-2000; Arco System, Kashiwa, Japan) and gas volume measured using a dry process gas flow meter (DC-1; Shinagawa, Tokyo, Japan) for the last 30 s of every stage. The number of revolutions for all ergometer trials was kept at 60 rpm to keep energy efficiency constant. V˙O2 was considered “peak” if two of the following criteria were met: 1) measured HRmax ≥ age-predicted HRmax − 10 beats·min−1; 2) V˙O2 increased by <100 mL·min−1 during a trial; 3) RERmax was ≥1.10; and/or 4) Borg scalemax was ≥19.
The present study used two open-circuit human calorimeters at the NIHN to measure oxygen consumption and carbon dioxide production. Details of the human calorimeter were previously reported (8,17). The accuracy of the chambers in measurement of EE as determined by an alcohol combustion test was 99.2 ± 0.7 (mean ± SD) over 6 h and 99.2 ± 3.0 (mean ± SD) over 30 min. The rooms were maintained at a temperature of 25°C, humidity of 55%, and a ventilation rate of 60 L·min−1. Ventilation rate was measured every 12 s using a pneumotachometer. Oxygen and carbon dioxide concentrations were also measured every 12 s using a mass spectrometer (ARCO-1000A-CH; Arco System). EE was calculated from V˙O2 and V˙CO2 using Weir equation (35). RER was defined as V˙CO2/V˙O2. Fat and carbohydrate oxidation were calculated from V˙O2 and V˙CO2 and protein oxidation using Jequier equation (15). Protein intake was substituted for protein oxidation.
PA evaluation using a triaxial accelerometer.
Participants wore the triaxial accelerometer on the waist until all experiments were completed. The accelerometer was developed especially for evaluating relatively low-intensity PA and nonlocomotive or household PA (20,21). Data were recorded in 10-s epoch length. Cycling PA measured by accelerometry while using the cycling ergometer in the chamber was converted to an acceleration value using Ohkawara equation (20). Nonwearing time while in the chamber was assigned a value of 0.9 METs based on Ohkawara’s article. Continuity of sedentary behavior (METs ≤1.5) in the chamber was scored using three cutoff points (3 or more, 5 or more, or 10 or more consecutive minutes) and analyzed using Microsoft Excel (2007; Microsoft Japan, Tokyo, Japan).
Blood samples for each participant were obtained under fasting condition at 0715 h outside the chamber on two consecutive mornings to identify metabolically abnormal subjects and to confirm whether there was an interaction with lipid metabolism between trials (lipid oxidation subsides during the night). Blood samples collected in prechilled tubes that contained a serum separating medium were centrifuged for 20 min at 3000 rpm 30 min after drawing blood, after which serum was immediately stored in a refrigerator. Blood samples collected in prechilled tubes that contained EDTA-2Na were centrifuged for 20 min at 3000 rpm, after which plasma was immediately stored in a freezer. Blood samples collected in prechilled tubes that contained EDTA-2Na and NaF were stored immediately in a refrigerator. Plasma concentrations of glucose, insulin, TG, nonesterified fatty acids, HDL cholesterol (HDL-C), LDL-C, and norepinephrine were analyzed at Mitsubishi Chemical Medience Corporation.
Data are presented as means ± SD. Twenty-three–hour RER from 0800 h on day 2 to 0700 h on day 3 was analyzed as the main outcome of this study. Descriptive statistics were calculated, and Student’s paired t-test, repeated-measures ANOVA, and Pearson (partial) correlations were performed using SPSS (18.0; IBM SPSS, Tokyo, Japan). Student’s paired t-test was used to assess differences between the trials. Because RER during sleeping time on day 1 was significantly different between trials and because sleeping RER was significantly correlated with 23-h RER, it was analyzed as a covariate. Multiple linear regression analysis was used to adjust for covariance. Biochemical data were statistically analyzed using repeated-measures ANOVA. The mean total EE (TEE) and EB were significantly different between trials. However, because neither TEE nor energy balance was significantly correlated with 23-h RER, these were not used as covariates. PA data were assessed for normality using a Kolmogorov–Smirnov test, and kurtosis and skewness were determined; however, all variables were normally distributed. Results were considered significant at P < 0.05.
Table 1 shows the characteristics of the nine participants. Participants were weight stable (within 1.5 kg) throughout the study period. The average TEE for 2 d before entering the chamber, measured using an accelerometer, was not significantly different between the continuous PA trial and the intermittent PA trial with 2450 ± 225 and 2522 ± 374 kcal, respectively. The same diets were provided between trials, and all were consumed before entering the chamber. The mean total EI was 2660 ± 225 kcal in both trials, and the mean macronutrient composition was 15.3% ± 0.0% protein, 15.8% ± 0.2% fat, and 68.9% ± 0.2% carbohydrate in both trials.
EI, EE, and substrate oxidation under HC conditions in the chamber.
Average EE and RER for each segment are shown in Tables 2 and 3. On the first night, EE and RER were not significantly different between trials except for sleeping time RER. During sleep on day 1, RER in the intermittent PA trial was significantly lower than that in the continuous PA trial (P = 0.01).
EI, EE, and substrate oxidation under HF conditions in the chamber.
On day 2 in the chamber, the mean total EI was 2413 ± 132 kcal in both trials, and the macronutrient composition was 16.4% ± 0.3% kcal from protein, 49.0% ± 0.7% from fat, and 34.6% ± 0.5% from carbohydrate in both trials. Table 2 shows EE and metabolic rate values during each segment in the chamber. The mean TEE in the intermittent PA trial (2456 ± 155 kcal) was higher than that in the continuous PA trial (2373 ± 198 kcal, P = 0.01). Table 3 shows RER (nonadjusted) during each segment in the chamber. Twenty-three–hour RER adjusted for RER on the preceding day in the intermittent PA trial was lower than that in the continuous trial (P = 0.021, Fig. 2). Nonsleeping RER (15-h) adjusted for RER on the preceding day in the intermittent PA trial was also lower than that in the continuous PA trial (P = 0.017). Sleeping RER adjusted for sleeping RER on the preceding day was not significantly different between trials. There was no interaction between trial and time for sleeping RER or postbreakfast RER. Although there was an effect of time between days 1 and 2 (P < 0.001) and a trial effect (P < 0.01) for sleeping RER, there was only an effect of time between days 2 and 3 (P < 0.001) for postbreakfast RER. Twenty-three–hour fat oxidation adjusted for TEE and sleeping fat oxidation rate on the preceding day was significantly higher in the intermittent PA trial (109.8 ± 6.8 g) than that in the continuous PA trial (101.1 ± 6.8 g; P = 0.001). There was no significant difference between trials in 23-h CHO oxidation adjusted for TEE and sleeping CHO oxidation rate on the preceding day.
PA in the chamber.
PA in the chamber was evaluated using an accelerometer. PA during the period without respiratory measurements (0700–0800 h) on days 2 and 3 was not significantly different between trials. There was no significant difference in cycling ergometer PA with either 5.5 METs or 20-W cycling between trials, whereas noncycling PA in the intermittent PA trial (1.33 ± 0.11 METs) was significantly higher than that in the continuous PA trial (1.25 ± 0.11 METs, P < 0.01). The difference of means of accumulated time in trials was larger with a greater number of consecutive minutes with METs ≤1.5 (Table 2).
PA in the chamber and substrate oxidation.
There was no significant relationship between total minutes with METs ≤1.5 and 23-h RER adjusted for sleeping RER on the preceding day (Fig. 3A), whereas adjusted 23-h RER was correlated with each level of accumulated consecutive minutes with METs ≤1.5 (3 min or more, r = 0.477; 5 min or more, r = 0.510; 10 min or more, r = 0.605; Fig. 3B). Moreover, because total minutes with METs ≤1.5 in the intermittent PA trial was significantly lower than that in the continuous PA trial, we examined the relationships between fractions of accumulated consecutive minutes with METs ≤1.5 relative to total minutes with METs ≤1.5 and adjusted 23-h RER to evaluate the influence of prolonged sedentary behavior independently of the PA trials. The relationships were comparable for each level (3 min or more, r = 0.488; 5 min or more, r = 0.516; 10 min or more, r = 0.625). The mean PA intensity for noncycling time was not significantly correlated with 23-hr RER adjusted for sleeping RER on the preceding day. In addition, neither PALsleep (TEE / sleeping metabolic rate × 23/24) nor PALBMR (TEE / estimated BMR × 23/24) evaluated in the respiratory chamber was significantly correlated with 23-h RER.
Plasma parameters were not significantly different between trials on day 2. For all variables, no significant interaction of trial and time was observed. The only significant effect of time was between days 2 and 3 on plasma parameters other than insulin and norepinephrine. Plasma glucose and TG decreased (P = 0.001 and P = 0.01, respectively), whereas nonesterified fatty acid, HDL-C, and LDL-C increased (P = 0.01, P < 0.05, and P < 0.001, respectively) (see Table, Supplementary Digital Content 1, https://links.lww.com/MSS/A209).
In the present study, we examined whether continuous and intermittent moderate-intensity PA differentially influence fat utilization over a whole day. Given the results of a recent study showing that the number of “breaks in sedentary” was associated with obesity-related parameters, we hypothesized that intermittent moderate-intensity PA throughout the day (e.g., walking, moving around, and intense household activity) would lead to greater fat utilization than a single bout of moderate-intensity PA. Twenty-three–hour RER in the intermittent PA trial was significantly lower than that in the continuous PA trial, although the difference in fat oxidation was only about 10 g·d−1. In the intermittent PA trial, there were 15 more instances of standing up, moving around, and ergometer preparation than that in the continuous PA trial. Twenty-three–hour TEE and EB were significantly different between trials, but both were not significantly associated with 23-h RER in this study, although EB is considered as a main determinant of fat oxidation. This result may reflect that interindividual relationships between EB and RER were masked by some other confounding factors. Incidentally, although the difference in TEE between trials was 83 kcal, most of this difference (70 kcal) can be explained by noncycling PA measured by accelerometry. In addition, PAL and noncycling PA (spontaneous PA) were not significantly associated with 23-h RER, although previous studies have indicated that a higher PAL leads to more rapid adaptation to an HF meal. This discrepancy may be due to a higher PAL in both trials in the present experiment. Hansen et al. (10) also showed that the change in RER at a PAL of 1.8 was similar to that at a PAL of 1.6. On the basis these results, even if PAL was the same, intermittent PA might induce greater utilization of ingested fat over the course of a day when switching from an HC meal to an HF meal than continuous PA.
It is plausible that consecutive time with METs ≤1.5 in the intermittent PA trial was less than that in the continuous PA trial. Figure 3 shows that there was a strong correlation between 10 or more consecutive minutes with METs ≤1.5 and adjusted 23-h RER. Recent studies presented by Hamilton et al. (1,39) suggest that prolonged sedentary behavior leads to decreased fat oxidation as a result of decreased heparin-releasable lipoprotein lipase (LPL) activity, which directs consumed fat toward muscle. Furthermore, the present study showed that the fraction of accumulated consecutive minutes with METs ≤1.5 relative to total minutes with METs ≤1.5 was strongly associated with 23-h RER adjusted for sleeping RER on the preceding day. Thus, our results may support the idea that “breaks in sedentary” prevent decreased fat oxidation.
Several studies performed under energy balanced conditions over 1 d showed that moderate-intensity exercise does not lead to relatively increased fat oxidation over the day (16). This phenomenon can be explained by the popular dogma that RER becomes equal to the food quotient (FQ) in the long term. Thus, when subjects eat meals with the same macronutrient balance on prechamber days and chamber days, fat and CHO utilization during exercise should compensate and become equal to the FQ. However, when FQ and EB change from day to day, a positive fat balance is probably always easy to retain. Then, because this possibly leads to weight gain, we need to investigate those conditions that are favorable for a positive fat balance. Thus, this was the motivation for the present study. Although the difference in fat oxidation was only about 10 g·d−1, if a positive fat balance (i.e., a negative CHO balance) accumulated rather than a threshold for stimulating appetite, this may lead to subsequent overeating. Actually, fat oxidation did not show compensation after exercise because the measurement was performed during the period of switching from HC to HF. In addition, because LPL protein remains elevated until about 20 h after exercise in humans (28), we continued our study until late morning on day 3. However, there were no significant interactions between pre- and postexercise for sleeping RER or postprandial RER in the morning (P = 0.19 and P = 0.64, respectively). Moreover, none of the biochemical variables on day 3 mornings showed any interactions between trials, although the sample size and only one point (fasted condition) for blood drawing were limited. Thus, excess fat oxidation after prolonged exercise during the continuous PA trial might have been completed in the morning. These data probably indicate that a positive fat balance may not be compensated and may accumulate day after day.
During switching from an HC meal to an HF meal, macronutrient utilization switches from predominantly CHO to fat until it becomes equal to the proportion of fat consumed. However, individuals cannot adapt as rapidly to changes in fat intake compared with changes in other macronutrients. More than a full day is needed to increase pyruvate dehydrogenase kinase (PDK) activity, a key factor for fat adaptation, after consumption of an HF diet (2,24). However, prolonged low- to moderate-intensity exercise can modulate PDK activity (34). In fact, Hansen et al. (10) showed that prolonged low-intensity exercise leads to faster adaptation to an HF meal than inactivity. A previous study reported that PDK activity was modulated 4 h after initiation of exercise. Moreover, LPL activity also began to increase 4 h after exercise (28). These data suggest that the beneficial effects of exercise on fat metabolism in response to an HF diet require at least 4 h. In the present study, however, increased fat utilization could be seen approximately 1–2 h after starting exercise in the intermittent PA trial (see Figure, Supplementary Digital Content 2, https://links.lww.com/MSS/A210), although protein oxidation could not be measured. An acute negative EB during an intermittent PA trial compared with during a continuous PA trial might lead to accelerating fat adaptation. Thus, a synergistic effect of rapidly increased fat consumption and excess of EE by only 5 min of exercise may have contributed to the acceleration of fat adaptation in the intermittent PA trial. Therefore, intermittent PA may lead to efficient utilization of ingested fat by preventing decreased fat oxidation and accelerating increased fat oxidation for adapting to fat consumption.
Multiple bouts of exercise have been reported to have beneficial effects for the prevention and management of obesity (9,19), although the results of these studies were not consistent with those of another study (14). Interestingly, Goto et al. (9) showed that splitting up exercise into short sessions may be beneficial for fat utilization, although this study did not evaluate all EE and PA over an entire day. That study compared RER during the 180 min after either a single 30-min bout of exercise or three 10-min bouts of exercise with a 10-min rest between each. The results showed that RER after intermittent exercise were lower than after continuous exercise. In the present study, RER postdinner in the intermittent PA trial on day 2 was significantly lower than that in the continuous PA trial (P < 0.01). However, EE postdinner in the intermittent PA trial tended to be higher than that in the continuous PA trial. Accelerometry data also showed that average PA in the intermittent PA trial (1.26 METs) was higher than that in the continuous PA trial (1.21 METs), but these differences were not significant (data not shown). We speculate that higher postprandial EE in the intermittent PA trial contributed to the lower postprandial RER relative to the continuous PA trial.
There are several limitations to our study. The first limitation is that EB was significantly different between trials. However, EB was not significantly correlated with RER in this study. Therefore, we thought that EB did not need to be taken into consideration for statistical analysis. However, this may reflect that a negative EB is associated with a higher RER in each participant, but these intraindividual relationships were masked in the larger interindividual distribution with almost no relationship. Therefore, we did a correlation analysis between intraindividual differences in RER and those in EB. There was a moderate correlation between differences in (delta) RER and differences in (delta) EB (r = 0.69). Thus, EB appears to influence RER in each subject. However, as far as we know, these intraindividual relationships between EB and RER cannot be statistically considered for comparing two PA patterns without significant interindividual relationships between EB and RER. In addition, because any consecutive minutes with sedentary behavior were not associated with EB (data not shown), we suggest that prolonged sedentary behavior influenced RER independently of EB. The second limitation is that protein consumption was used to estimate substrate oxidation. It is more accurate to estimate protein oxidation using urine samples. In the present study, however, all subjects consumed meals that contained 15% protein. Moreover, because this study used a crossover design, participants consumed the same diet in both trials. Previous studies using a similar protocol showed that protein oxidation was not different between trials, even if PAL (10) and meal frequency (29) were different. In addition, the duration of the experiment was shorter than previous studies. Previous studies have monitored fat adaptation over a 4-d period (3,10,30). However, participants in the present study consumed HC food that contained 70% CHO (FQ = 0.928, higher than in previous studies) for 2 d before entering the chamber to detect subsequent differences in adaptation speed to an HF diet. The present data showed that average 23-h RER rapidly decreased to about 0.84, approaching the FQ of 0.827, in both trials, although daily RER during HC consumption was not confirmed. Because a previous study also reported that RER decreased substantially within 1 d of consuming an HF diet (10), the experimental period of the present study appears to be appropriate. In addition, we did not sequentially observe any biochemical parameters. Although mean heart rate and variables of heart rate variability, an indicator of autonomic nervous activity, were measured during experiments in the chamber, these were not significantly different between trials (data not shown), because the intensity of exercise in these experiments was low.
Traditionally, prolonged exercise for 10 min or more in each session has been recommended to increase EE. A study (32) and a guideline (11) for adults suggested that a certain number of consecutive minutes (≥10 min) of MVPA contributed to weight control more than accumulated sporadic MVPA, although this evidence was limited to cross-sectional studies. However, the prevalence of obesity has continued to increase. In our study, the intermittent PA trial, in which exercise was performed for only 5 min per bout, was associated with greater fat utilization than the continuous PA trial. Thus, our data strongly suggest that at least five or more consecutive minutes of MVPA may contribute to preventing obesity as well as 10 or more consecutive minutes of MVPA, and may be a more achievable goal for many people, although further studies are needed to clarify the effects of PA lasting less than 5 min (sporadic PA). Partitioning exercise into short bouts of exercise throughout the day may be more practical for sedentary individuals who have low physical fitness. In addition, our study found that lower % V˙O2peak during exercise was strongly associated with lower 23-h RER adjusted for sleeping RER on the preceding day in both the continuous PA trial (r = 0.863, P < 0.01) and the intermittent PA trial (r = 0.653, P = 0.079). Nonlocomotive activity is typically categorized as relatively low- to moderate-intensity and intermittent PA. Thus, these variables may additively enhance the importance of nonlocomotive activity, such as household activity, and may support a new approach for weight management.
In summary, this study provides important information about the potential impact of PA continuity on substrate oxidation over a whole day. The present data indicate that there was greater fat oxidation in the intermittent PA trial than that in the continuous PA trial after exposure to an HF meal. In addition, our data also suggest that multiple bouts of exercise for only 5 min promote fat utilization better than prolonged exercise. This may be explained by the fact that a greater number of consecutive minutes of sedentary behavior (METs ≤1.5) was associated with higher RER (lower fat oxidation). Thus, the present study specifically suggests that the intervals between dynamic body movements should be as short as possible for more efficient utilization of ingested fat. However, because these results were obtained from only a few subjects during a short-term laboratory experiment, additional longitudinal studies and intervention studies are needed to confirm whether intermittent PA rather than continuous PA is effective for preventing obesity.
We thank Hiroko Kogure, a member of the NIHN staff, for her assistance in preparing diets and performing experiments. Heartfelt thanks are due to the subjects who participated in this study.
This work was supported by a grant for Waseda University Global COE “Sports Sciences for Promotion of Active life” (to S. Tanaka), a Grant-in-Aid for Scientific Research (A) (to S. Tanaka), and a Grant-in-Aid for Research Fellows of the Japan Society for the Promotion of Science (no. 23-40139, to C. Usui) .
None of the authors had a personal or financial conflict of interest.
The results of the present study do not constitute endorsement by American College of Sports Medicine.
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