Hourly 4-s Sprints Prevent Impairment of Postprandial Fat Metabolism from Inactivity : Medicine & Science in Sports & Exercise

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Hourly 4-s Sprints Prevent Impairment of Postprandial Fat Metabolism from Inactivity


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Medicine & Science in Sports & Exercise: October 2020 - Volume 52 - Issue 10 - p 2262-2269
doi: 10.1249/MSS.0000000000002367
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Over the past several decades, people living in modern societies have become more and more physically inactive because of technological innovations that have greatly increased “screen time” and reduced the need to move (1–3). As a result, people are spending an increasing amount of time sitting throughout the waking hours, and they are doing so with long periods that are devoid of meaningful physical activity. Physical inactivity impairs cardiometabolic health, and it is estimated to cause 16% of all deaths, largely through cardiovascular disease (2–4).

The identification of effective activity/exercise programs to counteract periods of inactivity from prolonged sitting is ongoing. One alarming statistic indicates that people who meet the recommended level of exercise (i.e., 150 min·wk−1 of moderate intensity [5,6]) are still at elevated risk of cardiovascular disease if they sit for prolonged periods throughout the day (2–4). A large epidemiological study (3), estimated that in order to counteract the effects of prolonged sitting, a person needs to exercise for 60–75 min·d−1 at moderate intensity. Furthermore, recent work by Kim et al. (7) and Akins et al. (8) reported that 60 min of running (e.g., 63%–67% V˙O2max) failed to improve postprandial lipemia after several days of sitting for 13.5 h·d−1, a condition termed “exercise resistance.” Therefore, it seems impractical to explore exercise bouts of longer than 1 h·d−1 to counteract the cardiometabolic risk of prolonged sitting due to adherence problems in the general population. Furthermore, the main reason people give for being inactive is lack of time to move and/or exercise throughout the day (9).

Another approach is to interrupt prolonged sitting with periodic bouts of activity/exercise throughout the day. Walking for 1–3 min every 15–30 min has been found to improve postprandial glucose metabolism on the day of the 1- to 3-min bouts, yet it did not improve postprandial lipemia (10–12). However, a recent study using the same protocol found postprandial lipemia to be improved the next day, agreeing with the idea that it takes 12–24 h for the effects of activity/exercise to be manifested in improved lipid metabolism (13).

Given that people claim a major reason for not being physically active or exercising is lack of time (9), it follows that a mode of exercise, which is as brief as possible, should be investigated. Very brief exercise performed with maximal effort has the advantage of being capable of producing very-high-power outputs and thus activation of a large mass of muscle. When sprints are performed maximally, both type I and type II muscle fibers are activated, and when the duration is very short (i.e., 4 s), there is little fatigue, thus allowing multiple sprints to be performed with 30- to 45-s rest in between sprints.

This study sought to determine if very brief (4-s) cycling performed at maximal intensity in blocks of five repetitions per hour is effective in counteracting the effects of prolonged sitting on postprandial lipid metabolism. In the control trial, subjects sat for 8 h and postprandial metabolism was measured the next day (SIT). This was compared with an exercise trial of repeated (5×) cycling sprints lasting only 4 s each, performed every hour for 8 h (SPRINTS). Sprints were performed on an inertial load ergometer (ILE) (14). Therefore, each hour, only 20 s of sprint exercise was performed and only 160 s of SPRINTS was performed for the entire day.



Eight healthy, untrained to recreationally active men (n = 4) and women (n = 4) were recruited to participate in this study. Subject characteristics can be seen in Table 1. Subjects were given written and verbal description of all the procedures and measurements used in this study, and written informed consent was obtained. The institutional review board of the University of Texas at Austin approved this study (ClinicalTrials.gov Identifier: NCT03856606).

TABLE 1 - Subject characteristics (n = 8; 4 men and 4 women).
Characteristic Mean ± SEM Male (n = 4) Female (n = 4)
Age (yr) 24.0 ± 1.8 26.0 ± 2.4 22.0 ± 2.1
Height (cm) 169.0 ± 4.6 176.8 ± 6.1 161.1 ± 2.6
Body mass (kg) 70.9 ± 6.0 81.3 ± 8.0 60.4 ± 3.1
BMI (kg·m−2) 24.5 ± 0.8 25.8 ± 1.0 23.2 ± 0.6
RMR (kcal·d−1) 1727 ± 210 20,367 ± 329 1418 ± 95

Research protocol

All subjects completed two trials in a randomized crossover design, with each trial occurring over 4 d with a minimum of 7 d between trials (Fig. 1). The first 2 d of each trial served as a control period allowing for familiarization and the control of physical activity and calorie consumption before the intervention. After each control period, subjects then performed one of the interventions on day 3. The interventions consisted of either 8 h of prolonged sitting (SIT) or 8 h of sitting interrupted every hour by five sprints lasting 4 s each using the ILE (SPRINTS). The sitting time of the trials was not different. The sprint on the ILE involves accelerating a flywheel with a known inertia from zero velocity to the highest RPM possible in approximately 4 s. Power per revolution of the cycle is calculated as the product of flywheel inertia and gearing, acceleration, and velocity (14).

Representation of experimental design. During SIT trial, subjects remained seated for 8 h, only getting up for the restroom and to prepare food. For the SPRINTS trial, subjects spent the same time seated, only getting up for the restroom and food. However, at the end of each hour, they performed five maximal sprints lasting 4 s in duration using the ILE (SPRINTS).

Controlled activity phase

During the 2-d controlled activity phase, subjects were asked to arrive at the laboratory at approximately 0900 h. Subjects were instructed to take between 5000 and 7500 steps per day, which is approximately equal to a nonsedentary, low physical activity step count (15). Subjects were then equipped with an activPAL activity monitor (activPAL, PAL Technologies, Glasgow, Scotland) to be secured onto a thigh for the assessment of body position and movement. Steps taken were not visible to the subjects, whereas the device was being worn; therefore, subjects were also asked to download a pedometer application on their mobile phones to provide visual feedback for daily step count. Subjects were also asked to refrain from exercise and to record all food intake and to minimize physical activity. They were then asked to repeat this diet and activity for the remaining trial.

Intervention phase

During the SIT trial, subjects remained seated for 8 h with the ability to get up for food and restroom usage. Estimates of the caloric intake were determined from preliminary tests of resting metabolic rate (RMR) and the addition of approximately 20% for the energy needed for the respective daily activity and maintenance of a stable body weight. Adherence to these guidelines was checked against the pedometer and activPAL, and food journals were analyzed to ensure participants duplicated their diet for the duration of the two trials.

During the SPRINTS trial, subjects were asked to report to the laboratory at 0900 h to begin the 8-h prolonged sit, interrupted by ILE sprints. During the prolonged sit and during the final 4 min of each hour, subjects performed five 4-s sprints separated by 45 s of rest, equating to 20 s of exercise per hour and 160 s of total time exercising on the SPRINT day. Given that each set of five SPRINTS required approximately 5 min to complete when resting for 45 s between SPRINTS and the fact that eight sets were completed, the total daily time required was 40 min. During the rest periods between sprints, subjects were seated. RPE was taken after five sprints using the standard Borg Scale (6–20). Food was provided at two times (lunch and dinner) over the duration of the trial, and the caloric content of these meals was such that energy balance was maintained.

High-fat/glucose tolerance test phase

The morning after each intervention day, subjects were asked to arrive to the laboratory to begin the high-fat/glucose tolerance test (HFGTT). Subjects remained seated for the 6-h duration of the test except for restroom usage. After a 5-min acclimatization period, a fasted blood sample was obtained via antecubital venous puncture into a 4-mL K2 EDTA vacutainer (BD Vacutainer; Fischer Scientific, Hampton, NH), and plasma was subsequently aliquoted into a microcentrifuge tube, labeled, and stored at −80°C for future batch analysis. This process was repeated for blood samples obtained 2, 4, and 6 h postprandially.

Subjects were asked to ingest a high-fat and carbohydrate shake, after which blood was sampled as described previously. At approximately 0, 2, 4, and 6 h postprandially, expired gasses were obtained from each subject, as they were asked to breathe into a meteorological balloon for a total of 15 min to monitor fat oxidation and metabolic rate. Subject body mass was taken by a digital scale (Ohaus, CW-11, Parsippany, NJ) and recorded to the nearest 0.5 kg, and height was measured using a standard stadiometer.

Blood sampling and analysis

After the collection into K2 EDTA tubes, blood was subsequently centrifuged at 3000 rpm at 4°C for 10 min. Plasma was then aliquoted and frozen at −80°C and later analyzed for triglyceride, glucose, and insulin concentrations. Triglyceride was measured using a spectrophotometric method from commercially available kits (Pointe Scientific, Inc., Canton, MI). Glucose was measured using a similar protocol from commercially available kits (Pointe Scientific). Plasma insulin was measured using a microplate reader and commercially available kits (LDN Immunoassays and Services, Nordhorn, Germany). Coefficients of variation for triglyceride, glucose, and insulin were 3.0%, 3.5%, and 4.9% respectively.

Diet control

The caloric content was roughly ~20% higher than each subject’s RMR, as measured during preliminary testing. Additional energy expenditure from exercise in the SPRINTS was estimated via indirect calorimetry. The postexercise meals were approximately 60% carbohydrate, 20% fat, and 20% protein. For the HFGTT, subjects were provided with a high-fat shake consisting of parts melted ice cream and heavy whipping cream, creating a macronutrient and caloric profile of 1.34 g·kg−1 fat, 0.92 g·kg−1 carbohydrate, 0.19 g·kg−1 protein, and 16.5 kcal·kg−1.

RMR and indirect calorimetry

All metabolic gas measurements were made using meteorological balloons. To determine RMR, subjects rested in a seated position for 15 min, followed by a 15-min period of gas collection. Subjects breathed through a one-way valve (Hans Rudolph, Kansas City, MO) directly attached to a meteorological balloon. A sample was then analyzed for concentrations of O2, CO2, and N2 by mass spectrometry (PerkinElmer MGA 1100, St. Louis, MI). Gas volume was then measured via spirometry (Vacumed, Ventura, CA). During each HFGTT, gas samples were analyzed following the procedures detailed previously at 0, 2, 4, and 6 h after shake ingestion for calculation of fat and carbohydrate oxidation rate, using the tables of Frayn (16).

Statistical analysis

Incremental (AUCI) and total area under the curve (AUCT) for concentrations of plasma triglyceride, insulin, and glucose were calculated. Once calculated, Student t-test with Bonferroni correction was used to test for differences. Plasma insulin, glucose, and triglyceride concentrations were analyzed using repeated-measures two-way ANOVA (trial–time). Likewise, daily step count and hourly distribution of posture were analyzed using repeated-measures two-way ANOVAs. Lastly, fasting and postprandial RER, as well as fat and carbohydrate oxidation, were analyzed using a repeated-measure two-way ANOVA. When interactions were significant, Tukey honest significant difference post hoc tests were run. Effect sizes were calculated as mean differences divided by the pooled SD (Cohen d); quantitative criteria for effect sizes used to explain practical significance of the findings were taken from Cohen (17). With eight participants, the study had 68% power to detect a difference of 1.0 SD (i.e., Cohen d = 1.0) between conditions.

All data were analyzed using GraphPad Prism 7 (GraphPad Software Inc., La Jolla, CA). All data are expressed as mean ± SEM; unless otherwise noted, the level for statistical significance was set at P < 0.05.


Daily steps and body posture

No significant differences were found comparing trials in daily steps, for C1, C2, or the intervention day (Table 2). The average number of steps taken on the intervention day was low (i.e., 3577 ± 953 and 2540 ± 969 for SPRINTS and SIT), respectively (P = 0.34). There were no significant differences between the groups for time spent sitting (P = 0.81) or time spent standing (P = 0.86). Furthermore, the caloric intake on the intervention day was similar for SPRINTS and SIT (2065 ± 235 and 2068 ± 232 kcal), respectively (P = 0.66).

TABLE 2 - Daily step count and hours per day spent sitting/supine and standing in SIT or SPRINT.
Trial Day of Trial
Control Day 1 Control Day 2 Intervention Day
Daily Steps (steps per day)
 SIT 6889 ± 1249 6626 ± 1111 2540 ± 969 a
 SPRINTS 7249 ± 1264 6537 ± 1198 3577 ± 954 a
Distribution of posture (h·d−1)
  SIT 12.6 ± 0.7 12.7 ± 0.8 15.2 ± 0.5 a
  SPRINT 12.7 ± 1.1 12.7 ± 0.8 14.9 ± 0.4
  SIT 2.7 ± 0.5 2.7 ± 0.6 0.8 ± 0.2 a
  SPRINTS 2.8 ± 0.8 3.2 ± 0.5 1.0 ± 0.2 a
The control days represent normal physical activity, and on the intervention day, sitting time was increased and steps per day were reduced.
aSignificantly different from control days by design.

Response to inertial load ergometry

During the SPRINTS trial, the average power generated by the 4-s sprints was 870 ± 139 W (male, 1107 ± 447 W; female, 632 ± 90 W) and RPE remained low (10.0 ± 0.7; very to fairly light).

Plasma triglyceride glucose and insulin responses

Postprandial plasma triglyceride responses are shown in Figure 2. There was a 31% reduction in incremental AUCI during the 6-h period in SPRINTS as compared with the SIT trial (408 ± 119 vs 593 ± 88 mg·dL−1; P = 0.009; Fig. 2; Table 3) and a medium effect size (d = 0.632). However, total AUCT for plasma triglyceride did not reach significance between trials (SPRINTS: 858 ± 154 mg·dL−1 vs SIT: 1003 ± 136 mg·dL−1; P = 0.11; Table 3). There were no significant differences between trials in the postprandial plasma glucose total AUCT (SPRINTS: 678 ± 49 mg·dL−1 vs SIT: 707 ± 32 mg·dL−1; P = 0.66) or incremental AUCI (SPRINTS: 150 ± 36 mg·dL−1 vs SIT: 159 ± 28 mg·dL−1; P = 0.88; Fig. 2; Table 3). Furthermore, there were no differences in insulin responses between trials in total AUC T (SPRINTS: 157 ± 16 μIU·mL−1 vs SIT: 159 ± 12 μIU·mL−1; P = 0.92) or incremental AUCI (SPRINTS: 85 ± 10 μIU·mL−1 vs SIT: 73 ± 11 μIU·mL−1; P = 0.46; Fig. 2; Table 3).

Postprandial plasma responses during the HFGTT. Plasma triglyceride concentration (A), plasma glucose concentration (B), and plasma insulin concentration (C).
TABLE 3 - Mean ± SE values for postprandial AUC responses over the 6-h postprandial period.
Variable Trial
Incremental AUCI
 Triglyceride (mg·dL−1 × 6 h) 593 ± 88 408 ± 119 a
 Glucose (mg·dL−1 × 6 h) 159 ± 81 150 ± 103
 Insulin (μIU·mL−1 × 6 h) 72.7 ± 31 84.9 ± 28
Total AUCT
 Triglyceride (mg·dL−1 × 6 h) 1003 ± 136 858 ± 154
 Glucose (mg·dL−1 × 6 h) 707 ± 91 678 ± 140
 Insulin (μIU·mL−1 × 6 h) 159 ± 33 157 ± 46
aSPRINTS significantly lower than SIT (P < 0.009).

Postprandial substrate oxidation

RER demonstrated both a significant trial effect (P = 0.001) and main effect of time (P = 0.02) but no interaction between the two, and exhibited a large effect size (d = 1.16 ± 0.04; Table 4). The average grams of fat oxidized over the 6-h period of the HFGTT was 43% higher (P < 0.001) during SPRINTS versus SIT (SPRINTS: 48.9 ± 17.7 g vs SIT: 34.1 ± 18.2 g; Table 4). Conversely, carbohydrate oxidation was significantly lower (P = 0.002) in SPRINTS versus SIT (SPRINTS: 13.0 ± 10.2 g vs SIT: 44.2 ± 22.3 g; Table 4).

TABLE 4 - Postprandial substrate oxidation in SIT vs SPRINT over the 6-h period.
Hours Postprandial Trial
RER (V˙CO2·V˙O2 −1)
 Hour 0 0.841 ± 0.034 0.752 ± 0.014*
 Hour 2 0.839 ± 0.033 0.750 ± 0.018*
 Hour 4 0.823 ± 0.044 0.725 ± 0.017*
 Hour 6 0.761 ± 0.022 0.709 ± 0.010
Substrate oxidation (%)
  Hour 0 52.8 ± 11.1 83.1 ± 4.7**
  Hour 2 53.5 ± 11.4 84.2 ± 6.0**
  Hour 4 60.3 ± 14.3 90.9 ± 5.2**
  Hour 6 79.1 ± 6.94 95.8 ± 3.0
  Hour 0 47.3 ± 11.1 16.9 ± 4.7*
  Hour 2 46.5 ± 11.4 15.9 ± 6.0*
  Hour 4 39.8 ± 14.3 9.1 ± 5.2*
  Hour 6 20.9 ± 6.94 4.2 ± 3.0
Substrate oxidation (g·min−1)
  Hour 0 0.066 ± 0.016 0.122 ± 0.019**
  Hour 2 0.075 ± 0.018 0.119 ± 0.016**
  Hour 4 0.102 ± 0.028 0.148 ± 0.022**
  Hour 6 0.136 ± 0.023 0.155 ± 0.019
  Hour 0 0.145 ± 0.051 0.038 ± 0.018*
  Hour 2 0.182 ± 0.055 0.055 ± 0.021*
  Hour 4 0.107 ± 0.027 0.027 ± 0.017*
  Hour 6 0.057 ± 0.018 0.011 ± 0.008
 Energy expenditure (kcal·min−1)
  Hour 0 1.19 ± 0.136 1.31 ± 0.168
  Hour 2 1.47 ± 0.191 1.35 ± 0.184
  Hour 4 1.40 ± 0.165 1.42 ± 0.179
  Hour 6 1.49 ± 0.131 1.32 ± 0.127
*SPRINTS different from SIT (P < 0.05).
**SPRINTS different from SIT (P < 0.01).


This study reports the effects of interrupting prolonged sitting with brief (4-s) maximal intensity cycling sprints on postprandial fat and carbohydrate metabolism measured the following day. This investigation’s major finding was that hourly maximal intensity 4-s sprints (performed five times per hour) on an ILE (SPRINTS) while sitting for 8-h reduced the next day’s postprandial plasma triglyceride incremental AUC by 31% (P = 0.009) compared with sitting for 8 continuous hours (SIT). Furthermore, SPRINTS significantly (P = 0.001) elevated fat oxidation by an average of 43% over the duration of HFGTT corresponding to a large effect size increase compared with SIT. This investigation did not use techniques that might determine if the two phenomena are causally related, yet it is possible that the postprandial lowering of plasma triglyceride concentration was due to increased tissue uptake and oxidation of the ingested plasma triglycerides.

When subjects who are physically active and taking approximately >8000 steps per day add a 1-h bout of running or a session of high-intensity interval training to their regime, they show an improvement in their next day’s postprandial plasma triglyceride response as well as increased fat oxidation (18–20). This can be considered the healthy “exercise response.” However, in people who are largely sedentary (i.e., 2000–4000 steps per day) (15), a 1-h bout of running does not improve the next day’s postprandial plasma triglyceride response or fat oxidation (7,8). This has been termed exercise resistance, as it seems that some aspect of the prolonged inactivity is preventing the acute bout of exercise from causing healthy adaptations in fat metabolism (7,8). In the present study, on the intervention days, the subjects in both trials were taking <4000 steps per day and thus sedentary, outside of the 160 s of exercise in SPRINTS. It is likely that the hourly sprints prevented exercise resistance from occurring and that is the reason for the enhanced fat metabolism in SPRINTS compared with SIT. The time course with which exercise resistance occurs from inactivity is unknown, but it seems that the present 20 s of hourly intermittent sprints, performed maximally in five bouts of 4 s each, was effective in counteracting it.

The hourly set of five sprints lasting 4 s each, with 45 s of rest, describes an exercise that is predominantly anaerobic, relying heavily on stores of ATP and PC for energy during exercise and oxidative metabolism for resynthesis of these stores during recovery (21). Given that the sprints elicited maximal power and involved maximal acceleration to an RPM of 120–160, the recruitment of both type I and type II muscle fibers should have reached maximal levels. It is likely that some aspect of high motor unit recruitment producing very high anaerobic power was responsible for the effectiveness of SPRINTS for enhancing fat metabolism (7,8). This is surprising in that fat oxidation is aerobic and it might be thought that aerobic exercise would be its specific stimulator. What seems to be truly different about the SPRINTS exercise is the high average maximal power (870 ± 139 W) and assumed type II fiber recruitment. Furthermore, perceived exertion was “very to fairly light” (10.0 ± 0.7) because of the only 4-s duration of each sprint and relatively long recovery period (45 s). Overall, the maximal intensity sprints of 4-s duration are a relatively nonfatiguing method of activating a large quantity of muscle, and it seems that fat oxidation is improved on the following day.

It is not clear why the present investigation observed an amelioration of postprandial lipemia when others, who also broke up prolonged sitting, did not (10,11). However, improvements in glucose and insulin metabolism have been typically seen on the day of the intervention and during the postprandial test, yet the improvement in postprandial lipemia has been observed the following day (12), which agrees with our present observations. Although this study did not directly investigate possible mechanisms, one hypothesis stems from the dysregulation of lipoprotein lipase (LPL), the rate-limiting enzyme for chylomicron and VLDL tissue uptake (22,23). Indeed, prolonged inactivity has been shown to decrease LPL activity up to 90% and influence the amount of heparin releasable LPL (24,25). The primary mechanism behind an attenuation of postprandial lipemia is hypothesized to be an upregulation of LPL after exercise. LPL activity typically peaks ≥8 h after exercise (26–28). Thus, it is feasible that the periodic interruption of sitting and a large amount of muscle fiber activation with SPRINTS prevented a decrease in LPL activity during the 8-h period of sitting used by this investigation. It is noteworthy that this might be achieved with only 20 s·h−1 of exercise, albeit at maximal power.

Previous research has shown that aerobic exercise at 30%–70% of V˙O2max with a minimum of ~360–950 kcal of energy expenditure is needed to reduce postprandial lipemia the next day (18,19,29–32). In the present study, participants expended much less energy with an amount that is below the health guidelines recommended for energy expenditure (33). However, a reduction in postprandial lipemia from small amounts of energy expenditure is not unprecedented, as resistance exercise as well as sprint interval cycling, without caloric replacement, has been shown to cause postprandial lipemia reduction (34–36). The low energy expenditure and low time commitment could be seen as a benefit to SPRINTS type exercise performed for only 4 s, and five times per hour, because the main reason people give for not exercising is lack of time (9). However, over the eight sets of hourly sprints of the present design, the total time involvement amounted to 40 min, which could be reduced by shortening the recovery period between sprints or by reducing the number of sets. Using similar test meals and design, we have shown significant reductions in integrated triglyceride AUCI with 1-h bouts of treadmill running, or cycling at intensities ranging from 50% to 90% V˙O2max (19,20). Kim et al. (19) found a 27% reduction in the AUCI after running at 65% V˙O2max for 1 h. Similar reductions in triglyceride AUCI (i.e., 31%) were seen in the present study with a total exercise time of only 160 s (2.7 min). The most salient aspect of the exercise bouts were that each 4-s sprint was performed at true maximal power output, which in these subjects averaged 870 W. This maximal power is roughly three to four times the power needed to elicit maximal oxygen uptake. Indeed, the 4-s sprints, by eliciting maximal power output, represent the highest possible rate of muscle fiber recruitment, especially of type II muscle fibers but without fatigue. This is unlike cycling sprints that last for 20–30-s durations and elicit an extreme accumulation of lactic acid and intense fatigue (37).

The negative health consequences of prolonged sitting and inactivity are often lumped together because most of the periods in which people are inactive; they spend sitting and sometimes standing (38). As a result, it could be thought that the act of sitting per se is unhealthy compared with other forms of inactivity. In the present study, the sitting time was the same in SIT and SPRINTS, given that so little time was spent exercising in SPRINTS and the recovery time was spent seated. Our observation that the next day’s postprandial hyperlipemia after 8 h of sitting could be successfully overcome by physical activity that amounted to only 160 s indicates that sitting may not be inherently negative beyond its inactivity, at least in terms of postprandial lipemia.

Although the present study adds to the body of literature regarding inactivity and postprandial responses, it is not without limitations. We did not control for phase of menstrual cycle in the female participants, as it has been previously shown that postprandial responses vary according to phase of menstrual cycle (39). This may have influenced the study findings. Furthermore, this study made use of a small number of subjects reducing the statistical power and increasing the likelihood of type II errors, as such potential differences between trials may not be fully represented. This also extends to the ability to detect sex differences within the study design. A previous quantitative review has suggested that sex may play a role in acute exercise-induced reductions of postprandial lipemia (18). In that review, sex was found to be a moderator with the effect size of the postexercise reductions being larger in females when compared with males (18). Lastly, this study investigated a young, lean, and apparently healthy population. Even within the SIT trial, subjects displayed favorable responses. It is unclear if SPRINT exercise might improve metabolism in those with a less than favorable metabolic profile. It might also depend on their level of background physical activity as reflected in their step count per day (7). Furthermore, mechanistic theorizing is beyond the scope of this study, as it was not designed to determine a mechanism as to how SPRINTS affect postprandial responses, rather if such a low volume of exercise could provide an impact.

In conclusion, these data indicate that hourly, maximal effort, 4-s sprints on an ILE, which interrupts prolonged sitting, lowers postprandial incremental plasma triglyceride concentration by 31% (P = 0.009) and simultaneously increases fat oxidation by an average of 43% (P < 0.001) during the next day. This is particularly significant when considering the small amount of energy expended, the low RPE reported by the subjects, and the minimal amount of time spent exercising (160 s·d−1). The brief nature and nonfatiguing aspect of the exercise might lead to better adherence when compared with current exercise recommendations (6). The clinical significance of these findings is centered on reductions in postprandial triglyceride incremental AUC and increased fat oxidation, which likely lead to improved cardiometabolic health.

We thank the subjects for their participation. As a matter of financial interest disclosure, E. F. Coyle owns equity in Sports Texas Nutrition Training and Fitness, Inc., a company that sells the inertial load ergometer used in this study. The results of this study do not constitute endorsement by the American College of Sports Medicine.

A. S. W. and E. F. C. conceived the research and designed the experiment; A. S. W., H. M. B., and E. V. recruited subjects and performed experiments; A. S. W. and E. F. C. interpreted results of experiments; A. S. W. prepared figures, performed statistical analyses, and drafted the manuscript; A. S. W., H. M. B., E. V., and E. F. C. edited and revised the manuscript; A. S. W., H. M. B., E. V., and E. F. C. approved the final version of the manuscript.

The results are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.


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