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| ORIGINAL ARTICLE |
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| Year : 2021 | Volume
: 64
| Issue : 5 | Page : 244-250 |
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Thirty minutes of moderate-intensity downhill or level running has no effect on postprandial lipemia: A randomized controlled trial
Tsung-Jen Yang1, Chih-Hui Chiu2, Ching-Lin Wu3, Yu-Sheng Liao4, Chen-Kang Chang5
1 Department of Physical Education, National Taiwan Normal University, Taipei, Taiwan
2 Graduate Program in Department of Exercise Health Science, National Taiwan University of Sport, Taichung, Taiwan
3 Graduate Institute of Sports and Health Management, National Chung Hsing University, Taichung, Taiwan
4 Department of Emergency, Everan Hospital, Taichung, Taiwan
5 Department of Sport Performance, National Taiwan University of Sport, Taichung, Taiwan
| Date of Submission | 04-Jul-2021 |
| Date of Decision | 17-Sep-2021 |
| Date of Acceptance | 21-Sep-2021 |
| Date of Web Publication | 27-Oct-2021 |
Correspondence Address:
Dr. Chen-Kang Chang
No. 16, Sec. 1, Shuang-Shih Rd., Taichung 404
Taiwan
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/cjp.cjp_61_21
Elevated postprandial triglyceride (TG) concentrations are linked to a relatively high risk of cardiovascular disease. Eccentric endurance exercise, such as downhill walking and running, can provide metabolic benefits similar to concentric exercise. However, whether eccentric exercise affects postprandial lipemia remains unknown. Nine healthy young men performed level running (trial) or downhill running (DR trial, −15% slope) at 60% VO2max or rest (CON trial) for 30 min in a randomized crossover design. The participants were fed a high-fat meal the next day. Blood and expired gas samples were collected before and 0.5, 1, 2, 3, 4, 5, and 6 h after the meal. Muscle soreness was measured using a visual analog scale. The DR trial induced mild muscle damage. During the 6-h postprandial period, serum TG concentrations and area under the curve (AUC) were similar across the three trials. The DR trial had a significantly higher AUC of nonesterified fatty acid concentrations and a significantly lower AUC of glucose concentrations than the CON trial. The results suggested that neither moderate-intensity DR nor running a level surface had a significant effect on lipemia after a high-fat meal. However, DR improved the postprandial glycemic response.
Keywords: Cardiovascular disease, eccentric exercise, fat oxidation, high-fat meal, nonesterified fatty acids, triglyceride
How to cite this article:
Yang TJ, Chiu CH, Wu CL, Liao YS, Chang CK. Thirty minutes of moderate-intensity downhill or level running has no effect on postprandial lipemia: A randomized controlled trial. Chin J Physiol 2021;64:244-50 |
How to cite this URL:
Yang TJ, Chiu CH, Wu CL, Liao YS, Chang CK. Thirty minutes of moderate-intensity downhill or level running has no effect on postprandial lipemia: A randomized controlled trial. Chin J Physiol [serial online] 2021 [cited 2023 Mar 24];64:244-50. Available from: https://www.cjphysiology.org/text.asp?2021/64/5/244/329362 |
| Introduction | |  |
Elevated triglyceride (TG) concentrations are linked to a higher risk of cardiovascular disease.[1] A prospective cohort study revealed that the hazard ratios for ischemic stroke per 1 mM increase in nonfasting TG levels were 1.14 for men and 1.33 for women.[2] People spend most of the waking hours in hyperlipidemia because plasma TG concentrations can remain elevated for more than 6 h after a meal.[3] Therefore, lowering postprandial TG concentrations can be an effective intervention strategy to prevent cardiovascular disease. Studies have reported that exercise can reduce postprandial lipemia effectively. For instance, individuals who performed a single bout of endurance,[4],[5] resistance,[6] or high-intensity interval[7] exercise 2 to 16 h before a high-fat meal had lower postprandial TG concentrations compared with controls who did not exercise. The mechanisms responsible for this effect include increased energy expenditure,[8] increased fatty acid oxidation, increased removal of very-low-density lipoprotein (VLDL)-TG from plasma by elevated lipoprotein lipase concentrations,[9] and reduced hepatic VLDL production.[10]
Eccentric endurance exercise, such as downhill walking and running, can provide metabolic benefits similar to those of concentric exercise. Regular downhill walking has been shown to result in similar improvement of blood lipid profile and glucose tolerance as uphill walking[11],[12] despite lower energy expenditure.[11] Moreover, weeks of downhill walking can increase resting energy expenditure, fat oxidation, and leg strength and reduce insulin resistance in healthy young adults.[13],[14] Thus, eccentric endurance exercise is suggested as an alternative for those who are unable to participate in strenuous exercise. Furthermore, the increased popularity of trail and marathon running has caused more people to perform considerable amounts of eccentric exercise on downhill courses.[15]
Acute eccentric exercise can, however, damage muscles, particularly type 2 muscle fibers,[16] which leads to impaired glucose metabolism. Following eccentric exercise, glucose uptake and glycogen resynthesis were reduced in the damaged skeletal muscle compared to the muscles that performed concentric exercise.[17],[18] The decrease in carbohydrate metabolism appeared to be the result of impaired insulin stimulation of insulin receptor substrate-1, phosphatidylinositol 3-kinase, and protein kinase B/Akt activity, potentially due to the elevated tumor necrosis factor α production after muscle damage.[19] By contrast, little is known about the effect of eccentric exercise on fat metabolism. A single bout of eccentric exercise was shown to improve fasting blood lipid profile.[20] Whether eccentric exercise affects postprandial lipemia is not clear.
The aim of this study was to investigate the effect of eccentric exercise, in the form of downhill running (DR) at 60%  , on plasma TG concentrations and substrate metabolism after a high-fat meal. The results were compared with those of participants who ran on a level surface with similar relative intensity and energy expenditure and controls who did not exercise.
| Materials and Methods | | |
Participants
Nine healthy young men (mean ± standard deviation (SD); age 24.0 ± 5.5 years, height 1.75 ± 0.06 m, body mass 71.9 ± 9.7 kg, body mass index 23.5 ± 3.0 kg/m2, and 45.9 ± 6.6 mL/min/kg) volunteered for this study. None of the participants had engaged in regular exercise, received any medication in the past 6 months, or had a history of cardiovascular disease, hypertension, hyperlipidemia, diabetes, atherosclerosis, or osteoporosis. The participants were free of any musculoskeletal injury during the study. This study was conducted according to the Declaration of Helsinki. Each participant signed an informed consent after the procedures and risks involved were explained by the research personnel. The study protocol was approved by the Research Ethics Committee of National Taiwan Normal University (201903HM011) and registered in ClinicalTrials.gov under the following identification: NCT04688073 (29/12/2020). All methods were performed in accordance with the relevant guidelines and regulations.
Experimental design
All participants underwent three experimental trials, namely, DR, level running (LR), and the control (CON) in a crossover design (four participants followed the order of CON → LR → DR, three followed LR → DR → CON, and two followed DR → CON → LR). The order of the trials was assigned to each participant by one of the authors (T. J. Y.) according to a random number generated by a computer program (Excel 2010, Microsoft, Redmond, WA, USA). The LR and CON trials were separated from the next trial by at least 7 days. The DR trial was separated from the next trial by at least 30 days to allow full recovery from muscle damage. The day after the exercise or control intervention, the participants ingested a high-fat meal and had their blood lipid profiles monitored for 6 h. All participants were prohibited from engaging in strenuous physical activities during the study period, except for the downhill and LR in the DR and LR trials, respectively. The study was performed at the National Taiwan University of Sport from May to August 2019. The participants were also asked to avoid medication, alcohol, massage, icing, hot treatment, or smoking during the study period.
The independent variable was intervention, and the primary outcome variables were serum concentrations of TG, glycerol, nonesterified fatty acids (NEFAs), and glucose during the 6-h postprandial period. Other dependent variables include the area under the curve (AUC) of the serum biochemical parameters, fat and glucose oxidation rates during the 6-h postprandial period, and muscle soreness.
Preliminary measurements
All participants underwent two preliminary measurements, the first one to measure and the second to determine the speed for 60% for the DR trial. The preliminary measurements were performed at least 7 days before the first experimental trial.
The test, the participants ran on a treadmill (Medtrack ST65, Quinton, Seattle, WA, USA) at 0% slope. The participants warmed up at a speed of 6 km/h for 5 min. The speed was then increased by 1.2 km/h in each 3-min stage until voluntary exhaustion. The breath-by-breath gas samples were analyzed using a gas analyzer (Vmax 29C, Sensormedics, Yorba Linda, CA, USA). VO2 at each stage and were recorded. The speed at 60% in the LR trial was predicted through linear regression [Table 1]. | Table 1: Running speed, respiratory quotient, and energy expenditure during the exercise intervention in the 3 trials
Click here to view |
On the day after the test, the participants ran on the same treadmill at a −15% slope. The breath-by-breath gas samples were analyzed. The participants warmed up at the speed of 6 km/h for 5 min. Then the speed was increased 0.5–1 km/h every 3 min until 60% was reached. The speed that elicited 60% was recorded and later used in the DR trial [Table 1].
Experimental protocol
Each trial lasted 2 days. The participants were asked to record their diet during the 3-day period before the first trial. They were asked to consume the same food during the 3 days before the second and third trials.
Day 1
The experimental procedure is shown in [Figure 1]. The participants were fed the same breakfast and lunch on day 1 in each trial. The participants arrived at the laboratory at 18:00 on day 1 and ran on the treadmill at 60% (DR or LR trials) or rested (CON trial) for 30 min. Their expired air was collected during the entire 30-min period by a gas analyzer. The average VO2 and VCO2 in the 30-min period were used to estimate the respiratory quotient and energy expenditure. Subsequently, they were fed a standardized dinner within 20 min. The participants were asked to refrain from eating any food and returned home after the standardized dinner. | Figure 1: Experimental protocol. The level running and downhill running (DR) trials exercise for 30 min, while the control trial (CON) rested for 30 min. Preliminary measurements: to determine VO2max and running speed at the DR trial. VAS: Visual analog scale for muscle soreness, 🠱 : Blood sample collection.
Click here to view |
Day 2
The participants returned to the laboratory at 07:30 am on day 2 after an overnight fast. After baseline blood and gas samples were collected (0 h), the participants were fed a high-fat meal within 20 min. Blood and expired gas samples were collected at 0.5, 1, 2, 3, 4, 5, and 6 h after the high-fat meal.
Test meal
Standardized dinner
The standardized dinner was purchased from a local convenience store. The standardized dinner contained chicken, vegetables, and rice. The total energy was 692 kcal, with 50% of energy from carbohydrates (86.5 g), 32% from fat (24.6 g), to 18% from protein (31.1 g).
High-fat meal
The high-fat meal included cereal, white bread, whipped cream, cheese, and butter. The high-fat meal provided fat 1.2 g/kg (65% energy), carbohydrate 1.1 g/kg (27% energy), protein 0.33 g/kg (8% energy), and 16.5 kcal/kg.[7] All the foods were purchased from the same local convenience store.
Blood sample collection and analysis
A 10-mL blood sample was collected from a forearm vein into nonheparinized tubes (Eppendorf 5810, Hamburg, Germany) before and immediately after exercise or rest on day 1. On day 2, postprandial blood samples were collected from forearm veins into nonheparinized tubes using an indwelling venous needle (Venflon 20G, Ohmeda, Sweden) and a three-way stopcock (Connecta., Helsingborg, Sweden). A 10-mL blood sample was collected before (0 h) and 0.5, 1, 2, 3, 4, 5, and 6 h after the high-fat meal. The blood samples were centrifuged at 500 g for 20 min at 4°C. Serum samples were collected and stored at − 80°C for further analysis. The serum samples were analyzed using an automated biochemical analyzer (Hitachi 7020, Tokyo, Japan) with commercial kits for the concentrations of TG (Wako, Osaka, Japan), glycerol (Randox., Antrim, UK), NEFA (NEFA; Wako, Neuss, Germany), glucose (Shino, Tokyo, Japan), creatine kinase (Kanto, Tokyo, Japan), and high-density lipoprotein (HDL)-cholesterol (Kyowa, Osaka, Japan). The intra-assay coefficients of variation of the blood sample measurement were TG: 4.9%; glycerol: 6.42%; NEFA: 4.51%; glucose: 6.9%; and HDL-C: 4.9%.
Expired gas analysis
Expired gas samples during the postprandial period were analyzed breath-by-breath for 5 min after each blood collection. Carbohydrate and fat oxidation rates were estimated using the following equations:[21]
Carbohydrate oxidation rate (g/min) =4.585 × VCO2 (L/min) −3.226 × VO2 (L/min)
Fat oxidation rate (g/min) =1.695 × VO2 (L/min) −1.701 × VCO2 (L/min)
Muscle soreness
Perceived soreness of the knee extensors was estimated using a visual analog scale before the 30-min exercise or rest on day 1 and before being fed the high-fat meal on day 2. The visual analog scale had a continuous 100 mm line, with 0 mm on the left representing “not sore” and 100-mm on the right representing “very, very sore.”[22]
Statistical analyses
All data are presented as mean ± SD. The AUCs of blood parameters and substrate oxidation rates were calculated using the trapezoidal rule.[23] The normality of each variable was analyzed using the Shapiro–Wilk test. Differences in serum biochemical parameters before and after exercise in the same trial were analyzed using a paired-sample t-test if normally distributed or the Wilcoxon signed-rank test if not normally distributed. Differences among the three trials at the same time point during the 6-h postprandial period were analyzed with the Friedman test, a nonparametric equivalent to one-way repeated measures analysis of variance (ANOVA). Differences in the AUC among the three trials were analyzed with one-way repeated measures ANOVA if the data were normally distributed or the Friedman test if the data were not normally distributed. If a significant main effect was found, the Bonferroni post hoc test was performed to compare the three trials if the data were normally distributed or the Wilcoxon signed-rank test with Bonferroni adjustment of P values if the data were not normally distributed. The data were analyzed using SPSS for Windows, version 23.0 (IBM, Armonk, NY, USA). The significance level was set at α = 0.05.
| Results | | |
Running speed, respiratory quotient, and energy expenditure data during the intervention in the three trials are presented in [Table 1]. The subjects ran significantly faster in the DR trial than in the LR trial. The respiratory quotient and energy expenditure were significantly higher in the DR and LR trial than in the CON trial. No significant differences were observed in respiratory quotient and energy expenditure between the DR and LR trials. [Table 2] shows the serum concentrations of biochemical parameters before and after 30 min of rest or exercise in the three trials. The two running interventions resulted in significant increases in NEFA, glycerol, and creatine kinase concentrations. The magnitude of increase in creatine kinase concentrations in the DR trial (25.1% ± 10.3%) was significantly higher than that in the LR (7.5% ± 6.5%) and CON (−2.0% ± 33.8%) trials. DR also resulted in a significant increase in TG, glucose, and HDL-cholesterol concentrations. | Table 2: Serum concentrations of biochemical parameters before and after 30 min of rest or exercise in the 3 trials
Click here to view |
Before the high-fat meal on the morning of day 2, serum creatine kinase concentrations were significantly higher in the DR trial (456.7 ± 176.0 U/L) than they were in the LR (212.4 ± 48.3 U/L) and CON (178.9 ± 46.0 U/L) trials. Serum TG concentrations during the 6-h postprandial period after a high-fat meal in the three trials are shown in [Figure 2]a. The trial, time, and trial × time interaction effects were insignificant. Moreover, TG AUC was similar across the three trials [Figure 2]b. Postprandial serum glycerol concentrations and AUC were also similar among the three trials [Figure 3]a and [Figure 3]b. The DR trial had a significantly higher NEFA concentration than did the CON trial at 0 h after the high-fat meal [Figure 4]a. The DR trial also had a significantly higher NEFA AUC than did the CON trial [DR: 4.71 ± 1.29; CON: 3.63 ± 1.24 mmol/L × 6 h, P < 0.05, [Figure 4]b. The NEFA AUC was similar between the DR and LR (4.13 ± 1.02 mmol/L × 6 h) trials. Serum glucose concentrations were not significantly different between the three trials at any time point [Figure 5]a. The DR trial (36.16 ± 3.65 mmol/L×6 h) had a significantly lower glucose AUC than did the CON trial (39.74 ± 4.21 mmol/L×6 h), but it was similar to that of the LR trial [37.09 ± 4.33 mmol/L × 6 h; [Figure 5]b]. The three trials had similar carbohydrate oxidation rates (CON, 0.15 ± 0.08 g/min; LR, 0.17 ± 0.07 g/min; DR, 0.19 ± 0.08 g/min) and fat oxidation rates (CON, 0.10 ± 0.04 g/min; LR, 0.11 ± 0.05 g/min; DR, 0.09 ± 0.04 g/min) during the 6-h postprandial period. | Figure 2: Postprandial serum TG concentrations after a high-fat meal (a) and the area under the curve (b) in the three trials. P >0.05.
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 | Figure 3: Postprandial serum glycerol concentrations after a high-fat meal (a) and the area under the curve (b) in the 3 trials. P >0.05.
Click here to view |
 | Figure 4: Postprandial serum nonesterified fatty acid concentrations after a high-fat meal (a) and the area under the curve (b) in the 3 trials. *Significantly different between DR and CON, P < 0.05. #Significantly different from CON, P < 0.05.
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 | Figure 5: Postprandial serum glucose concentrations after a high-fat meal (a) and the area under the curve (b) in the 3 trials. #Significantly different from CON, P < 0.05.
Click here to view |
Before the exercise intervention or rest in day 1, none of the participants reported muscle soreness. Muscle soreness scores were 0.0 ± 0.0 in all three trials. Muscle soreness scores on the morning of day 2 were significantly higher in the DR trial (30.2 ± 17.8) than in the LR (2.2 ± 5.1) and CON (0.0 ± 0.0) trials.
| Discussion | | |
The results of this study suggest that running at 60% for 30 min downhill or on a level surface did not affect serum TG concentrations after a high-fat meal. Downhill and LR also elicited similar postprandial AUCs in serum glycerol, NEFA, and glucose concentrations. However, DR resulted in a significantly higher serum NEFA and lower glucose responses after a high-fat meal compared with the controls who did not exercise.
The DR protocol in this study elicited a mild (1.8-fold) increase in plasma creatine kinase concentration on the morning of day 2 (456.7 ± 176.0 U/L) compared with the pre-exercise level (162.6 ± 49.1 U/L). The postexercise muscle soreness score (30.2 ± 17.8) in the DR trial, although significantly higher than that after LR, also indicated mild muscle damage. To our knowledge, only one study investigated the effect of eccentric exercise on postprandial lipemia.[24] A 4.4-fold increase in plasma creatine kinase concentration was elicited after eight sets of six repetitions of eccentric leg press at six repetitions maximum. However, the incremental AUC of postprandial TG concentrations was similar between baseline and after eccentric exercise.[24] This suggested that eccentric exercise with moderate muscle damage did not significantly affect postprandial lipemia, similar to the present results.
The energy expenditure of prior exercise is proposed to be a key determinant of the benefit in postprandial lipemia.[25] Previous studies have revealed that a single bout of 60–90 min of moderate exercise is effective in reducing postprandial lipemia.[4],[5],[26] The estimated average energy expenditure in the present study was 269 and 301 kcal in the LR and DR trials, respectively, which was lower than the values in the aforementioned studies. The lower energy expenditure in the DR and LR trials may have been insufficient to elicit a favorable change in postprandial lipemia. Consistently, two studies that used moderate exercise, lasting 30–36 min, reported no effect on plasma TG concentrations after a high-fat meal.[7],[27] The type of exercise intervention may not be a crucial factor as long as it induces sufficient energy expenditure or exercise duration. A previous study reported that 60 min of endurance exercise at 60%–65% or high-intensity resistance exercise were equally effective in reducing postprandial plasma TG concentrations.[28] Other studies have shown that prior resistance[6] and high-intensity interval exercise[7] significantly alleviated postprandial lipemia.
The intensity of prior exercise can be another factor in reducing postprandial lipemia. A previous study revealed that whole-body high-intensity intermittent exercise significantly reduced postprandial plasma TG concentrations compared with continuous moderate exercise with higher total energy expenditure.[7] In addition, high-intensity exercise is more effective in reducing postprandial lipemia than isoenergetic moderate exercise.[29],[30] The exercise intensity at 60% for 30 min in both DR and LR trials appeared insufficient to elicit significant changes in postprandial plasma TG concentrations.
The significantly higher AUC of postprandial NEFA in the DR trial compared with the CON trial may result from reduced fatty acid uptake and lower intramyocellular lipid recovery in damaged muscles. Hughes et al. reported that there is no replenishment of intramyocellular lipid between 24 and 48 h after unilateral eccentric contractions of the quadriceps. By contrast, the intramyocellular lipid content of the contralateral leg that undertook the same repetitions of the concentric exercise was significantly increased during that period.[31] However, the AUC of postprandial NEFA was reported to be unchanged after eccentric resistance exercise.[24] Only limited postexercise intramyocellular lipid recovery would occur because the high-intensity and low-energy exercise protocol used in the aforementioned study required little intramuscular TG as the energy source. The significantly higher AUC of postprandial NEFA in the DR trial in the present study was not the result of a difference in the substrate utilization because fat and carbohydrate oxidation rates were similar across the three trials during the 6-h postprandial period.
Although impaired insulin sensitivity after eccentric exercise has been reported,[19] this study did not find such effect. By contrast, the AUC of postprandial glucose concentrations in the DR trial was significantly lower than that in the CON trial. The role of insulin sensitivity in the effect of exercise on postprandial lipemia remains unclear. However, endurance exercise can still alleviate postprandial lipemia in men with impaired insulin sensitivity.[32]
Strengths and limitations
The strength of this study is that the participants in the DR and LR trial exercised at the same relative intensity with similar energy expenditure levels and substrate oxidation rates. This design minimized the potential effect of energy deficit and carbohydrate and fat replenishment on postprandial responses in the two running trails.
This study has several limitations. Muscle TG uptake and intramuscular TG concentrations during the postprandial period were not measured. Therefore, the direct evidence that reduced intramyocellular lipid recovery caused a higher postprandial NEFA response in the DR trial is lacking. In addition, postexercise creatine kinase concentrations among the participants varied widely. Thus, the possibility that individual differences in the level of muscle damage resulted in various lipemia responses cannot be ruled out.
| Conclusion | | |
This study revealed that running downhill or on a level surface at moderate intensity for 30 min had no effect on postprandial lipemia. In addition, DR improved glycemic response after a high-fat meal. For people who cannot participate in strenuous exercise, eccentric endurance exercise such as DR provides an alternative form of physical activity with health benefits.
Acknowledgments
The authors thank Ms. Yu-Fang Huang for her assistance with blood collection and analysis. The authors would like to appreciate Sports Science Research Center of National Taiwan University of Sports for providing the equipment to collect data and complete this study.
Financial support and sponsorship
This study was supported by the Ministry of Science and Technology, Taiwan (grant number MOST 107-2410-H-028-006).
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2]
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