Interval Exercise Characteristics
During INT, the mean V˙O2 and V˙E were constant across the final 60% and 50% of exercise duration, respectively (Figs. 1A and B, respectively; P > 0.05). There were no significant differences between V˙CO2 values during INT (Fig. 1C; P = 0.77). The mean RER was stable across the final 70% of INT duration (Fig. 1D; P > 0.05). There were no significant differences between PaCO2 values during the final 40% of INT period (Fig. 1E; P > 0.05). Thus, respiratory gas exchange data for indirect calorimetry collected in the initial 60% of INT duration were excluded from analysis due to the potential instability of plasma bicarbonate in this period.
Postexercise Recovery Characteristics
For each exercise trial, there were no significant differences in V˙E and V˙CO2 during the 3-h postexercise recovery (Table 3; P > 0.05). After C45%, the mean PaCO2 was significantly lower in the first hour than in the third hour of postexercise recovery (Table 3; P = 0.048). During recovery after INT, the mean PaCO2 was significantly lower in the first hour than in the second and third hours (Table 3; P = 0.041 and 0.003, respectively). In contrast, there was no significant difference in PaCO2 during the second and third hours of recovery after each exercise trial (Table 3; P > 0.05). There were no significant differences in V˙E, V˙CO2, or PaCO2 during the 3-h postexercise recovery of CON (Table 3; P > 0.05). Considering the second and third hours of postexercise recovery, there were no significant differences in V˙E, V˙CO2, or PaCO2 values among trials (Table 3; P = 0.10, 0.14, and 0.61, respectively) and from corresponding preexercise resting values (Table 3; P > 0.05).
Because V˙E, V˙CO2, and PaCO2 values were stable in the second and third hours of postexercise recovery of each trial, respiratory gas exchange data for indirect calorimetry to determinate substrate oxidation rates collected in the first hour of recovery were excluded from statistical analysis due to the potential instability of plasma bicarbonates in this period. Therefore, for all metabolic variables, only the second and third hours of recovery were considered as total postexercise recovery.
Oxygen Uptake and Rating Perceived Exertion Scale
The mean resting V˙O2 in INT was significantly higher than in CON (Table 4; P = 0.004). The mean exercise duration was significantly lower in INT (34.7 ± 1.2 min) than in C45% (60 min; P < 0.001), and there were no significant differences in mechanical work performed between exercise trials (C45% = 426 ± 24 kJ; INT = 423 ± 24 kJ; P = 0.14). The mean relative intensity was 47.7 ± 1.0% of V˙O2max in C45% and 79.5 ± 1.4% of V˙O2max in INT, and the mean V˙O2 in INT was significantly higher than in C45% (Table 4; P < 0.001) and in CON (Table 4; P < 0.001). The mean RPE after INT (17.5 ± 0.4; range = 15-20) was significant higher than after C45% (11.8 ± 0.4; range = 9-14; P < 0.001). During postexercise recovery, the mean V˙O2 was significantly higher in INT than in C45% and CON (Table 4; P < 0.05).
Respiratory Exchange Ratio
There were no significant differences in RER values during the preexercise resting period among experimental trials (Table 4; P = 0.81). During exercise, the mean RER in C45% was significantly lower than in INT (Table 4; P < 0.001). RER values in both exercise trials were significantly higher as compared with CON and the corresponding preexercise resting values (Table 4; P < 0.001 for both). During postexercise recovery, the mean RER was significantly lower in INT and C45% compared with CON (Table 4; P = 0.002 and 0.003, respectively), and for all trials, RER values were significantly lower relative to the preexercise resting periods (Table 4; P ≤ 0.02). The mean values for RER during preexercise resting period, exercise, and postexercise recovery are shown in Figure 2.
Total Energy Expenditure
During the preexercise resting period, the total energy expenditure was significantly higher in the INT relative to the CON trial (Table 5; P = 0.004). There was no significant difference in total energy expenditure during the C45% and the INT exercise trials (Table 5; P = 0.55). During postexercise recovery, there was no significant difference in total energy expenditure among trials (Table 5; P = 0.054). Considering exercise plus recovery, the mean total energy expenditures in INT and C45% were significantly higher than that in CON (Table 5; P < 0.001 for both).
Absolute substrate oxidation.
During the preexercise resting period, there were no significant differences in absolute substrate oxidation among the various trials (Tables 4 and 5; P > 0.05). The contribution of CHO to energy expenditure and the CHO oxidation rates during exercise were significantly higher in INT than in C45% and CON (Tables 4 and 5; P < 0.001 for all). The contribution of lipids to energy expenditure and the lipid oxidation rate during exercise were significantly higher in C45% than in INT and CON (Tables 4 and 5; P < 0.001 for all). On the other hand, there were no significant differences in these variables between INT and CON (Tables 4 and 5; P = 0.94 and 0.57, respectively). Figures 3 and 4 show the lipid and the CHO oxidation rates during postexercise recovery in the three experimental trials. The mean total lipid oxidation rates and the mean contribution of lipids to energy yield were significantly higher in INT and C45% compared with CON (Tables 4 and 5; P ≤ 0.007). After 120 min postexercise, the lipid oxidation rate was higher in the exercise trials than in CON (Fig. 3; P ≤ 0.03). The mean total CHO oxidation rate and the mean contribution to energy yield were significantly lower in INT and C45% compared with CON (Tables 4 and 5; P ≤ 0.02). Considering exercise plus recovery, the total amount of lipid oxidized was significantly higher in C45% (25.7 ± 2.9 g) than in INT (12.0 ± 1.7 g) and CON (11.9 ± 0.7 g; P < 0.001 for both). The total amount of CHO was significantly higher in INT (136 ± 6.9 g) than in other trials (P < 0.001 for both) and in C45% (109 ± 5.4 g) compared with CON (22.5 ± 1.1 g; P < 0.001). A significantly larger contribution of lipids to energy expenditure was found in C45% compared with INT and CON during exercise plus recovery (Table 5; P < 0.001 for both). The mean total lipid oxidation rate during postexercise recovery was positively correlated with total energy expenditure of exercise trials (Fig. 5; r = 0.47; P = 0.02).
Relative substrate oxidation.
During the preexercise resting period, there were no significant differences in relative substrate oxidation among the various trials (Table 6; P = 0.79). During exercise, a larger relative contribution of CHO oxidation was found during INT than in other trials (Table 6; P < 0.001 for both). A greater relative lipid contribution to energy expenditure was found in C45% compared with INT (Table 6; P < 0.001). Also, relative lipid oxidation was higher in CON than in both exercise trials (Table 6; P < 0.001 for both). During the second and third hours of postexercise recovery, a significantly greater relative lipid oxidation and a lower relative CHO contribution were found in INT and C45% than in CON (Table 6; P ≤ 0.003 for both).
The aim of this study was to examine the energy substrate partitioning difference during 3 h of postexercise recovery after continuous or interval exercise matched for mechanical work output on a cycle ergometer in fit young men. The main finding of this investigation indicated that the lipid oxidation rate and the contribution of lipids to energy yield during postexercise recovery were increased by a similar amount on high-intensity interval submaximal exercise and moderate-intensity continuous exercise compared with the no-exercise control trial. Contrary to our preliminary hypothesis, the greater CHO oxidation rate during interval exercise was probably too small to lead to larger muscle glycogen depletion and to enhance lipid oxidation during postexercise recovery. Moreover, the postexercise lipid oxidation rate was positively correlated with total energy expenditure of exercise trials. Therefore, postexercise lipid oxidation may be more dependent upon the energy expenditure of exercise than on the intensity of the prior isoenergetic exercise (17,22).
In the present study, substrate oxidation was quantified by indirect calorimetry. The calculation of substrate oxidation rates by this technique is based on the assumption that V˙O2 and V˙CO2 measured at the mouth reflect the O2 consumption and the CO2 production at the tissue level, and thus the RER equals the cellular respiratory quotient (RQ) (14). Although O2 uptake measured at the mouth follows whole-body O2 consumption very quickly due to the absence of large O2 reserves in the body, cellular production of CO2 is not instantaneously translated to changes in V˙CO2 at the mouth because the body stores of CO2 are large and have complex kinetics (4). Indeed, in exercise intensity above VT1, as with INT in this study, lactate production and hyperventilation affect bicarbonate kinetics (i.e., buffering of the lactic acid by bicarbonates). Therefore, V˙CO2, as measured in expired air, reflects the metabolic production of CO2 as well as the depletion of bicarbonate pools (14). This will result in RER exceeding RQ and can potentially lead to an overestimation of CHO and an underestimation of lipid oxidation during exercise. Consequently, the presence of a stable bicarbonate pool is required for the reliable estimation of tissue CO2 production from measurement of expired V˙CO2 during high-intensity interval exercise (11,28). Nevertheless, during acute metabolic acidosis of high-intensity exercise, RER exceeds RQ until a new steady state is attained (i.e., the CO2 size is again constant although depleted), at which time RER again equals RQ (40). In fact, it has been suggested that constant lactate concentrations are associated with a stable bicarbonate level during sustained constant heavy work rate exercise, despite an initial decrease in bicarbonate concentration corresponding to initial increase in lactate (39). Christmass et al. (11) have shown that capillary bicarbonates, PaCO2, and pH decrease in the initial 10 min of interval exercise (12 s at 120% V˙O2max and 18 s of passive recovery for 90 min) but subsequently remain stable in the presence of a constant blood lactate as well as V˙E and V˙CO2. Taken together, these results suggest the presence of stable plasma lactate and bicarbonate pools and support the use of indirect calorimetry for estimating substrate oxidation rates across the final 75 min of high-intensity supramaximal interval exercise (11). Therefore, in the present study, indirect calorimetry was used for INT when constant V˙E, V˙CO2, and PaCO2 responses were observed (i.e., the final 40% of exercise duration) to avoid potential instability of the plasma bicarbonates due to the high exercise intensity during work periods. Moreover, it has been shown that close agreement exists between the estimates of substrate oxidation rates measured with indirect calorimetry and by an isotope method during strenuous exercise at ∼85% of V˙O2max (i.e., >80% V˙O2max of the present study) (28) and that there was good agreement between the leg RQ and the RER during high-intensity interval exercise (15 s at V˙O2max and 15 s of rest for 60 min) (13).
Skeletal muscle (30) and arterial blood bicarbonate pools (33) that are depleted during exercise in an intensity-dependent manner (33) would be replenished during the postexercise recovery, providing a nonpulmonary destination for metabolically produced CO2. Therefore, RER is lower than RQ, and the lipid oxidation rate may be overestimated during recovery. Recently, Henderson et al. (17) have shown that bicarbonate/CO2 retention is transiently increased for the first hour of postexercise recovery after 1 h of exercise at 65% V˙O2max but is not increased after isoenergetic bouts of exercise at a lower endurance (45% V˙O2max). In addition, it has been demonstrated that after exercise at 75% V˙O2max, blood bicarbonate levels return to baseline during the 30-min postexercise recovery period (27). In the present study, there were no significant differences in V˙E, V˙CO2, and PaCO2 for each experimental trial during the second and third hours of postexercise recovery. Combining these results with those of previous studies (17,27), respiratory gas exchange data for indirect calorimetry to determine substrate oxidation rates collected in the first hour of recovery were excluded from statistical analysis, and the use of the mean RER value during the second and third hours of postexercise recovery thus appears to be a valid indicator of substrate partitioning.
During the preexercise resting period, V˙O2 and the total energy expenditure in INT were significantly higher than in CON (4.5% and 6%, respectively). To evaluate the day-to-day variability of these variables, we calculated the coefficient of variation among trials. The resting V˙O2 and the total energy expenditure exhibited variations of approximately 10.5 ± 1.1% and 10.3 ± 1.1%, respectively. These values are similar to the 9% coefficient of variation for resting V˙O2 reported by Carter and Jeukendrup (10), who suggested that this variation is probably linked to significant biological variability in the responses (10). Moreover, the differences in the mean resting V˙O2 and the total energy expenditure between INT and CON during the preexercise resting period are 15.6 mL·min−1 and 0.5 kcal, respectively. These magnitudes are very small and confirm the lack of any significant physiological change.
During exercise, lipid oxidation rates were approximately three times lower in INT as compared with C45%, despite similar overall energy expenditure in both exercise trials. Higher CHO oxidation rates during INT (∼2 times) compensated for the lower lipid contribution. These results agree with previous findings, which showed similar substrate partitioning during supramaximal interval exercise on a treadmill (12 s at 120% V˙O2max and 18 s of passive recovery) compared with continuous submaximal exercise (60% V˙O2max) matched for total energy expenditure (11). However, to obtain two isoenergetic exercise bouts and to compare INT with a continuous exercise with a recommended duration (60 min) and intensity (40-50% V˙O2max) for weight management (8) and to enhance lipid oxidation (37) in obese individuals, the mean exercise duration was significantly lower in INT (∼35 min) than in C45% (60 min). Thus, the contribution of CHO to energy expenditure was significantly but only slightly higher in INT compared with C45% (+20%; ΔCHOINT-C45% = 106.4 kcal ∼ 26 g). Moreover, it has been shown that the duration and the intensity of exercise influence EPOC and postexercise substrate use (7). However, the mean RPE (∼17 = "very hard") and the mean relative intensity (∼80% V˙O2max) in INT indicated that our healthy fit subjects were close to the upper limit of the exercise duration that may be borne during INT session.
The results of the present study show that during the postexercise recovery period, the mean lipid oxidation rate and the mean contribution of lipids to energy yield were increased by a similar amount in INT and C45% compared with CON, and the contribution of CHO to energy expenditure and the relative CHO oxidation after INT and C45% were lower as compared with CON. Moreover, the postexercise lipid oxidation rate in INT and C45% was positively correlated with total energy expenditure of exercise trials. These results are in line with previous findings (17,22), which showed that the contribution of lipid oxidation to energy expenditure after isoenergetic low- and moderate-intensity exercise (45% and 65% V˙O2max, respectively) was higher during postexercise recovery compared with time-matched no-exercise control period values. These authors further suggested that isoenergetic exercises result in similar elevations in postexercise lipid oxidation with no significant effect of exercise intensity on substrate oxidation in recovery. To our knowledge, our study is the first to confirm this evidence comparing two isoenergetic exercises of different forms (i.e., interval vs continuous) and intensities (i.e., 45% vs 80% V˙O2max) in healthy male subjects. In the present study, the mean RER after exercise was lower than preexercise and CON values in both trials. These results confirm the difference in substrate partitioning between exercise and no-exercise control trials and corroborate previous findings concerning postexercise recovery (1 h , 2 h , and 4 h ) after high-intensity interval exercise. It has been shown that RER is lower in recovery after supramaximal interval exercise (20 × 1-min intervals at 105% V˙O2max with intervening 2-min rest periods ; 3 × 2-min intervals at 108% V˙O2max with intervening 3-min rest periods ) compared with the no-exercise control trial. Moreover, our findings are in line with those of Saris and Schrauwen (31), which showed that 24 h of postexercise RER was similar after INT (3 × 30 min of 2.5-min intervals at 80% W˙max with intervening 2.5-min active rest periods at 50% W˙max) and continuous exercise (38% W˙max) in obese men. On the other hand, our results partially agree with findings of McGarvey et al. (24) who have shown that RER is lower in postexercise recovery after interval submaximal exercise (7 × 2-min intervals at 90% V˙O2max with intervening 3-min active recovery at 30% V˙O2max) compared with preexercise values but also in recovery after continuous exercise (∼30 min at 65% V˙O2max). This difference may be explained by the fact that exercise bouts were not matched by energy expenditure and that authors did not verify the validity of indirect calorimetry to determine substrate oxidation across postexercise recovery. In fact, the dip in RER values during the first hour of recovery after both interval and continuous exercise is indicative of CO2 retention to replenish bicarbonate stores with the more pronounced dip after interval likely the result of greater lactate buffering.
As a result, the data in the present study support the assertion that greater lipid oxidation during postexercise recovery may be due to sparing CHO and facilitating subsequent muscle glycogen restoration, which represents a priority during recovery (19,21). Recently, Henderson et al. (17) have shown that lipolysis and NEFA mobilization are elevated in postexercise recovery and plasma NEFA oxidation is also increased, leading to an elevation of total lipid oxidation after exercise. It has been suggested that noradrenaline and growth hormone are involved in the elevated postexercise lipolysis in men. In addition, the increased NEFA use in recovery may have been related to depletion of CHO removing energy substrate competition between oxidative glycolysis and β-oxidation (17).
Considering exercise plus recovery, these results show that the total amount of lipid oxidized and the contribution of lipid to energy expenditure were approximately 2.5 times higher in C45% than in INT due to the higher lipid oxidation in C45% during exercise. The mean relative intensity of C45% was close to the level at which lipid oxidation reached a maximum in healthy subjects (i.e., Fatmax) and may represent a crucial intensity to recommend exercise training to promote lipid oxidation in healthy and obese subjects. Furthermore, it has been shown that at this intensity, 12-wk low-intensity endurance training (three training sessions per week: approximately 50 min at 40% V˙O2max on a cycle ergometer) increases the ability to oxidize lipids during both rest and exercise in healthy male subjects (32). However, although INT does not acutely generate a greater postexercise lipid oxidation compared with C45%, the chronic influence of such an approach may lead to a different outcome. Indeed, Tremblay et al. (36) have shown that the increase in lipid oxidation is greater after a 15-wk high-intensity interval training program than after a 20-wk moderate-intensity continuous training program. The metabolic adaptations taking place in the skeletal muscle in response to the high-intensity interval training program appear to favor the process of lipid oxidation. Moreover, it has recently been shown that only seven sessions of high-intensity submaximal interval training (4 min at 90% V˙O2max with 2-min rest between intervals) over 2 wk induced an increase in whole body lipid oxidation during exercise in moderately active women (34). These findings reveal the potency of high-intensity interval exercise associated with short duration sessions and training periods (i.e., 3 h·wk−1 for 2 wk) to improve the skeletal muscle capacity to oxidize lipids, which has implications for improving fitness and health (34). Obviously, INT requires a high level of motivation and causes a feeling of severe fatigue resulting in poor adherence, soreness, and significant risk of injury for individuals with health problems or for obese subjects who are not accustomed to exercise. Especially in these specific populations, low-intensity continuous training should be performed during the first training period to develop the endurance necessary to support high-intensity interval exercise sessions. Subsequently, INT associated with short duration sessions and low volume may be added to a training program to further improve metabolic effects. Thus, high-intensity interval exercise may be an important complementary training tool to traditional low-intensity continuous exercise and could make an important contribution to weight management in individuals at risk for obesity and in obese subjects (31).
Some methodological limitations exist and need to be addressed. First, participants were healthy, active, and normal-weight individuals, so the response observed may not be representative of very physically fit, sedentary, overweight, or obese subjects. Furthermore, the precise sources of lipids (i.e., NEFA and intramuscular or plasma TAG) and CHO (i.e., muscle glycogen, blood glucose, blood, or muscle lactate) oxidized during exercise and recovery could not be determined or differentiated.
In conclusion, this study shows that lipid oxidation during postexercise recovery was increased by similar amount on high-intensity interval submaximal exercise and moderate-intensity continuous exercise compared with the no-exercise control trial. Despite a significant but slightly greater CHO oxidation that likely leads to larger muscle glycogen depletion during interval exercise, the two isoenergetic exercises of different forms and intensities promote similar shifts in the pattern of substrate use toward lipids during postexercise recovery, when lipid oxidation predominates. Thus, postexercise lipid oxidation may be more dependent upon the energy expenditure of exercise than on the intensity of the prior isoenergetic exercise. Because the data reported are of potential interest for exercise prescription in obese individuals, future research should compare the effect of these two forms of exercise between fit young and obese subjects.
This work was supported by Office Fédéral du Sport Macolin (Switzerland). The results of the present study do not constitute endorsement by ACSM.
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Keywords:©2009The American College of Sports Medicine
SUBSTRATE USE; ENERGY EXPENDITURE; EXCESS POSTEXERCISE OXYGEN CONSUMPTION; INDIRECT CALORIMETRY; WEIGHT MANAGEMENT