Exercise routines in which intensity fluctuates, such as Spinning and Treading, are gaining in popularity in fitness industry (6,17). Such a variable intensity exercise is typically accomplished by a systematic change in intensity throughout an exercise bout to reach different target heart rates (HRs). The scheme of a variable intensity exercise may be viewed as similar to an interval training protocol. However, its overall intensity is rather moderate because the protocol does not involve ultrashort bursts of intense exercise performed intermittently. Performing such dynamic exercise has a unique advantage in that it would allow participants, especially those with lower exercise tolerance, to experience some moments of more intense exercise without undue fatigue, thereby gaining proper benefits associated with physical activity. It has been shown that an exercise regimen in which intensity varies is more effective in improving muscle oxidative capacity (10,26), glucose tolerance (18), insulin sensitivity (21,29), and metabolic syndrome characteristics (27).
To date, data as to whether and how this dynamic protocol may affect the exercise metabolism remains scarce and largely controversy in part because of the nonsteady-state nature of the exercise that makes metabolic measurement difficult. Inserting multiple periods of more intense exercise may help increase metabolic cost during exercise. It has been documented that once an exercise is performed with intensity near or above lactate threshold, there would be an additional rise in V[Combining Dot Above]O2, often regarded as a slow component, despite unchanging intensity (8). This phenomenon, however, has not been demonstrated during variable intensity exercise that contains intermittent periods of intense effort. It is also unclear whether variegating intensity without a concurrent change in overall intensity will alter substrate utilization. Essen et al. (5) reported no differences in respiratory exchanged ratio (RER) and patterns of substrate utilization between intermittent and continuous exercise matched for the overall intensity. However, by using a similar experimental design, Christmass et al. (4) observed a significantly higher carbohydrate oxidation (COX) concomitant with lower fat oxidation (FOX) during intermittent than continuous exercise.
We have previously compared the acute metabolic effect between a Spinning protocol and a conventional steady-state exercise of the same overall intensity (11). Although no between-protocol differences in oxygen uptake (V[Combining Dot Above]O2) were found during exercise, V[Combining Dot Above]O2 was higher during recovery following the Spinning protocol. A higher intensity exercise that elicits greater carbohydrate utilization has been shown to produce a greater lipid oxidation during recovery (14,20). Given that a variable intensity exercise encompasses multiple periods of intense effort, one may expect that this exercise scheme could also elicit a greater FOX during recovery. This speculation, however, has not been uniformly confirmed. McGarvey et al. (16) observed a lower RER during postexercise recovery following a variable intensity protocol as compared with a continuous exercise. However, when controlling for the total energy output during exercise, Malatesta et al. (15) and Warren et al. (28) reported no differences in RER and substrate oxidation rates after an interval or a continuous exercise protocol.
The present investigation was undertaken to provide additional data concerning the acute effect of intensity fluctuation and its magnitude on energy output and substrate utilization during exercise and recovery. This research objective was accomplished by using three 30-minute exercise protocols that matched for the total power output, but differed in intensity fluctuation, and each protocol was immediately followed by a 25-minute recovery period. Intensity fluctuation was achieved through modulating break resistance on a cycle ergometer, while maintaining the same pedal revolution. Protocols were kept within moderate intensity domain to minimize metabolic acidosis, which can otherwise distort CO2 production and thus affect the estimation of substrate utilization. It was hypothesized that because of the inclusion of multiple periods of intense exercise, a variable intensity exercise would elicit greater oxygen uptake during both exercise and recovery. It was also hypothesized that this dynamic protocol would produce greater COX during exercise and greater FOX during recovery.
Experimental Approach to the Problem
A between-subject design was used in this study in which each group of participants received a different experimental treatment. All participants completed a familiarization session, a maximal oxygen uptake (V[Combining Dot Above]O2peak) test, and an experimental trial on 3 separate occasions. During the familiarization session, participants were provided with specific details regarding the study and the opportunity to familiarize with exercise protocol and measurement apparatus including cycle ergometer, metabolic system, HR monitor, and lactate analyzer. During the V[Combining Dot Above]O2peak test, participants performed a maximal graded cycle exercise test to determine their aerobic fitness and ventilatory threshold (VT). During the experimental trial, participants within the same gender performed 1 of the following 3 exercise protocols: (a) a 30-minute cycling exercise performed at a constant power output of 75 W (P1), (b) a 30-minute cycling exercise with power output being alternated between 50 and 100 W every 5 minutes (P2), (c) same as P2 except power output was alternated between 25 and 125 W (P3). Each exercise protocol was immediately followed by a 25-minute recovery period, and all 3 protocols produced the same total power output. Dependent variables such as oxygen uptake (V[Combining Dot Above]O2), carbon dioxide production (V[Combining Dot Above]CO2), RER, and HR were measured at rest and during exercise and recovery. The 3 exercise protocols were illustrated in Figure 1.
Thirty participants including 15 men and 15 women (age range: 19-24 years) volunteered to participate in this study. These participants were healthy, physically active, and free of any orthopedic injury as revealed by their responses to a medical and physical activity questionnaire. All women participants had regular menstrual cycles, and those who had used contraceptive agents or devices at the time of the investigation or within the past year were excluded from the study. Participants were informed of the purpose and testing procedures of the study, and each gave their written consent to participate. All experimental procedures were evaluated and approved by The College of New Jersey Institutional Review Board for Human Subjects Experimentation. The physical and physiological characteristics of participants are presented in Table 1.
Participants were requested to attend a familiarization session before the start of the study. During this session, instructions with regard to the testing protocols, instrumentation, and measurement were provided. In addition, height was measured using a wall-mounted stadiometer, and body mass was measured using an electronic scale. Participants were also given the opportunity to perform an incremental exercise on a cycle ergometer up to an ∼85% of their age-predicted HR. Participants also received instructions of the proper physical activity and dietary guidelines that they would need to follow before each experimental trial.
V[Combining Dot Above]O2peak and Ventilatory Threshold
The test was conducted on a stationary cycle ergometer by using an incremental exercise protocol previously described (13). Briefly, the protocol began with riding at a workload of 25 W for female participants and 50 W for male participants. Workload was then increased by 25 W every 2 minutes in both genders. Each subject was verbally encouraged to continue exercise until volitional exhaustion. The test was terminated when the subjects met at least 2 of the following 3 criteria: (a) failing to maintain the peak power output for 15 consecutive seconds, (b) an increase in V[Combining Dot Above]O2 of <100 ml·min−1 despite an increase in workload, and (c) a RER >1.05. The V[Combining Dot Above]O2 and RER were measured every 30 seconds. Heart rate was measured at the end of every minute. The maximal value for V[Combining Dot Above]O2 was determined as the average of the 2 highest consecutive values.
Data from the V[Combining Dot Above]O2peak test were also used to quantify VT. This procedure was based on the “V-slope” method described previously (2). Briefly, this method was built into the metabolic system and consists of plotting V[Combining Dot Above]CO2 as a function of V[Combining Dot Above]O2. This plot has 2 major linear components. The lower component has a slope between 0.8 and 1.0, whereas the upper component has a slope >1.15. The break point between the 2 components has been shown to coincide with the V[Combining Dot Above]O2 at which metabolic acidosis occurs (2,25). V[Combining Dot Above]O2 at this break point was then converted to %V[Combining Dot Above]O2peak.
Upon arrival at the laboratory, participants first rested quietly by sitting in a chair for 15 minutes while being attached to a metabolic system. They then began a 5-minute resting measurement period during which V[Combining Dot Above]O2, RER, and HR were measured every minute. At the end of this resting phase, baseline blood lactate concentrations ([La]) were also determined.
The exercise session began immediately after the completion of resting measurement. Participants performed a 30-minute exercise bout on an electronic cycle ergometer (Ergo 800; SensorMedics, Inc., Yorba Linda, CA, USA) by following the protocol they were assigned. The ergometer has the digital display that illustrates power in watts and real-time pedal frequency in revolutions per minute performed by the participant. This ergometer also allows pedal frequency to be altered without affecting power output. In light of the evidence that an increase in pedal frequency can elevate V[Combining Dot Above]O2 despite the maintenance of power output (9), all participants were instructed to maintain their pedal frequency at 65 rpm throughout exercise, and therefore any alteration in power output can be solely attributed to a change in brake resistance. During trials in which intensity varied, participants were prompted to make a change at the point where power output needed to be increased or decreased. Each change in power output was verified by an investigator. Throughout exercise, V[Combining Dot Above]O2, V[Combining Dot Above]CO2, and RER were measured every minute, whereas HR was recorded every 5 minutes. In addition, [La] was determined immediately after the cessation of the exercise.
The exercise session was followed by a 25-minute recovery phase during which the participant remained seated in a chair. During this phase, V[Combining Dot Above]O2, V[Combining Dot Above]CO2, and RER were measured every minute, whereas HR was recorded every 5 minutes. In addition, [La] was determined once again at the end of recovery.
All trials were conducted in the morning with participants being in a minimum of 4-hour postprandial to maintain a similar circadian rhythm across all experimental trials and to minimize the confounding effect of prior eating on exercise metabolism. On the day before the experimental trial, participants were instructed not to participate in vigorous physical activities. They were also instructed to refrain from alcohol and caffeine and to follow a moderate carbohydrate diet that elicited ∼50% of the total caloric intake derived from carbohydrate. Each participant was provided with individualized dietary instructions and sample meal plans to ensure that they adhere to the prescribed diets. Female participants were tested within the first 10 days after the onset of menses.
Respiratory gas exchanges were measured breath-by-breath using a 2-way T-shape breathing valve (2700 series; Hans Rudolph, Inc., Kansas City, MO, USA) and an open-circuit respiratory-metabolic system (Metabolic Measurement Cart 2900; SensorMedics, Inc.). This system was calibrated regularly using gases of known O2 and CO2 concentrations. For further analysis, breath-by-breath V[Combining Dot Above]O2, V[Combining Dot Above]CO2, and RER were averaged at a 30-second (for V[Combining Dot Above]O2peak test) or a 1-minute interval (for exercise trials). Heart rate was determined using a HR monitor (Pacer; Polar CIC, Inc., Port Washington, NY, USA). [La] was analyzed from sampling of fingertip whole capillary blood using a lancet procedure and a portable lactate analyzer (Accusport Portable Lactate Analyzer; Sports Resource Group, Hawthorne, NY, USA). All trials were conducted in the laboratory where the mean barometric pressure and laboratory temperature were 757 ± 2 mm Hg and 24 ± 1° C, respectively.
Calculations of Substrate Oxidation
V[Combining Dot Above]O2 and V[Combining Dot Above]CO2 were also used to further calculate the rates of COX and FOX using the stochiometric equations (7). Stochiometric calculations are made based on relative quantities of reactants (i.e., O2) and products (CO2) in chemical reactions to quantify rates of substrate oxidation. These equations are illustrated as follows:
In these equations, n represents nitrogen excretion rate, which was estimated to be 135 µg·kg−1·min−1 according to the study of Romijn et al. (23). For between-group comparisons, both COX and FOX were further divided by participant's body mass to be expressed in mg·kg−1·min−1.
All dependent variables including V[Combining Dot Above]O2, RER, HR, [La] and rates of COX and FOX were averaged for every 5-minute stage and for the entire 30 minutes of exercise. These averaging processes were also used for the recovery period. One-way (i.e., protocol) analysis of co-variance with participants' V[Combining Dot Above]O2max as a covariate was used to compare all dependent variables across the 3 protocols and this was performed separately for (a) rest, (b) exercise, and (c) recovery. In addition, 2-way (i.e., protocol by time) analysis of variance with repeated measure on time was used to compare stage-specific rates of substrate oxidation across the 3 protocols over time and this was performed separately for (a) exercise and (b) recovery. A significant F ratio was followed by post hoc comparisons using the Sheffé procedure to detect significant pair-wise differences. For all statistical tests, a probability level of 0.05 was established to denote statistical significance. All analyses were carried out using the Statistical Package for the Social Sciences version 21 (SPSS, Inc., Chicago, IL, USA).
V[Combining Dot Above]O2
No between-protocol differences in V[Combining Dot Above]O2 were observed at rest (Table 2). During exercise, despite divergent metabolic responses over time in different exercise protocols as show in Figure 2, no between-protocol differences in V[Combining Dot Above]O2 were observed. During recovery, a significant F ratio was observed for V[Combining Dot Above]O2 (F(2,26) = 5.602, p = 0.009). The post hoc comparisons revealed that V[Combining Dot Above]O2 was lower (p ≤ 0.05) in P1 than in P2 or P3, whereas no differences in V[Combining Dot Above]O2 were observed between P2 and P3.
COX and FOX
No between-protocol differences in COX and FOX were observed at rest (Table 3). However, there were significant main effects for COX (F(2,26) = 4.723, p = 0.018) and FOX (F(2,26) = 4.192, p = 0.026) during exercise. Post hoc comparisons revealed that COX was higher (p ≤ 0.05), whereas FOX was lower (p ≤ 0.05) in P3 than in either P1 or P2. No differences in COX or FOX were seen between P1 and P2. During recovery, there was a significant main effect for COX (F(2,26) = 4.707, p = 0.018), whereas FOX remained indifferent across the 3 protocols. Post hoc comparisons revealed that COX was higher (p ≤ 0.05) in P than in P1 or P2, whereas no differences in COX were seen between P1 and P2.
Stage-specific analysis revealed that COX was higher in P3 than in P1 or P2 (p ≤ 0.05) during all but the first 5 minutes, whereas COX remained the same between P1 and P2 throughout the exercise (Figure 3). However, the significant main effect of protocol for FOX was only seen at those low-intensity stages where FOX was lower (p ≤ 0.05) in P3 than in either P1 or P2, whereas no differences in FOX were seen between P1 and P2 (Figure 4). As for recovery, the significant between-protocol differences in COX and FOX were seen during the first 10 minutes (Figures 3 and 4). COX was higher (p ≤ 0.05), whereas FOX was lower (p ≤ 0.05) in P3 than in P1 or P2, and no differences in COX or FOX between P1 and P2 were seen during both the first and second 5-minute periods of recovery.
HR, RER, and [La]
No between-protocol differences in HR were observed at rest (Table 2). During exercise, despite divergent metabolic responses as show in Figure 2, no between-protocol differences in HR were observed. During recovery, HR remained the same across the 3 protocols.
No between-protocol differences in [La] were observed at rest (Table 2). There was a significant main-effect for [La] during exercise (F(2,26) = 3.831, p = 0.035). Post hoc comparisons revealed that [La] in mM at the end of exercise was greater (p ≤ 0.05) in P3 than in P1. There were no differences between P1 and P2 and between P2 and P3, though a trend toward a greater [La] in P3 than P2 (p = 0.13) was observed. No significant between-protocol differences in [La] were seen during recovery.
No between-protocol differences in RER were observed at rest (Table 2). There was a significant main effect for RER during exercise (F(2,26) = 7.229, p = 0.003). Post hoc comparisons revealed that RER was higher (p ≤ 0.05) in P3 than in either P1 or P2, whereas no differences in RER were observed between P1 and P2. No significant between-protocol differences in RER were seen during recovery.
It was our initial hypothesis that for an exercise regimen containing some moments of higher intensity exercise, there would be a more profound elevation in overall V[Combining Dot Above]O2 especially in P3 that was associated with greater intensity fluctuation. This assumption was based on the notion that V[Combining Dot Above]O2 can rise progressively during constant-rate exercise of sufficient intensity and such a rise will be more significant as intensity approaches to or exceeds lactate threshold (8). However, our findings did not prove this hypothesis. Although V[Combining Dot Above]O2 was somewhat higher in P3 (20.09 ± 2.09 ml·kg−1·min−1) than in P1 (18.68 ± 2.21 ml·kg−1·min−1) and P2 (18.41 ± 2.07 ml·kg−1·min−1), these differences did not reach statistical significance (Table 2). The lack of difference in V[Combining Dot Above]O2 could be attributed to modest nature of the protocols in which metabolic demand produced during exercise was largely below lactate threshold. For example, the highest intensity achieved was ∼52% and ∼65% V[Combining Dot Above]O2peak in P2 and P3, respectively, whereas VT, a measure that coincides with lactate threshold (2,21), of our participants ranged from 56 to 57% V[Combining Dot Above]O2peak (Table 1). It seems that under the moderate-intensity domain, energy expenditure during exercise would not be affected by intensity fluctuation so long as the total power output or overall intensity stays the same.
Postexercise V[Combining Dot Above]O2 was greater in P2 or P3 than in P1 (Table 2). Compared with P1, recovery V[Combining Dot Above]O2 was 18 and 19% higher in P2 and P3, respectively. The observation that oxygen cost during recovery was higher after P2 or P3 suggests that variegating exercise intensity without a concurrent change in the overall exertion can play a role in augmenting postexercise energy expenditure. The underlying mechanism for these findings cannot be determined in this study. However, they could be related to an increased oxygen deficit associated with intensity oscillation during exercise. Almuzaini et al. (1) found that splitting a 30-minute session into two 15-minute sessions elicited a greater postexercise V[Combining Dot Above]O2. In this study, there were 3 intensity increments made at a 10-minute interval during 30 minutes of exercise in P2 and P3, whereas this was not the case during P1. During these changing periods, there should be physiological adjustments necessary to meet the increased oxygen demand just as those during rest-to-exercise transition. As a result, some degree of oxygen deficit may have occurred because an increase in cardiopulmonary function that supplies oxygen usually lags behind an increase in muscular force production (19). The similarity of postexercise V[Combining Dot Above]O2 between P2 and P3 may be explained by the fact that the 2 protocols yielded the same total power output despite a difference in intensity fluctuation (i.e., 50–100 W in P2 vs. 25–125 W in P3).
Intensity fluctuation seems to affect the pattern of substrate utilization during exercise. For example, RER was higher in P3 than in either P1 or P2, whereas no differences in RER were observed between P1 and P2 (Table 3). Further calculations revealed that COX was higher, whereas FOX was lower in P3 than in either P1 or P2, respectively, and no differences in COX or FOX were seen between P1 and P2. The high carbohydrate utilization in P3 can also be evidenced by the fact that [La] at the end of P3 was the highest among the 3 protocols (Table 2). The fact that the altered pattern of substrate utilization occurred only in P3 not P2 is an interesting phenomenon. Both P2 and P3 were associated with intensity fluctuation except that its magnitude was twice as much in P3. As a result, P3 elicited a greater span of change in metabolic demand (i.e., 32–65% V[Combining Dot Above]O2peak) as compared with P2 (i.e., 37–52% V[Combining Dot Above]O2peak). In this context, the greater carbohydrate utilization seen in P3 may be attributable to the severity of intensity fluctuation or, more specially, the highest metabolic demand achieved. Indeed, the intensity achieved during the 3 high-intensity stages of P3 was above VT, whereas this was not the case in P2 (Table 4). It seems that intensifying some periods of exercise without changing an overall effort can alter substrate utilization, but this would require augmenting intensity to a greater extent, preferably above lactate threshold.
Our stage-specific analysis further revealed that in P3 COX remained elevated and FOX remained suppressed even during the low-intensity periods (Figures 3 and 4). This finding is in agreement with those of Christmass et al. (4) who demonstrated consistently higher COX rates throughout an interval protocol as compared with continuous exercise of the same total energy expenditure. A greater rate of COX seen in P3 could be explained by accelerated glycogenolysis associated with high-intensity phases of the protocol (4), and such accelerated glycogenolysis can be further attributed to increases in cytosolic calcium release, higher levels of circulating catecholamines, more rapid depletion of phosphocreatine, and greater recruitment of type II muscle fibers (3). The increased carbohydrate utilization may have in turn caused a concomitant decrease in FOX even during the low-intensity phases where FOX is expected to increase. Romijn et al. (22) demonstrated lower rates of FOX when COX was higher during high-intensity continuous exercise. It has been evidenced that carbohydrate availability could suppress FOX during exercise in reverse of classic glucose-fatty acid cycle (24).
Previous studies have shown that an exercise of higher intensity would produce greater lipid oxidation during postexercise recovery (14,20). It seems that when muscle and liver glycogen stores are mobilized to support most of the energy expenditure during exercise, lipids will become the predominant energy stores during recovery. In this study, COX during exercise was greater in P3. However, no differences in FOX were seen during recovery (Table 3). This finding may be in part attributable to the modest nature of the exercise protocols. It is likely that carbohydrate utilization in P3 may not be sufficiently high enough to induce appreciable increases in fat utilization after exercise. Previous studies demonstrating postexercise increases in fat utilization have used an ∼60 minutes of continuous exercise at 65–75% V[Combining Dot Above]O2max (14,20). The lack of differences in postexercise FOX can also be ascribed to the equivalency of the total power output or overall intensity across the 3 protocols. Even with greater intensity fluctuation (i.e., 40–85% V[Combining Dot Above]O2max) and sufficient exercise duration (i.e., ∼60 minutes), Malatesta et al. (15) and Warren could not detect any differences in RER and substrate oxidation rates after interval and continuous exercise (15,24). In these latter studies, higher RER and greater COX were identified during an interval exercise, but no corresponding increases in FOX were observed during recovery.
The upper end of metabolic demand elicited by our protocols (i.e., P2 and P3) is less than those reported by previous studies (i.e., ∼80–85% V[Combining Dot Above]O2max) (3,4,13,14,24). As such, from a practical standpoint, results of this study may be applicable to those who have lower exercise tolerance, but would like to experience some moments of intense exercise to gain proper benefits associated with physical activity. However, as mentioned earlier, it was our intent to keep the protocols within moderate-intensity domain so that estimation of substrate utilization through pulmonary respiration can be more accurate. The most demanding protocol such as P3 was created as such because we have previously observed that on a cycle ergometer, participants of an average fitness, as used presently, would reach their VT at power outputs near 125 W (12). The calculation of substrate oxidation rates using the stochiometric equations is based on the assumption that V[Combining Dot Above]O2 and V[Combining Dot Above]CO2 within the tissue are represented accurately by measurement of V[Combining Dot Above]O2 and V[Combining Dot Above]CO2 in expired air (7). During intense exercise in which lactate production increases, V[Combining Dot Above]CO2 will increase because of the use of HCO−1 pool for buffering. This can potentially lead to a higher RER and an overestimation of carbohydrate concomitant with an underestimation of FOX. We are cognizant that these potential errors may have impacted the results of P3 to a certain degree.
In summary, we found that intensity fluctuation of sufficient magnitude can alter exercise metabolism independent of the overall intensity or total power output. The 2 variable intensity protocols used presently seem to be equally effective in elevating postexercise V[Combining Dot Above]O2, but the one with greater intensity fluctuation can also elicit greater COX coupled with reduced FOX during exercise. Intensity fluctuation does not seem to affect substrate utilization during recovery so long as the overall intensity or total power output of the proceeding exercise remains the same.
This study revealed that by variegating exercise intensity as was performed in P2 and P3, one can expect greater postexercise energy expenditure without necessarily changing the overall effort of exercise. Intensity fluctuation of sufficient magnitude can also alter substrate utilization patterns despite the fact that the overall intensity of the exercise stays the same. For example, COX was higher and FOX was lower in P3 that was associated with greater intensity fluctuation, whereas the total power output remained the same across the 3 protocols. Training involving a high use of carbohydrate has proven effective in improving insulin-mediated glucose disposal or insulin sensitivity (21,27,29). Therefore, fitness professionals may consider incorporating variable intensity exercise routines into their prescription especially for those who are overweight or at risk for insulin resistance. To apply these results, one may exercise on a treadmill at 60% of HRmax, but to maximize exercise benefits he could vary his HR between 50 and 70% HRmax by modulating speed or incline of the treadmill periodically. A high use of carbohydrate can lead to a higher use of fat during recovery. However, our findings did not support this contention in part because of modest nature of the protocols. The protocols used presently did not involve short bursts of very intense exercise performed intermittently. As such, results of the study may be of interest to a clinical setting where participants are generally less fit, but would like to experience some moments of intense exercise to maintain a proper gain in cardiorespiratory and metabolic benefits.
1. Almuzaini KS, Potteiger JA, Green SB. Effects of split exercise sessions on excess postexercise oxygen consumption and resting metabolic rate. Can J Appl Physiol 23: 433–443, 1998.
2. Beaver WL, Wasserman K, Whipp BJ. A new method for detecting anaerobic threshold by gas exchange. J Appl Physiol (1985) 60: 2020–2027, 1986.
3. Chasiotis D. The regulation of glycogen phosphorylase and glycogen breakdown in human skeletal muscle. Acta Physiol Scand Suppl 518: 1–68, 1983.
4. Christmass MA, Dawson B, Passeretto P, Arthur PG. A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise. Eur J Appl Physiol Occup Physiol 80: 423–435, 1999.
5. Essén B, Hagenfeldt L, Kaijser L. Utilization of blood-borne and intramuscular substrates during continuous and intermittent exercise in man. J Physiol 265: 489–506, 1977.
6. Francis PR, Witucki AS, Buono MJ. Physiological response to a typical studio cycling session. ACSM's Health Fit J 3: 30–36, 1990.
7. Frayn KN. Calculation of substrate oxidation rates in vivo from gaseous exchange. J Appl Physiol Respir Environ Exerc Physiol 55: 628–634, 1983.
8. Gaesser GA, Poole DC. The slow component of oxygen uptake kinetics in humans. Exerc Sport Sci Rev 24: 35–71, 1996.
9. Hagan RD, Weis SE, Raven PB. Effect of pedal rate on cardiorespiratory responses during continuous exercise. Med Sci Sports Exerc 24: 1088–1095, 1992.
10. Hood MS, Little JP, Tarnopolsky MA, Myslik F, Gibala MJ. Low-volume interval training improves muscle oxidative capacity in sedentary adults. Med Sci Sports Exerc 43: 1849–1856, 2011.
11. Kang J, Chaloupka EC, Mastrangelo MA, Hoffman JR, Ratamess NA, O'Connor E. Metabolic and perceptual responses to cycling at a constant intensity and with Spinning® exercise protocol. Med Sci Sports Exerc 37: 853–859, 2005.
12. Kang J, Hoffman JR, Ratamess NA, Faigenbaum AD, Falvo M, Wendell M. Effect of exercise intensity on fat utilization in males and females. Res Sports Med 15: 175–188, 2007.
13. Kang J, Robertson RJ, Goss FL, DaSilva SG, Suminski RR, Utter AC, Zoeller RF, Metz KF. Metabolic efficiency of arm cranking and leg cycling at the same mode-specific relative exercise intensity. Med Sci Sports Exerc 29: 377–382, 1997.
14. Kuo CC, Fattor JA, Henderson GC, Brooks GA. Lipid oxidation in fit young adults during postexercise recovery
. J Appl Physiol (1985) 99: 349–356, 2005.
15. Malatesta D, Werlen C, Bulfaro S, Chenevière X, Borrani F. Effect of high-intensity interval exercise on lipid oxidation during postexercise recovery
. Med Sci Sports Exerc 41: 364–374, 2009.
16. McGarvey W, Jones R, Petersen S. Excess post-exercise oxygen consumption following continuous and interval cycling exercise. Int J Sport Nutr Exerc Metab 15: 28–37, 2005.
17. Nichols JF, Sherman CL, Abbott E. Treading is new and hot. ACSM's Health Fit J 4: 12–17, 2000.
18. Nybo L, Sundstrup E, Jakobsen MD, Mohr M, Hornstrup T, Simonsen L, Bülow J, Randers MB, Nielsen JJ, Aagaard P, Krustrup P. High-intensity training versus traditional exercise interventions for promoting health. Med Sci Sports Exerc 42: 1951–1958, 2010.
19. Palmer GS, Borghouts LB, Noakes TD, Hawley JA. Metabolic and performance responses to constant-load vs. variable intensity exercise in trained cyclists. J Appl Physiol 87: 1186–1196, 1999.
20. Phelain JF, Reinke E, Harris MA, Melby CL. Postexercise energy expenditure and substrate oxidation in young women resulting from exercise bouts of different intensity. J Am Coll Nutr 16: 140–146, 1997.
21. Richards JC, Johnson TK, Kuzma JN, Lonac MC, Schweder MM, Voyles WF, Bell C Short-term sprint interval training increases insulin sensitivity in healthy adults but does not affect the thermogenic response to beta-adrenergic stimulation. J Physiol 588: 2961–2972, 2010.
22. Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, Wolfe RR. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 265: E380–E391, 1993.
23. Romijn JA, Coyle EF, Sidossis LS, Rosenblatt J, Wolfe RR. Substrate metabolism during different exercise intensities in endurance-trained women. J Appl Physiol 88: 1707–1714, 2000.
24. Sidossis LS, Gastaldelli A, Klein S, Wolfe RR. Regulation of plasma fatty acid oxidation during low- and high-intensity exercise. Am J Physiol 272: E1065–E1070, 1997.
25. Simon J, Young JL, Blood DK, Segal KR, Case RB, Gutin B. Plasma lactate and ventilation thresholds in trained and untrained cyclists. J Appl Physiol (1985) 60: 777–781, 1986.
26. Talanian JL, Galloway SD, Heigenhauser GJ, Bonen A, Spriet LL. Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women. J Appl Physiol 102: 1439–1447, 2007.
27. Tjønna AE, Lee SJ, Rognmo Ø, Stølen TO, Bye A, Haram PM, Loennechen JP, Al-Share QY, Skogvoll E, Slørdahl SA, Kemi OJ, Najjar SM, Wisløff U. Aerobic interval training versus continuous moderate exercise as a treatment for the metabolic syndrome: A pilot study. Circulation 118: 346–354, 2008.
28. Warren A, Howden EJ, Williams AD, Fell JW, Johnson NA. Postexercise fat oxidation: Effect of exercise duration, intensity, and modality. Int J Sport Nutr Exerc Metab 19: 607–623, 2009.
29. Whyte LJ, Gill JM, Cathcart AJ. Effect of 2 weeks of sprint interval training on health-related outcomes in sedentary overweight/obese men. Metabolism 59: 1421–1428, 2010.