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Two Weeks of High-Intensity Aerobic Interval Training Increases The Capacity For Fat Oxidation During Exercise in Women. Journal of A
Two Weeks of High-Intensity Aerobic Interval Training Increases The Capacity For Fat Oxidation During Exercise in Women. Journal of A
Talanian JL, Galloway SD, Heigenhauser GJ, Bonen A, Spriet ing exercise and also for athletes attempting to spare carbohy-
LL. Two weeks of high-intensity aerobic interval training increases drate during competition.
the capacity for fat oxidation during exercise in women. J Appl It has commonly been observed that 6 12 wk of exercise
Physiol 102: 1439 1447, 2007. First published December 14, 2006; training at a moderate intensity [MIT, 60 75% peak O2 con-
doi:10.1152/japplphysiol.01098.2006.Our aim was to examine the sumption (VO2 peak)] can improve aerobic capacity and maxi-
effects of seven high-intensity aerobic interval training (HIIT) ses-
Address for reprint requests and other correspondence: J. L. Talanian, Dept. The costs of publication of this article were defrayed in part by the payment
of Human Health and Nutritional Sciences, Univ. of Guelph, Guelph, ON, of page charges. The article must therefore be hereby marked advertisement
Canada N1G 2W1 (e-mail: [email protected]). in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
http://www. jap.org 8750-7587/07 $8.00 Copyright 2007 the American Physiological Society 1439
1440 FAT METABOLISM DURING HIGH-INTENSITY INTERVAL TRAINING
in the study. On average, subjects engaged in recreational physical (Fig. 1). All training sessions were supervised. Each session
activity 23 days/wk. Most subjects did not limit their exercise to one consisted of ten 4-min cycling bouts at 90% VO2 peak separated by 2
type, but common activities included weight lifting, soccer, cycling, min of rest. Heart rate (HR) was recorded throughout training and was
swimming, and walking. Subjects were fully informed of the purpose held constant at 90% of maximal by increases in the power output
of the study and of potential risks before giving written consent. This as training progressed. Required adjustments in training power output
study was approved by the Ethics Committees at McMaster Univer- were made at the beginning of sessions, and all subjects experienced
sity and the University of Guelph. three power output increases during the initial six training sessions.
During training session 7, subjects cycled at the same power output as
Preliminary Testing during training session 2 to enable training-related comparisons.
Before the study, subjects reported to the laboratory on two During training sessions 2 and 7, respiratory gases and venous blood
occasions. On the first visit, subjects performed an incremental cy- samples (Teflon catheter) were collected before and immediately after
cling (Lode Excalibur, Quinton Instrument, Grogingen The Nether- bouts 1, 3, 5, and 10. Throughout the 2 wk of training, subjects
lands) test to exhaustion for determination of VO2 peak. Respiratory continued the recreational activities in which they were engaged
gases were collected and analyzed using a metabolic cart (Vmax 229, before training.
Sensormedic, Yorba Linda, CA). On the second visit, appropriate
power outputs for the experimental trials were verified. Subjects Analyses
cycled for 15 min at 60% VO2 peak to establish the power output for the
60-min trial. They then performed four to six bouts of cycling at 90% Blood measurements. Venous blood was collected in heparin so-
VO2 peak, with each bout lasting 4 min and separated by 2 min of rest, dium tubes. A portion (1.5 ml) was added to 30 l of EGTA and
to establish power outputs for the HIIT sessions. After 2 wk (7 reduced glutathione and centrifuged (10,000 g for 3 min), and the
RESULTS
Table 1. Respiratory, heart rate, and venous blood measurements during HIIT sessions 2 and 7
Bout 1 Bout 3 Bout 5 Bout 10
VO2, l/min
Session 2 2.030.17 2.190.16 2.190.17 2.240.15
Session 7 2.070.17 2.170.19 2.210.26 2.250.20
VO2 peak
Session 2, % pre training VO2 peak 86.12.5 92.82.5 92.92.5 94.82.3
Session 7, % post training VO2 peak 77.72.3* 81.52.6* 83.03.5* 84.42.6*
Heart rate, beats/min
Session 2 722 1712 1254 1802 1333 1812 1323 1811
Session 7 694 1672 1253 1742* 1293 1772* 1264 1772*
Lactate, mM
Session 2 0.60.1 2.10.3 3.10.2 3.40.2 3.50.1 3.60.2 3.20.2 3.30.2
Session 7 0.60.1 2.00.2 2.80.1 3.00.2 2.90.1 3.30.2 3.30.2 3.50.2
Glucose, mM
Session 2 4.840.12 4.580.25 4.900.23 4.530.21 5.160.32 4.940.17 5.340.19 4.510.18
Session 7 4.910.14 4.680.10 4.460.19 4.110.17 4.800.20 4.5850.21 5.340.28 4.770.24
FFA, mM
Session 2 0.440.10 0.270.04 0.340.06 0.260.03 0.430.11 0.280.04 0.590.14 0.380.11
Session 7 0.320.06 0.270.04 0.280.03 0.220.03 0.310.03 0.270.03 0.420.04 0.270.03
Glycerol, M
Session 2 35.46.3 41.67.6 59.28.0 67.07.5 87.211.9 84.210.4 109.412.0 127.713.5
Session 7 45.84.6 55.93.8 64.04.6 65.26.0 74.74.6 79.25.6 88.63.9* 97.65.9*
Values are means SE, (n 8). HIIT, high-intensity interval training; VO2, O2 consumption; FFA, free fatty acids. *Significantly lower (P 0.05) than the
same time point during session 2. Significantly higher (P 0.05) than the same time point during bout 1.
cycling during session 7. Whole blood glucose and plasma HSL protein content (13%) after training (Fig. 6). Total
FFA concentrations were unchanged throughout the training muscle FABPpm content increased 25% after training, while
bouts in both training sessions (Table 1). Whole blood glycerol muscle FAT/CD36 protein content was unchanged (Fig. 6).
concentrations increased during the training bouts in sessions 2 Resting muscle glycogen content was unaffected by training,
and 7 but were significantly lower before and after bout 10 in but net muscle glycogen utilization was decreased by 12% after
session 7 (Table 1). 60 min of exercise after training (Table 4). IMTG content
decreased 12% and 17% after 60 min of cycling before and
Cycling at 60% VO2 peak Before and After Training after training, respectively, but there was no difference be-
Subjects cycled for 60 min at 101.3 4.2 W before and after tween the trials (Table 4).
HIIT. This power output represented 63.9 2.6% of the Resting muscle PCr was similar in both trials, but PCr was
pretraining and 55.2 2.2% of the posttraining VO2 peak (Table higher 60 min after training, such that net PCr degradation was
2). The RER was significantly lower after HIIT (Table 2), and significantly decreased by 40% after HIIT. Muscle ATP was
the estimated whole body fat oxidation was significantly higher unchanged by exercise after both trials, but ATP contents were
at 30, 45, and 60 min of cycling (Fig. 2). Total fat oxidation lower after than before training at 60 min (Table 4). Muscle
during the 60-min trial before training was 15.0 2.4 g and free ADP at 60 min was lower after the posttraining trial (Table
increased by 36% after HIIT to 20.4 2.5 g. There was a 4). Muscle lactate contents increased from rest after 60 min of
reciprocal decrease in whole body carbohydrate oxidation at exercise to the same extent in both trials (Table 4).
30, 45, and 60 min after training (Fig. 3). Total carbohydrate
Table 2. Effects of HIIT on VO2 and RER during cycling at 60% pretraining VO2 peak
Cycling at 60% VO2 peak
VO2, l/min
Pre 1.470.06 1.500.06 1.510.05 1.510.05
Post 1.460.06 1.450.06 1.440.05 1.450.06
VO2 peak
Pre, % pretraining VO2 peak 62.12.6 64.12.9 64.62.3 64.83.1
Post, % posttraining VO2 peak 55.52.3* 55.42.6* 54.92.2* 55.22.9*
RER
Pre 0.920.02 0.910.02 0.880.01* 0.880.02
Post 0.890.02 0.850.02* 0.840.02* 0.840.02*
Values are means SE, (n 8). RER, respiratory exchange ratio; Pre, pretraining; Post, posttraining. *Significantly different (P 0.05) from the same time
point during pretraining trial. Significantly different (P 0.05) from 15 min of the same trial.
Table 3. Effects of HIIT on venous blood measurements during cycling at 60% pretraining VO2 peak
Cycling at 60% VO2 peak
FFA, mM
Pre 0.600.14 0.390.06 0.490.10 0.650.14 0.870.16
Post 0.520.11 0.420.06 0.480.06 0.560.14 0.720.16
Glycerol, M
Pre 60.05.6 67.25.1 89.65.1 118.97.1 140.510.5
Post 54.43.8 79.23.8 110.012.6* 131.312.8 166.413.6*
Glucose, mM
Pre 4.40.2 4.80.3 4.70.3 4.50.3 4.40.3
Post 5.20.2* 4.80.3 5.10.4 5.20.3* 5.20.4*
Values are means SE, (n 8). *Significantly different (P 0.05) from the same time point during pretraining trial. Significantly different (P 0.05)
from 0 min of the same trial.
increases in -HAD activity were observed after only seven oxidation during exercise (62). Therefore, HIIT offers a short-
training sessions. In contrast, with other protocols in which duration stimulus for elite endurance athletes to increase fat
subjects trained for 2 h/day for 57 days (46, 47) and six sprint oxidation during exercise above an already high endurance
Glycogen, mmol/kg dry mass 468.625.0 136.517.4 474.625.8 182.415.5* 332.119.1 292.222.3*
IMTG, mmol/kg dry mass 46.42.6 41.03.0 43.13.3 35.83.4 5.43.5 7.33.7
PCr, mmol/kg dry mass 76.93.3 53.54.3 77.23.2 63.13.3 23.45.8 14.13.3*
ATP, mmol/kg dry mass 24.11.2 24.21.6 22.40.8 21.50.8* 0.11.1 0.90.3
Free ADP, mol/kg dry mass 101.810.5 198.041.5 88.12.3 120.19.7* 96.139.9 32.19.7*
Free AMP, mol/kg dry mass 0.460.12 1.870.81 0.330.01 0.660.08 1.410.8 0.330.09*
Lactate, mmol/kg dry mass 3.90.4 11.10.9 3.70.5 9.90.8 7.21.0 6.21.6
Values are means SE, (n 8). PCr, phosphocreatine; IMTG, intramuscular triacylglycerol; , change. *Significantly different (P 0.05) from the same
time point during pretraining trial. Significantly different (P 0.05) from 0 min of the same trial.
Skeletal Muscle Fat Metabolism similar to that of oxidative capacity within tissue types
(heart red muscle white muscle) in rodents (7). Therefore,
Increases in skeletal muscle fat oxidation likely result from it remains possible that there was a shift in the fractional
a number of adaptations, including an increase in mitochon- concentrations of FAT/CD36 on the mitochondria and plasma