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Metabolic and Hormonal Responses To Isoenergetic High-Intensity Interval Exercise and Continuous Moderate-Intensity Exercise
Metabolic and Hormonal Responses To Isoenergetic High-Intensity Interval Exercise and Continuous Moderate-Intensity Exercise
Peake JM, Tan SJ, Markworth JF, Broadbent JA, Skinner TL, out” effort or at intensities close to maximum oxygen con-
yield any detailed information on specific metabolic responses and adding this to the power output in the prior completed stage of the
to exercise (51). Subsequently, metabolomics and proteomics test. The test was repeated at least 48 h later, and the higher V̇O2 max
have been used to determine responses to acute exercise (34, and associated peak power output were used to determine power
42, 43, 48) and in response to exercise training (49, 67). output during the experimental trials.
Familiarization trial. To determine whether the athletes could
However, we are not aware of any studies that have system-
complete the HIIT session, they completed a familiarization trial at
atically employed metabolomics to compare metabolic re- least 48 h following the second V̇O2 max test. This required them to
sponses to different modes of exercise. complete 10 ⫻ 4 min intervals at a power output corresponding to
CHO and fat metabolism during exercise is regulated by ⬃80% V̇O2 max, with a 2-min recovery at 50 W (11.4 ⫾ 0.9% peak
various hormones, including insulin, glucagon, cortisol, adre- power output) between the intervals. The work completed during each
nocorticotrophic hormone (ACTH), growth hormone, epineph- interval was calculated by multiplying the power output for each
rine, and norepinephrine (37). The cytokine interleukin (IL)-6 athlete at 80% V̇O2 max by the duration of the interval (240 s). The
also influences metabolism during exercise in a hormone-like work completed during each recovery period was calculated by
manner (50). Combining metabolomics with a range of coun- multiplying the power output (50 W) by the duration of the recovery
terregulatory hormones provides a more complete perspective period (120 s). These two figures were added together and then
multiplied by 10 to calculate the total amount of work that each athlete
on cross talk between the endocrine system and metabolic
Table 1. Exercise intensity and substrate oxidation during during exercise was not significantly different between the
exercise HIIT and MOD trials (P ⫽ 0.71) (Table 1). HR, V̇O2,
%V̇O2 max, power output, %peak power output, and the rate of
HIIT MOD
energy expenditure were all higher during HIIT compared with
Heart rate, beats/min 179.9 ⫾ 9.6* 154.3 ⫾ 10.7 the corresponding periods during MOD (P ⬍ 0.05) (Table 1).
V̇O2, l/min 3.7 ⫾ 0.3* 2.9 ⫾ 0.2
V̇O2max, % 81.6 ⫾ 3.7* 66.7 ⫾ 3.5
The rates of CHO oxidation (Table 1) and blood lactate
Power output, W 319 ⫾ 26* 216 ⫾ 26 concentration (Fig. 1) were also higher during HIIT compared
Peak power output, % 72.0 ⫾ 3.2 48.5 ⫾ 3.1 with MOD (P ⬍ 0.01). Conversely, the rate of fat oxidation
CHO oxidation, g/min 4.20 ⫾ 1.04* 2.75 ⫾ 0.64 tended to be lower (P ⫽ 0.037), whereas respiratory exchange
Fat oxidation, g/min 0.41 ⫾ 0.26 0.47 ⫾ 0.25
RER 0.95 ⫾ 0.04 0.91 ⫾ 0.04
ratio tended to be higher (P ⫽ 0.063), during HIIT compared
Lactate, mmol/l 7.5 ⫾ 1.2* 1.5 ⫾ 1.1 with MOD (Table 1).
Rate of EE, kJ/min 19.4 ⫾ 1.6* 15.7 ⫾ 1.5 Glucose, lactate, and free fatty acids. Blood lactate was
Total work, kJ 792 ⫾ 95 797 ⫾ 95 higher throughout HIIT compared with MOD (P ⬍ 0.01;
Data are means ⫾ SD. HIIT, high-intensity interval training; MOD, mod- Fig. 1A). Compared with preexercise values, plasma glucose
concentration (P ⬍ 0.01; Fig. 1B) and total serum free fatty
#
Blood lactate (mmol/l)
0.9
10
0.6
5
0.3
10
mean ⫾ 95% confidence interval for plasma
Glucose (mmol/l)
ST
1H
2H
ST
1H
2H
ST
1H
2H
ST
1H
2H
PR
PR
PR
PR
PO
PO
PO
PO
Fig. 2. Network map (A) and KEGG classification of metabolomic species (B) identified and quantified in plasma by gas chromatography-mass spectrometry.
Numbered nodes represent measured metabolites. Nodes with colored letters represent a significant change with time for specific species after HIIT (H) and MOD
(M) exercise. Numbered nodes with red boarders represent those metabolites that had a significantly different response between high-intensity intervals and
continuous, moderate-intensity exercise. The Venn diagram (C) illustrates the distribution of common and trial-specific changes in metabolomic species after
exercise.
Fig. 3. Heat map showing fold changes in metabolomic compounds after high-intensity intervals and continuous, moderate-intensity exercise. PUFA,
polyunsaturated fatty acids; SFA, saturated fatty acids; MUFA, monounsaturated fatty acids. Numbers on the right correspond to compound numbers in Fig. 2
and KEGG compound identifiers.
A 0.25 C 0.015
#
# *
0.20 *
0.010
Citric acid
Aconitic acid
0.15
0.10
0.005
0.05
0.04
0.001
0.02
0.00 0.000
H
H
ST
E
E
E
ST
ST
ST
1H
1H
2H
1H
2H
R
2
2
PR
PR
PR
PO
P
PO
O
P
P
H IIT MOD H IIT MOD
The saturated fatty acids myristic acid (Fig. 6A), dodecanoic plasma concentrations of ACTH, free cortisol, and growth
acid (Fig. 6B), and decanoic acid (Fig. 6C) all increased after hormone were all higher immediately after HIIT (P ⬍ 0.05).
both trials (P ⬍ 0.01). The monounsaturated fatty acids palmi- During the postexercise recovery period, growth hormone
toleic acid (Fig. 6D) and heptadecenoic acid (data not shown) concentration remained elevated up to 1 h after MOD and up
increased after both trials (P ⬍ 0.01), whereas myristoleic acid to 2 h after HIIT (P ⬍ 0.05), whereas IL-6 remained elevated
(Fig. 6E) and oleic acid (Fig. 6F) increased only after HIIT up to 2 h after both HIIT and MOD (P ⬍ 0.01). Norepinephrine
(P ⬍ 0.05) (Fig. 6). The polyunsaturated fatty acid ␥-linolenic was also higher 1 h after MOD (P ⬍ 0.01), whereas ACTH was
acid increased after MOD (P ⫽ 0.005), and there was a trend lower than preexercise values 2 h after HIIT (P ⬍ 0.01).
toward an increase after HIIT (P ⫽ 0.037) (data not shown). Plasma insulin concentration did not change significantly fol-
The increase in some of these fatty acids (e.g., oleic acid, lowing HIIT (P ⫽ 0.14) or MOD (P ⫽ 0.055) (Fig. 7G).
myristoleic acid) after exercise was relatively brief, whereas However, during the postexercise recovery period, insulin was
other fatty acids (e.g., myristic acid, palmitoleic acid) remained lower than preexercise values at 1 and 2 h after both HIIT and
elevated during the 2-h recovery period. MOD (P ⬍ 0.01). Plasma glucagon also did not change
The percentage molar distribution of all nonesterified fatty significantly during HIIT (P ⫽ 0.12) or MOD (P ⫽ 0.32) (Fig.
acid (NEFA) detected in plasma was calculated using normal- 7H), whereas it was lower than preexercise values at 2 h after
ized peak heights as previously described (39) and is presented both HIIT and MOD (P ⬍ 0.05).
in Table 2. Among the fatty acids that increased after exercise,
oleic acid was the most abundant fatty acid, whereas myristo- DISCUSSION
leic acid was the least abundant. The molar distribution of
dodecanoic acid, myristic acid, and palmitoleic acid increased In this study, we systematically compared the metabolic and
after both HIIT and MOD (P ⬍ 0.05), the molar distribution of hormonal responses to matched-work high-intensity interval
octanoic acid decreased after MOD (P ⬍ 0.05), and the molar and continuous moderate-intensity exercise. CHO oxidation,
distribution of linoleic acid decreased after HIIT (P ⬍ 0.05). plasma glucose, and lactate were markedly higher after high-
Other metabolomic species that were present in plasma intensity interval exercise compared with continuous moder-
(including glycine, phenylalanine, cysteine, threonine, orni- ate-intensity exercise, whereas fat oxidation and total serum
thine, arachidonic acid, adrenic acid, docosahexaenoic acid, eico- NEFA were not significantly different between the two exer-
sapentaenoic acid, bis-homo-␥-linolenic acid, azelaic acid, oc- cise trials. Targeted metabolomic analysis of plasma samples
tanoylcarnitine, palmitic acid, stearic acid, arachidic acid, quinic revealed detailed insights into the exercise intensity-dependent
acid, heptadecanoic acid, phenylacetic acid) did not change changes in TCA cycle intermediates, specific NEFA, and
significantly after exercise (P ⬎ 0.05). amino acids. Although there was no significant difference in
Hormones. The plasma concentrations of growth hormone total serum NEFA between the two trials after exercise, we did
(Fig. 7A), norepinephrine (Fig. 7B), and IL-6 (Fig. 7C) in- notice some differences in the abundance of individual fatty
creased after both HIIT and MOD, whereas ACTH (Fig. 7D), acids. This finding highlights the importance of considering
free cortisol (Fig. 7E), and epinephrine (Fig. 7F) increased more than changes in total serum NEFA when evaluating the
only after HIIT (P ⬍ 0.05) (Fig. 7). Compared with MOD, the metabolic demands of exercise. The significant increase in
A 2.0
#
D 0.9
* * *
0.8
1.5 #
0.7
Alanine
Valine
1.0
0.6
0.5
0.5
0.0 0.4
B 0.05 E 0.05
* * *
0.04 0.04
0.00 0.00
C 0.5
* * F 1.5
*
0.4
1.0
0.3
Leucine
Proline
0.2
0.5
0.1
0.0 0.0
E
ST
1H
2H
ST
1H
2H
ST
1H
2H
ST
1H
2H
PR
PR
PR
PR
PO
PO
PO
PO
H IIT MOD H IIT MOD
TCA cycle intermediates suggests that during exercise these (48), urinary succinate (12), plasma/serum succinate, malate,
metabolic compounds spill over from muscle into the circula- fumarate, citrate-isocitrate, aconitic acid, and ␣-ketoglutarate
tion and/or are released systemically from other metabolic (34, 42) after exercise. Lewis et al. (34) observed that succi-
organs (e.g., the liver). The individual NEFA that were most nate, malate, and fumarate (but not citrate-isocitrate, aconitic
responsive to exercise were not necessarily the most abundant acid, or ␣-ketoglutarate) were higher in plasma from fast
NEFA in plasma. This finding raises some questions about the marathon runners compared with slow marathon runners. This
factors that determine the preference(s) for mobilization of finding also provides some indirect evidence of the intensity-
NEFA during exercise. Furthermore, the changes in the per- dependent changes in these TCA intermediates after exercise
centage molar distribution of NEFA contrast with previous that we observed. The biological role (if any) of TCA inter-
findings after exercise and challenge the previously held notion mediates in urine and plasma after exercise is unclear because
that changes in plasma NEFA composition reflect the compo- they are primarily active in skeletal muscle (14, 15) and the
sition of adipose tissue. These metabolic changes were accom- liver (24) during exercise. It is likely that the presence of TCA
panied by changes in counterregulatory hormones, some of intermediates in urine and plasma after exercise likely reflects
which increased only after HIIT. Collectively, these findings “spillover” from skeletal muscle or the liver.
highlight the value of targeted metabolomics to obtain more The intensity-dependent increase in plasma TCA intermedi-
detailed and specific information on metabolic responses to ates in the present study agrees with other reports that the
exercise beyond basic measures of substrate oxidation, glu- concentration of TCA intermediates in skeletal muscle also
cose, and free fatty acids. increases with exercise intensity (15). The increase in the
TCA intermediates, including citric acid (1.8-fold), succinic concentration of TCA intermediates in skeletal muscle, and
acid (3.0-fold), aconitic acid (2.0-fold), and malonic acid possibly plasma too, during high-intensity exercise may result
(1.6-fold), all increased in plasma during high-intensity inter- from epinephrine-induced accumulation of pyruvate (54). Gi-
val exercise in the present study. Of the TCA intermediates, bala et al. (15) found that of all of the TCA intermediates in
only succinic acid increased in response to moderate-intensity skeletal muscle, malate increased to the greatest extent (7.5⫻)
exercise, and this response was considerably lower than the during exercise and contributed the most to the expansion of
response following high-intensity interval exercise. Others the pool of TCA intermediates at the end of exercise. By
have reported an increase in urinary citrate and ␣-ketoglutarate contrast, succinic acid showed the greatest fold change in
A 0.25 E 0.06
* * * *
0.20
0.04
Palmitoleic acid
Myristic acid
0.15
0.10
0.02
0.05
0.00 0.00
B 0.10 C 0.0015
* * * *
0.08
Myristoleic acid
0.06
0.04
Fig. 6. Plasma fatty acids following HIIT and
0.0005 MOD. Data are in arbitrary units and repre-
sent means ⫾ SD. *P ⬍ 0.05 vs. preexercise.
0.02
0.00 0.0000
D 0.04 F 0.5
* *
0.4
*
0.03
Decanoic acid
0.3
Oleic acid
0.02
0.2
0.01
0.1
0.00 0.0
E
E
ST
2H
ST
ST
ST
1H
E
E
1H
2H
1H
2H
PR
2H
PR
1
PR
PR
PO
PO
PO
PO
plasma after exercise in the present study. One explanation for hetadecenoic acid (C17:1), and palmitoleic acid (C16:1), after
the rise in succinic acid is that carbon skeletons may enter the both exercise trials. Myristoleic acid (C14:1) and oleic acid
cycle at the level of 2-oxoglutarate through the alanine ami- (C18:1n-9) increased only after HIIT, whereas ␥-linolenic acid
notransferase reaction, thereby causing accumulation of inter- (C18:3) increased only after continuous, moderate-intensity
mediates in the second span of the TCA cycle (i.e., malate, exercise.
fumarate, succinate) (15). Typically, TCA intermediates accu- Among the NEFA that increased after exercise in the present
mulate in skeletal muscle early during exercise and then study, dodecanoic acid increased to the greatest extent (3.2-
progressively decline thereafter (18). In the present study, the fold), palmitoleic acid and myristic acid increased moderately
plasma concentrations of TCA intermediates may therefore (2.5-fold), and oleic acid increased only slightly (1.3-fold). The
have been higher during exercise compared with the end of percentage molar distribution of these NEFA also increased
exercise. after exercise (Table 2). Interestingly, with the exception of
Most exercise studies have focused on changes in plasma/ oleic acid, these NEFA generally comprised ⬍4% of the sum
serum NEFA; comparatively little research has investigated of all NEFA that we measured in plasma. Palmitoleic acid and
exercise-induced changed in other lipid classes (e.g., phospho- myristic acid also make up only a small proportion of fatty
lipids, mono-, di- or triacylglcerols, diacylglycerols, choles- acids in adipose tissue (23, 29). Changes in plasma fatty acids
teryl esters) (44). NEFA represent a relatively small proportion during exercise represent the balance between fatty acid release
of fatty acids in tissues. Nevertheless, they are important in the from adipose tissue and fatty acid uptake into skeletal muscle
context of exercise from both a physiological standpoint (i.e., and the liver (41). There are several possible explanations as to
alterations in the composition of fatty acids delivered to tis- why dodecanoic acid, palmitoleic acid, and myristic acid were
sues) and a practical perspective (i.e., increasing the likelihood preferentially mobilized during exercise despite their low rel-
of detecting significant changes) (44). In addition to an in- ative abundance in plasma and adipose tissue. One possibility
crease in total serum NEFA, we detected increases in the is that transport proteins for these particular fatty acids are
plasma concentration of specific NEFA, including myristic more abundant in skeletal muscle and adipose tissue, and/or
acid (C14:0), decanoic acid (C10:0), dodecanoic acid (C12:0), they are more sensitive to muscle contractions and hormones.
Octanoic acid (C8:0) 0.4 (0.3) 0.3 (0.3) 0.3 (0.1) 0.2 (0.1) 0.3 (0.1) 0.3 (0.1) 0.2 (0.1)* 0.2 (0.1)*
Decanoic acid (C10:0) 0.3 (0.2) 0.5 (0.3) 0.5 (0.3) 0.4 (0.3) 0.4 (0.2) 0.6 (0.2) 0.4 (0.2) 0.5 (0.3)
Dodecanoic acid (C12:0) 0.6 (0.2) 1.5 (0.6)* 1.0 (0.8) 1.3 (0.9)* 0.7 (0.4) 1.8 (0.5)* 1.1 (0.6)* 1.3 (0.8)*
Myristic acid (C14:0) 1.8 (0.5) 3.4 (0.9)* 2.7 (1.0)* 3.4 (1.6)* 2.0 (0.7) 4.4 (1.2)* 3.1 (0.9)* 3.3 (1.0)*
Palmitic acid (C16:0) 30 (0.8) 29 (0.8) 30 (0.8) 30 (0.8) 32 (5.8) 29 (1.3) 30 (0.7) 30 (1.0)
Margaric acid (C17:0) 1.1 (0.2) 1.3 (0.3) 1.2 (0.2) 1.2 (0.3) 1.0 (1.0) 1.2 (0.3) 1.2 (0.2) 1.3 (0.2)
Stearic acid (C18:0) 24 (1.2) 23 (1.2) 23 (2.3) 23 (3.2) 22 (3.5) 21 (2.2) 23 (1.6) 22 (1.0)
Arachidic acid (C20:0) 0.2 (0.34) 0.2 (0.19) 0.1 (0.09) 0.1 (0.02) 0.2 (0.17) 0.1 (0.03) 0.1 (0.02) 0.1 (0.01)
Myristoleic acid (C14:1) 0.02 (0.004) 0.03 (0.005) 0.02 (0.005) 0.02 (0.003) 0.06 (0.127) 0.02 (0.005) 0.02 (0.003) 0.03 (0.004)
Palmitoleic acid (C16:1) 0.3 (0.1) 0.6 (0.2)* 0.5 (0.2)* 0.7 (0.3)* 0.4 (0.1) 0.9 (0.4)* 0.6 (0.2)* 0.7 (0.2)*
Vaccenic acid (C18:1n-7) 9.1 (0.1) 8.7 (0.7) 9.0 (0.6) 8.7 (0.6) 8.8 (1.6) 8.5 (0.9) 8.7 (0.6) 8.7 (0.5)
Oleic acid (C18:1n-9) 7.5 (1.0) 8.1 (1.0) 7.9 (0.9)* 8.7 (1.1) 8.1 (0.8) 8.8 (0.7) 8.2 (0.7) 8.3 (0.7)
Linoleic acid (C18:2) 16 (0.9) 15 (1.1)* 16 (1.3) 15 (0.9)* 16 (1.6) 15 (1.8) 15 (1.1) 15 (0.8)
Up to five different fatty acid transport proteins are expressed exercise trials. Consistent with other studies, there were no
in skeletal muscle and adipose tissue (20). It is yet to be significant differences in plasma fatty acid concentrations dur-
determined whether these individual proteins transport specific ing recovery from the high-intensity exercise and the continu-
fatty acids. However, the expression or function of specific ous moderate-intensity exercise (22, 41). In support of the
substrate transporters may be adaptable to alter preferences for present study in relation to postexercise lipid metabolism,
certain cellular substrates (20). Another possibility is that the several studies have found no difference in fat oxidation or
chemical structure of these fatty acids favors a greater ATP respiratory exchange ratio after high-intensity exercise com-
yield (relative to O2 demand) during exercise compared with pared with moderate-intensity exercise (30, 31). By contrast,
other fatty acids. Further research is needed to examine in more others have reported that fat oxidation was higher while respi-
detail why certain fatty acids are mobilized into the circulation ratory exchange ratio was lower after high-intensity exercise
to a greater or lesser extent during exercise. compared with moderate-intensity exercise (36, 63). These
We observed that the ratio of unsaturated/saturated NEFA in discrepancies may reflect differences between these studies in
plasma did not change after exercise, which contrasts with exercise protocols and the training status of participants. It also
other research reporting an increase in this ratio. Mougios et al. remains unclear whether differences in intensity and substrate
(39) reported that the molar distribution of palmitic acid and metabolism during exercise translate to differences in energy
stearic acid increased, whereas the molar distribution of oleic expenditure during recovery from exercise (31, 38).
acid and linoleic acid decreased, after exercise. It is difficult to In the present study, changes in the concentration of NEFA
compare these studies with our results because we measured a and other specific fatty acids (e.g., dodecanoic acid, myristic
greater number of plasma NEFA. Consequently, the ratio of acid, palmitoleic acid) remained high for 2 h after exercise.
unsaturated/saturated fatty acids was lower in the present Mulla et al. (41) reported similar changes in NEFA and
study. Nevertheless, we observed that the molar distribution of glycerol output from adipose tissue during and after exercise.
palmitic acid and stearic acid did not change, oleic acid Together, these findings reflect a shift in substrate oxidation in
increased slightly, and linoleic acid decreased slightly (Table favor of lipid metabolism (28, 30). This response may occur to
2). The changes in these specific NEFA after exercise are continue supplying energy while facilitating restoration of
generally consistent with other studies (6, 39). In addition to glucose homeostasis and glycogen restoration (30).
differences in the number of NEFA that we detected, the This is the first study to compare the effects of exercise
variation between our findings and others (39) may be related intensity on changes in a broad range of amino acids in plasma.
to the intensity and duration of exercise and the sex and The plasma concentrations of alanine, glutamate, and tyrosine
training status of the participants. increased significantly only during high-intensity interval ex-
A strength of the present study is that we monitored meta- ercise. Furthermore, alanine was significantly higher after
bolic changes not only immediately following completion of high-intensity interval exercise compared with continuous
exercise but additionally during the early hours of recovery moderate-intensity exercise. Other studies have reported an
from exercise. We found that total serum NEFA remained increase in alanine concentration in both venous plasma (3) and
elevated 2 h after both high-intensity interval exercise and arterial plasma in response to exercise (40, 59). This rise in
continuous, moderate-intensity exercise. Among the individual alanine within the circulation reflects its synthesis and release
fatty acids that we measured in plasma by metabolomics, from skeletal muscle (58). Previous research indicates that
heptadecenoic acid, dodecanoic acid, myristic acid, oleic acid, alanine release from skeletal muscle is more sustained during
and palmitoleic acid were also still elevated 2 h after both exercise with low vs. normal muscle glycogen (59). We did not
A * # E
#
16384
*
150 *
8192
4096
log 2 GH (pg/ml)
2048 100
*
Freecortisol
1024
*
512
256 50
128
64
32 0
B 40 F 1.5
*
*
Adrenaline (nmol/l)
1.0
20
*
0.5
10 * Fig. 7. Plasma hormones following HIIT and
MOD. Data represent means ⫾ SD for gluca-
0 0.0 gon; geometric mean ⫾ 95% confidence in-
terval for ACTH, insulin, and growth hor-
mone; and median ⫾ interquartile range for
C 5 * G 200 norepinephrine, epinephrine, cortisol, and in-
terleukin (IL)-6. *P ⬍ 0.05 vs. preexercise.
4 #P ⬍ 0.05 for HIIT vs. MOD. NB, free
150 cortisol represents the ratio between total cor-
* tisol and cortisol-binding globulin.
Insulin (pmol/l)
3
IL-6 (pg/ml)
100
2
* *
50
1
0 0
D 40 H 300
#
*
30
* *
200
Glucagon (pg/ml)
ACTH (pmol/l)
20
100
10
*
0 0
E
E
1H
2H
1H
2H
1H
2H
1H
2H
ST
ST
ST
ST
PR
PR
PR
PR
PO
PO
PO
PO
measure muscle glycogen in the present study, but the greater We can only speculate, but the increase in venous plasma
reliance on CHO metabolism could possibly account for the glutamate concentration that we observed may have served
higher plasma concentration of alanine after high-intensity to generate more TCA intermediates during high-intensity
interval exercise. In contrast with our findings, other studies interval exercise. We detected increases in the plasma con-
have reported a decrease (40) or no change (59) in the con- centrations of 4-methyl-2-oxopentanoic acid and 3-methyl-
centration of glutamate in arterial plasma. In skeletal muscle, 2-oxopentanoic acid after high-intensity intermittent exer-
glutamate consumption increases markedly during the first few cise. These carboxylic acids may represent breakdown prod-
minutes of exercise, particularly when muscle glycogen is low ucts of leucine (46).
(59). The consumption of glutamate in muscle may shift the The other amino acids that we measured in plasma (i.e.,
alanine aminotransferase reaction in favor of the formation of threonine, phenylalanine, glycine, cysteine, proline, and orni-
alanine and TCA intermediates such as ␣-oxoglutarate (58). thine) did not change significantly during either exercise trial.
Some of these amino acids, such as threonine, phenylalanine, role for these hormones in regulating fat metabolism during
and glycine, are not metabolized in skeletal muscle (58), which exercise. At rest, IL-6 induces lipolysis in skeletal muscle (but
could explain why they did not change after exercise in this not adipose tissue) (66), yet its role in regulating lipid metab-
study. It is possible that phenylalanine is converted to tyrosine, olism during exercise remains unresolved (62). Cortisol medi-
which might partially account for the rise in plasma tyrosine ates protein metabolism during exercise (11) and could possi-
concentration that occurred during high-intensity interval ex- bly account for the higher plasma alanine concentration after
ercise. high-intensity intermittent exercise in the present study.
During recovery from exercise, branched-chain amino acids, There were several limitations to the present study. First, we
methionine, alanine, and proline were all significantly lower could not determine the precise intensity for high-intensity
compared with preexercise, particularly after continuous mod- interval exercise and continuous moderate-intensity exercise
erate-intensity exercise. This sustained decline in these amino that would elicit the greatest difference in CHO and fat me-
acids during recovery from exercise reflects their role in tabolism. Second, the short 30-s stages that we employed
gluconeogenesis. Wahren et al. (61) provided early evidence during the V̇O2 max test may not have provided stable readings
that amino acids (particularly alanine), pyruvate and lactate to determine relative workloads in an accurate manner. Last,
assist in restoring hepatic glucose metabolism after exercise. we did not assess the metabolic and hormonal response to
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and degradation in intact hind-limb muscle of lambs. Biochem J 233: Loennechen JP, Al-Share QY, Skogvoll E, Slordahl SA, Kemi OJ,
417–425, 1986. Najjar SM, Wisloff U. Aerobic interval training versus continuous
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com/Library/. . ./5990 –3638en_lo%20CMS.pdf. amino acid metabolism during prolonged knee-extensor exercise in hu-
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