Physiology and Biochemistry
Effects of a Training Taper on Tissue Damage Indices, Serum
Antioxidant Capacity and Half-Marathon Running Performance
R. B. Child, D. M. Wilkinson, J. L. Fallowfield
Exercise Physiology Research Group, University College Chichester, Chichester, UK
Child RB, Wilkinson DM, Fallowfield JL. Effects of a Training
Taper on Tissue Damage Indices, Serum Antioxidant Capacity
and Half-Marathon Running Performance. Int J Sports Med
2000; 21: 325 – 331
Accepted after revision: December 20, 1999
■■■■ This study investigated the effects of a training taper on
muscle damage indices and performance. Two matched groups
of seven male runners each performed two self paced half-mara-
thons on a motorised treadmill. After the first half-marathon one
group maintained their normal weekly training volume, while
the taper group progressively reduced weekly training volume
by 85 %. Venous blood was drawn immediately before and after
the first half-marathon. Subsequent samples were taken 7 days
later, immediately before and after the second half-marathon.
Serum samples were analysed for antioxidant capacity, urate
concentration and creatine kinase activity (CK). The plasma con-
centration of malondialdehyde (MDA) was used as a marker of
lipid peroxidation. There were no differences in running per-
formance either between the first and second half-marathon
within each group, or between groups (86.75 ± 2.65 min and
87.67 ± 2.87 min for the “normal training” group vs 85.62 ± 2.81
min and 85.39 ± 3.52 min for the “training taper” group). Serum
antioxidant capacity and CK were increased over time (P < 0.05,
ANOVA), with significant elevations after each half-marathon
(P < 0.025, t-test). Elevations in MDA attained significance for
the first half-marathon (P < 0.05, t-test) when data for both sub-
ject groups were pooled. There were no differences in serum an-
tioxidant capacity, or urate concentration between groups. Post-
exercise CK was lower following the training taper (149 ± 22 %
baseline, for the training taper vs 269 ± 55 % baseline for the nor-
mal training group, P < 0.05, t-test). Despite evidence that the
training taper reduced muscle damage, relative to the normal
training group, half-marathon performance was not enhanced.
■ Key words: Reduced training, overreaching, training volume,
free radicals, exercise.
Int J Sports Med 2000; 21: 325 – 331
© Georg Thieme Verlag Stuttgart · New York
ISSN 0172-4622
325
Introduction
Muscle contraction increases free radical formation [12, 24],
which has been implicated in muscle fatigue [38] and exercise
induced myocellular injury in humans [8, 27, 32]. The rise in
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oxidative stress during physical activity has been partially at-
tributed to increased mitochondrial respiration [43], which
has been estimated to rise up to 200 fold in active muscle fi-
bres [28]. Exercise such as running can elevate markers of oxi-
dative damage, such as malondialdehyde [12, 32] and pro-
duces damage to muscle membranes [37, 45]. These events
are often associated with the release of myocellular proteins
[17] and compromised membrane function [12,17]. Antioxi-
dant defences include enzymes such as superoxide dismutase
and glutathione peroxidase, and non-enzymatic compounds
such as vitamins and reduced glutathione. Some aspects of an-
tioxidant protection can be increased by training [26, 41, 45] ,
especially the enzymes of glutathione synthesis [30, 41].
It has been suggested that heavy exercise (either high intensity
or long duration) may deplete the pool of antioxidant vitamins
[25]. As a consequence, athletes who train regularly are
thought to be particularly susceptible to free radical mediated
damage [5, 25]. Experiments using rodents provide some evi-
dence to support such proposals; typically these show that
acute exercise reduces the vitamin E content of skeletal muscle
[4, 39, 40], while exercise training compromises myocellular
vitamin E status in whole muscle [11] and mitochondria [19].
These observations may have led Brooks et al. [5] to suggest
that repeated sessions of exercise might produce a progressive
reduction in membrane antioxidants. Such compounds in-
clude vitamin E and carotenoids, the presence of which can in-
hibit peroxidation of membrane lipids [44, 48]. Animals defi-
cient in vitamin E are more susceptible to exercise induced
muscle damage, assessed by the release of muscle enzymes
[12]; peroxidative damage [12] and fatigue [12, 34]. Such ob-
servations indicate that compromised myocellular free radical
protection can increase susceptibility to exercise induced lipid
peroxidation oxidative injury and fatigue, which may have
profound effects on exercise performance.
A training taper is defined as a systematic reduction in training
volume [22], and the application of this intervention prior to
distance running can enhance performance [22, 42]. Previous
training taper studies have focused on running events of less
than 20 minutes duration [22, 42], and little information is
326 Int J Sports Med 2000; 21 Child RB et al

available on endurance events such as marathon and half- Table 1 Profiles of subjects in normal and training taper groups, prior
marathon running [47]. Houmard et al. [22] reported im- to the first half-marathon
proved running performance during a 5 km time trial, which
was attributed to a 6 % decrease in submaximal oxygen con- Parameter Taper group Normal group
n=7 n=7
sumption (i.e. improved running economy). As this is an im-
portant contributor to middle and long, distance running per-
Age (years) 31 ± 2 30 ± 1
formance [3, 35], it has been proposed that reduced training
Running experience (years) 15 ± 1 14 ± 1
volumes might result in even greater performance benefits
for endurance events [23]. At present however, there are no Mass (kg) 72.4 ± 2.1 71.2 ± 1.6
empirical data to support this view [16]. Height (m) 1.77 ± 0.02 1.76 ± 0.02
Peak VO2 (ml · kg–1 · min–1) 63.2 ± 1.7 61.8 ± 1.4
Little is known about the mechanisms by which a training ta- Distance run (km · week–1) 50 ± 7 45 ± 7
per can improve exercise performance. Most studies have fo-
Running time (min · week–1) 215 ± 33 202 ± 28
cused on changes in glycogen availability and/or muscle oxida-
Average training speed (km · h–1) 14.8 ± 0.5 14.6 ± 0.4
tive capacity to explain the positive effects of reduced training
–1
[23, 33, 42]. However, beneficial effects could also arise by Urate (µmol · l ) 258 ± 18 270 ± 19
mechanisms unrelated to these factors. Distance running dis- TAC (µmol Trolox Eq · l–1) 456 ± 29 503 ± 39
rupts the muscle ultrastructure [20, 29] and the frequency of Plasma MDA (µmol · l–1) 1.43 ± 0.17 1.49 ± 0.16
such injuries appears to increase with training distance [29]. Serum CK (IU · l–1) 90 ± 32 115 ± 24
Muscle damage may be a limiting factor to long distance run-
ning performance [22, 29] and performing a training taper pro-
vides several potential mechanisms to reduce exercise induced

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myocellular injury.
Reducing training volume decreases myocellular oxygen utili-
sation, which in turn decreases the oxidative load on the mus-
cle. This could result in a more reductive myocellular redox en-
vironment and experiments in mice have shown this can im-
prove exercise performance and increase resistance to free
radical mediated muscle injury [45].
The objectives of this study were to reproduce the taper regi-
men of Houmard et al. [22] to test the hypotheses that a con-
trolled training taper could enhance half-marathon running
performance by improving serum antioxidant protection and
attenuating indices of lipid peroxidation and exercise induced
muscle damage.
After the first half-marathon the “normal training” group
maintained their usual weekly training volume at (100 %). This
was split as 15 % (day 1), 25 % (day 3), 25% (day 4), and 20 % (day
6) and was performed as long slow runs below half-marathon
pace. This group also performed 15 % weekly training as 400 m
repetitions at 10 km race pace, with a 1 : 1 work to rest ratio.
Repetition training was divided equally into two training ses-
sions which were performed on days 2 and 5 after the first
half-marathon. The day prior to the second half-marathon
was a rest day. A schematic representation of the training in-
terventions is shown in Fig. 1. Venous blood samples were
taken immediately prior to and following the first half-mara-
thon, at time-points A and B, respectively. Further blood sam-
ples were taken immediately prior to and following the second
half-marathon, at time points C and D, respectively.

Methods Experimental protocol

Prior to the study, subjects were interviewed to determine the
number of years they had been involved in running training.
Each subject was asked to keep a training diary for the one
month period prior to the first simulated half-marathon. From
the training diary average weekly running time and training
distance were calculated, from which average training speed
was derived. No attempt was made to control training in the
one month period prior to exercise. Based on the training data,
physiological characteristics (Table 1) and running ability, sub-
jects were matched into “normal training”, or “training taper”
groups. All subjects had run a half-marathon in under 95 min-
utes during the previous year.
The training taper was based on the regime used by Houmard
et al. [22]. In the training taper group total weekly training vol-
ume was reduced by 85 %. The 15 % weekly training performed
was split as 30 % (day 2), 25 % (day 3), 20 % (day 4), 15 % (day 5),
10 % day (day 6). Sessions were performed as 400 m repetitions
at 10 km race pace, with a 1 : 1 work to rest ratio. The day after
the first half-marathon and the day preceding the second half
marathon were rest days. Such a progressive training taper is
thought to be an effective way of improving exercise perform-
ance [33].
Subjects refrained from exercise for 36 hours before each la-
boratory testing session and performed only light training in
the 2 days prior to each half-marathon.
Within a 2 week period before the first half-marathon, each
subject completed a graded exercise test to derive individual
speed-oxygen uptake regression equations. The test involved
completion of four to six 4-minute stages, on a motorised
treadmill (Quinton Q65, Quinton Instruments, Seattle, USA).
Expired gas was collected in the final minute of each stage
using standard Douglas bag techniques. A fingertip blood sam-
ple was collected at the end of each exercise stage to deter-
mine the capillary blood lactate concentration (BLa). Following
collection of capillary blood, running velocity was increased
progressively by 1.5 km · h–1 and the test was terminated when
(BLa) exceeded 4 mmol · l–1. Following a 30 minute recovery
period, subjects performed an incremental graded test to es-
tablish peak VO2. Initial running velocity was set 2 km · h–1
slower than the velocity which elicited a BLa of 4 mmol · l–1 in
the previous test. The gradient was increased by 1.5 % every
90 s throughout the test. Expired gas was collected continu-
ously from 5 minutes, to test termination. Interpolation of the
Effects of a Training Taper on Tissue Damage
speed oxygen uptake regression was used to determine the
running velocity required to elicit 50 % and 70 % of peak VO2.
On the day of each half-marathon subjects reported to the la-
boratory following a 3 hour fast and stood for 20 minutes prior
to exercise, to normalise for postural changes in blood volume.
Immediately before exercise a 13 ml blood sample was drawn
from an antecubital vein. Each subject then performed a con-
trolled warm up on the treadmill, at a predetermined speed
corresponding to 50 % peak VO2 for 5 minutes. During the first
10 min of the half-marathon treadmill speed was held con-
stant at 70 % peak VO2, thereafter subjects were allowed to
run self paced and were encouraged to cover the remaining
distance in the shortest possible time. This was achieved by
enabling the subjects to adjust the velocity of the treadmill
during the run. Capillary BLa was measured pre-exercise, after
the warm up period, at 5 min, 10 min, 4, 8, 12, 16 and 20 km
during the half-marathon, and then again immediately post-
exercise. A further 13 ml of venous blood was drawn from an
antecubital vein immediately after exercise. Oxygen uptake
was recorded during exercise, just prior to collection of capil-
lary blood. To simulate race conditions subjects were allowed
water ad libitum at 5, 10, 15 and 19 km.
The volume of expired air was measured using a previously
calibrated dry gas meter (Harvard Apparatus, Kent, UK). Gas
fractions were determined using a paramagnetic oxygen ana-
lyser and infra red carbon dioxide analyser (Servomex 1400,
Crowborough, UK), calibrated with nitrogen, two gravimetri-
cally determined calibration gases (Linde Gases UK Ltd., Lon-
don, UK) and ambient air. Prior to analysis all gases were satu-
rated with water by passage throuch Nafion tubing (Omnifit
Ltd, Cambridge, UK) immersed in distilled water.
Biochemical analysis
The whole blood lactate concentration of capillary blood sam-
ples was determined immediately following collection. This
was performed using an automated analyser (Model 2300 Stat
plus, Yellow Springs Inc., Ohio, USA).
In venous blood, haemoglobin concentrations were deter-
mined by the cyanmethaemoglobin method using a diagnostic
Int J Sports Med 2000; 21 327
Fig. 1 Training regi-
mens in normal and
training taper groups
after the first half-
marathon.
kit (No. 124 729, Boehringer Mannheim, Mannheim, Germa-
ny). Haematocrit was determined in triplicate following mi-
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crocentrifugation (Hawksley and Sons Ltd, Lancing, UK). The
remaining venous blood was split between potassium EDTA
tubes, to be centrifuged immediately at 2500 g for 10 minutes
and plain tubes (to be centrifuged using the same protocol
after clotting at room temperature for 1 hour). Plasma and se-
rum were removed, and stored at – 20 8C until analysis. Post-
exercise measurements in venous blood were corrected for
plasma volume changes using procedures described by Dill
and Costill [13].
Serum total antioxidant capacity (TAC) was determined by the
method of Whitehead et al. [46], relative to 6-hydroxy-2,5,7,8-
tetramethylchroman-2-carboxylic acid (Trolox), a soluble vita-
min E analogue. Each analysis was performed in duplicate and
was expressed as Trolox Equivalents per litre (Trolox Eq · l–1).
MDA was measured following the method of Young and Trim-
ble [49], with slight modifications described by Child et al. [9].
The assay uses HPLC and fluorescence to distinguish the MDA
adduct from contaminating compounds.
Serum creatine kinase activity (CK) was measured using a di-
agnostic kit (Sigma No. 47-10, Sigma Chemicals, Poole, UK). At
least duplicate analyses were performed on each sample, and
creatine kinase activities were calculated as a mean of two val-
ues that differed by no more than 10 % of the lower value. The
serum urate concentration (UA) was measured using a diag-
nostic kit (Sigma No. 686), based on the uricase-peroxidase
system.
Statistics
All data are presented as arithmetic means ± SEM. To illustrate
relative changes prior to running the first half-marathon bio-
chemical measurements are presented as a percentage of each
subject’s baseline measurements. Physiological and biochem-
ical data were analysed using repeated measures analysis of
variance (ANOVA). Where significant differences were ob-
served using the ANOVA, post-hoc paired t-tests (with Bonfer-
roni correction), were used to evaluate exercise induced
changes within groups. Where significant differences were ob-
328 Int J Sports Med 2000; 21
Table 2 Oxygen uptake during each half-marathon in normal and training taper groups
Oxygen uptake (l · min–1)
Group Half- Minute 5 Minute 5 Minute 10
marathon @ 50 % @ 70 % @ 70 %
peak VO2 peak VO2 peak VO2
Normal Run 1 2.23 ± 0.06 2.95 ± 0.05 2.99 ± 0.08
Run 2 2.18 ± 0.04 2.96 ± 0.03 2.93 ± 0.05
Taper Run 1 2.35 ± 0.07 3.13 ± 0.11 3.13 ± 0.11
Run 2 2.31 ± 0.07 3.08 ± 0.15 3.11 ± 0.14
served between groups using the ANOVA, post-hoc tests were
performed using unpaired t-tests. Significance was set at
P < 0.05.
Results
Baseline physiological and biochemical measurements sug-
gested that the groups were well matched (Table 1). Perform-
ance times for the first and second half-marathons were
86.75 ± 2.65 min and 87.67 ± 2.87 min for the normal training
group and 85.62 ± 2.81 min and 85.39 ± 3.52 min for the train-
ing taper group. Differences in performance both between and
within groups were non-significant. Completion of the half-
marathon represented 52 ± 7 % of weekly training volume in
the normal training group and 48 ± 8 % weekly training volume
in the taper group. The first half-marathon was performed at
an intensity of 111 ± 6 % average training speed in the normal
training group, and 108 ± 2 % average training speed in the ta-
per group. At the start of each half-marathon there were no
differences either within or between groups in oxygen con-
sumption, at running speeds which elicited either 50 % or 70 %
V̇O2max (Table 2).
During the self paced run average exercise intensity for the
normal training group was 77.5 ± 0.4% peak VO2 during run 1
and 75.1 ± 0.7% peak VO2 during run 2. For the training taper
group average exercise intensity was 77.0 ± 0.8 % peak VO2 dur-
ing run 1 and 76.4 ± 1.0 % peak VO2 during run 2. Oxygen up-
take measurements made during exercise are reported in
Table 2.
Plasma volume decreased immediately after exercise, by
6.9 ± 1.2 % after run 1 and 8.3 ± 1.1 % after run 2 in the normal
training group, and 8.5 ± 1.6 % and 7.1 ± 1.2 % after run 1 and 2
respectively in the training taper group. Serum urate was
elevated over time in both groups (P < 0.001, ANOVA), although
there was no difference in this response between groups. Se-
rum TAC also was elevated over time in both normal training
and taper groups (P < 0.001, ANOVA), but there was no differ-
ence in this response over time between groups. When MDA
data for each group were pooled, such that the t-test was ap-
plied to 14 paired data sets, the rise in plasma MDA was signif-
icant (P < 0.05). However, when the same statistical proce-
dures were applied to MDA data for each group of seven sub-
jects, the rise in MDA was found to be non-significant. These
findings suggest that the small size of each group resulted in
insufficient statistical power, to determine if the exercise in-
duced rise in MDA was significant. Changes in MDA over time
did not differ either between or within groups (P > 0.05, ANO-
VA). Serum CK was elevated over time in both normal training
Child RB et al
4 km 8 km 12 km 16 km 20 km
3.34 ± 0.05 3.43 ± 0.06 3.38 ± 0.05 3.39 ± 0.07 3.45 ± 0.10
3.26 ± 0.06 3.29 ± 0.06 3.25 ± 0.08 3.25 ± 0.04 3.41 ± 0.08
3.44 ± 0.09 3.42 ± 1.2 3.50 ± 0.12 3.59 ± 1.0 3.60 ± 0.12
3.40 ± 0.22 3.38 ± 0.20 3.51 ± 0.11 3.53 ± 0.17 3.63 ± 0.40
and taper groups (P < 0.01, ANOVA), however there was a great-
er rise in serum CK in the normal training group than the train-
ing taper group (P < 0.05, ANOVA). Resting CK was elevated in
the normal training group, rising from 90 ± 32 IU · l–1 at base-
line to 106 ± 23 IU · l–1 immediately prior to the second half-
marathon (P = 0.2037). In the training taper group baseline CK
was 115 ± 24 IU · l–1 and decreased to 108 ± 24 IU · l–1 prior to
the second half marathon. In the normal training group CK
was higher than in the taper group over the time course of
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the study and at the end of the second half-marathon (Fig. 5).
This reflected both a higher resting CK prior to the second half-
marathon (P = 0.2240) and a greater relative rise during exer-
cise (P = 0.2144). When expressed relative to CK activity imme-
diately before exercise CK rose by 80 ± 24 IU · l–1 in the normal
training group and only 53 ± 19 IU · l–1. The greater relative rise
in CK in the normal training group (74 ± 20 %) relative to the
taper group, where CK rose by 49 ± 11 % was not significant
(P = 0.2141). These changes in CK suggest that the higher activ-
ity observed in the normal training, group reflected both the
higher resting CK prior to the second half-marathon and the
greater relative rise during exercise.
Discussion
There is accumulating evidence that a training taper can im-
prove performance in a variety of sports [22, 23, 33], but the
biochemical mechanisms which produce this effect have re-
ceived little attention. Free radical and mechanically induced
skeletal muscle damage occurs during distance running
[2, 29], which may impair muscle performance [6, 8,10]. A
training taper could improve skeletal muscle function by al-
lowing training induced myocellular injuries and antioxidant
deficits to recover, prior to exercise. Such a transient reduction
in training volume is unlikely to compromise the activities of
enzymes important for glutathione metabolism in locomotory
muscles [41]. Despite the potential benefits of reducing train-
ing loads, the effects of this intervention on indices of muscle
damage, lipid peroxidation and antioxidant protection have
not been investigated.
In the present investigation treadmill time trials were chosen
to assess distance running performance, as in previous training
taper studies [22, 42]. This exercise model has the advantage of
closely simulating a competitive race situation by allowing self
pacing through the given distance, yet minimises variability in
environmental and psychological factors which may confound
measurements made during actual competition. The half-
marathon runs were performed at a pace which exceeded the
average running speed during training, furthermore for most
subjects, completion of each half-marathon involved perform-
Effects of a Training Taper on Tissue Damage
Fig. 2 Serum urate concentration in normal and training taper
groups. A (baseline, immediately before run 1); B (immediately
after run 1); C (immediately before run 2); D (immediately after
run 2). * P < 0.025 relative to pre-exercise, NS: not significant rela-
tive to baseline.
Fig. 3 Serum TAC in normal and training taper groups. A (base-
line, immediately before run 1); B (immediately after run 1); C (im-
mediately before run 2); D (immediately after run 2). * P < 0.025
relative to pre-exercise.
ing almost half the weekly training volume in a single exercise
session. This finding suggests that each half-marathon
represented a considerable exercise challenge to these sub-
jects and would typically compromise exercise performance
for 2 to 3 days after the event. Therefore each half-marathon
would have resulted in overreaching as described by Fry et al.
[16] and Hooper et al. [21]. It is clear that the subjects were not
in an overreached state prior to the second half-marathon, as
performance was not significantly slower than that for the first
run.
Indices of exercise induced muscle damage, such as elevations
in serum CK, can be significantly attenuated by the prior per-
formance of a single session of exercise which produces myo-
cellular injury [6, 7]. Furthermore, oxidative stress (as experi-
enced during an acute session of running) can differentially af-
fect the components of myocellular antioxidant defences
[11, 26, 40, 41]. Such responses could alter susceptibility to oxi-
dative muscle injury when subsequent damaging exercise is
performed. To compensate for “order effects” arising from such
responses, a normal training group was evaluated in parallel to
the training taper group. Thus, the differences reported be-
Int J Sports Med 2000; 21 329
Fig. 4 MDA in normal and training taper groups. A (baseline, imme-
diately before run 1); B (immediately after run 1); C (immediately be-
fore run 2); D (immediately after run 2).
tween groups following the taper cannot simply be attributed
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to the effects of the first half-marathon.
The subjects studied utilised a large fraction of peak VO2 and
maintained high rates of oxygen utilisation during the half-
marathon run (Table 2). This suggests that the exercise was in-
tense, and produced a considerable increase in the formation
of reactive oxygen species. Despite this rise in oxidative stress,
the half-marathons performed by both normal training and
training taper groups resulted in significant increases in serum
TAC (Fig. 3). This response was partially attributable to increas-
es in serum urate (Fig. 2) and the mobilisation of labile antiox-
idants [18]. The rise in serum TAC during the first half-mara-
thon did not prevent the exercise induced increase in lipid per-
oxidation in normal training and training taper groups respec-
tively (Fig. 4).
Each half-marathon resulted in significant elevations in serum
CK (Fig. 5). Both resting serum CK and the exercise induced rise
in serum CK are consistent with previous studies on half-
marathon running [14]. Increases in serum CK during exercise
may arise from sarcolemmal rupture, which has been reported
in humans immediately following a marathon [20]. When
compared with the normal training group, the training taper
resulted in lower CK after the second half-marathon (Fig. 5).
There is evidence that exercise induced myocellular injury
can arise from increased mechanical loading on the muscle
[2,10,15] and oxidative stress [8, 27, 32]. As there were no dif-
ferences in performance between the two groups, the attenu-
ated release of creatine kinase was unlikely to be a conse-
quence of lower muscle force generation, or reduced oxidative
stress. Furthermore, the reduction in CK as a consequence of
the training taper did not appear to be caused by increased ex-
tracellular antioxidant protection, as there were no differences
in serum TAC between groups (Fig. 3). The higher CK in the
normal training group (relative to the taper group) after the
second half-marathon, was a consequence of higher CK imme-
diately before exercise and a greater relative rise during exer-
cise. These data suggest that the maintenance of normal train-
ing volumes may have slowed recovery processes following
the first half-marathon, resulting in a higher resting level of
muscle injury prior to the second half-marathon. There also
330 Int J Sports Med 2000; 21
Fig. 5 Serum CK in normal and training taper groups. A (baseline,
immediately before run 1); B (immediately after run 1); C (immedi-
ately before run 2); D (immediately after run 2). P < 0.05 ANOVA
between groups, δ P < 0.05, t-test between groups at timepoint D,
* P < 0.025 relative to pre-exercise.
appeared to be a reduced tolerance to exercise induced muscle
injury in the normal training group. Therefore in relative
terms, the training taper may have facilitated muscle recovery,
such that CK returned to resting values prior to the second
half-marathon level and that resistance to exercise induced in-
jury was similar to that observed prior to reduced training.
In conclusion the training taper did not enhance serum free
radical scavenging capacity prior to, or during exercise. Despite
evidence that the training taper reduced muscle damage, rela-
tive to the normal training aroup, half-marathon performance
was not improved. Further studies evaluating muscle damage
and indices of antioxidant status within active skeletal muscle
are necessary to determine if the changes produced by the
training taper are a consequence of reduced myocellular in-
jury.
Acknowledgements
The authors gratefully acknowledge the support of the runners
who participated in this project and critical input from Mr. J.D.
Chance.
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