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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

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-marathons 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 concentration of malondialdehyde (MDA) was used as a marker of
lipid peroxidation. There were no differences in running performance 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 subject groups were pooled. There were no differences in serum antioxidant capacity, or urate concentration between groups. Postexercise CK was lower following the training taper (149 22 %
baseline, for the training taper vs 269 55 % baseline for the normal 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.

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
oxidative stress during physical activity has been partially attributed to increased mitochondrial respiration [43], which
has been estimated to rise up to 200 fold in active muscle fibres [28]. Exercise such as running can elevate markers of oxidative damage, such as malondialdehyde [12, 32] and produces damage to muscle membranes [37, 45]. These events
are often associated with the release of myocellular proteins
[17] and compromised membrane function [12,17]. Antioxidant defences include enzymes such as superoxide dismutase
and glutathione peroxidase, and non-enzymatic compounds
such as vitamins and reduced glutathione. Some aspects of antioxidant protection can be increased by training [26, 41, 45] ,
especially the enzymes of glutathione synthesis [30, 41].

Key words: Reduced training, overreaching, training volume,

free radicals, exercise.

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 evidence 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 include vitamin E and carotenoids, the presence of which can inhibit peroxidation of membrane lipids [44, 48]. Animals deficient 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 observations 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.

Int J Sports Med 2000; 21: 325 331

Georg Thieme Verlag Stuttgart New York
ISSN 0172-4622

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

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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

Int J Sports Med 2000; 21

available on endurance events such as marathon and halfmarathon running [47]. Houmard et al. [22] reported improved running performance during a 5 km time trial, which
was attributed to a 6 % decrease in submaximal oxygen consumption (i.e. improved running economy). As this is an important contributor to middle and long, distance running performance [3, 35], it has been proposed that reduced training
volumes might result in even greater performance benefits
for endurance events [23]. At present however, there are no
empirical data to support this view [16].
Little is known about the mechanisms by which a training taper can improve exercise performance. Most studies have focused on changes in glycogen availability and/or muscle oxidative capacity to explain the positive effects of reduced training
[23, 33, 42]. However, beneficial effects could also arise by
mechanisms unrelated to these factors. Distance running disrupts the muscle ultrastructure [20, 29] and the frequency of
such injuries appears to increase with training distance [29].
Muscle damage may be a limiting factor to long distance running performance [22, 29] and performing a training taper provides several potential mechanisms to reduce exercise induced
myocellular injury.

Child RB et al
Table 1 Profiles of subjects in normal and training taper groups, prior
to the first half-marathon

Taper group

Normal group

Age (years)

31 2

30 1

Running experience (years)

15 1

14 1

Mass (kg)

72.4 2.1

71.2 1.6

Height (m)

1.77 0.02

1.76 0.02

Peak VO2 (ml kg1 min1)

63.2 1.7

61.8 1.4

Distance run (km week1)

50 7

45 7

Running time (min week1)

215 33

202 28

Average training speed (km h1)

14.8 0.5

14.6 0.4

258 18

270 19

TAC (mol Trolox Eq l1)

456 29

503 39

Plasma MDA (mol l1)

1.43 0.17

1.49 0.16

Serum CK (IU l1)

90 32

115 24

Urate (mol l

The objectives of this study were to reproduce the taper regimen of Houmard et al. [22] to test the hypotheses that a controlled 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 sessions 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 interventions is shown in Fig. 1. Venous blood samples were
taken immediately prior to and following the first half-marathon, at time-points A and B, respectively. Further blood samples were taken immediately prior to and following the second
half-marathon, at time points C and D, respectively.


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, subjects were matched into normal training, or training taper
groups. All subjects had run a half-marathon in under 95 minutes during the previous year.

Subjects refrained from exercise for 36 hours before each laboratory testing session and performed only light training in
the 2 days prior to each half-marathon.

Reducing training volume decreases myocellular oxygen utilisation, which in turn decreases the oxidative load on the muscle. This could result in a more reductive myocellular redox environment and experiments in mice have shown this can improve exercise performance and increase resistance to free
radical mediated muscle injury [45].

The training taper was based on the regime used by Houmard

et al. [22]. In the training taper group total weekly training volume 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 performance [33].

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 sample was collected at the end of each exercise stage to determine the capillary blood lactate concentration (BLa). Following
collection of capillary blood, running velocity was increased
progressively by 1.5 km h1 and the test was terminated when
(BLa) exceeded 4 mmol l1. Following a 30 minute recovery
period, subjects performed an incremental graded test to establish peak VO2. Initial running velocity was set 2 km h1
slower than the velocity which elicited a BLa of 4 mmol l1 in
the previous test. The gradient was increased by 1.5 % every
90 s throughout the test. Expired gas was collected continuously from 5 minutes, to test termination. Interpolation of the

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Effects of a Training Taper on Tissue Damage

Int J Sports Med 2000; 21


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 laboratory 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 controlled 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 constant 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 postexercise. 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 capillary 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 analyser and infra red carbon dioxide analyser (Servomex 1400,
Crowborough, UK), calibrated with nitrogen, two gravimetrically determined calibration gases (Linde Gases UK Ltd., London, UK) and ambient air. Prior to analysis all gases were saturated 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 samples 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 determined by the cyanmethaemoglobin method using a diagnostic

kit (No. 124 729, Boehringer Mannheim, Mannheim, Germany). Haematocrit was determined in triplicate following microcentrifugation (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 serum were removed, and stored at 20 8C until analysis. Postexercise 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-2,5,7,8tetramethylchroman-2-carboxylic acid (Trolox), a soluble vitamin E analogue. Each analysis was performed in duplicate and
was expressed as Trolox Equivalents per litre (Trolox Eq l1).
MDA was measured following the method of Young and Trimble [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 diagnostic 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 values that differed by no more than 10 % of the lower value. The
serum urate concentration (UA) was measured using a diagnostic kit (Sigma No. 686), based on the uricase-peroxidase

All data are presented as arithmetic means SEM. To illustrate
relative changes prior to running the first half-marathon biochemical measurements are presented as a percentage of each
subjects baseline measurements. Physiological and biochemical data were analysed using repeated measures analysis of
variance (ANOVA). Where significant differences were observed using the ANOVA, post-hoc paired t-tests (with Bonferroni correction), were used to evaluate exercise induced
changes within groups. Where significant differences were ob-

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Fig. 1 Training regimens in normal and

training taper groups
after the first halfmarathon.

Int J Sports Med 2000; 21

Table 2

Child RB et al

Oxygen uptake during each half-marathon in normal and training taper groups



Minute 5
@ 50 %
peak VO2

Minute 5
@ 70 %
peak VO2

Oxygen uptake (l min1)

Minute 10
4 km
8 km
@ 70 %
peak VO2


Run 1
Run 2

2.23 0.06
2.18 0.04

2.95 0.05
2.96 0.03

2.99 0.08
2.93 0.05

3.34 0.05
3.26 0.06


Run 1
Run 2

2.35 0.07
2.31 0.07

3.13 0.11
3.08 0.15

3.13 0.11
3.11 0.14

3.44 0.09
3.40 0.22

served between groups using the ANOVA, post-hoc tests were

performed using unpaired t-tests. Significance was set at
P < 0.05.

Baseline physiological and biochemical measurements suggested that the groups were well matched (Table 1). Performance 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 training taper group. Differences in performance both between and
within groups were non-significant. Completion of the halfmarathon 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 taper group. At the start of each half-marathon there were no
differences either within or between groups in oxygen consumption, at running speeds which elicited either 50 % or 70 %
VO2max (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 during run 1 and 76.4 1.0 % peak VO2 during run 2. Oxygen uptake 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. Serum TAC also was elevated over time in both normal training
and taper groups (P < 0.001, ANOVA), but there was no difference in this response over time between groups. When MDA
data for each group were pooled, such that the t-test was applied to 14 paired data sets, the rise in plasma MDA was significant (P < 0.05). However, when the same statistical procedures were applied to MDA data for each group of seven subjects, 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 induced rise in MDA was significant. Changes in MDA over time
did not differ either between or within groups (P > 0.05, ANOVA). Serum CK was elevated over time in both normal training

12 km

16 km

20 km

3.43 0.06
3.29 0.06

3.38 0.05
3.25 0.08

3.39 0.07
3.25 0.04

3.45 0.10
3.41 0.08

3.42 1.2
3.38 0.20

3.50 0.12
3.51 0.11

3.59 1.0
3.53 0.17

3.60 0.12
3.63 0.40

and taper groups (P < 0.01, ANOVA), however there was a greater rise in serum CK in the normal training group than the training taper group (P < 0.05, ANOVA). Resting CK was elevated in
the normal training group, rising from 90 32 IU l1 at baseline to 106 23 IU l1 immediately prior to the second halfmarathon (P = 0.2037). In the training taper group baseline CK
was 115 24 IU l1 and decreased to 108 24 IU l1 prior to
the second half marathon. In the normal training group CK
was higher than in the taper group over the time course of
the study and at the end of the second half-marathon (Fig. 5).
This reflected both a higher resting CK prior to the second halfmarathon (P = 0.2240) and a greater relative rise during exercise (P = 0.2144). When expressed relative to CK activity immediately before exercise CK rose by 80 24 IU l1 in the normal
training group and only 53 19 IU l1. 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 activity 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.

There is accumulating evidence that a training taper can improve performance in a variety of sports [22, 23, 33], but the
biochemical mechanisms which produce this effect have received 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 allowing 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 training 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 halfmarathon 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-

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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 relative to baseline.

Int J Sports Med 2000; 21

Fig. 4 MDA 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).

tween groups following the taper cannot simply be attributed

to the effects of the first half-marathon.

Fig. 3 Serum TAC 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.

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 subjects 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
Indices of exercise induced muscle damage, such as elevations
in serum CK, can be significantly attenuated by the prior performance of a single session of exercise which produces myocellular injury [6, 7]. Furthermore, oxidative stress (as experienced during an acute session of running) can differentially affect the components of myocellular antioxidant defences
[11, 26, 40, 41]. Such responses could alter susceptibility to oxidative 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-


The subjects studied utilised a large fraction of peak VO2 and

maintained high rates of oxygen utilisation during the halfmarathon run (Table 2). This suggests that the exercise was intense, 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 increases in serum urate (Fig. 2) and the mobilisation of labile antioxidants [18]. The rise in serum TAC during the first half-marathon did not prevent the exercise induced increase in lipid peroxidation in normal training and training taper groups respectively (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 halfmarathon 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 differences in performance between the two groups, the attenuated release of creatine kinase was unlikely to be a consequence 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 extracellular 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 immediately before exercise and a greater relative rise during exercise. These data suggest that the maintenance of normal training 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

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Effects of a Training Taper on Tissue Damage

Int J Sports Med 2000; 21

Child RB et al

Fig. 5 Serum CK 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 < 0.05 ANOVA
between groups, 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 injury 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, relative 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 injury.

The authors gratefully acknowledge the support of the runners
who participated in this project and critical input from Mr. J.D.


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Corresponding Author:
Robert B. Child, Ph.D.
Exercise Physiology Research Group
University College Chichester
College Lane
West Sussex, PO19 4PE

+ 44 (1243) 816-387
+ 44 (1243) 816-080

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