Physiology and Biochemistry

325

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.

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
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

Downloaded by: University of Thessaly. Copyrighted material.

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
Parameter

Taper group
n=7

Normal group
n=7

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.

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, 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

Downloaded by: University of Thessaly. Copyrighted material.

326

Effects of a Training Taper on Tissue Damage

Int J Sports Med 2000; 21

327

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
system.

Statistics
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-

Downloaded by: University of Thessaly. Copyrighted material.

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

Group

Halfmarathon

Minute 5
@ 50 %
peak VO2

Minute 5
@ 70 %
peak VO2

Oxygen uptake (l min1)

Minute 10
4 km
8 km
@ 70 %
peak VO2

Normal

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

Taper

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.

Results
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.

Discussion
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-

Downloaded by: University of Thessaly. Copyrighted material.

328

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
run.
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-

329

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

Downloaded by: University of Thessaly. Copyrighted material.

Effects of a Training Taper on Tissue Damage

Int J Sports Med 2000; 21

Child RB et al
7

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.

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

References
1

Aikawa KM, Quintanilha AT, de Lumen BO, Brooks GA, Packer L.

Exercise endurance-training alters vitamin E tissue levels and
red cell hemolysis in rodents. Biosci Rep 1984; 4: 253 257
2
Armstrong RB, Warren GL, Warren JA. Mechanisms of exercise-induced muscle fibre injury. Sports Med 1991; 12: 184 207
3
Brandon LJ. Physiological factors associated with middle and long
distance running performance. Sports Med 1995; 19: 268 277
4
Bowles DK, Torgan CE, Ebner S, Kehrer JP, Ivy JL, Starnes JW. Effects of acute submaximal exercise on skeletal muscle vitamin E.
Free Rad Res Commun 1991; 14: 139 143
5
Brooks G, Gillam I, Kanter M, Packer L. Proceedings of the panel
discussion: Antioxidants and the elite athlete. LaGrange: Henkel
Fine Chemicals, 1992: 1 21
6
Brown SJ, Child RB, Day SH, Donnelly AE. Exercise-induced skeletal muscle damage and adaptation following repeated bouts of
eccentric muscle contractions. J Sports Sci 1997; 15: 215 222

Byrnes WC, Clarkson PM, White JS, Hsieh SS, Frykman PN,
Maughan RJ. Delayed onset muscle soreness following repeated
bouts of downhill running. J Appl Physiol 1985; 59: 710 715
8
Child RB, Brown SJ, Day SH, Donnelly AE. Functional and biochemical changes in indices of muscle damage, lipid peroxidation
and lysosomal enzyme release, following eccentric exercise in
humans. J Physiol 1998; 509.P: 46P 47P
9
Child RB, Brown SJ, Day SH, Donnelly AE, Roper H, Saxton JM.
Changes in indices of antioxidant status, lipid peroxidation and
inflammation in human skeletal muscle after eccentric muscle
actions. Clin Sci 1999; 96: 105 115
10
Child RB, Brown SJ, Day SH, Saxton JM, Donnelly AE. Manipulation of knee extensor force using percutaneous electrical myostimulation during eccentric actions: Effects on indices of muscle
damage in humans. Int J Sports Med 1998; 19: 468 473
11
Corbucci GG, Montanari G, Cooper MB, Jones DA, Edwards RHT.
The effect of exertion on mitochondrial oxidative capacity and
on some antioxidant mechanisms in muscle from marathon runners. Int J Sports Med 1984; 5: 135
12
Davies KJA, Quintanilha AT, Brooks GA, Packer L. Free radicals and
tissue damage produced by exercise. Biochem Biophys Res Com
1982; 107: 1198 1205
13
Dill DB, Costill DL. Calculation of percentage changes in volumes
of blood, plasma and red cells in dehydration. J Appl Physiol 1974;
37: 247 248
14
Duthie GG, Robertson JD, Maughan RJ, Morrice PC. Blood antioxidant status and erythrocyte lipid peroxidation following distance
running. Arch Biochem Biophys 1990; 282: 73 83
15
Faulkner JA, Brooks S, Opiteck J. Injury to skeletal muscle fibers
during contractions: Conditions of occurrence and prevention.
Physical Therapy 1993; 73: 911 921
16
Fry RW, Morton AR, Keast D. Periodisation of training stress: A review. Can J Spt Sci 1992; 17: 234 240
17
Gauduel Y, Menasche P, Duvelleroy M. Enzyme release and mitochondrial activity in reoxygenated cardiac muscle. Relationship
with oxygen induced lipid peroxidation. Gen Physiol Biophys
1989; 8: 327 340
18
Gleeson M, Robertson JD, Maughan RJ. Influence of exercise on
ascorbic acid status in man. Clin Sci 1987; 73: 501 505
19
Gohil K, Rothfuss L, Lang J, Packer L. Effect of exercise training on
tissue vitamin E and ubiquinone content. J Appl Physiol 1987; 63:
1638 1641
20
Hikida RS, Staron RS, Hagerman FC, Sherman WM, Costill DL.
Muscle fiber necrosis associated with human marathon runners.
J Neurol Sci 1983; 59: 185 203
21
Hooper SL, Makinnon LT. Monitoring overtraining in athletes.
Sports Med 1995; 20: 321 327
22
Houmard JA, Scott BK, Justice CL, Chenier TC. The effects of taper
on performance in distance runners. Med Sci Sports Exerc 1994;
26: 624 631
23
Houmard JA. Impact of reduced training on performance in endurance athletes. Sports Med 1991; 12: 380 393
24
Jackson MJ, Edwards RHT, Symons MCR. Electron spin resonance
studies of intact mammalian skeletal muscle. Biochem Biophys
Acta 1985; 847: 185 190
25
Ji L. Gatorade Sports Science Exchange. Roundtable. Exercise nutrition and free radicals: Whats the connection? 1994; 15: Vol 5:
380 393
26
Ji LL. Exercise and oxidative stress: Role of cellular antioxidant
systems 1995. Exerc Sport Sci Rev 1995; 23: 135 166
27
Kanter MM, Lesmes GR, Kaminsky LA, La Ham-Saeger J, Nequin
ND. Serum creatine kinase and lactate dehydrogenase changes
following an eighty kilometer race. Eur J Appl Physiol 1988; 57:
60 63

Downloaded by: University of Thessaly. Copyrighted material.

330

Effects of a Training Taper on Tissue Damage

Keul J, Doll E, Koppler D. Oxidative energy supply. In: Jokl E (ed).
Energy metabolism in human muscle. Basel: Karger, 1972
29
Kuipers H, Janssen GME, Bosman F, Frederik PM, Geurten P. Structural and ultrastructural changes in skeletal muscle associated
with long-distance training and running. Int J Sports Med 1989;
10: S156 S159
30
Marin E, Kretzschmar M, Arokoski J, Hanninen O, Klinger W. Enzymes of glutathione synthesis in dog skeletal muscles and their
response to training. Acta Physiol Scand 1993; 147: 369 373
31
McKenzie DC. Markers of excessive exercise. Can J Appl Physiol
1999; 24: 66 73
32
Maughan RJ, Donnelly AE, Gleeson M, Whiting PH, Walker KA,
Clough PJ. Delayed-onset muscle damage and lipid peroxidation
in man after a downhill run. Muscle Nerve 1989; 12: 322 336
33
Mujika I. The influence of training characteristics and tapering on
the adaptation in highly trained individuals: A review. Int J Sports
Med 1998; 19: 439 446
34
Novelli GP, Bracciotti G, Falsini S. Spin-trappers and vitamin E
prolong endurance to muscle fatigue in mice. Free Rad Biol Med
1990; 8: 9 13
35
Peronnet F, Thibault G. Mathematical analysis of running performance and world running records. J Appl Physiol 1989; 67:
453 465
36
Pfafferott C, Meiselman H, Hochstein P. The effect of malondialdehyde on erythrocyte deformability. Blood 1982; 59: 12 15
37
Rajguru SU, Yeargans GS, Seidler NW. Exercise causes oxidative
damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls. Life Sciences 1994; 54: 149 157
38
Reid MB, Stokic DS, Koch SM, Khawli FA, Leis AA. N-Acetylcysteine inhibits muscle fatigue in humans. J Clin Invest 1994; 94:
2468 2474
39
Reznick AZ, Witt E, Matsumoto M, Packer L. Vitamin E inhibits
protein oxidation in skeletal muscle of resting and exercised rats.
Biochem Biophys Res Commun 1992; 189: 801 806
40
Salminen A, Vihko V. Lipid peroxidation in exercise myopathy.
Exp Mol Pathol 1983; 38: 380 388
41
Sen CK, Marin E, Kretzschmar M, Hanninen O. Skeletal muscle
and liver glutathione homeostasis in response to training, exercise, and immobilization. J Appl Physiol 1992; 73: 1265 1272
42
Sheply B, MacDougall JD, Cipriano N, Sutton JR, Tarnopolsky MA,
Coates G. Physiologic effects of tapering in highly trained athletes. J Appl Physiol 1992; 72: 706 711
43
Sjodin B, Hellsten-Westing Y, Apple FS. Biochemical mechanisms
for free radical formation during exercise. Sports Med 1990; 10:
236 254
44
van den Berg JJM, Kuypers FA, Roelofsen B, Op den Kamp JAF. The
cooperative action of vitamins E and C in the protection against
peroxidation of parinaric acid in human erythrocyte membranes.
Chem Phys Lipids 1990; 53: 309 320
45
Venditti P, Di Meo S. Effect of training on antioxidant capacity, tissue damage, and endurance of adult male rats. Int J Sports Med
1997; 18: 497 502
46
Whitehead T, Thorpe GHG, Maxwell S. Enhanced chemiluminescent assay for antioxidant capacity in biological fluids. Anal Chim
Acta 1992; 226: 265 277
47
Wilmore JH, Costill DL. Optimizing performance in sport. Physiology of Sport and Exercise. Champaign, Illinois: Human Kinetics,
1994: 309
48
Woodhall A, Britton G, Jackson M. Carotenoids and protection of
phospholipids in solution or in liposomes against oxidation by
peroxyl radicals: Relationship between carotenoid structure and
protective ability. Biochim Biophys Acta 1997; 1336: 575 586
49
Young IS, Trimble ER. Measurement of malondialdehyde in plasma by high performance liquid chromatography with fluorimetric detection. Ann Clin Biochem 1991; 28: 504 508

331

Corresponding Author:
Robert B. Child, Ph.D.
Exercise Physiology Research Group
University College Chichester
College Lane
Chichester
West Sussex, PO19 4PE
UK
Phone:
Fax:
E-mail:

+ 44 (1243) 816-387
+ 44 (1243) 816-080
rchild@chihe.ac.uk

Downloaded by: University of Thessaly. Copyrighted material.

28

Int J Sports Med 2000; 21