You are on page 1of 7

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

Child RB, Wilkinson DM, Fallowfield JL. Effects of a Training Introduction


Taper on Tissue Damage Indices, Serum Antioxidant Capacity
and Half-Marathon Running Performance. Int J Sports Med Muscle contraction increases free radical formation [12, 24],
2000; 21: 325 – 331 which has been implicated in muscle fatigue [38] and exercise
induced myocellular injury in humans [8, 27, 32]. The rise in

Downloaded by: University of Thessaly. Copyrighted material.


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

Downloaded by: University of Thessaly. Copyrighted material.


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

Methods Experimental protocol

Prior to the study, subjects were interviewed to determine the Subjects refrained from exercise for 36 hours before each la-
number of years they had been involved in running training. boratory testing session and performed only light training in
Each subject was asked to keep a training diary for the one the 2 days prior to each half-marathon.
month period prior to the first simulated half-marathon. From
the training diary average weekly running time and training Within a 2 week period before the first half-marathon, each
distance were calculated, from which average training speed subject completed a graded exercise test to derive individual
was derived. No attempt was made to control training in the speed-oxygen uptake regression equations. The test involved
one month period prior to exercise. Based on the training data, completion of four to six 4-minute stages, on a motorised
physiological characteristics (Table 1) and running ability, sub- treadmill (Quinton Q65, Quinton Instruments, Seattle, USA).
jects were matched into “normal training”, or “training taper” Expired gas was collected in the final minute of each stage
groups. All subjects had run a half-marathon in under 95 min- using standard Douglas bag techniques. A fingertip blood sam-
utes during the previous year. ple was collected at the end of each exercise stage to deter-
mine the capillary blood lactate concentration (BLa). Following
The training taper was based on the regime used by Houmard collection of capillary blood, running velocity was increased
et al. [22]. In the training taper group total weekly training vol- progressively by 1.5 km · h–1 and the test was terminated when
ume was reduced by 85 %. The 15 % weekly training performed (BLa) exceeded 4 mmol · l–1. Following a 30 minute recovery
was split as 30 % (day 2), 25 % (day 3), 20 % (day 4), 15 % (day 5), period, subjects performed an incremental graded test to es-
10 % day (day 6). Sessions were performed as 400 m repetitions tablish peak VO2. Initial running velocity was set 2 km · h–1
at 10 km race pace, with a 1 : 1 work to rest ratio. The day after slower than the velocity which elicited a BLa of 4 mmol · l–1 in
the first half-marathon and the day preceding the second half the previous test. The gradient was increased by 1.5 % every
marathon were rest days. Such a progressive training taper is 90 s throughout the test. Expired gas was collected continu-
thought to be an effective way of improving exercise perform- ously from 5 minutes, to test termination. Interpolation of the
ance [33].
Effects of a Training Taper on Tissue Damage Int J Sports Med 2000; 21 327

Fig. 1 Training regi-


mens in normal and
training taper groups
after the first half-
marathon.

speed oxygen uptake regression was used to determine the kit (No. 124 729, Boehringer Mannheim, Mannheim, Germa-
running velocity required to elicit 50 % and 70 % of peak VO2. ny). Haematocrit was determined in triplicate following mi-

Downloaded by: University of Thessaly. Copyrighted material.


crocentrifugation (Hawksley and Sons Ltd, Lancing, UK). The
On the day of each half-marathon subjects reported to the la- remaining venous blood was split between potassium EDTA
boratory following a 3 hour fast and stood for 20 minutes prior tubes, to be centrifuged immediately at 2500 g for 10 minutes
to exercise, to normalise for postural changes in blood volume. and plain tubes (to be centrifuged using the same protocol
Immediately before exercise a 13 ml blood sample was drawn after clotting at room temperature for 1 hour). Plasma and se-
from an antecubital vein. Each subject then performed a con- rum were removed, and stored at – 20 8C until analysis. Post-
trolled warm up on the treadmill, at a predetermined speed exercise measurements in venous blood were corrected for
corresponding to 50 % peak VO2 for 5 minutes. During the first plasma volume changes using procedures described by Dill
10 min of the half-marathon treadmill speed was held con- and Costill [13].
stant at 70 % peak VO2, thereafter subjects were allowed to
run self paced and were encouraged to cover the remaining Serum total antioxidant capacity (TAC) was determined by the
distance in the shortest possible time. This was achieved by method of Whitehead et al. [46], relative to 6-hydroxy-2,5,7,8-
enabling the subjects to adjust the velocity of the treadmill tetramethylchroman-2-carboxylic acid (Trolox), a soluble vita-
during the run. Capillary BLa was measured pre-exercise, after min E analogue. Each analysis was performed in duplicate and
the warm up period, at 5 min, 10 min, 4, 8, 12, 16 and 20 km was expressed as Trolox Equivalents per litre (Trolox Eq · l–1).
during the half-marathon, and then again immediately post-
exercise. A further 13 ml of venous blood was drawn from an MDA was measured following the method of Young and Trim-
antecubital vein immediately after exercise. Oxygen uptake ble [49], with slight modifications described by Child et al. [9].
was recorded during exercise, just prior to collection of capil- The assay uses HPLC and fluorescence to distinguish the MDA
lary blood. To simulate race conditions subjects were allowed adduct from contaminating compounds.
water ad libitum at 5, 10, 15 and 19 km.
Serum creatine kinase activity (CK) was measured using a di-
The volume of expired air was measured using a previously agnostic kit (Sigma No. 47-10, Sigma Chemicals, Poole, UK). At
calibrated dry gas meter (Harvard Apparatus, Kent, UK). Gas least duplicate analyses were performed on each sample, and
fractions were determined using a paramagnetic oxygen ana- creatine kinase activities were calculated as a mean of two val-
lyser and infra red carbon dioxide analyser (Servomex 1400, ues that differed by no more than 10 % of the lower value. The
Crowborough, UK), calibrated with nitrogen, two gravimetri- serum urate concentration (UA) was measured using a diag-
cally determined calibration gases (Linde Gases UK Ltd., Lon- nostic kit (Sigma No. 686), based on the uricase-peroxidase
don, UK) and ambient air. Prior to analysis all gases were satu- system.
rated with water by passage throuch Nafion tubing (Omnifit
Ltd, Cambridge, UK) immersed in distilled water. Statistics

Biochemical analysis All data are presented as arithmetic means ± SEM. To illustrate
relative changes prior to running the first half-marathon bio-
The whole blood lactate concentration of capillary blood sam- chemical measurements are presented as a percentage of each
ples was determined immediately following collection. This subject’s baseline measurements. Physiological and biochem-
was performed using an automated analyser (Model 2300 Stat ical data were analysed using repeated measures analysis of
plus, Yellow Springs Inc., Ohio, USA). variance (ANOVA). Where significant differences were ob-
served using the ANOVA, post-hoc paired t-tests (with Bonfer-
In venous blood, haemoglobin concentrations were deter- roni correction), were used to evaluate exercise induced
mined by the cyanmethaemoglobin method using a diagnostic changes within groups. Where significant differences were ob-
328 Int J Sports Med 2000; 21 Child RB et al

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 4 km 8 km 12 km 16 km 20 km
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 3.34 ± 0.05 3.43 ± 0.06 3.38 ± 0.05 3.39 ± 0.07 3.45 ± 0.10
Run 2 2.18 ± 0.04 2.96 ± 0.03 2.93 ± 0.05 3.26 ± 0.06 3.29 ± 0.06 3.25 ± 0.08 3.25 ± 0.04 3.41 ± 0.08
Taper Run 1 2.35 ± 0.07 3.13 ± 0.11 3.13 ± 0.11 3.44 ± 0.09 3.42 ± 1.2 3.50 ± 0.12 3.59 ± 1.0 3.60 ± 0.12
Run 2 2.31 ± 0.07 3.08 ± 0.15 3.11 ± 0.14 3.40 ± 0.22 3.38 ± 0.20 3.51 ± 0.11 3.53 ± 0.17 3.63 ± 0.40

served between groups using the ANOVA, post-hoc tests were and taper groups (P < 0.01, ANOVA), however there was a great-
performed using unpaired t-tests. Significance was set at er rise in serum CK in the normal training group than the train-
P < 0.05. 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-
Results line to 106 ± 23 IU · l–1 immediately prior to the second half-
marathon (P = 0.2037). In the training taper group baseline CK
Baseline physiological and biochemical measurements sug- was 115 ± 24 IU · l–1 and decreased to 108 ± 24 IU · l–1 prior to
gested that the groups were well matched (Table 1). Perform- the second half marathon. In the normal training group CK
ance times for the first and second half-marathons were was higher than in the taper group over the time course of

Downloaded by: University of Thessaly. Copyrighted material.


86.75 ± 2.65 min and 87.67 ± 2.87 min for the normal training the study and at the end of the second half-marathon (Fig. 5).
group and 85.62 ± 2.81 min and 85.39 ± 3.52 min for the train- This reflected both a higher resting CK prior to the second half-
ing taper group. Differences in performance both between and marathon (P = 0.2240) and a greater relative rise during exer-
within groups were non-significant. Completion of the half- cise (P = 0.2144). When expressed relative to CK activity imme-
marathon represented 52 ± 7 % of weekly training volume in diately before exercise CK rose by 80 ± 24 IU · l–1 in the normal
the normal training group and 48 ± 8 % weekly training volume training group and only 53 ± 19 IU · l–1. The greater relative rise
in the taper group. The first half-marathon was performed at in CK in the normal training group (74 ± 20 %) relative to the
an intensity of 111 ± 6 % average training speed in the normal taper group, where CK rose by 49 ± 11 % was not significant
training group, and 108 ± 2 % average training speed in the ta- (P = 0.2141). These changes in CK suggest that the higher activ-
per group. At the start of each half-marathon there were no ity observed in the normal training, group reflected both the
differences either within or between groups in oxygen con- higher resting CK prior to the second half-marathon and the
sumption, at running speeds which elicited either 50 % or 70 % greater relative rise during exercise.
V̇O2max (Table 2).
Discussion
During the self paced run average exercise intensity for the
normal training group was 77.5 ± 0.4% peak VO2 during run 1 There is accumulating evidence that a training taper can im-
and 75.1 ± 0.7% peak VO2 during run 2. For the training taper prove performance in a variety of sports [22, 23, 33], but the
group average exercise intensity was 77.0 ± 0.8 % peak VO2 dur- biochemical mechanisms which produce this effect have re-
ing run 1 and 76.4 ± 1.0 % peak VO2 during run 2. Oxygen up- ceived little attention. Free radical and mechanically induced
take measurements made during exercise are reported in skeletal muscle damage occurs during distance running
Table 2. [2, 29], which may impair muscle performance [6, 8,10]. A
training taper could improve skeletal muscle function by al-
Plasma volume decreased immediately after exercise, by lowing training induced myocellular injuries and antioxidant
6.9 ± 1.2 % after run 1 and 8.3 ± 1.1 % after run 2 in the normal deficits to recover, prior to exercise. Such a transient reduction
training group, and 8.5 ± 1.6 % and 7.1 ± 1.2 % after run 1 and 2 in training volume is unlikely to compromise the activities of
respectively in the training taper group. Serum urate was enzymes important for glutathione metabolism in locomotory
elevated over time in both groups (P < 0.001, ANOVA), although muscles [41]. Despite the potential benefits of reducing train-
there was no difference in this response between groups. Se- ing loads, the effects of this intervention on indices of muscle
rum TAC also was elevated over time in both normal training damage, lipid peroxidation and antioxidant protection have
and taper groups (P < 0.001, ANOVA), but there was no differ- not been investigated.
ence in this response over time between groups. When MDA
data for each group were pooled, such that the t-test was ap- In the present investigation treadmill time trials were chosen
plied to 14 paired data sets, the rise in plasma MDA was signif- to assess distance running performance, as in previous training
icant (P < 0.05). However, when the same statistical proce- taper studies [22, 42]. This exercise model has the advantage of
dures were applied to MDA data for each group of seven sub- closely simulating a competitive race situation by allowing self
jects, the rise in MDA was found to be non-significant. These pacing through the given distance, yet minimises variability in
findings suggest that the small size of each group resulted in environmental and psychological factors which may confound
insufficient statistical power, to determine if the exercise in- measurements made during actual competition. The half-
duced rise in MDA was significant. Changes in MDA over time marathon runs were performed at a pace which exceeded the
did not differ either between or within groups (P > 0.05, ANO- average running speed during training, furthermore for most
VA). Serum CK was elevated over time in both normal training subjects, completion of each half-marathon involved perform-
Effects of a Training Taper on Tissue Damage Int J Sports Med 2000; 21 329

Fig. 2 Serum urate concentration in normal and training taper Fig. 4 MDA in normal and training taper groups. A (baseline, imme-
groups. A (baseline, immediately before run 1); B (immediately diately before run 1); B (immediately after run 1); C (immediately be-
after run 1); C (immediately before run 2); D (immediately after fore run 2); D (immediately after run 2).
run 2). * P < 0.025 relative to pre-exercise, NS: not significant rela-
tive to baseline.

tween groups following the taper cannot simply be attributed

Downloaded by: University of Thessaly. Copyrighted material.


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-
Fig. 3 Serum TAC in normal and training taper groups. A (base- oxidation in normal training and training taper groups respec-
line, immediately before run 1); B (immediately after run 1); C (im- tively (Fig. 4).
mediately before run 2); D (immediately after run 2). * P < 0.025
relative to pre-exercise. 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-
ing almost half the weekly training volume in a single exercise marathon running [14]. Increases in serum CK during exercise
session. This finding suggests that each half-marathon may arise from sarcolemmal rupture, which has been reported
represented a considerable exercise challenge to these sub- in humans immediately following a marathon [20]. When
jects and would typically compromise exercise performance compared with the normal training group, the training taper
for 2 to 3 days after the event. Therefore each half-marathon resulted in lower CK after the second half-marathon (Fig. 5).
would have resulted in overreaching as described by Fry et al. There is evidence that exercise induced myocellular injury
[16] and Hooper et al. [21]. It is clear that the subjects were not can arise from increased mechanical loading on the muscle
in an overreached state prior to the second half-marathon, as [2,10,15] and oxidative stress [8, 27, 32]. As there were no dif-
performance was not significantly slower than that for the first ferences in performance between the two groups, the attenu-
run. ated release of creatine kinase was unlikely to be a conse-
quence of lower muscle force generation, or reduced oxidative
Indices of exercise induced muscle damage, such as elevations stress. Furthermore, the reduction in CK as a consequence of
in serum CK, can be significantly attenuated by the prior per- the training taper did not appear to be caused by increased ex-
formance of a single session of exercise which produces myo- tracellular antioxidant protection, as there were no differences
cellular injury [6, 7]. Furthermore, oxidative stress (as experi- in serum TAC between groups (Fig. 3). The higher CK in the
enced during an acute session of running) can differentially af- normal training group (relative to the taper group) after the
fect the components of myocellular antioxidant defences second half-marathon, was a consequence of higher CK imme-
[11, 26, 40, 41]. Such responses could alter susceptibility to oxi- diately before exercise and a greater relative rise during exer-
dative muscle injury when subsequent damaging exercise is cise. These data suggest that the maintenance of normal train-
performed. To compensate for “order effects” arising from such ing volumes may have slowed recovery processes following
responses, a normal training group was evaluated in parallel to the first half-marathon, resulting in a higher resting level of
the training taper group. Thus, the differences reported be- muscle injury prior to the second half-marathon. There also
330 Int J Sports Med 2000; 21 Child RB et al

7
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 bio-
chemical 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. Manipula-
tion of knee extensor force using percutaneous electrical myo-
stimulation 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.
Fig. 5 Serum CK in normal and training taper groups. A (baseline,
The effect of exertion on mitochondrial oxidative capacity and
immediately before run 1); B (immediately after run 1); C (immedi-
on some antioxidant mechanisms in muscle from marathon run-
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, ners. Int J Sports Med 1984; 5: 135
12
* P < 0.025 relative to pre-exercise. 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
appeared to be a reduced tolerance to exercise induced muscle Dill DB, Costill DL. Calculation of percentage changes in volumes

Downloaded by: University of Thessaly. Copyrighted material.


injury in the normal training group. Therefore in relative of blood, plasma and red cells in dehydration. J Appl Physiol 1974;
terms, the training taper may have facilitated muscle recovery, 37: 247 – 248
14
Duthie GG, Robertson JD, Maughan RJ, Morrice PC. Blood antioxi-
such that CK returned to resting values prior to the second
dant status and erythrocyte lipid peroxidation following distance
half-marathon level and that resistance to exercise induced in-
running. Arch Biochem Biophys 1990; 282: 73 – 83
jury was similar to that observed prior to reduced training. 15
Faulkner JA, Brooks S, Opiteck J. Injury to skeletal muscle fibers
during contractions: Conditions of occurrence and prevention.
In conclusion the training taper did not enhance serum free Physical Therapy 1993; 73: 911 – 921
radical scavenging capacity prior to, or during exercise. Despite 16
Fry RW, Morton AR, Keast D. Periodisation of training stress: A re-
evidence that the training taper reduced muscle damage, rela- view. Can J Spt Sci 1992; 17: 234 – 240
tive to the normal training aroup, half-marathon performance 17
Gauduel Y, Menasche P, Duvelleroy M. Enzyme release and mito-
was not improved. Further studies evaluating muscle damage chondrial activity in reoxygenated cardiac muscle. Relationship
and indices of antioxidant status within active skeletal muscle with oxygen induced lipid peroxidation. Gen Physiol Biophys
are necessary to determine if the changes produced by the 1989; 8: 327 – 340
18
training taper are a consequence of reduced myocellular in- Gleeson M, Robertson JD, Maughan RJ. Influence of exercise on
jury. 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:
Acknowledgements 1638 – 1641
20
Hikida RS, Staron RS, Hagerman FC, Sherman WM, Costill DL.
The authors gratefully acknowledge the support of the runners
Muscle fiber necrosis associated with human marathon runners.
who participated in this project and critical input from Mr. J.D.
J Neurol Sci 1983; 59: 185 – 203
Chance. 21
Hooper SL, Makinnon LT. Monitoring overtraining in athletes.
Sports Med 1995; 20: 321 – 327
References 22
Houmard JA, Scott BK, Justice CL, Chenier TC. The effects of taper
on performance in distance runners. Med Sci Sports Exerc 1994;
1
Aikawa KM, Quintanilha AT, de Lumen BO, Brooks GA, Packer L. 26: 624 – 631
Exercise endurance-training alters vitamin E tissue levels and 23
Houmard JA. Impact of reduced training on performance in en-
red cell hemolysis in rodents. Biosci Rep 1984; 4: 253 – 257 durance athletes. Sports Med 1991; 12: 380 – 393
2
Armstrong RB, Warren GL, Warren JA. Mechanisms of exercise-in- 24
Jackson MJ, Edwards RHT, Symons MCR. Electron spin resonance
duced muscle fibre injury. Sports Med 1991; 12: 184 – 207 studies of intact mammalian skeletal muscle. Biochem Biophys
3
Brandon LJ. Physiological factors associated with middle and long Acta 1985; 847: 185 – 190
distance running performance. Sports Med 1995; 19: 268 – 277 25
Ji L. Gatorade Sports Science Exchange. Roundtable. Exercise nu-
4
Bowles DK, Torgan CE, Ebner S, Kehrer JP, Ivy JL, Starnes JW. Ef- trition and free radicals: What’s the connection? 1994; 15: Vol 5:
fects of acute submaximal exercise on skeletal muscle vitamin E. 380 – 393
Free Rad Res Commun 1991; 14: 139 – 143 26
Ji LL. Exercise and oxidative stress: Role of cellular antioxidant
5
Brooks G, Gillam I, Kanter M, Packer L. Proceedings of the panel systems 1995. Exerc Sport Sci Rev 1995; 23: 135 – 166
discussion: Antioxidants and the elite athlete. LaGrange: Henkel 27
Kanter MM, Lesmes GR, Kaminsky LA, La Ham-Saeger J, Nequin
Fine Chemicals, 1992: 1 – 21 ND. Serum creatine kinase and lactate dehydrogenase changes
6
Brown SJ, Child RB, Day SH, Donnelly AE. Exercise-induced skele- following an eighty kilometer race. Eur J Appl Physiol 1988; 57:
tal muscle damage and adaptation following repeated bouts of 60 – 63
eccentric muscle contractions. J Sports Sci 1997; 15: 215 – 222
Effects of a Training Taper on Tissue Damage Int J Sports Med 2000; 21 331

28
Keul J, Doll E, Koppler D. Oxidative energy supply. In: Jokl E (ed). Corresponding Author:
Energy metabolism in human muscle. Basel: Karger, 1972
29
Kuipers H, Janssen GME, Bosman F, Frederik PM, Geurten P. Struc- Robert B. Child, Ph.D.
tural and ultrastructural changes in skeletal muscle associated
Exercise Physiology Research Group
with long-distance training and running. Int J Sports Med 1989;
University College Chichester
10: S156 – S159
30
College Lane
Marin E, Kretzschmar M, Arokoski J, Hanninen O, Klinger W. En-
Chichester
zymes of glutathione synthesis in dog skeletal muscles and their
West Sussex, PO19 4PE
response to training. Acta Physiol Scand 1993; 147: 369 – 373
31 UK
McKenzie DC. Markers of excessive exercise. Can J Appl Physiol
1999; 24: 66 – 73
32 Phone: + 44 (1243) 816-387
Maughan RJ, Donnelly AE, Gleeson M, Whiting PH, Walker KA,
Fax: + 44 (1243) 816-080
Clough PJ. Delayed-onset muscle damage and lipid peroxidation
E-mail: rchild@chihe.ac.uk
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 per-
formance and world running records. J Appl Physiol 1989; 67:
453 – 465

Downloaded by: University of Thessaly. Copyrighted material.


36
Pfafferott C, Meiselman H, Hochstein P. The effect of malondial-
dehyde 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 cel-
lular sulfhydryls. Life Sciences 1994; 54: 149 – 157
38
Reid MB, Stokic DS, Koch SM, Khawli FA, Leis AA. N-Acetylcys-
teine 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, exer-
cise, 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 ath-
letes. 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, tis-
sue damage, and endurance of adult male rats. Int J Sports Med
1997; 18: 497 – 502
46
Whitehead T, Thorpe GHG, Maxwell S. Enhanced chemilumines-
cent assay for antioxidant capacity in biological fluids. Anal Chim
Acta 1992; 226: 265 – 277
47
Wilmore JH, Costill DL. Optimizing performance in sport. Physiol-
ogy 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 plas-
ma by high performance liquid chromatography with fluorimet-
ric detection. Ann Clin Biochem 1991; 28: 504 – 508