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Biomedical subjects

R B Child

Publications and source records attributed to R B Child.

10 recordsLinked to original sources

Time course of responses of human skeletal muscle to oxidative stress induced by nondamaging exercise.

Previous studies in animals have demonstrated that a single period of aerobic exercise induces a rise in the skeletal muscle activity of the antioxidant enzymes superoxide dismutase and catalase and an increase in the muscle content of heat shock proteins (HSPs). The purpose of this study was to examine the time course of response of human skeletal muscle superoxide dismutase and catalase activities and the content of HSP60 and HSP70 after a period of exhaustive, nondamaging aerobic exercise. Seven volunteers undertook one-legged cycle ergometry at 70% maximal oxygen uptake for 45 min. Biopsies were obtained from the vastus lateralis muscle 7 days before and at 1, 2, 3, and 6 days after exercise. Muscle superoxide dismutase activity increased to a peak at 3 days postexercise, muscle catalase activities were unchanged, and muscle content of HSP60 and the inducible HSP70 increased by variable amounts to reach means of 190% and 3,100% of preexercise values, respectively, by 6 days postexercise. These data indicate that human skeletal muscle responds to a single bout of nondamaging exercise by increasing superoxide dismutase activity and provide the first evidence of an increase in HSP content of human skeletal muscle after a submaximal exercise bout.

Adult↗

Effects of a training taper on tissue damage indices, serum antioxidant capacity and half-marathon running performance.

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.

Adult↗

Resting serum antioxidant status is positively correlated with peak oxygen uptake in endurance trained runners.

BACKGROUND: This study tested the hypothesis that the ability to scavenge free radicals in serum was compromised in trained runners. METHODS EXPERIMENTAL DESIGN: peak VO2, the ability to scavenge free radicals in serum and the plasma concentration of malondialdehyde (MDA) were assessed in 18 male runners. PARTICIPANTS: subject characteristics (mean +/- SEM) were height 1.77 +/- 0.01 m, mass 71.4 +/- 1.2 kg, age 31 +/- 1 years and weekly training distance 45 +/- 5 km.week-1. MEASURES: venous blood samples were collected at rest. Serum total antioxidant capacity (TAC) was determined using a chemiluminescent technique. This involved the oxidation of luminol, in a reaction catalysed by horseradish peroxidase. Serum antioxidant protection was quantified relative to a soluble vitamin E analogue (Trolox) and expressed as Trolox equivalents (Trolox Eq.). MDA was determined using a highly specific assay, using HPLC with fluorimetric detection. Peak VO2 was determined from expired gas measurements collected during an incremental running test on a motorised treadmill. Data were analysed using Pearson correlations. RESULTS: Serum TAC was 500 +/- 26 mumol Trolox Eq.l-1, with a plasma MDA concentration of 1.5 +/- 0.1 mmol.l-1 and serum urate concentration of 274 +/- 12 mmol.l-1. Peak VO2 was 63 +/- 1 ml.kg-1.min-1. Significant correlations were observed between peak VO2 and serum TAC (r = 0.365, p < 0.05); peak VO2 and serum urate (r = 0.463, p < 0.05) and serum urate and serum TAC (r = 0.807, p < 0.001). Plasma MDA and serum TAC were not significantly correlated (r = 0.026, p > 0.05). CONCLUSIONS: These data demonstrate that the ability to quench free radicals in serum in increased in relation to the maximum ability to consume oxygen, however this response does not appear to provide any additional protection against peroxidative damage at rest.

Adult↗

Electromyogram activity and mean power frequency in exercise-damaged human muscle.

Eight volunteers performed two bouts of 50 voluntary maximal eccentric contractions of the knee extensors of one leg 3 weeks apart. During maximal voluntary isometric contractions performed at intervals after each bout, electromyogram (EMG) mean power frequency declined after bout one (P < 0.01 Duncan's test), whereas integrated EMG did not change after either bout. These results suggest that unaccustomed eccentric contractions produce a temporary reduction in mean muscle activation frequency during subsequent maximal isometric contractions.

Adult↗

Manipulation of knee extensor force using percutaneous electrical myostimulation during eccentric actions: effects on indices of muscle damage in humans.

Percutaneous electrical myostimulation (PES) was used to manipulate the force produced by the knee extensor muscles during eccentric exercise, thereby providing a model to investigate the role of force in muscle damage. Two eccentric exercise bouts of equal work were performed by nine subjects, using fixed voltage PES at 20 Hz (to produce moderate muscle forces) and 100 Hz (to produce high muscle forces). Muscle contractility, serum creatine kinase activity (CK) and muscle soreness (MS) were evaluated before, and up to 14 days after exercise. Data are presented as means+/-SEM, and were analysed using repeated measures analysis of variance (ANOVA), t-tests and Wilcoxon tests. Peak forces were higher during the 100 Hz bout than the 20 Hz bout for repetitions 1 (472+/-60 vs 237+/-23 Newtons), 10 (381+/-26 vs 233+/-26 Newtons), 20 (310+/-24 vs 218+/-24 Newtons), all p < 0.01, t-test and 30 (297+/-27 vs 204+/-21 Newtons), p < 0.05, t-test. Following the 100 Hz bout, maximum voluntary contractile force (MVC) was lower (p<0.01, ANOVA), and CK was higher (p<0.0001, ANOVA) than after the 20 Hz bout. Subjects also reported greater MS on days 2 to 6 (p<0.05, Wilcoxon test) following the 100 Hz bout. Despite a decline in the stimulated 20:100 Hz tetanic force ratio after each bout (p<0.01, ANOVA) there was no difference between bouts (p>0.05, ANOVA). The higher rise in CK and MS after the 100 Hz bout, together with the greater deficit in MVC, suggest that in humans, muscle force is a contributing factor to muscle injury during eccentric actions.

Adolescent↗

Comparison of eccentric knee extensor muscle actions at two muscle lengths on indices of damage and angle-specific force production in humans.

In this study, we investigated the effects of knee extensor length during eccentric exercise on indices of muscle damage and adaptation. Subjects (n = 7) performed two bouts of 75 maximal voluntary eccentric muscle actions at a knee joint angular velocity of 1.57 rad s(-1). One bout was performed at a short muscle length (bout S) with a knee joint range of motion of 2.79 to 1.40 radians (160 degrees to 80 degrees), and a second with the contralateral knee extensors at a long muscle length (bout L) with a range of motion of 2.01 to 0.7 radians (120 degrees to 40 degrees). The maximum voluntary contractile force (MVC) was measured before and 5 min after exercise, and again on days 3, 5, 7, 10 and 12, at knee angles of 160 degrees, 120 degrees and 80 degrees. Muscle soreness was measured before exercise and on each day after exercise. Serum creatine kinase activity was measured before exercise and on days 3, 5, 7, 10 and 12 post-exercise. The MVC declined after each bout (P < 0.01), with a greater decline after bout L (P < 0.05). Muscle soreness was higher relative to bout S on days 1, 2, 3, 5 and 6 (P < 0.05). Although serum creatine kinase activity was elevated after both exercise bouts (P < 0.01), there was no difference between bouts. Functional muscle damage markers and muscle soreness suggest greater damage after bout L. Post-exercise angle-specific force decrements suggest a transient increase in muscle length after bout L but not bout S.

Adaptation, Physiological↗

Elevated serum antioxidant capacity and plasma malondialdehyde concentration in response to a simulated half-marathon run.

PURPOSE AND METHODS: Indices of antioxidant status, membrane permeability, and lipid peroxidation were investigated in venous blood immediately before and after a simulated half-marathon run. In serum, these included the ability to scavenge free radicals (total antioxidant capacity, TAC), the concentration of uric acid (UA), and the activities of creatine kinase (CK) and beta-glucuronidase (beta G). The plasma concentration of malondialdehyde (MDA) was used as a marker of lipid peroxidation. Data were analyzed with paired t-tests. After a standardized warm-up, 17 trained male runners (mean +/- SD, age 31 +/- 4 yr, peak VO2 63.2 +/- 4.8 mL.kg-1.min-1) each completed a self-paced half-marathon run, on a motorized treadmill. Average exercise intensity was 77.1 +/- 1.0% peak VO2, with a performance time of 87.1 +/- 7.0 min. RESULTS: After exercise, elevations were observed in MDA from 1.48 +/- 0.39 mmol.L-1 to 1.65 +/- 0.32 mmol.L-1 (P < 0.05), TAC from 475 +/- 84 to 564 +/- 113 mmol Trolox Eq.L-1 (P < 0.0001), UA from 268 +/- 45 to 312 +/- 51 mmol.L-1 (P < 0.001), serum cortisol concentration from 339 +/- 95 to 557 +/- 157 nmol.L-1 (P < 0.01), CK from 98 +/- 67 to 133 +/- 89 IU.L-1 (P < 0.0001), and beta G from 15.39 +/- 5.34 to 17.05 +/- 5.7 Sigma Units.mL-1 (P < 0.001). CONCLUSIONS: The rise in TAC did not prevent exercise-induced lipid peroxidation and muscle damage as both MDA and CK were elevated after exercise. This may indicate inadequacies in the antioxidant defense system during the half-marathon run.

Adult↗

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions.

Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU.l-1 and 375 (198) IU.l-1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response.

Adult↗

Exercise-induced skeletal muscle damage and adaptation following repeated bouts of eccentric muscle contractions.

Repeated bouts of eccentric muscle contractions were used to examine indirect indices of exercise-induced muscle damage and adaptation in human skeletal muscle. Twenty-four subjects (18 females, 6 males) aged 20.0 +/- 1.4 years (mean +/- S.D.) performed an initial bout of either 10 (n = 7), 30 (n = 9) or 50 (n = 8) maximum voluntary eccentric contractions of the knee extensors, followed by a second bout of 50 contractions 3 weeks later using the same leg. Muscle soreness was elevated after all bouts (P < 0.05, Wilcoxon test), although the initial bout reduced the soreness associated with the second bout. Force loss and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio were observed after all exercise bouts (P < 0.01). Serum creatine kinase activity was elevated following the initial bouts of 30 and 50 repetitions (P < 0.01), but there was no increase following 10 repetitions. No increase in serum creatine kinase activity was observed in any group following the second bout of contractions (P > 0.05). We conclude that skeletal muscle adaptation can be brought about by a single bout of relatively few eccentric muscle contractions. Increasing the number of eccentric muscle repetitions did not result in an increased prophylactic effect on skeletal muscle.

Adaptation, Physiological↗

Changes in human skeletal muscle contractile function following stimulated eccentric exercise.

Indices of human skeletal muscle contractile function were examined in nine subjects for up to 9 days following a single bout of stimulated eccentric exercise. Eccentric muscle actions of the knee extensor muscles were evoked by percutaneous electrical myostimulation (PES). Delayed onset muscle soreness (DOMS), elevated serum creatine kinase activity, chronic force loss, and a decline in the 20:100 Hz force ratio were observed in the days postexercise. The exercised knee extensor muscles demonstrated an impaired ability to respond to PES. This was evident by an increased time delay between the start of 100 Hz PES and the onset of contraction immediately postexercise [22.3 (SD 15.9)%, P < 0.01] and 3 days postexercise [14.9 (SD 18.1)%, P < 0.05]. Muscle relaxation rates appeared unaffected by the eccentric exercise protocol, where the muscles showed no differences in the time between the end of PES and the onset of relaxation (P > 0.05). During the days following the exercise, no significant differences were observed in the time between the start of contraction and attainment of 70% of the mean tetanic force following a single 1-s pulse of PES. Similarly, no significant differences were observed in the time between the start of relaxation and attainment of 70% of the total relaxation during the same time. The increased delay in excitation-contraction coupling observed immediately postexercise and 3 days after the exercise, may reflect a damage-induced delay in action potential propagation. Muscle relaxation rates postexercise remained unchanged, which would seem to indicate normal functioning of the sarcoplasmic reticulum, suggesting this was not the site of failure in excitation-contraction coupling.

Adult↗