PubMed Health⌕ Search

Biomedical subjects

Roger Eston

Publications and source records attributed to Roger Eston.

7 recordsLinked to original sources
PubMed2005

The effects of exercise-induced muscle damage on maximal intensity intermittent exercise performance.

Exercise-induced muscle damage (EIMD) is a common occurrence following activities with a high eccentric component. Alterations to the torque-velocity relationship following EIMD would appear to have serious implications for athletic performance, particularly as they relate to impairment of maximal intensity exercise. However, this has been studied infrequently. The purpose of this study was to assess the effects of EIMD on maximal intermittent sprint performance. Ten male participants (age 22.4 +/- 3.2 years, height 178.6 +/- 5.2 cm, mass 80.6 +/- 10.7 kg) performed 10 x 6 s cycle ergometer sprints, interspersed with 24 s recovery against a load corresponding to 0.10 kp/kg and 10 x 10 m sprints from a standing start, each with 12 s active (walking) recovery. All variables were measured immediately before and at 30 min, 24, 48 and 72 h following a plyometric exercise protocol comprising of 10 x 10 maximal counter movement jumps. Repeated measures ANOVA showed significant changes over time (all P<0.05) for perceived soreness, plasma creatine kinase activity (CK), peak power output (PPO), sprint time and rate of fatigue. Soreness was significantly higher (P<0.01) than baseline values at all time intervals (3.1, 4.9, 5.5 and 3.2 at 30 min, 24, 48 and 72 h, respectively). CK was significantly elevated (P<0.05) at 24 h (239 IU/l) and 48 h (245 IU/l) compared to baseline (151 IU/l). PPO was significantly lower (P<0.05) than baseline (1,054 W) at all time intervals (888, 946, 852 and 895 W, at 30 min, 24, 48 and 72 h, respectively). The rate of fatigue over the ten cycling sprints was reduced compared to baseline, with the greatest reduction of 48% occurring at 48 h (P<0.01). This was largely attributed to the lower PPO in the initial repetitions, resulting in a lower starting point for the rate of fatigue. Values returned to normal at 72 h. Sprint times over 10 m were higher (P<0.05) at 30 min, 24 h and 48 h compared to baseline (1.96 s) with values corresponding to 2.01, 2.02 and 2.01 at 30 min, 24 h and 48 h, respectively. Values returned to baseline by 72 h. The results provide further evidence that, following a plyometric, muscle-damaging exercise protocol, the ability of the muscle to generate power is reduced for at least 3 days. This is also manifested by a small, but statistically significant reduction in very short-term (approximately 2 s) intermittent sprint running performance. These findings have implications for appropriate training strategies in multiple sprint sports.

Adaptation, Physiological↗
PubMed2004

Neuromuscular function after exercise-induced muscle damage: theoretical and applied implications.

Exercise-induced muscle damage is a well documented phenomenon particularly resulting from eccentric exercise. When eccentric exercise is unaccustomed or is performed with an increased intensity or duration, the symptoms associated with muscle damage are a common outcome and are particularly associated with participation in athletic activity. Muscle damage results in an immediate and prolonged reduction in muscle function, most notably a reduction in force-generating capacity, which has been quantified in human studies through isometric and dynamic isokinetic testing modalities. Investigations of the torque-angular velocity relationship have failed to reveal a consistent pattern of change, with inconsistent reports of functional change being dependent on the muscle action and/or angular velocity of movement. The consequences of damage on dynamic, multi-joint, sport-specific movements would appear more pertinent with regard to athletic performance, but this aspect of muscle function has been studied less often. Reductions in the ability to generate power output during single-joint movements as well as during cycling and vertical jump movements have been documented. In addition, muscle damage has been observed to increase the physiological demand of endurance exercise and to increase thermal strain during exercise in the heat. The aims of this review are to summarise the functional decrements associated with exercise-induced muscle damage, relate these decrements to theoretical views regarding underlying mechanisms (i.e. sarcomere disruption, impaired excitation-contraction coupling, preferential fibre type damage, and impaired muscle metabolism), and finally to discuss the potential impact of muscle damage on athletic performance.

Action Potentials↗
PubMed2002

The effect of exercise-induced muscle damage on isometric and dynamic knee extensor strength and vertical jump performance.

In this study, we assessed the effect of exercise-induced muscle damage on knee extensor muscle strength during isometric, concentric and eccentric actions at 1.57 rad x s(-1) and vertical jump performance under conditions of squat jump, countermovement jump and drop jump. The eight participants (5 males, 3 females) were aged 29.5+/-7.1 years (mean +/- s). These variables, together with plasma creatine kinase (CK), were measured before, 1 h after and 1, 2, 3, 4 and 7 days after a bout of muscle damaging exercise: 100 barbell squats (10 sets x 10 repetitions at 70% body mass load). Strength was reduced for 4 days (P< 0.05) but no significant differences (P> 0.05) were apparent in the magnitude or rate of recovery of strength between isometric, concentric and eccentric muscle actions. The overall decline in vertical jump performance was dependent on jump method: squat jump performance was affected to a greater extent than countermovement (91.6+/-1.1% vs 95.2+/-1.3% of pre-exercise values, P< 0.05) and drop jump (95.2+/-1.4%, P< 0.05) performance. Creatine kinase was elevated (P < 0.05) above baseline 1 h after exercise, peaked on day 1 and remained significantly elevated on days 2 and 3. Strength loss after exercise-induced muscle damage was independent of the muscle action being performed. However, the impairment of muscle function was attenuated when the stretch-shortening cycle was used in vertical jumping performance.

Adult↗
PubMed2002

Maximal-intensity isometric and dynamic exercise performance after eccentric muscle actions.

A well-documented observation after eccentric exercise is a reduction in maximal voluntary force. However, little is known about the ability to maintain maximal isometric force or generate and maintain dynamic peak power. These aspects of muscle function were studied in seven participants (5 males, 2 females). Knee extensor isometric strength and rate of fatigue were assessed by a sustained 60 s maximal voluntary contraction at 80 degrees and 40 degrees knee flexion, corresponding to an optimal and a shortened muscle length, respectively. Dynamic peak power and rate of fatigue were assessed during a 30 s Wingate cycle test. Plasma creatine kinase was measured from a fingertip blood sample. These variables were measured before, 1 h after and 1, 2, 3 and 7 days after 100 repetitions of the eccentric phase of the barbell squat exercise (10 sets x 10 reps at 80% concentric one-repetition maximum). Eccentric exercise resulted in elevations in creatine kinase activity above baseline (274+/-109 U x l(-1); mean +/- s(x)) after 1 h (506+/-116 U x l(-1), P < 0.05) and 1 day (808+/-117 U x l(-1), P < 0.05). Isometric strength was reduced (P < 0.05) for 7 days (35% at 1 h, 5% at day 7) and the rate of fatigue was lower (P < 0.05) for 3 days at 80 degrees and for 1 day at 40 degrees. Wingate peak power was reduced to a lesser extent (P < 0.05) than isometric strength at 1 h (13%) and, although the time course of recovery was equal, the two variables differed in their pattern of recovery. Eccentrically exercised muscle was characterized by an inability to generate high force and power, but an improved ability to maintain force and power. Such functional outcomes are consistent with the proposition that type II fibres are selectively recruited or damaged during eccentric exercise.

Adult↗
PubMed2002

Exercise-induced muscle damage and the potential protective role of estrogen.

Exercise-induced muscle damage is a well documented phenomenon that often follows unaccustomed and sustained metabolically demanding activities. This is a well researched, but poorly understood area, including the actual mechanisms involved in the muscle damage and repair cycle. An integrated model of muscle damage has been proposed by Armstrong and is generally accepted. A more recent aspect of exercise-induced muscle damage to be investigated is the potential of estrogen to have a protective effect against skeletal muscle damage. Estrogen has been demonstrated to have a potent antioxidant capacity that plays a protective role in cardiac muscle, but whether this antioxidant capacity has the ability to protect skeletal muscle is not fully understood. In both human and rat studies, females have been shown to have lower creatine kinase (CK) activity following both eccentric and sustained exercise compared with males. As CK is often used as an indirect marker of muscle damage, it has been suggested that female muscle may sustain less damage. However, these findings may be more indicative of the membrane stabilising effect of estrogen as some studies have shown no histological differences in male and female muscle following a damaging protocol. More recently, investigations into the potential effect of estrogen on muscle damage have explored the possible role that estrogen may play in the inflammatory response following muscle damage. In light of these studies, it may be suggested that if estrogen inhibits the vital inflammatory response process associated with the muscle damage and repair cycle, it has a negative role in restoring normal muscle function after muscle damage has occurred. This review is presented in two sections: firstly, the processes involved in the muscle damage and repair cycle are reviewed; and secondly, the possible effects that estrogen has upon these processes and muscle damage in general is discussed. The muscle damage and repair cycle is presented within a model, with particular emphasis on areas that are important to understanding the potential effect that estrogen has upon these processes.

Calcium↗