Biomedical subjects

Jonathan M Peake

Publications and source records attributed to Jonathan M Peake.

8 recordsLinked to original sources

PubMed2006

The influence of antioxidant supplementation on markers of inflammation and the relationship to oxidative stress after exercise.

Interest in the relationship between inflammation and oxidative stress has increased dramatically in recent years, not only within the clinical setting but also in the fields of exercise biochemistry and immunology. Inflammation and oxidative stress share a common role in the etiology of a variety of chronic diseases. During exercise, inflammation and oxidative stress are linked via muscle metabolism and muscle damage. Because oxidative stress and inflammation have traditionally been associated with fatigue and impaired recovery from exercise, research has focused on nutritional strategies aimed at reducing these effects. In this review, we have evaluated the findings of studies involving antioxidant supplementation on alterations in markers of inflammation (e.g., cytokines, C-reactive protein and cortisol). This review focuses predominantly on the role of reactive oxygen and nitrogen species generated from muscle metabolism and muscle damage during exercise and on the modulatory effects of antioxidant supplements. Furthermore, we have analyzed the influence of factors such as the dose, timing, supplementation period and bioavailability of antioxidant nutrients.

Antioxidants↗

PubMed2006

Systemic inflammatory responses to maximal versus submaximal lengthening contractions of the elbow flexors.

We compared changes in markers of muscle damage and systemic inflammation after submaximal and maximal lengthening muscle contractions of the elbow flexors. Using a cross-over design, 10 healthy young men not involved in resistance training completed a submaximal trial (10 sets of 60 lengthening contractions at 10% maximum isometric strength, 1 min rest between sets), followed by a maximal trial (10 sets of three lengthening contractions at 100% maximum isometric strength, 3 min rest between sets). Lengthening contractions were performed on an isokinetic dynamometer. Opposite arms were used for the submaximal and maximal trials, and the trials were separated by a minimum of two weeks. Blood was sampled before, immediately after, 1 h, 3 h, and 1-4 d after each trial. Total leukocyte and neutrophil numbers, and the serum concentration of soluble tumor necrosis factor-alpha receptor 1 were elevated after both trials (P < 0.01), but there were no differences between the trials. Serum IL-6 concentration was elevated 3 h after the submaximal contractions (P < 0.01). The concentrations of serum tumor necrosis factor-alpha, IL-1 receptor antagonist, IL-10, granulocyte-colony stimulating factor and plasma C-reactive protein remained unchanged following both trials. Maximum isometric strength and range of motion decreased significantly (P < 0.001) after both trials, and were lower from 1-4 days after the maximal contractions compared to the submaximal contractions. Plasma myoglobin concentration and creatine kinase activity, muscle soreness and upper arm circumference all increased after both trials (P < 0.01), but were not significantly different between the trials. Therefore, there were no differences in markers of systemic inflammation, despite evidence of greater muscle damage following maximal versus submaximal lengthening contractions of the elbow flexors.

Adult↗

PubMed2005

Plasma cytokine changes in relation to exercise intensity and muscle damage.

The purpose of this study was to compare the effects of exercise intensity and exercise-induced muscle damage on changes in anti-inflammatory cytokines and other inflammatory mediators. Nine well-trained male runners completed three different exercise trials on separate occasions: (1) level treadmill running at 60% VO2max (moderate-intensity trial) for 60 min; (2) level treadmill running at 85% VO2max (high-intensity trial) for 60 min; (3) downhill treadmill running (-10% gradient) at 60% VO2max (downhill running trial) for 45 min. Blood was sampled before, immediately after and 1 h after exercise. Plasma was analyzed for interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-5, IL-10, IL-12p40, IL-13, monocyte chemotactic protein-1 (MCP-1), prostaglandin E(2), leukotriene B(4) and heat shock protein 70 (HSP70). The plasma concentrations of IL-1ra, IL-12p40, MCP-1 and HSP70 increased significantly (P<0.05) after all three trials. Plasma prostaglandin E(2) concentration increased significantly after the downhill running and high-intensity trials, while plasma IL-10 concentration increased significantly only after the high-intensity trial. IL-4 and leukotriene B(4) did not increase significantly after exercise. Plasma IL-1ra and IL-10 concentrations were significantly higher (P<0.05) after the high-intensity trial than after both the moderate-intensity and downhill running trials. Therefore, following exercise up to 1 h duration, exercise intensity appears to have a greater effect on anti-inflammatory cytokine production than exercise-induced muscle damage.

Adult↗

PubMed2005

Exercise-induced muscle damage, plasma cytokines, and markers of neutrophil activation.

INTRODUCTION: Unaccustomed eccentric exercise often results in muscle damage and neutrophil activation. We examined changes in plasma cytokines stress hormones, creatine kinase activity and myoglobin concentration, neutrophil surface receptor expression, degranulation, and the capacity of neutrophils to generate reactive oxygen species in response to in vitro stimulation after downhill running. METHODS: Ten well-trained male runners ran downhill on a treadmill at a gradient of -10% for 45 min at 60% VO2max. Blood was sampled immediately before (PRE) and after (POST), 1 h (1 h POST), and 24 h (24 h POST) after exercise. RESULTS: At POST, there were significant increases (P < 0.01) in neutrophil count (32%), plasma interleukin (IL)-6 concentration (460%), myoglobin (Mb) concentration (1100%), and creatine kinase (CK) activity (40%). At 1 h POST, there were further increases above preexercise values for neutrophil count (85%), plasma Mb levels (1800%), and CK activity (56%), and plasma IL-6 concentration remained above preexercise values (410%) (P < 0.01). At 24 h POST, neutrophil counts and plasma IL-6 levels had returned to baseline, whereas plasma Mb concentration (100%) and CK activity (420%) were elevated above preexercise values (P < 0.01). There were no significant changes in neutrophil receptor expression, degranulation and respiratory burst activity, and plasma IL-8 and granulocyte-colony stimulating factor concentrations at any time after exercise. Neutrophil count correlated with plasma Mb concentration at POST (r = 0.64, P < 0.05), and with plasma CK activity at POST (r = 0.83, P < 0.01) and 1 h POST (r = 0.78, P < 0.01). CONCLUSION: Neutrophil activation remains unchanged after downhill running in well-trained runners, despite increases in plasma markers of muscle damage.

Adult↗

PubMed2005

Influence of high-intensity interval training on adaptations in well-trained cyclists.

The purpose of the present study was to examine the influence of 3 different high-intensity interval training regimens on the first and second ventilatory thresholds (VT(1) and VT(2)), anaerobic capacity (ANC), and plasma volume (PV) in well-trained endurance cyclists. Before and after 2 and 4 weeks of training, 38 well-trained cyclists (Vo(2)peak = 64.5 +/- 5.2 ml.kg(-1).min(-1)) performed (a) a progressive cycle test to measure Vo(2)peak, peak power output (PPO), VT(1), and VT(2); (b) a time to exhaustion test (T(max)) at their Vo(2)peak power output (P(max)); and (c) a 40-km time-trial (TT(40)). Subjects were assigned to 1 of 4 training groups (group 1: n = 8, 8 x 60% T(max) at P(max), 1:2 work-recovery ratio; group 2: n = 9, 8 x 60% T(max) at P(max), recovery at 65% maximum heart rate; group 3: n = 10, 12 x 30 seconds at 175% PPO, 4.5-minute recovery; control group: n = 11). The TT(40) performance, Vo(2)peak, VT(1), VT(2), and ANC were all significantly increased in groups 1, 2, and 3 (p < 0.05) but not in the control group. However, PV did not change in response to the 4-week training program. Changes in TT(40) performance were modestly related to the changes in Vo(2)peak, VT(1), VT(2), and ANC (r = 0.41, 0.34, 0.42, and 0.40, respectively; all p < 0.05). In conclusion, the improvements in TT(40) performance were related to significant increases in Vo(2)peak, VT(1), VT(2), and ANC but were not accompanied by significant changes in PV. Thus, peripheral adaptations rather than central adaptations are likely responsible for the improved performances witnessed in well-trained endurance athletes following various forms of high-intensity interval training programs.

Adaptation, Physiological↗

PubMed2003

Vitamin C: effects of exercise and requirements with training.

Ascorbic acid or vitamin C is involved in a number of biochemical pathways that are important to exercise metabolism and the health of exercising individuals. This review reports the results of studies investigating the requirement for vitamin C with exercise on the basis of dietary vitamin C intakes, the response to supplementation and alterations in plasma, serum, and leukocyte ascorbic acid concentration following both acute exercise and regular training. The possible physiological significance of changes in ascorbic acid with exercise is also addressed. Exercise generally causes a transient increase in circulating ascorbic acid in the hours following exercise, but a decline below pre-exercise levels occurs in the days after prolonged exercise. These changes could be associated with increased exercise-induced oxidative stress. On the basis of alterations in the concentration of ascorbic acid within the blood, it remains unclear if regular exercise increases the metabolism of vitamin C. However, the similar dietary intakes and responses to supplementation between athletes and nonathletes suggest that regular exercise does not increase the requirement for vitamin C in athletes. Two novel hypotheses are put forward to explain recent findings of attenuated levels of cortisol postexercise following supplementation with high doses of vitamin C.

Animals↗

PubMed2002

Interval training program optimization in highly trained endurance cyclists.

PURPOSE: The purpose of this study was to examine the influence of three different high-intensity interval training (HIT) regimens on endurance performance in highly trained endurance athletes. METHODS: Before, and after 2 and 4 wk of training, 38 cyclists and triathletes (mean +/- SD; age = 25 +/- 6 yr; mass = 75 +/- 7 kg; VO(2peak) = 64.5 +/- 5.2 mL x kg(-1) min(-1)) performed: 1) a progressive cycle test to measure peak oxygen consumption (VO(2peak)) and peak aerobic power output (PPO), 2) a time to exhaustion test (T(max)) at their VO(2peak) power output (P(max)), as well as 3) a 40-km time-trial (TT(40)). Subjects were matched and assigned to one of four training groups (G(2), N = 8, 8 x 60% T(max) at P(max), 1:2 work:recovery ratio; G(2), N = 9, 8 x 60% T(max) at P(max), recovery at 65% HR(max); G(3), N = 10, 12 x 30 s at 175% PPO, 4.5-min recovery; G(CON), N = 11). In addition to G(1), G(2), and G(3) performing HIT twice per week, all athletes maintained their regular low-intensity training throughout the experimental period. RESULTS: All HIT groups improved TT(40) performance (+4.4 to +5.8%) and PPO (+3.0 to +6.2%) significantly more than G(CON) (-0.9 to +1.1%; P < 0.05). Furthermore, G(1) (+5.4%) and G(2) (+8.1%) improved their VO(2peak) significantly more than G(CON) (+1.0%; P < 0.05). CONCLUSION: The present study has shown that when HIT incorporates P(max) as the interval intensity and 60% of T(max) as the interval duration, already highly trained cyclists can significantly improve their 40-km time trial performance. Moreover, the present data confirm prior research, in that repeated supramaximal HIT can significantly improve 40-km time trial performance.

Adult↗

PubMed2002

Exercise-induced alterations in neutrophil degranulation and respiratory burst activity: possible mechanisms of action.

Neutrophils constitute 50-60% of all circulating leukocytes; they present the first line of microbicidal defense and are involved in inflammatory responses. To examine immunocompetence in athletes, numerous studies have investigated the effects of exercise on the number of circulating neutrophils and their response to stimulation by chemotactic stimuli and activating factors. Exercise causes a biphasic increase in the number of neutrophils in the blood, arising from increases in catecholamine and cortisol concentrations. Moderate intensity exercise may enhance neutrophil respiratory burst activity, possibly through increases in the concentrations of growth hormone and the inflammatory cytokine IL-6. In contrast, intense or long duration exercise may suppress neutrophil degranulation and the production of reactive oxidants via elevated circulating concentrations of epinephrine (adrenaline) and cortisol. There is evidence of neutrophil degranulation and activation of the respiratory burst following exercise-induced muscle damage. In principle, improved responsiveness of neutrophils to stimulation following exercise of moderate intensity could mean that individuals participating in moderate exercise may have improved resistance to infection. Conversely, competitive athletes undertaking regular intense exercise may be at greater risk of contracting illness. However, there are limited data to support this concept. To elucidate the cellular mechanisms involved in the neutrophil responses to exercise, researchers have examined changes in the expression of cell membrane receptors, the production and release of reactive oxidants and more recently, calcium signaling. The investigation of possible modifications of other signal transduction events following exercise has not been possible because of current methodological limitations. At present, variation in exercise-induced alterations in neutrophil function appears to be due to differences in exercise protocols, training status, sampling points and laboratory assay techniques.

Cell Degranulation↗