It is widely recognized that an athlete’s ‘pacing strategy’, or how an athlete distributes work and energy throughout an exercise task, can have a significant impact on performance. By applying mathematical modelling (i.e. power/velocity and force/time relationships) to athletic performances, coaches and researchers have observed a variety of pacing strategies. These include the negative, all-out, positive, even, parabolic-shaped and variable pacing strategies. Research suggests that extremely short-duration events (≤30 seconds) may benefit from an explosive ‘all—out’ strategy, whereas during prolonged events (>2 minutes), performance times may be improved if athletes distribute their pace more evenly. Knowledge pertaining to optimal pacing strategies during middle—distance (1.5–2 minutes) and ultra-endurance (>4 hours) events is currently lacking. However, evidence suggests that during these events well trained athletes tend to adopt a positive pacing strategy, whereby after peak speed is reached, the athlete progressively slows. The underlying mechanisms influencing the regulation of pace during exercise are currently unclear. It has been suggested, however, that self-selected exercise intensity is regulated within the brain based on a complex algorithm involving peripheral sensory feedback and the anticipated workload remaining. Furthermore, it seems that the rate and capacity limitations of anaerobic and aerobic energy supply/utilization are particularly influential in dictating the optimal pacing strategy during exercise. This article outlines the various pacing profiles that have previously been observed and discusses possible factors influencing the self-selection of such strategies.

Describing and Understanding Pacing Strategies during Athletic Competition

This investigation determined the efficacy of a tart cherry juice in aiding recovery and reducing muscle damage, inflammation and oxidative stress. Twenty recreational Marathon runners assigned to either consumed cherry juice or placebo for 5 days before, the day of and for 48 h following a Marathon run. Markers of muscle damage (creatine kinase, lactate dehydrogenase, muscle soreness and isometric strength), inflammation [interleukin-6 (IL-6), C-reactive protein (CRP) and uric acid], total antioxidant status (TAS) and oxidative stress [thiobarbituric acid reactive species (TBARS) and protein carbonyls] were examined before and following the race. Isometric strength recovered significantly faster (P=0.024) in the cherry juice group. No other damage indices were significantly different. Inflammation was reduced in the cherry juice group (IL-6, P<0.001; CRP, P<0.01; uric acid, P<0.05). TAS was ∼10% greater in the cherry juice than the placebo group for all post-supplementation measures (P<0.05). Protein carbonyls was not different; however, TBARS was lower in the cherry juice than the placebo at 48 h (P<0.05). The cherry juice appears to provide a viable means to aid recovery following strenuous exercise by increasing total antioxidative capacity, reducing inflammation, lipid peroxidation and so aiding in the recovery of muscle function.

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Influence of tart cherry juice on indices of recovery following marathon running.

Production, detection, and adaptive responses to free radicals in exercise

The aim of this article is to present the effects of acute muscle-damaging exercise on oxidative stress/damage of animal and human tissues using a quantitative approach and focusing on the time-course of exercise effects. The reviewed studies employed eccentric contractions on a dynamometer or downhill running. The statistical power of each study to detect a 20% or 40% post-exercise change compared with pre-exercise value in each oxidative stress/damage biomarker was calculated. Muscle-damaging exercise can increase free radical levels and augment oxidation of lipids, proteins, glutathione and possibly DNA in the blood. In contrast, the effect of muscle-damaging exercise on concentration of antioxidants in the blood, except for glutathione, was little. Muscle-damaging exercise induces oxidative stress/damage in skeletal muscle, even though this is not fully supported by the original statistical analysis of some studies. In contrast, muscle-damaging exercise does not appear to affect--at least to similar extent as the oxidative stress/damage markers--the levels of antioxidants in skeletal muscle. Based on the rather limited data available, the oxidative stress response of skeletal muscle to exercise was generally independent of muscle fibre type. Most of the changes in oxidative stress/damage appeared and were sustained for days after muscle-damaging exercise. The major part of the delayed oxidative stress/damage production that follows muscle-damaging exercise probably comes from phagocytic cells that are activated and recruited to the site of the initial damage. A point that emerged and potentially explains much of the lack of consensus among studies is the low statistical power of many of them. In summary, muscle-damaging exercise can increase oxidative stress/damage in blood and skeletal muscle of rats and humans that may persist for and/or appear several days after exercise.

The effect of muscle-damaging exercise on blood and skeletal muscle oxidative stress: magnitude and time-course considerations.

Ultra-endurance exercise, such as an Ironman triathlon, induces muscle damage and a systemic inflammatory response. As the resolution of recovery in these parameters is poorly documented, we investigated indices of muscle damage and systemic inflammation in response to an Ironman triathlon and monitored these parameters 19 days into recovery. Blood was sampled from 42 well-trained male triathletes 2 days before, immediately after, and 1, 5 and 19 days after an Ironman triathlon. Blood samples were analyzed for hematological profile, and plasma values of myeloperoxidase (MPO), polymorphonuclear (PMN) elastase, cortisol, testosterone, creatine kinase (CK) activity, myoglobin, interleukin (IL)-6, IL-10 and high-sensitive C-reactive protein (hs-CRP). Immediately post-race there were significant (P < 0.001) increases in total leukocyte counts, MPO, PMN elastase, cortisol, CK activity, myoglobin, IL-6, IL-10 and hs-CRP, while testosterone significantly (P < 0.001) decreased compared to prerace. With the exception of cortisol, which decreased below prerace values (P < 0.001), these alterations persisted 1 day post-race (P < 0.001; P < 0.01 for IL-10). Five days post-race CK activity, myoglobin, IL-6 and hs-CRP had decreased, but were still significantly (P < 0.001) elevated. Nineteen days post-race most parameters had returned to prerace values, except for MPO and PMN elastase, which had both significantly (P < 0.001) decreased below prerace concentrations, and myoglobin and hs-CRP, which were slightly, but significantly higher than prerace. Furthermore, significant relationships between leukocyte dynamics, cortisol, markers of muscle damage, cytokines and hs-CRP after the Ironman triathlon were noted. This study indicates that the pronounced initial systemic inflammatory response induced by an Ironman triathlon declines rapidly. However, a low-grade systemic inflammation persisted until at least 5 days post-race, possibly reflecting incomplete muscle recovery.

Recovery after an Ironman triathlon: sustained inflammatory responses and muscular stress

We investigated the effects of an Ironman triathlon race on markers of muscle damage, inflammation and heat shock protein 70 (HSP70). Nine well-trained male triathletes (mean +/- SD age 34 +/- 5 years; VO(2peak) 66.4 ml kg(-1) min(-1)) participated in the 2004 Western Australia Ironman triathlon race (3.8 km swim, 180 km cycle, 42.2 km run). We assessed jump height, muscle strength and soreness, and collected venous blood samples 2 days before the race, within 30 min and 14-20 h after the race. Plasma samples were analysed for muscle proteins, acute phase proteins, cytokines, heat shock protein 70 (HSP70), and clinical biochemical variables related to dehydration, haemolysis, liver and renal functions. Muscular strength and jump height decreased significantly (P < 0.05) after the race, whereas muscle soreness and the plasma concentrations of muscle proteins increased. The cytokines interleukin (IL)-1 receptor antagonist, IL-6 and IL-10, and HSP70 increased markedly after the race, while IL-12p40 and granulocyte colony-stimulating factor (G-CSF) were also elevated. IL-4, IL-1beta and tumour necrosis factor-alpha did not change significantly, despite elevated C-reactive protein and serum amyloid protein A on the day after the race. Plasma creatinine, uric acid and total bilirubin concentrations and gamma-glutamyl transferase activity also changed after the race. In conclusion, despite evidence of muscle damage and an acute phase response after the race, the pro-inflammatory cytokine response was minimal and anti-inflammatory cytokines were induced. HSP70 is released into the circulation as a function of exercise duration.

Changes in markers of muscle damage, inflammation and HSP70 after an Ironman triathlon race

A nonlinear dynamic systems model has previously been proposed to explain pacing strategies
employed during exercise. This study was conducted to examine the pacing strategies used under varying conditions during
the cycle phase of an Ironman triathlon.

Rob Surriano

Papers

Changes in markers of muscle damage, inflammation and HSP70 after an Ironman triathlon race

Dynamic pacing strategies during the cycle phase of an Ironman triathlon.