Oxidant stress in sled dogs subjected to repetitive endurance exercise

Hinchcliff, Kenneth W.; Reinhart, Gregory A.; DiSilvestro, Robert A.; Reynolds, Arleigh J.; Blostein-Fujii, Ashley; Swenson, Richard A.

doi:10.2460/ajvr.2000.61.512

Cited by 91 publications

(97 citation statements)

References 28 publications

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“…This result is in accord with other studies (22,48,50,52,62). These increases presumably reflect persistent damage to the muscles, resulting in a loss of cell membrane integrity, and consequent leakage of proteins into the blood.…”

Section: Figsupporting

confidence: 82%

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Plasma antioxidant status and cell injury after severe physical exercise

Chevion

Moran

Heled

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

221

137

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Strenuous exercise leads to an increase in metabolic rate, increased production of reactive oxygen species, and compromised antioxidant defense systems. To study the effects of oxidative stress during strenuous exercise, a homogeneous group of 31 male subjects participated in a 6-month, 5 days͞week training schedule involving two extreme marches of 50 km and 80 km at sea level, separated by 2 weeks of regular training. Each participant carried 35 kg of extra weight. Blood samples were drawn imediately before and after each march. Twenty-nine subjects completed the 50-km march, and only 16 completed the 80-km march. Plasma levels of reduced ascorbic acid, total ascorbate, and dehydroascorbate did not undergo significant changes during either march. However, the 50-and 80-km marches led to 25% and 37% increases, respectively, in plasma levels of uric acid; due presumably to increases in the metabolic rate and consequent pyrimidine nucleotide metabolism. Both marches led to Ϸ10-fold increase leakage of creatine phosphokinase into the plasma. Likewise, plasma levels of aspartate transaminase, a characteristic marker of liver injury, increased Ϸ4-fold. Plasma levels of bilirubin, creatine, urea, and glucose also increased. Plasma protein carbonyl content, a marker of protein oxidative damage, decreased significantly during each march. These results are discussed with respect to the consideration that elevation of the respiration rate during exercise leads to production of more reactive oxygen species than the antioxidant systems can scavenge. Plausible explanations for leakage of molecules into the plasma are discussed.

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Section: Figsupporting

confidence: 82%

“…No change in OSAA was recorded in our study (Table 2). This is in accord with other studies of the antioxidant capacity after severe exercise (46,52). By contrast, some other reports have demonstrated an unexpected increase in the antioxidant capacity of athletes after exercise (23,48,53).…”

Section: Figsupporting

confidence: 36%

Plasma antioxidant status and cell injury after severe physical exercise

Chevion

Moran

Heled

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

221

137

View full text Add to dashboard Cite

show abstract

“…Exhaustive exercise, i.e., human ultramarathon or endurance sled dog racing, increased production of free radicals (particularly oxygen-and nitrogen-centered radicals)leads to exercise-induced oxidative stress, including increased formation of F 2 -isoprostanes [13] [14]. Four groups of F 2 -isoprostane regioisomers (5-, 8-, 12-, and 15-series F 2 -isoprostanes) can be formed during free-radical mediated oxidation of arachidonic acid.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Low Intensity Endurance Activity on Various Physiological Parameters and Exercise Induced Oxidative Stress in Dogs

Huntingford¹,

Levine²,

Mustacich³

et al. 2014

OJVM

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The study of canine athlete physiology has focused on endurance sled dog racing and high intensity short duration Greyhound racing, yet the number of dogs competing in low intensity endurance activities is rising due to the increased numbers of hunting and companion dog activities. There is little information on the physiological effect of longer duration low intensity endurance activities. We set out to evaluate the serum biochemistry, oxidative stress, and cortisol response before and after two consecutive days of exercise in ten healthy unconditioned male dogs. Exercise sessions consisted of 120 minutes on an exercise wheel at 11 km/hour on 2 consecutive days. Blood was collected at four time points: 24 hours pre-exercise (sample 1, Day 0, resting); 2 min post-exercise on days 1 and 2, (samples 2 and 3, respectively); and 20 hours post-exercise, collected on day 3(sample 4). Hematocrit, blood gases, serum chemistry, uric acid, cortisol, and F2-isoprostanes were determined. Serum biochemistry and hematocrit suggested hemoconcentration, mild muscle damage and respiratory alkalosis during exercise, which was expected in the unconditioned canine athlete. In addition, plasma indices of oxidative damage (F2-isoprostanes) increased, as did plasma uric acid (an endogenous antioxidant). Importantly, similar to human studies, plasma F2-isoprostanes decreased 24 hours after exercise suggesting a protective effect of exercise. Serum cortisol concentrations were also markedly elevated at the end of exercise on both days suggesting that timing of sampling may play a role in interpreting cortisol results when looking at previous field studies.

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“…In the diet of sled dog, ROS scavengers such as vitamin E have been used to diminish cellular damage due to exercise (Hinchcliff et al, 2000). Some antioxidants are used to protect gastrointestinal mucosa and apical epithelial membrane.…”

Section: Antioxidant Therapymentioning

confidence: 99%

“…In acute events of inflammation free radicals may play a major role in gastric mucosal barrier dysfunction. In humans oxidative stress occurs during exercise leads to decrease gastric and mesenteric blood flow ( Qamar et al, 1987;Mastaloudis et al, 1994;Hinchcliff et al, 2000;Otte et al, 2001;Radak et al, 2003) along with mitochondrial electron transport chain inefficiency during respiration leading reperfusion injury mediated by ROS. In the disease condition, exercise has been activated to pro-inflammatory cascades which are able to trigger the leukocytes (Cooper et al, 2007).…”

Section: Etiopathogenesis Of Gastritis and Peptic Ulcer Diseasesmentioning

confidence: 99%