Effect of maximal dynamic exercise on exhaled ethane and carbon monoxide levels in human, equine, and canine athletes

Wyse, Cathy; Cathcart, Andrew J.; Sutherland, Rona; Ward, Susan A.; McMillan, Lesley C; Gibson, Graham M.; Padgett, Miles J.; Skeldon, K. D.

doi:10.1016/j.cbpb.2005.05.046

Cited by 18 publications

(19 citation statements)

References 36 publications

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“…While there is considerable evidence showing that membrane fatty acid composition affects the rate of lipid peroxidation measured in vitro, there is less evidence that it has an effect on in vivo lipid peroxidation. One of the products of n-3 PUFA peroxidation is ethane, and the rate of ethane exhalation has been used as a noninvasive method for assessing in vivo lipid peroxida- (178), and values from the literature are for mice (79), rats (179,245,356), dogs and horses (375), and humans (178). Oxygen consumption is the basal metabolic rate of each species (317).…”

Section: ϫ030mentioning

confidence: 99%

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Hulbert¹,

Pamplona²,

Buffenstein

et al. 2007

Physiological Reviews

752

725

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Maximum life span differences among animal species exceed life span variation achieved by experimental manipulation by orders of magnitude. The differences in the characteristic maximum life span of species was initially proposed to be due to variation in mass-specific rate of metabolism. This is called the rate-of-living theory of aging and lies at the base of the oxidative-stress theory of aging, currently the most generally accepted explanation of aging. However, the rate-of-living theory of aging while helpful is not completely adequate in explaining the maximum life span. Recently, it has been discovered that the fatty acid composition of cell membranes varies systematically between species, and this underlies the variation in their metabolic rate. When combined with the fact that 1) the products of lipid peroxidation are powerful reactive molecular species, and 2) that fatty acids differ dramatically in their susceptibility to peroxidation, membrane fatty acid composition provides a mechanistic explanation of the variation in maximum life span among animal species. When the connection between metabolic rate and life span was first proposed a century ago, it was not known that membrane composition varies between species. Many of the exceptions to the rate-of-living theory appear explicable when the particular membrane fatty acid composition is considered for each case. Here we review the links between metabolic rate and maximum life span of mammals and birds as well as the linking role of membrane fatty acid composition in determining the maximum life span. The more limited information for ectothermic animals and treatments that extend life span (e.g., caloric restriction) are also reviewed.

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Section: ϫ030mentioning

confidence: 99%

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Hulbert¹,

Pamplona²,

Buffenstein

et al. 2007

Physiological Reviews

752

725

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“…Similarly, alterations in redox homeostasis have been reported in mdx mice [an animal model for Duchenne muscular dystrophy, which lacks dystrophin (Radley-Crabb et al, 2011)], C57/BL6J mice (Yokota et al, 2009), BALB/c mice (De la Fuente et al, 1995), Swiss mice (Prigol et al, 2009), Hsd:ICR mice, which had been selected for high wheel-running activity (Vaanholt et al, 2008), and guinea pigs (De la Fuente et al, 1995). Finally, exercise has been reported to induce alterations in redox homeostasis in fish (Aniagu et al, 2006), birds (Costantini et al, 2008;Costantini and Lipp, 2010;Larcombe et al, 2010), dogs (Wyse et al, 2005) and horses (Kinnunen et al, 2009). Based on the above-mentioned analysis, it is evident that exercise-induced changes in redox homeostasis are a ubiquitous fundamental response of most (if not all) animal species, irrespective of definite differences in redox composition across species and between non-human animal models and humans.…”

Section: Acute Exercise Alters Redox Homeostasis Across Strains and Smentioning

confidence: 99%

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Nikolaidis

Kyparos

Spanou

et al. 2012

Journal of Experimental Biology

124

152

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SummaryThe central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to redefine ʻoxidative stressʼ as well as to introduce the term ʻalterations in redox homeostasisʼ to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscledamaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30s and isometric exercise lasting 1-3min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, ʻexercise-induced oxidative stressʼ is not an ʻoddityʼ associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Key words: antioxidant, biomarker, eccentric, free radical, training. THE JOURNAL OF EXPERIMENTAL BIOLOGY 1616The ʻgoodʼ (antioxidants), the ʻbadʼ (reactive species) and the ʻuglyʼ (oxidative stress) 1 The distinction drawn in the section heading is schematically used to parody the popular manichaeistic view that antioxidants are considered 'useful' entities, reactive species are considered 'harmful' entities and oxidative stress is considered a 'negative' state. Certainly, the reality is much more complicated and antioxidants, reactive species and oxidative stress can serve both useful and detrimental roles, which are dependent on the biological context (within an organism), which in turn are greatly dependent on the environmental context (outside an organism). AntioxidantsAdmittedly, to define the term 'antioxidant' is a difficult task. In this paper, antioxidant is defined as any mechanism, structure and/or substance that delays, prevents or removes oxidative modifications to a target molecule (Halliwell and Gutteridge, 2007;Pamplona and Costantini, 2011). Antioxidants can be complex molecules such as the superoxide dismutases and peroxiredoxins, or simpler ones such as uric acid and glutathione (Gutteridge and Halliwell, 2010). They can be broa...

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“…It was concluded that CO exhalation Introduction It has been demonstrated that carbon monoxide (CO) is produced endogenously from various types of cells and has many pathophysiological roles, including neurotransmission, vascular regulation, anti-inflammatory, anti-proliferative, and anti-apoptotic responses, similar to those of other gaseous transmitters such as nitric oxide and hydrogen sulfide [1][2][3]. It has also been shown that the concentration of exhaled CO is affected by normal and the pathophysiological conditions, including airway and lung inflammation [4][5][6][7], cigarette smoking [8][9][10][11], exercise [5,12] and aging [13].…”

mentioning

confidence: 99%

Effect of ramp bicycle exercise on exhaled carbon monoxide in humans

Yasuda

Miyamura

et al. 2011

J Physiol Sci

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The effect of exercise on the increase of exhaled CO in smokers compared to non-smokers has not been clarified yet. In this study we compared the dynamics of exhaled CO before, during and after exercise between smokers and non-smokers. A group of 8 smokers and a group of 8 non-smokers underwent a bicycle exercise in a ramp fashion to near maximum intensity. Ventilation and gas exchange, and CO exhalation were continuously measured every 30-s before, during and after the exercise. The fraction of CO (F (CO)) in the exhaled air decreased gradually, but the total amount of exhaled CO (V(CO)) increased in a linear manner during the ramp exercise, and F (CO) and returned to the pre-exercise level within several minutes after exercise in all subjects. A linear relationship was observed between V (O(2)) and V (CO) and between V (E) and V (CO) in both the whole period of measurement and during the ramp exercise period in all subjects. However, the at V (CO) 0 W, the peak V (CO) and the slope coefficients in the regression equation between V (CO) and V (O(2)) and between V (CO) and V (E) in the ramp exercise as well as the entire periods of measurement were significantly higher in smokers compared with those in non-smokers, and these were correlated with the number of cigarettes smoked per day. It was concluded that CO exhalation increases linearly with the increase of V (O(2)) and V (E) during exercise, and habitual smoking shifts these relationships upward depending on the number of cigarettes smoked daily.

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Effect of maximal dynamic exercise on exhaled ethane and carbon monoxide levels in human, equine, and canine athletes

Cited by 18 publications

References 36 publications

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Effect of ramp bicycle exercise on exhaled carbon monoxide in humans

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