Hyperthermia Increases Exercise-induced Oxidative Stress

McAnulty, Steven R.; McAnulty, Lisa S.; Pascoe, David D.; Gropper, Sareen S.; Keith, Robert E.; Morrow, Jason D.; Gladden, L. Bruce

doi:10.1055/s-2004-820990

Cited by 83 publications

(88 citation statements)

References 26 publications

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“…These aggregates may sequester components of the chaperone and degradation systems and thereby reduce their activity (Jiang and Chang 2007). As HSP70 and other heat-inducible chaperones reduce oxidative stress (Kalmar and Greensmith 2009), impairments in heat shock responses may enhance oxidative stress and thereby contribute to the augmented cell death (Burdon et al 1987;Skibba et al 1991;McAnulty et al 2005). Misfolded, dysfunctional proteins have also been shown to be more susceptible to carbonylation compared to their native forms.…”

Section: Sarcomeric Proteins: Elastic Filamentsmentioning

confidence: 99%

A change of heart: oxidative stress in governing muscle function?

Breitkreuz

Hamdani

2015

Biophys Rev

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Redox/cysteine modification of proteins that regulate calcium cycling can affect contraction in striated muscles. Understanding the nature of these modifications would present the possibility of enhancing cardiac function through reversible cysteine modification of proteins, with potential therapeutic value in heart failure with diastolic dysfunction. Both heart failure and muscular dystrophy are characterized by abnormal redox balance and nitrosative stress. Recent evidence supports the synergistic role of oxidative stress and inflammation in the progression of heart failure with preserved ejection fraction, in concert with endothelial dysfunction and impaired nitric oxide-cyclic guanosine monophosphate-protein kinase G signalling via modification of the giant protein titin. Although antioxidant therapeutics in heart failure with diastolic dysfunction have no marked beneficial effects on the outcome of patients, it, however, remains critical to the understanding of the complex interactions of oxidative/nitrosative stress with pro-inflammatory mechanisms, metabolic dysfunction, and the redox modification of proteins characteristic of heart failure. These may highlight novel approaches to therapeutic strategies for heart failure with diastolic dysfunction. In this review, we provide an overview of oxidative stress and its effects on pathophysiological pathways. We describe the molecular mechanisms driving oxidative modification of proteins and subsequent effects on contractile function, and, finally, we discuss potential therapeutic opportunities for heart failure with diastolic dysfunction.

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Section: Sarcomeric Proteins: Elastic Filamentsmentioning

confidence: 99%

A change of heart: oxidative stress in governing muscle function?

Breitkreuz

Hamdani

2015

Biophys Rev

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“…However, even nonlethal hyperthermia can lead to a whole range of detrimental effects, which include elevated protein damage, increased inflammatory responses, apoptosis, increased DNA damage in germ cells, oxidative stress, mitochondrial dysfunction, liver damage, cerebral ischaemia, disrupted blood-brain barrier function and embryonic death in pregnant females (e.g. Arnaud et al, 2002;McAnulty et al, 2005;Yan et al, 2006;Chang et al, 2007;Lee et al, 2008;Hansen, 2009). In contrast, mild hypothermia appears to bring a range of benefits including neuroprotection (Salerian and Saleri, 2006;Cheng et al, 2008;Salerian and Saleri, 2008) and enhanced lifespan (Conti et al, 2006;Conti, 2008).…”

Section: New Ideas On Limits To Sustained Energy Intakementioning

confidence: 99%

Limits to sustained energy intake. XIII. Recent progress and future perspectives

Speakman

Król

2011

Journal of Experimental Biology

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Summary Several theories have been proposed to explain limits on the maximum rate at which animals can ingest and expend energy. These limits are likely to be intrinsic to the animal, and potentially include the capacity of the alimentary tract to assimilate energy – the ‘central limitation’ hypothesis. Experimental evidence from lactating mice exposed to different ambient temperatures allows us to reject this and similar ideas. Two alternative ideas have been proposed. The ‘peripheral limitation’ hypothesis suggests that the maximal sustained energy intake reflects the summed demands of individual tissues, which have their own intrinsic limitations on capacity. In contrast, the ‘heat dissipation limit’ (HDL) theory suggests that animals are constrained by the maximal capacity to dissipate body heat. Abundant evidence in domesticated livestock supports the HDL theory, but data from smaller mammals are less conclusive. Here, we develop a novel framework showing how the HDL and peripheral limitations are likely to be important in all animals, but to different extents. The HDL theory makes a number of predictions – in particular that there is no fixed limit on sustained energy expenditure as a multiple of basal metabolic rate, but rather that the maximum sustained scope is positively correlated with the capacity to dissipate heat.

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“…The adverse effects of excessive body temperature include apoptosis, hypoxia, oxidative stress, mitochondrial dysfunction, liver damage, DNA damage to germ cells, and cerebral ischemia, among others (e.g. Cui et al, 2004;McAnulty et al, 2005;Chang et al, 2007;Bloomer et al, 2008;Lee et al, 2008;Haak et al, 2009;Paul et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Heat dissipation does not suppress an immune response in laboratory mice divergently selected for basal metabolic rate (BMR)

Książek

Konarzewski

2016

Journal of Experimental Biology

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The capacity for heat dissipation is considered to be one of the most important constraints on rates of energy expenditure in mammals. To date, the significance of this constraint has been tested exclusively under peak metabolic demands, such as during lactation. Here, we used a different set of metabolic stressors, which do not induce maximum energy expenditures and yet are likely to expose the potential constraining effect of heat dissipation. We compared the physiological responses of mice divergently selected for high (H-BMR) and low basal metabolic rate (L-BMR) to simultaneous exposure to the keyhole limpet haemocyanin (KLH) antigen and high ambient temperature (T a ). At 34°C (and at 23°C, used as a control), KLH challenge resulted in a transient increase in core body temperature (T b ) in mice of both line types (by approximately 0.4°C). Warm exposure did not produce line-type-dependent differences in T b (which was consistently higher by ca. 0.6°C in H-BMR mice across both T a values), nor did it result in the suppression of antibody synthesis. These findings were also supported by the lack of between-line-type differences in the mass of the thymus, spleen or lymph nodes. Warm exposure induced the downsizing of heatgenerating internal organs (small intestine, liver and kidneys) and an increase in intrascapular brown adipose tissue mass. However, these changes were similar in scope in both line types. Mounting a humoral immune response in selected mice was therefore not affected by ambient temperature. Thus, a combined metabolic challenge of high T a and an immune response did not appreciably compromise the capacity to dissipate heat, even in the H-BMR mice.

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Hyperthermia Increases Exercise-induced Oxidative Stress

Cited by 83 publications

References 26 publications

A change of heart: oxidative stress in governing muscle function?

A change of heart: oxidative stress in governing muscle function?

Limits to sustained energy intake. XIII. Recent progress and future perspectives

Heat dissipation does not suppress an immune response in laboratory mice divergently selected for basal metabolic rate (BMR)

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