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This qualitative study examined the sporting experiences of individuals of diverse sexual orientation and gender identity (SOGI) in rural and remote areas of Australia - contexts where marginalised groups can feel excluded based on gender or sexuality, and where physical activity options may be limited. Twelve participants (aged 29-73 years) identifying as female or gender fluid, and as queer, bisexual, gay, lesbian or pansexual, completed an online, qualitative survey. Thematic analysis and an integrative theory of belonging were used to interpret the experiences and feelings of belonging, exclusion and resistance to heteronormativity found in the data. The development of viable opportunities for sport participation and physical activities that foster a sense of belonging and health in rural or remote Australian communities requires strategies based on a deep understanding of the needs and identities of individuals of diverse SOGI, as well as the cultural and social contexts in which people live. [ABSTRACT FROM AUTHOR]

The mediators of acute exercise-induced preconditioning against ischemia-reperfusion injury are not understood. This study assesses the role of nitric oxide synthase (NOS), a reported mediator of other forms of preconditioning. Male Fischer 344 rats were divided into five groups (n = 6-7): sedentary (Sed); exercised 2 days on a treadmill at 20 m/min, 6[degrees] grade, for 60 min (Run); sedentary, perfused with 100 [micro] M [N.sup.[omega]]-nitro-L-arginine methyl ester hydrochloride (L-NAME) to inhibit NOS (Sed/L-N); exercised, perfused with L-NAME (Run/L-N); and exercised in a 4[degrees]C environment, perfused with L-NAME (CRun/L-N). Twenty-four hours following exercise, isolated, perfused working hearts were subjected to 22.5 min of global ischemia plus 30 min of normoxic reperfusion. Left ventricle contents of several putative preconditioning mediators were determined. Postischemic recovery of cardiac output times systolic pressure was better in Run than Sed (78.4 vs. 50.2% of preischemia, P < 0.05). Inhibition of NOS did not abrogate the improved recovery in the exercise groups or alter recovery in Sed. All exercise groups also displayed improved myocardial efficiency (cardiac output times systolic pressure/oxygen consumption) postischemia and less lactate dehydrogenase release (P < 0.05). L-NAME appeared to lower lactate dehydrogenase release independent of exercise. The only change in antioxidant enzyme activity was a decrease in manganese superoxide dismutase in CRun/L-N (P < 0.05). Heat shock protein 72 expression increased only in Run and Run/L-N and endothelial NOS only in CRun/ L-N (P < 0.05). Acute exercise-induced preconditioning of the Fischer 344 rat heart is not mediated by NOS and does not require increases in heat shock protein 72 or antioxidant enzymes. reactive oxygen species; reperfusion injury; oxygen consumption; stunning; contractile function

Exercise provides cardioprotection against ischemia-reperfusion injury, a process involving mitochondrial reactive oxygen species (ROS) generation and calcium overload. This study tested the hypotheses that isolated mitochondria from hearts of endurance-trained rats have decreased ROS production and improved tolerance against Ca2+-induced dysfunction. Male Fischer 344 rats were either sedentary (Sed, n = 8) or endurance exercise trained (ET, n = 11) by running on a treadmill for 16 wk (5 days/wk, 60 min/day, 25 m/min, 6° grade). Mitochondrial oxidative phosphorylation measures were determined with glutamate-malate or succinate as substrates, and H2O2 production and permeability transition pore (PTP) opening were determined with succinate. All assays were carried out in the absence and presence of calcium. In response to 25 and 50 µM CaCl2, Sed and ET displayed similar decreases in state 3 respiration, respiratory control ratio, and ADP:O ratio. Ca2+-induced PTP opening was also similar. However, H2O2 production by ET was lower than Sed (P < 0.05) in the absence of calcium (323 ± 12 vs. 362 ± 11 pmol·min-1 · mg protein-1) and the presence of 50 µM CaCl2 (154 ± 3 vs. 197 ± 7 pmol · min-1 · mg protein-1). Rotenone, which blocks electron flow from succinate to complex 1, reduced H2O2 production and eliminated differences between ET and Sed. Mitochondrial superoxide dismutase and glutathione peroxidase were not affected by exercise. Catalase activity was extremely low but increased 49% in ET (P < 0.05). In conclusion, exercise reduces ROS production in myocardial mitochondria through adaptations specific to complex 1 but does not improve mitochondrial tolerance to calcium overload. [ABSTRACT FROM AUTHOR]