Abstract

IntroductionElimination of CO2 from skeletal muscle (mCO2) during exercise is important for the regulation of intramuscular [H+] ([mH+]). Carbonic anhydrase (CA) catalyses the hydration/dehydration reaction of CO2 to facilitate its elimination. We hypothesised that extracellular CA inhibition and subsequent increase in PCO2 will result in increased m[H+] and decreased exercise performance.MethodsSix horses were exercised on a treadmill until fatigue without (Con) and with acetazolamide (CA inhibitor) treatment (Acz; 30 mg/kg, 30 min before exercise). Arterial and mixed‐venous blood was sampled, and biopsies collected from gluteal muscles at fatigue. Whole blood (wb) arteriovenous difference across the muscle (a‐v) of [Na+], [K+], [Cl−], [Lac−], [SID], and PCO2, mCO2 and m[H+] were determined. Paired t‐test was used to assess statistical significance (P<0.05).ResultsDuration of exercise to fatigue was not affected by Acz. Compared to Con, Acz increased mCO2 (Con 16.5(mean) ± 3.6(SE), Acz 20.5 ± 2 mmol/L) and mixed‐venous and arterial PCO2 but had no effect on VCO2. No difference was observed in m[H+] between Con (118 ± 18 nmol/L) and Acz (99 ± 16 nmol/L). Acetazolamide did not affect plasma [H+]. Based on the a‐v differences Acz increased [Na+]wb and [K+]wb release, increased [Cl‐]wb uptake and did not affect [Lac‐]wb release by the muscle. Acz decreased a‐v[SID]wb (Con 6.2 ± 2.8 mmol/L, Acz −0.3 ± 2 mmol/L).ConclusionsAlthough PCO2 and mCO2 were elevated no difference in [mH+] was observed. An increase in m[H+] due to elevated mCO2 was attenuated by strong ion fluxes between intramuscular and vascular spaces. Strong ion exchanges are important in attenuating m[H+] and maintaining exercise performance.Ethical Animal ResearchThe study protocols were approved by the Animal Care Committee of the University of Guelph according to the Guide to the Care and Use of Experimental Animals (Canadian Council on Animal Care, Ottawa, Ontario). Sources of funding: Ontario Ministry of Agriculture and Food ‐ Equine Program, Department of Clinical Studies at the University of Guelph, Canadian Institutes of Health Research and the Slovenian Research Agency grant P4‐0053. Competing interests: none.

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