Alveolar air and oxidative metabolic demand during exercise in healthy adults: the role of single‐nucleotide polymorphisms of the β2AR gene. Issue 20 (23rd October 2017)

• Record Type: Journal Article
• Authors: Van Iterson, Erik H.; Snyder, Eric M.; Johnson, Bruce D.
• Is Part Of: Physiological reports. Volume 5:Issue 20(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-10-23
• Subjects: Aerobic exercise -- codon 16 -- exercise capacity -- genetic polymorphism -- β2‐adrenergic receptor; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.13476
• Languages: English
• ISSNs: 2051-817X

Abstract

Abstract: The predominating β ‐adrenergic receptor subtype expressed on human alveolar tissue is the β 2 AR. The homozygous arginine (Arg16Arg) single‐nucleotide polymorphism (SNP) at codon 16 of the β 2 AR gene has been associated with abnormal β 2 AR function accompanied by decreased resting alveolar‐capillary membrane gas‐transfer in certain healthy adults. Although not previously studied in the context of the β 2 AR gene, pulmonary gas‐transfer is also influenced by alveolar volume ( V A ) and with it the availability of alveolar surface area, particularly during exercise. Small V A implies less alveolar surface area available for O2 transport. We tested the following hypothesis in healthy adults during exercise: compared with Gly16Gly and Arg16Gly β2AR genotypes, Arg16Arg will demonstrate reduced V A and ventilation ( V̇ A ) relative to V̇ E and oxidative metabolic demand. Age‐ BMI‐ and gender‐matched groups of Arg16Arg ( N = 16), Gly16Gly ( N = 31), and Arg16Gly ( N = 17) performed consecutive low (9‐min, 40%‐peak workload) and moderate (9‐min, 75%‐peak workload) intensity exercise. We derived V A and V̇ A using "ideal" alveolar equations via arterialized gases combined with breath‐by‐breath ventilation and gas‐exchange measurements; whereas steady‐state V̇ O2 was used in metabolic equations to derive exercise economy (EC = workload÷ V̇ O2 ). Variables at rest did not differ across β 2 AR genotype. Strongest β 2 AR genotype effects occurred during moderate exercise. Accordingly, while V̇ E did not differ across genotype ( P > 0.05), decreased in Arg16Arg versus Arg16Gly and Gly16Gly were V̇ O2 (1110 ± 263, 1269 ± 221, 1300 ± 319 mL/(min·m 2 ), respectively, both P < 0.05), V̇ A (59 ± 21, 70 ± 16, 70 ± 21 L/min, respectively, both P < 0.05), and V A (1.43 ± 0.37, 1.95 ± 0.61, 1.93 ± 0.65 L, respectively, both P < 0.05). Also reduced was EC in Arg16Arg versus Arg16Gly ( P < 0.05) and Gly16Gly ( P > 0.05) (1.81 ± 0.23, 1.99 ± 0.30, and 1.94 ± 0.26 kcal/(L·m 2 ), respectively). Compared with Gly16Gly and Arg16Gly genotypes, these data suggest the Arg16Arg β 2 AR genotype plays a role in the loss of oxidative metabolic efficiency coupled with an inadaptive V A and, hence, smaller alveolar surface area available for O2 transport during submaximal exercise in healthy adults. Abstract : β 2ARs are the predominating β AR subtype expressed on alveolar tissue and play an important role in pulmonary gas exchange. This study demonstrates the homozygous Arg16Arg single‐nucleotide polymorphism (SNP) of the β 2AR gene is associated with reduced alveolar volume (i.e., smaller alveolar surface area) contributions to total ventilatory and oxidative metabolic demand during submaximal exercise in healthy adults.