Nitric oxide (NO) has been demonstrated to enhance the maximal shortening velocity and maximal power of rodent muscle. Dietary nitrate (NO3-) intake has been demonstrated to increase NO bioavailability in humans. We therefore hypothesized that acute dietary NO3- intake (in the form of a concentrated beetroot juice (BRJ) supplement) would improve muscle speed and power in humans. To test this hypothesis, healthy men and women (n=12; age=22-50 y) were studied using a randomized, double-blind, placebo-controlled crossover design. After an overnight fast, subjects ingested 140 mL of BRJ either containing or devoid of 11.2 mmol of NO3-. After 2 h, knee extensor contractile function was assessed using a Biodex 4 isokinetic dynamometer. Breath NO levels were also measured periodically using a Niox Mino analyzer as a biomarker of whole-body NO production. No significant changes in breath NO were observed in the placebo trial, whereas breath NO rose by 61% (P<0.001; effect size=1.19) after dietary NO3- intake. This was accompanied by a 4% (P<0.01; effect size=0.74) increase in peak knee extensor power at the highest angular velocity tested (i.e., 6.28 rad/s). Calculated maximal knee extensor power was therefore greater (i.e., 7.90±0.59 vs. 7.44±0.53 W/kg; P<0.05; effect size=0.63) after dietary NO3- intake, as was the calculated maximal velocity (i.e., 14.5±0.9 vs. 13.1±0.8 rad/s; P<0.05; effect size=0.67). No differences in muscle function were observed during 50 consecutive knee extensions performed at 3.14 rad/s. We conclude that acute dietary NO3- intake increases whole-body NO production and muscle speed and power in healthy men and women.

Background Skeletal muscle strength, velocity, and power are markedly reduced in heart failure (HF) patients, which contributes to their impaired exercise capacity and lower quality of life. This muscle dysfunction may be partially due to decreased nitric oxide (NO) bioavailability. We therefore sought to determine whether ingestion of inorganic nitrate (NO3−) would increase NO production and improve muscle function in patients with HF due to systolic dysfunction. Methods and Results Using a double-blind, placebo-controlled, randomized crossover design, we determined the effects of dietary NO3− in nine HF patients. After fasting overnight, subjects drank beetroot juice containing or devoid of 11.2 mmol NO3−. Two hours later, muscle function was assessed using isokinetic dynamometry. Dietary NO3− increased (P<0.05–0.001) breath NO by 35–50%. This was accompanied by 9% (P=0.07) and 11% (P<0.05) increases in peak knee extensor power at the two highest movement velocities tested (i.e., 4.71 and 6.28 rad/s). Maximal power (calculated by fitting peak power data with a parabola) was therefore greater (i.e., 4.74±0.41 vs. 4.20±0.33 W/kg; P<0.05) after dietary NO3− intake. Calculated maximal velocity of knee extension was also higher following NO3− ingestion (i.e., 12.48±0.95 vs. 11.11±0.53 rad/s; P<0.05). Blood pressure was unchanged, and no adverse clinical events occurred. Conclusions In this pilot study, acute dietary NO3− intake was well-tolerated and enhanced NO bioavailability and muscle power in patients with systolic HF. Larger-scale studies should be conducted to determine whether the latter translates into an improved quality of life in this population. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01682356.

Maximal neuromuscular power is an important determinant of athletic performance and also quality of life, independence, and perhaps even mortality in patient populations. We have shown that dietary nitrate (NO 3 −), a source of nitric oxide (NO), improves muscle power in some, but not all, subjects. The present investigation was designed to identify factors contributing to this interindividual variability. Healthy men (n = 13) and women (n = 7) 22–79 year of age and weighing 52.1–114.9 kg were studied using a randomized, double‐blind, placebo‐controlled, crossover design. Subjects were tested 2 h after ingesting beetroot juice (BRJ) either containing or devoid of 12.3 ± 0.8 mmol of NO 3 −. Plasma NO 3 − and nitrite (NO 2 −) were measured as indicators of NO bioavailability and maximal knee extensor speed (V max), power (P max), and fatigability were determined via isokinetic dynamometry. On average, dietary NO 3 − increased (P < 0.05) P max by 4.4 ± 8.1%. Individual changes, however, ranged from −9.6 to +26.8%. This interindividual variability was not significantly correlated with age, body mass (inverse of NO 3 − dose per kg), body mass index (surrogate for body composition) or placebo trial V max or fatigue index (in vivo indicators of muscle fiber type distribution). In contrast, the relative increase in Pmax was significantly correlated (r = 0.60; P < 0.01) with the relative increase in plasma NO 2 − concentration. In multivariable analysis female sex also tended (P = 0.08) to be associated with a greater increase in Pmax. We conclude that the magnitude of the dietary NO 3 −‐induced increase in muscle power is dependent upon the magnitude of the resulting increase in plasma NO 2 − and possibly female sex.

Acute dietary NO intake increases VOpeak and performance in patients with HFrEF. These data, in conjunction with our recent data demonstrating that dietary NO also improves muscle contractile function, suggest that dietary NO supplementation may be a valuable means of enhancing exercise capacity in this population.

Myocarditis is a recognized but underdiagnosed cause of cardiomyopathy due to its wide clinical spectrum and nonspecific presentation. Accurate diagnosis is important because 25% of patients with acute myocarditis develop cardiomyopathy, and of those, approximately 5% per year require heart transplantation or die. Current guidelines for the recognition and treatment of the inflammatory cardiomyopathies are limited. The gold standard for diagnosis, endomyocardial biopsy, has low sensitivity, and thus, multimodality imaging of inflammation plays a crucial role in defining the cardiac abnormalities and in assisting with diagnosis and management. The literature on inflammatory cardiomyopathies is limited to small studies of selected populations due to the diverse etiologies and inherent difficulties in definitive diagnosis. This review focuses on the current and projected use of various imaging modalities, including echocardiography, cardiac magnetic resonance, and nuclear imaging to better define inflammatory cardiomyopathies and aid in their management; it specifically focuses on cardiac sarcoidosis, and giant cell, eosinophilic, and lymphocytic myocarditis.