LAUSR

Obesity decreases respiratory compliance, increasing energy expenditure and fatigue during breathing, contributing to perceived shortness of breath, elevating respiratory drive in an exhaustive positive feedback manner. The additional demand on the diaphragm can contribute to increased production of reactive oxygen species deleterious to function. Similarly, obesity drives cardiac morphological abnormalities, for example, fatty infiltration, fibrosis and cardiac hypertrophy, which can cause pulmonary congestion, contributing to dyspnoea and thusmore work. In this issue of Experimental Physiology, Kelley et al. (2022) investigated in rats the effects of an obesogenic diet (high saturated fat/high sucrose) on the structure and function of the dual pumps of life. The ‘cafeteria’ diet was adequate to provoke morphological and functional changes in the heart characterised by hypertrophy, hypercontractility and diastolic dysfunction; however, interestingly, no changes were observed in the diaphragm. Dietary supplementation with N-acetylcysteine partially or fully prevented cardiac remodelling pointing to redox mechanisms as pivotal to obesity-related morbidity. N-acetylcysteine is a substrate for endogenous glutathioneproduction, and it also has general widespread antioxidant effects. The cardiorespiratory systems are centred on dual pumps working interdependently to maintain systemic oxygen delivery and metabolic waste removal. Reciprocal interactions between the pumps are at play in health and disease. People with end-stage heart failure often manifest diaphragm dysfunction characterized by deleterious