Metabolic changes during exercise testing of patients with ischaemic heart disease

Abstract

Nineteen patients who had recovered from a mild to moderately severe myocardial infraction 6--18 months previously were studied in order to investigate the relationship between the severity of myocardial insufficiency and metabolic changes developing during and after exercise. The patients were compared with six controls by means of a graded exercise test on a treadmill. Electrocardiographic records were made and blood pressure measured during and after the exercise and venous blood samples were taken for measurement of lactate, pyruvate, glycerol and free fatty acids. In five patients with moderate or advanced ischaemic electrocardiograph changes the blood lactate and pyruvate mean concentrations continued to rise up to a further 50% after they stopped exercising. The other patients, including some who developed symptoms suggestive of myocardial ischaemia, and all the controls, failed to show these marked increases in blood concentrations after the exercise. We conclude that the development of myocardial insufficiency during exercise is associated with marked increases in lactate and pyruvate concentrations in the peripheral blood particularly after the exercise has ceased.

Graded Maximal Exercise Testing to Assess Mouse Cardio-Metabolic Phenotypes

“…Thus, with GXT m , AT was lower in dysfunctional mice; a finding similar to those from human research looking at AT in patients with cardiac disease above functional class I (S5 Text, [ 90 ]). Together, these results demonstrated that the GXT m , like the GXT h [ 4 , 72 , 74 , 89 , 91 ], was able to simultaneously elicit exhaustive efforts, true VO 2max , and shift to anaerobic metabolism [ 4 , 72 , 74 , 89 , 91 ].…”

“…With the GXT m , Casq2 -/- mice had significantly greater LA delta compared to WT; however, with the PXT m, this parameter was decreased compared to controls ( Fig 4B , S9 Table). In humans with myocardial ischemia, a hallmark response to a GXT h is a significant increase in circulating blood LA concentrations compared to healthy subjects [ 89 ]. Thus, this response was replicated with the GXT m in the genetic model of cardiac insufficiency (9.32 ±1.53mmol/L, Casq2 -/- v. 6.63 ±17mmol/L; WT; Student’s t-Test, alpha = .05; Fig 4B , S9 Table).…”