Acute progressive resistance exercise alters intracardiac pressure in ponies

Abstract

AbstractFive male ponies (3–6 years, 208±11 kg) were used to examine the haemodynamic effects of resistance exercise. The experiment consisted of a 30 min catheterization period and a 15 min equilibration period followed by the test. Initially, the ponies stood quietly on a treadmill for collection of 5 min of baseline data. They then walked at 1.9 m s−1 for 1 min sets while carrying 0 kg, 67 kg or 134 kg of weight loaded on the saddle area. Weights were applied in a randomized order using a chain hoist and sling. The ponies rested unloaded for 2 min between sets and all cardiovascular parameters returned to baseline before beginning the next set. Haemodynamic measurements (heart rate (HR), carotid artery systolic (SP), diastolic (DP), pulse (PP) and mean pressure (MAP), right atrial pressure (RAP), right ventricular pressure (RVP) and right ventricular maximum rate of pressure rise (dP/dtmax)) were recorded continuously and data collected during the last 18 s of each set were averaged and analysed. HR increased (P<0.05) with unloaded exercise (201%) and with increases in load (252 and 271% at 67 and 134 kg, respectively). RAP increased (P<0.05) with exercise, with differences (P<0.05) between the response to the 0 kg (66%), 67 kg (121%) and 134 kg (138%) loads. RVP increased (P<0.05) incrementally with load during exercise (58, 110 and 136%, respectively), with differences (P<0.05) between 0 versus 67 kg and 67 versus 134 kg. Right ventricular dP/dtmax increased (P<0.05) incrementally and showed differences (P<0.05) between loads (131, 191 and 252% at 0, 67 and 134 kg, respectively). There were increases (P<0.05) in MAP (20%), SP (20%) and DP (27) with exercise, but no difference (P>0.05) between the response to 67 versus 134 kg load (43 and 51%; 40 and 46%; 49 and 62, respectively). Pulse pressure did not change (P>0.05) from baseline values. These data suggest that resistance exercise in the form of weight carried increases intraventricular pressure through a significant increase in both cardiac pre-load and after-load.