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Background: Exaggerated blood pressure (BP) during submaximal exercise independently predicts cardiovascular mortality and identifies uncontrolled high BP not detected at rest. However, thresholds for submaximal exercise BP during clinical exercise testing have never been defined from a large representative sample, which was the aim of this study. Methods: Records from 13,949 people referred for a clinical exercise stress test (aged 52 ± 13 years, 61% male) using the Bruce treadmill protocol (stages 1 to 4 plus peak) were extracted from 4 Australian hospitals over the years 2000–2018. Exercise records were linked to administrative health datasets (hospital admissions and emergency presentations) to define clinical characteristics, including cardiovascular disease history. Thresholds denoting exaggerated BP were defined as > 90th centile at each exercise stage. Results: SBP and DBP thresholds across all stages were higher in males vs. females (stage-1: 180/90 vs 175/90 mmHg; stage-2: 196/94 vs 190/90 mmHg; stage-3: 204/97 vs 196/91 mmHg; stage-4: 210/100 vs 196/92 mmHg; peak: 215/100 vs 206/95 mmHg). SBP at all stages increased stepwise from the 1st to 4th age quartile (p < 0.05), whilst DBP remained similar (stage-1: 163/90 to 185/92 mmHg; stage-2: 180/90 to 204/95 mmHg; stage-3: 193/90 to 210/95 mmHg, stage-4: 200/91, to 210/96 mmHg; peak: 201/95 to 217/100 mmHg). Results were similar irrespective of cardiovascular disease history. Conclusions: This is the first study to define submaximal exercise BP thresholds during clinical exercise testing. Thresholds were higher in males compared to females and increased with age. These thresholds may help clinicians to identify people at increased high BP-related risk.

Low density lipoprotein (LDL) particle diameters were determined by non-denaturing gradient gel electrophoresis in 53 subjects with previously unrecognised coronary heart disease (CHD) and 167 control subjects matched by age, sex and total plasma cholesterol. The mean diameter of the major LDL peak was found not to be significantly different between the two groups, but the CHD subjects were found to have a broader distribution of the predominant LDL species ((25.0 (24.7-25.3)nm versus 24.8 (24.7-24.9)nm)) (median (25-75%)), a greater proportion of larger particles (chi 2 = 19.8, P0.001) and to be more likely to have multiple numbers of LDL species than the control subjects (chi 2 = 22.7, P0.001). A negative correlation was found between the diameter of the predominant LDL species and fasting plasma triglyceride (r = -0.21, P = 0.0015), waist to hip ratio (WHR) (r = -0.15, P = 0.026) and body mass index (BMI) (r = -0.20, P = 0.002), and in a subgroup of subjects (n = 106), postprandial analysis revealed a negative correlation with the incremental postprandial response of plasma insulin (r = -0.19, P = 0.025). Male subjects had a significantly smaller diameter of the major LDL peak (24.8 +/- 0.0 nm) than female subjects (25.0 +/- 0.0 nm, P0.001). The present study failed to confirm an association between small LDL particles and the presence of coronary heart disease but did demonstrate more LDL heterogeneity in those with CHD. In addition, significant relationships were evident between the diameter of the major LDL peak and a number of other risk factors for coronary disease.