Differences in cardiovascular function between sexes have been documented at rest and maximal exercise. The purpose of this study was to examine the sex differences in cardiovascular function during submaximal constant-load exercise, which is not well understood.
Thirty-one male and 33 female subjects completed nine minutes moderate and nine minutes vigorous intensity submaximal exercise (40 and 75% of peak watts determined by maximal exercise test). Measurements included: intra-arterial blood pressure (SBP and DBP), cardiac index (QI), heart rate (HR), oxygen consumption (VO2) and arterial catecholamines (epinephrine = EPI and norepinephrine = NE), and blood gases. Mean arterial pressure (MAP), stroke volume index (SVI), systemic vascular resistance index (SVRI), arterial oxygen content (CaO2), arterial to venous O2 difference (AVO2) and systemic oxygen transport (SOT) were calculated.
This study demonstrates sex differences in the cardiovascular response to constant-load submaximal exercise. Specifically, females presented limitations in cardiac performance in which they are unable to compensate for reductions in stroke volume through increases in HR, potentially a consequence of a female’s blunted sympathetic response and higher vasodilatory state. Females demonstrated greater cardiac work needed to meet the same external work demand, and relied on increased peripheral oxygen extraction, lower energy expenditure and improvements in mechanical efficiency as compensatory mechanisms.
At rest and during submaximal exercise QI, SVI, SBP, MAP, NE, CaO2, and SOT were lower in females compared to males. VO2, AVO2, EPI were lower in females throughout exercise. When corrected for wattage, females had a higher Q, HR, SV, VO2 and AVO2 despite lower energy expenditure and higher mechanical efficiency.
Bibliographical noteFunding Information:
We would like to thank Kathy O’Malley, Chris Johnson, and Shelly Roberts for their assistance with data collection. We also thank the participants for their effort. This work was supported by grant numbers HL71478 (BDJ) and 1KL2RR024151 (TPO) from the National Institutes of Health (NIH) and grant number 56051Z (EMS) from the American Heart Association. We also thank the staff of the Clinical Research Unit (CRU) for their assistance throughout this study. The Mayo Clinic CRU is supported by grant number 1UL1RR024150 from the National Center for Research Resources (NCRR).
© 2014, Wheatley et al.; licensee Springer.
- Arterial pressure
- Cardiac output
- Energy expenditure
- Systemic vascular resistance