Sex differences in calf muscle hemoglobin oxygen saturation in patients with intermittent claudication
Received 2 October 2008; accepted 21 December 2008. published online 17 February 2009.
Purposes
We tested the hypotheses that women have greater impairment in calf muscle hemoglobin oxygen saturation (StO2) in response to exercise than men, and that the sex-related difference in calf muscle StO2 would partially explain the shorter claudication distances of women.
Methods
The study comprised 27 men and 24 women with peripheral arterial disease limited by intermittent claudication. Patients were characterized on calf muscle StO2 before, during, and after a graded treadmill test, as well as on demographic and cardiovascular risk factors, ankle-brachial index (ABI), ischemic window, initial claudication distance (ICD), and absolute claudication distance (ACD).
Results
Women had a 45% lower ACD than men (296 ± 268 m vs 539 ± 288 m; P = .001) during the treadmill test. Calf muscle StO2 declined more rapidly during exercise in women than in men; the time to reach minimum StO2 occurred 54% sooner in women (226 ± 241 vs 491 ± 426 seconds; P = .010). The recovery time for calf muscle StO2 to reach the resting value after treadmill exercise was prolonged in women (383 ± 365 vs 201 ± 206 seconds; P = .036). Predictors of ACD included the time from start of exercise to minimum calf muscle StO2, the average rate of decline in StO2 from rest to minimum StO2 value, the recovery half-time of StO2, and ABI (R2 = 0.70; P < .001). The ACD of women remained lower after adjusting for ABI (mean difference, 209 m; P = .003), but was no longer significantly lower (mean difference, 72 m; P = .132) after further adjustment for the StO2 variables for the three calf muscles.
Conclusion
In patients limited by intermittent claudication, women have lower ACD and greater impairment in calf muscle StO2 during and after exercise than men, the exercise-mediated changes in calf muscle StO2 are predictive of ACD, and women have similar ACD as men after adjusting for calf StO2 and ABI measures.
aCMRI Diabetes and Metabolic Research Program, University of Oklahoma Health Sciences Center, Oklahoma City, Okla
bDepartment of Biostatistics and Epidemiology, University of Oklahoma Health Sciences Center, Oklahoma City, Okla
cGeneral Internal Medicine Section, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Okla
dCardiovascular Section, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Okla
eEndocrinology Section, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Okla
Reprint requests: Andrew W. Gardner, PhD, Hobbs-Recknagel Professor, General Clinical Research Center, University of Oklahoma Health Sciences Center, 1122 NE 13th St, Ste 150, Oklahoma City, OK 73117
This research was supported by grants from the National Institute on Aging (NIA) (R01-AG-24296) to Dr Gardner, by a Oklahoma Center for the Advancement of Science and Technology grant (HR04-113S) to Dr Gardner, and by the University of Oklahoma Health Sciences Center General Clinical Research Center grant (M01-RR-14467), sponsored by the National Center for Research Resources from the National Institutes of Health.
ABSTRACT