BACKGROUND: Obesity is linked with numerous physiological impairments; however, its impact on orthostatic tolerance (OT) remains unknown. This study tested the hypothesis that OT is reduced in obese individuals, and that reduced heart rate (HR) reserve and impaired cerebral autoregulation contribute to impaired OT. METHODS: Eleven obese (8 females) and 22 non-obese (10 females) individuals were exposed to incremental lower body negative pressure (LBNP) to presyncope while HR, arterial blood pressure, and cerebral perfusion (middle cerebral artery blood velocity; MCA V mean) were measured. OT was quantified with a cumulative stress index (CSI). RESULTS: OT was reduced in obese subjects, and there was an inverse relationship between body mass index (BMI) and OT (R = -0.47). HR was higher at rest and during each level of LBNP completed by all subjects. Similar peak HR (HRpeak) during LBNP between obese and non-obese subjects resulted in obese having a higher %peak HR at rest and at each stage of LBNP compared. Relationships existed for BMI and resting %HRpeak (R = 0.45) and resting %HRpeak and CSI (R = -0.52). Despite lower CSI in obese, MCA V mean and indices of cerebral autoregulation were similar between groups at all time points. CONCLUSIONS: These data suggest that OT is reduced in obese and a higher resting HR, but not impaired regulation of cerebral perfusion, may contribute to this reduction.
BACKGROUND: Obesity is linked with numerous physiological impairments; however, its impact on orthostatic tolerance (OT) remains unknown. This study tested the hypothesis that OT is reduced in obese individuals, and that reduced heart rate (HR) reserve and impaired cerebral autoregulation contribute to impaired OT. METHODS: Eleven obese (8 females) and 22 non-obese (10 females) individuals were exposed to incremental lower body negative pressure (LBNP) to presyncope while HR, arterial blood pressure, and cerebral perfusion (middle cerebral artery blood velocity; MCA V mean) were measured. OT was quantified with a cumulative stress index (CSI). RESULTS: OT was reduced in obese subjects, and there was an inverse relationship between body mass index (BMI) and OT (R = -0.47). HR was higher at rest and during each level of LBNP completed by all subjects. Similar peak HR (HRpeak) during LBNP between obese and non-obese subjects resulted in obese having a higher %peak HR at rest and at each stage of LBNP compared. Relationships existed for BMI and resting %HRpeak (R = 0.45) and resting %HRpeak and CSI (R = -0.52). Despite lower CSI in obese, MCA V mean and indices of cerebral autoregulation were similar between groups at all time points. CONCLUSIONS: These data suggest that OT is reduced in obese and a higher resting HR, but not impaired regulation of cerebral perfusion, may contribute to this reduction.
Authors: Ann M Schreihofer; Daniel A Mandel; Susan C Mobley; David W Stepp Journal: Am J Physiol Heart Circ Physiol Date: 2007-08-17 Impact factor: 4.733
Authors: Allison W Peng; Lawrence J Appel; Noel T Mueller; Olive Tang; Edgar R Miller; Stephen P Juraschek Journal: J Clin Hypertens (Greenwich) Date: 2019-01-28 Impact factor: 3.738