Affiliation:
1. Manaaki Manawa – The Centre for Heart Research, Department of Physiology, Faculty of Medical and Health Sciences University of Auckland Auckland New Zealand
2. Department of Anesthesiology University of Kansas Medical Center Kansas City KS USA
3. Department of Kinesiology, Health Promotion and Recreation, College of Education The University of North Texas Denton TX USA
4. Department of Kinesiology, College of Nursing and Health Innovation University of Texas at Arlington Arlington TX USA
Abstract
AbstractType 2 diabetes (T2D) is often accompanied by hypertension, exaggerated blood pressure (BP) responses to sympatho‐excitatory stressors, and raised cardiovascular disease risk. Appropriate respiratory–sympathetic coupling and sympathetic transduction to BP are important for short‐ and longer‐term BP control. We tested the hypotheses that respiratory modulation of muscle sympathetic nerve activity (MSNA) and its transduction to BP would be impaired in T2D and associated with higher BP and respiratory‐coupled BP variability. Resting MSNA, respiration and beat‐to‐beat BP were recorded in 20 T2D (49.1 ± 7.4 years; mean ± SD) and 13 healthy control (46.3 ± 9.4 years) participants. MSNA and the transduction of sympathetic bursts (signal‐averaging) to mean arterial pressure (MAP) were compared at low and high lung volume phases. The peak MAP response following a sympathetic burst was lower during the high lung volume than low lung volume phase in controls (P = 0.005), whereas it was unchanged with phase in T2D participants (P = 0.522). Respiratory modulation of MSNA was impaired in T2D participants, who had an attenuated reduction in burst incidence from low to the high lung volume phase, versus controls (27.8 ± 38.4% vs. 49.4 ± 24.6%, respectively; P = 0.043). The T2D participants were grouped into unimpaired respiratory modulators (burst incidence modulation median or above) or impaired respiratory modulators (below median). Impaired modulators had higher systolic BP (133 ± 14 vs. 121 ± 11 mmHg, P = 0.046), greater Traube–Hering wave amplitudes (6.3 ± 2.4 vs. 4.6 ± 1.1 mmHg; P = 0.028) and higher BP variability (MAP average real variability, 2.0 ± 0.7 vs. 1.4 ± 0.3, P = 0.033). Respiratory modulation of MSNA and sympathetic transduction to BP are altered in T2D patients and may contribute to their increased hypertension and cardiovascular risk.
imageKey points
Respiratory–sympathetic coupling and sympathetic transduction to blood pressure (BP) contribute to short‐ and longer‐term BP control. Our understanding of these processes in health and type 2 diabetes (T2D), a condition with high prevalence of hypertension and cardiovascular risk, is incomplete.
We found that respiration and sympathetic transduction to BP are coupled in healthy individuals. The mean arterial pressure response to a sympathetic burst was reduced during the high lung volume compared to the low lung volume phase. This coupling was absent in T2D.
Respiratory modulation of muscle sympathetic nerve activity (MSNA) is impaired in T2D, with a blunted reduction of MSNA observed during the high lung volume phase.
T2D patients with impaired respiratory MSNA modulation had augmented systolic BP, respiratory‐related BP excursions (Traube–Hering waves) and BP variability.
Abnormal respiratory modulation of MSNA and sympathetic transduction to BP in T2D may contribute to altered blood pressure control and cardiovascular risk in this population.