PURPOSE: The purpose of this study was to determine the cardiac mechanisms involved in cardiovascular adjustments during postexercise circulatory occlusion (OCCL). METHOD:Heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance (total peripheral resistance (TPR)) were assessed in nine healthy volunteers duringrest and static exercise at 30% of maximum voluntary contraction followed by either OCCL for 3 min or non-OCCL in a randomized crossover protocol. RESULTS: During handgrip, HR (+20%; P < 0.001), CO (+11%; P = 0.003), MAP (+18%; P = 0.001), and TPR (+6%; P = 0.004) increased, SV (-8%; P = 0.001) and EDV (-5%; P < 0.001) decreased, while ESV did not change (P > 0.05). These responses were similar between conditions (P > 0.05). During OCCL, HR, SV, and CO returned to baseline, whereas MAP (+19%; P < 0.001) and TPR (+9%; P = 0.004) remained elevated. EDV (+12%; P < 0.001) and ESV (+23%; P < 0.001) increased in parallel above resting values. CONCLUSION: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying the involvement of the Frank-Starling mechanism.
RCT Entities:
PURPOSE: The purpose of this study was to determine the cardiac mechanisms involved in cardiovascular adjustments during postexercise circulatory occlusion (OCCL). METHOD: Heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance (total peripheral resistance (TPR)) were assessed in nine healthy volunteers during rest and static exercise at 30% of maximum voluntary contraction followed by either OCCL for 3 min or non-OCCL in a randomized crossover protocol. RESULTS: During handgrip, HR (+20%; P < 0.001), CO (+11%; P = 0.003), MAP (+18%; P = 0.001), and TPR (+6%; P = 0.004) increased, SV (-8%; P = 0.001) and EDV (-5%; P < 0.001) decreased, while ESV did not change (P > 0.05). These responses were similar between conditions (P > 0.05). During OCCL, HR, SV, and CO returned to baseline, whereas MAP (+19%; P < 0.001) and TPR (+9%; P = 0.004) remained elevated. EDV (+12%; P < 0.001) and ESV (+23%; P < 0.001) increased in parallel above resting values. CONCLUSION: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying the involvement of the Frank-Starling mechanism.
Authors: Marty D Spranger; Jasdeep Kaur; Javier A Sala-Mercado; Tiago M Machado; Abhinav C Krishnan; Alberto Alvarez; Donal S O'Leary Journal: Am J Physiol Regul Integr Comp Physiol Date: 2015-01-28 Impact factor: 3.619
Authors: Marty D Spranger; Javier A Sala-Mercado; Matthew Coutsos; Jasdeep Kaur; Doug Stayer; Robert A Augustyniak; Donal S O'Leary Journal: Am J Physiol Regul Integr Comp Physiol Date: 2013-02-20 Impact factor: 3.619
Authors: Javier A Sala-Mercado; Marty D Spranger; Rania Abu-Hamdah; Jasdeep Kaur; Matthew Coutsos; Douglas Stayer; Robert A Augustyniak; Donal S O'Leary Journal: Am J Physiol Heart Circ Physiol Date: 2013-09-06 Impact factor: 4.733
Authors: James P Fisher; Ahmed M Adlan; Alena Shantsila; J Frederik Secher; Henrik Sørensen; Niels H Secher Journal: J Physiol Date: 2013-05-27 Impact factor: 5.182