Jeann L Sabino-Carvalho1,2, Tiago Obeid-Freitas2,3, Marcelle Paula-Ribeiro1,3, Thiago R Lopes2,3,4, Thiago H N Ferreira1,2, José E Succi5, Antônio C Silva2,3, Bruno Moreira Silva6,7,8. 1. Post-graduate Program in Translational Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. 2. Laboratory of Exercise Physiology, Olympic Center of Training and Research, São Paulo, SP, Brazil. 3. Department of Physiology, Federal University of São Paulo, Botucatu street 862, Biomedical Sciences Building, 5th floor, São Paulo, 04023-062, SP, Brazil. 4. São Paulo Association for Medicine Development, São Paulo, Brazil. 5. Department of Surgery, Federal University of São Paulo, São Paulo, SP, Brazil. 6. Post-graduate Program in Translational Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. silva.bruno@unifesp.br. 7. Laboratory of Exercise Physiology, Olympic Center of Training and Research, São Paulo, SP, Brazil. silva.bruno@unifesp.br. 8. Department of Physiology, Federal University of São Paulo, Botucatu street 862, Biomedical Sciences Building, 5th floor, São Paulo, 04023-062, SP, Brazil. silva.bruno@unifesp.br.
Abstract
PURPOSE: High cardiac vagal control in endurance athletes has been generally associated with adequate recovery from training and readiness to cope high-intensity training. A method that improves cardiac vagal control in endurance athletes could therefore be advantageous. Accordingly, we sought to test whether ischemic preconditioning (IPC) could enhance cardiac vagal control in endurance runners. METHODS:Fifteen subjects underwentIPC, sham ultrasound (SHAM) or control (CT), in random order. Subjects were informed both IPC and SHAM would be beneficial vs. CT (i.e., similar placebo induction), and IPC would be harmless despite ischemia sensations (i.e., nocebo avoidance). Resting cardiac vagal control was assessed via respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) indexes. Post-exercise cardiac vagal control was assessed via heart rate recovery [HR time constant decay (T30) and absolute HR decay (HRR30s)] during 30-s breaks of a discontinuous incremental test. Capillary blood samples were collected for lactate threshold identification. RESULTS:RSA and HRV were similar among interventions at pre- and post-intervention assessments. Lactate threshold occurred at 85 ± 4% of maximal effort. T30 was similar among interventions, but IPC increased HRR30s at 70% and 75% of maximal effort vs. SHAM and CT (70%: IPC = 31 ± 2 vs. SHAM = 26 ± 3 vs. CT = 26 ± 2 bpm, mean ± SEM, P < 0.01; 75%: IPC = 29 ± 2 vs. SHAM = 25 ± 2 vs. CT = 24 ± 2 bpm, P < 0.01). CONCLUSION:IPC did not change resting cardiac vagal control, but boosted fast post-exercise cardiac vagal reactivation at exercise intensities below lactate threshold in endurance runners.
RCT Entities:
PURPOSE: High cardiac vagal control in endurance athletes has been generally associated with adequate recovery from training and readiness to cope high-intensity training. A method that improves cardiac vagal control in endurance athletes could therefore be advantageous. Accordingly, we sought to test whether ischemic preconditioning (IPC) could enhance cardiac vagal control in endurance runners. METHODS: Fifteen subjects underwent IPC, sham ultrasound (SHAM) or control (CT), in random order. Subjects were informed both IPC and SHAM would be beneficial vs. CT (i.e., similar placebo induction), and IPC would be harmless despite ischemia sensations (i.e., nocebo avoidance). Resting cardiac vagal control was assessed via respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) indexes. Post-exercise cardiac vagal control was assessed via heart rate recovery [HR time constant decay (T30) and absolute HR decay (HRR30s)] during 30-s breaks of a discontinuous incremental test. Capillary blood samples were collected for lactate threshold identification. RESULTS: RSA and HRV were similar among interventions at pre- and post-intervention assessments. Lactate threshold occurred at 85 ± 4% of maximal effort. T30 was similar among interventions, but IPC increased HRR30s at 70% and 75% of maximal effort vs. SHAM and CT (70%: IPC = 31 ± 2 vs. SHAM = 26 ± 3 vs. CT = 26 ± 2 bpm, mean ± SEM, P < 0.01; 75%: IPC = 29 ± 2 vs. SHAM = 25 ± 2 vs. CT = 24 ± 2 bpm, P < 0.01). CONCLUSION: IPC did not change resting cardiac vagal control, but boosted fast post-exercise cardiac vagal reactivation at exercise intensities below lactate threshold in endurance runners.
Authors: Clint R Bellenger; Joel T Fuller; Rebecca L Thomson; Kade Davison; Eileen Y Robertson; Jonathan D Buckley Journal: Sports Med Date: 2016-10 Impact factor: 11.136
Authors: Ville Vesterinen; Ari Nummela; Sami Ayramo; Tanja Laine; Esa Hynynen; Jussi Mikkola; Keijo Häkkinen Journal: Int J Sports Physiol Perform Date: 2015-08-26 Impact factor: 4.010