Effects of high-intensity interval training on central haemodynamics and skeletal muscle oxygenation during exercise in patients with chronic heart failure

Background High-intensity interval training (HIT) improves exercise capacity in patients with chronic heart failure (CHF). Moreover, HIT was associated with improved resting cardiac function. However, the extent to which these improvements actually contribute to training-induced changes in exercise capacity remains to be elucidated. Therefore, we evaluated the effects of HIT on exercising central haemodynamics and skeletal muscle oxygenation. Methods Twenty-six CHF patients were randomised to a 12-week 4 × 4 minute HIT program at 85-95% of peak VO2 or usual care. Patients performed maximal and submaximal cardiopulmonary exercise testing with simultaneous assessment of cardiac output and skeletal muscle oxygenation by near infrared spectroscopy, using the amplitude of the tissue saturation index (TSIamp). Results Peak workload increased by 11% after HIT (p between group = 0.01) with a non-significant increase in peak VO2 (+7%, p between group = 0.19). Cardiac reserve increased by 37% after HIT (p within group = 0.03, p between group = 0.08); this increase was not related to improvements in peak workload. Oxygen uptake recovery kinetics after submaximal exercise were accelerated by 20% (p between group = 0.02); this improvement was related to a decrease in TSIamp (r = 0.71, p = 0.03), but not to changes in cardiac output kinetics. Conclusion HIT induced improvements in maximal exercise capacity and exercising haemodynamics at peak exercise. Improvements in recovery after submaximal exercise were associated with attenuated skeletal muscle deoxygenation during submaximal exercise, but not with changes in cardiac output kinetics, suggesting that the effect of HIT on submaximal exercise capacity is mediated by improved microvascular oxygen delivery-to-utilisation matching

The relation between cardiac output kinetics and skeletal muscle oxygenation during moderate exercise in moderately impaired patients with chronic heart failure

Oxygen uptake (V̇O2) kinetics are prolonged in patients with chronic heart failure (CHF). This may be caused by impaired oxygen delivery or skeletal muscle derangements. We investigated whether impaired cardiac output (Q) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the VAT to assess V̇O2 kinetics (τVO2). Q kinetics (τQ) were assessed by a radial artery pulse contour analysis method. Skeletal muscle deoxygenation was assessed by near infrared spectroscopy at the m. vastus lateralis, using the minimal value of the tissue saturation index during onset of exercise (TSImin). Patients were categorized in slow and normal Q responders relative to metabolic demands (τQ/ V̇O2 ≥ 1 and τQ/ VO2 < 1, respectively) τQ (62 +/- 29s) and τV̇O2 (60+/-21s) were significantly related (r=0.66, p= 0.001). There was a significant correlation between τQ and TSImin in the slow Q responders (rs= -0.57, p=0.005, n=22 (51%)) In conclusion, in moderately impaired CHF patients with relatively slow Q kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise

High intensity interval training after cardiac resynchronization therapy : An explorative randomized controlled trial

BACKGROUND: CRT leads to improvement in exercise capacity, cardiac function and mortality in selected CHF patients. Exercise capacity improves even greater when combining CRT with moderate-intensity exercise training (ET). However, high-intensity interval training (HIT) as additional therapy to CRT has not yet been established. Given the complementary physiological effects of HIT, we hypothesized that HIT after CRT may have additional effects on exercise capacity. METHODS: 24 CHF patients, NYHA class II/III and accepted for CRT underwent an echocardiogram, QoL questionnaire and CPET with cardiac output (CO) measurements before implantation, at 3 and 6 months. After 3 months, patients were randomized to usual care (UC) or HIT, consisting of 36 sessions at 85-95% of peak V̇O 2. RESULTS: Peak V̇O 2 increased after CRT (17±5.3 to 18.7±6.2 ml/kg/min, p < 0.05); after HIT there was a non-significant increase of 1.4 ml/kg/min (p = 0.12). Peak workload increased after CRT (109±45 to 118±44 W, p = 0.001). An additional significant within- and between group increase after HIT was found in the intervention group (128±42 to 148±48 W, versus 110±50 to 110±50, respectively, p = 0.03). Peak CO did not change significantly after CRT or HIT. V̇O 2 recovery kinetics speeded by 27% after CRT (p = 0.04), no further improvement after HIT was observed. LVEF increased 25% after CRT (p = 0.0001), no additional increase was seen after HIT. CONCLUSION: This study demonstrates that HIT provides additional improvement of exercise capacity without a concomitant change in peak V̇O 2 or CO suggesting that the additional effect of HIT is mainly mediated by an improvement of anaerobic performance

High intensity interval training after cardiac resynchronization therapy: An explorative randomized controlled trial

Background: CRT leads to improvement in exercise capacity, cardiac function and mortality in selected CHF patients. Exercise capacity improves even greater when combining CRT with moderate-intensity exercise training (ET). However, high-intensity interval training (HIT) as additional therapy to CRT has not yet been established. Given the complementary physiological effects of HIT, we hypothesized that HIT after CRT may have additional effects on exercise capacity. Methods: 24 CHF patients, NYHA class II/III and accepted for CRT underwent an echocardiogram, QoL questionnaire and CPET with cardiac output (CO) measurements before implantation, at 3 and 6 months. After 3 months, patients were randomized to usual care (UC) or HIT, consisting of 36 sessions at 85–95% of peak V̇O 2. Results: Peak V̇O 2 increased after CRT (17±5.3 to 18.7±6.2 ml/kg/min, p < 0.05); after HIT there was a non-significant increase of 1.4 ml/kg/min (p = 0.12). Peak workload increased after CRT (109±45 to 118±44 W, p = 0.001). An additional significant within- and between group increase after HIT was found in the intervention group (128±42 to 148±48 W, versus 110±50 to 110±50, respectively, p = 0.03). Peak CO did not change significantly after CRT or HIT. V̇O 2 recovery kinetics speeded by 27% after CRT (p = 0.04), no further improvement after HIT was observed. LVEF increased 25% after CRT (p = 0.0001), no additional increase was seen after HIT. Conclusion: This study demonstrates that HIT provides additional improvement of exercise capacity without a concomitant change in peak V̇O 2 or CO suggesting that the additional effect of HIT is mainly mediated by an improvement of anaerobic performance

Characterization of exercise limitations by evaluating individual cardiac output patterns : A prospective cohort study in patients with chronic heart failure

Background: Patients with chronic heart failure (CHF) suffer from exercise intolerance due to impaired central hemodynamics and subsequent alterations in peripheral skeletal muscle function and structure. The relative contribution of central versus peripheral factors in the reduced exercise capacity is still subject of debate. The main purpose was to investigate heterogeneity in the nature of exercise intolerance by evaluating individual cardiac output (Q) patterns. The secondary purpose was to evaluate whether patient and disease characteristics were associated with a central hemodynamic exercise limitation. Methods: Sixty-four stable CHF patients performed a symptom limited incremental exercise test with respiratory gas analysis and simultaneous assessment of Q, using a radial artery pulse contour analysis method. A central hemodynamic exercise limitation was defined as a plateau or decline in Q from 90 to 100 % of exercise duration. Results: Data from 61 patients were analyzed. A central hemodynamic exercise limitation was observed in 21 patients (34 %). In these patients, a higher occurrence of a plateau/decrease in oxygen uptake (VO2) (52 % vs 23 %, p=0.02), stroke volume (SV) (100 % vs. 75 %, p=0.01) and chronotropic incompetence (31 % vs. 2.5 %, p=0.01) was observed, while presence of a left bundle branch block (LBBB) occurred significantly less (19 % vs 48 %, p=0.03) There was no difference in disease characteristics such as etiology, duration, NYHA class, mitral regurgitation or ischemia. Conclusions: The study revealed considerable heterogeneity in the nature of exercise limitations between moderately impaired CHF patients. In one third of the study population a plateau or decrease in Q towards peak exercise was demonstrated, which is indicative of a central hemodynamic exercise limitation. A central hemodynamic exercise limitation was associated with an impairment to augment stroke volume and heart rate

The utility of the oxygen pulse recovery as a marker of the cardiac output response to exercise in patients with chronic heart failure

PURPOSE: The cardiac output (CO) response to exercise is a useful marker to grade the prognosis and severity of chronic heart failure (CHF). The recovery of the oxygen pulse (OP) is a non-invasive parameter, which is related to exercise capacity in cardiac patients. However, the relation between OP recovery and the central haemodynamic response to exercise remains to be determined. We hypothesized that an impaired OP recovery is associated with a reduced CO response to exercise in CHF patients. METHODS: Sixty one CHF patients performed cardiopulmonary exercise test with simultaneous measurement of CO. Impaired OP recovery was defined as an overshoot during the first minute of recovery or OP at 1-min recovery as a percentage of peak OP (OPRR ). RESULTS: An OP overshoot was observed in 9% (n = 5) of patients. In these patients, peak CO and VO2 were significantly lower (peak CO 7.9 ± 0.8 versus 11.2 ± 4.3 L/min and peak VO2 14.1 ± 4.7 versus 19.6 ± 5.8 ml min-1 kg-1 ). Mean relative recovery of OP was 78 ± 20%. Slow OP recovery (negative OPRR ) was seen in 13% (n = 8). Peak CO and VO2 were significantly lower in the negative OPRR group (11 ± 4 versus 8 ± 0.7 L/min and 19.7 ± 5.9 versus 14.6 ± 3.7 ml kg min-1 ). There was a significant relation between OPRR and stroke volume (SV) RR (r = .57), as well as between OPRR and a-v O2 diff RR (rs = .4). CONCLUSION: An impaired OP recovery is associated with a reduced CO response to exercise and worse functional status. Therefore, the OP recovery can be used to grade the severity of CHF

The utility of the oxygen pulse recovery as a marker of the cardiac output response to exercise in patients with chronic heart failure

PURPOSE: The cardiac output (CO) response to exercise is a useful marker to grade the prognosis and severity of chronic heart failure (CHF). The recovery of the oxygen pulse (OP) is a non-invasive parameter, which is related to exercise capacity in cardiac patients. However, the relation between OP recovery and the central haemodynamic response to exercise remains to be determined. We hypothesized that an impaired OP recovery is associated with a reduced CO response to exercise in CHF patients. METHODS: Sixty one CHF patients performed cardiopulmonary exercise test with simultaneous measurement of CO. Impaired OP recovery was defined as an overshoot during the first minute of recovery or OP at 1-min recovery as a percentage of peak OP (OPRR ). RESULTS: An OP overshoot was observed in 9% (n = 5) of patients. In these patients, peak CO and VO2 were significantly lower (peak CO 7.9 ± 0.8 versus 11.2 ± 4.3 L/min and peak VO2 14.1 ± 4.7 versus 19.6 ± 5.8 ml min-1 kg-1 ). Mean relative recovery of OP was 78 ± 20%. Slow OP recovery (negative OPRR ) was seen in 13% (n = 8). Peak CO and VO2 were significantly lower in the negative OPRR group (11 ± 4 versus 8 ± 0.7 L/min and 19.7 ± 5.9 versus 14.6 ± 3.7 ml kg min-1 ). There was a significant relation between OPRR and stroke volume (SV) RR (r = .57), as well as between OPRR and a-v O2 diff RR (rs = .4). CONCLUSION: An impaired OP recovery is associated with a reduced CO response to exercise and worse functional status. Therefore, the OP recovery can be used to grade the severity of CHF

Skeletal muscle fiber characteristics in patients with chronic heart failure: impact of disease severity and relation with muscle oxygenation during exercise

Skeletal muscle function in patients with heart failure and reduced ejection fraction (HFrEF) greatly determines exercise capacity. However, reports on skeletal muscle fiber dimensions, fiber capillarization, and their physiological importance are inconsistent. Twenty-five moderately impaired patients with HFrEF and 25 healthy control (HC) subjects underwent muscle biopsy sampling. Type I and type II muscle fiber characteristics were determined by immunohistochemistry. In patients with HFrEF, enzymatic oxidative capacity was assessed, and pulmonary oxygen uptake (VO2) and skeletal muscle oxygenation during maximal and moderateintensity exercise were measured using near-infrared spectroscopy. While muscle fiber cross-sectional area (CSA) was not different between patients with HFrEF and HC, the percentage of type I fibers was higher in HC (46 ± 15 vs. 37 ± 12%, respectively, P = 0.041). Fiber type distribution and CSA were not different between patients in New York Heart Association (NYHA) class II and III. Type I muscle fiber capillarization was higher in HFrE.compared with HC[capillary- to-fiber perimeter exchange (CFPE) index: 5.70 ± 0.92 vs. 5.05 ± 0.82, respectively, P = 0.027]. Patients in NYHA class III had slower VO2 and muscle deoxygenation kinetics during onset of exercise and lower muscle oxidative capacity than those in class II (P < 0.05). Also, fiber capillarization was lower but no.compared with HC. Higher CFPE index was related to faster deoxygenation (rspearman±±0.682, P±0.001), however, not to muscle oxidative capacity (r±±0.282, P± 0.216). Type I muscle fiber capillarization is higher in HFrE.compared with HC but not in patients with greater exercise impairment. Greater capillarization may positively affect VO2 kinetics by enhancing muscle oxygen diffusion. NEW & NOTEWORTHY The skeletal myopathy of chronic heart failure (HF) includes a greater percentage of fatigable type II fibers and, for less impaired patients, greater skeletal muscle fiber capillarization. Near-infrared spectroscopy measurements of skeletal muscle oxygenation indicate that greater capillarization ma.compensate for reduced blood flow in mild HF by enhancing the diffusive capacity of skeletal muscle. This thereby augments and speeds oxygen extraction during contractions, which is translated into faster pulmonary oxygen uptake kinetics