Does recovery from submaximal exercise predict response to cardiac resynchronisation therapy?

BACKGROUND: Exercise parameters are not routinely incorporated in decision making for cardiac resynchronisation therapy (CRT). Submaximal exercise parameters better reflect daily functional capacity of heart failure patients than parameters measured at maximal exertion, and may therefore better predict response to CRT. We compared various exercise parameters, and sought to establish which best predict CRT response. METHODS: In 31 patients with chronic heart failure (61% male; age 68±7 years), submaximal and maximal cycling testing was performed before and 3 months after CRT. Submaximal oxygen onset (τVO(2) onset) and recovery kinetics (τVO(2) recovery), peak oxygen uptake (VO(2) peak) and oxygen uptake efficiency slope (OUES) where measured. Response was defined as ≥15% relative reduction in end-systolic volume. RESULTS: After controlling for age, New York Heart Association and VO(2) peak, fast submaximal VO(2) kinetics were significantly associated with response to CRT, measured either during onset or recovery of submaximal exercise (area under the curve, AUC=0.719 for both; p<0.05). By contrast, VO(2) peak (AUC=0.632; p=0.199) and OUES (AUC=0.577; p=0.469) were not associated with response. Among patients with fast onset and recovery kinetics, below 60 s, a significantly higher percentage of responders was observed (91% and 92% vs 43% and 40%, respectively). CONCLUSIONS: Impaired VO(2) kinetics may serve as an objective marker of submaximal exercise capacity that is age-independently associated with non-response following CRT, whereas maximal exercise parameters are not. Assessment of VO(2) kinetics is feasible and easy to perform, but larger studies should confirm their clinical utility

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

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

\u3cp\u3eBackground 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 VO\u3csub\u3e2\u3c/sub\u3e 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 VO\u3csub\u3e2\u3c/sub\u3e (+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.\u3c/p\u3