scholarly journals 97 Increasing skeletal muscle oxygenation by prior moderate-intensity exercise increases aerobic energy provision in chronic heart failure

Heart ◽  
2011 ◽  
Vol 97 (Suppl 1) ◽  
pp. A56-A56
Author(s):  
T. S. Bowen ◽  
D. T. Cannon ◽  
S. R. Murgatroyd ◽  
K. K. Witte ◽  
H. B. Rossiter
2016 ◽  
Vol 311 (6) ◽  
pp. H1530-H1539 ◽  
Author(s):  
Victor M. Niemeijer ◽  
Ruud F. Spee ◽  
Thijs Schoots ◽  
Pieter F. F. Wijn ◽  
Hareld M. C. Kemps

The extent and speed of transient skeletal muscle deoxygenation during exercise onset in patients with chronic heart failure (CHF) are related to impairments of local O2 delivery and utilization. This study examined the physiological background of submaximal exercise performance in 19 moderately impaired patients with CHF (Weber class A, B, and C) compared with 19 matched healthy control (HC) subjects by measuring skeletal muscle oxygenation (SmO2) changes during cycling exercise. All subjects performed two subsequent moderate-intensity 6-min exercise tests (bouts 1 and 2) with measurements of pulmonary oxygen uptake kinetics and SmO2 using near-infrared spatially resolved spectroscopy at the vastus lateralis for determination of absolute oxygenation values, amplitudes, kinetics (mean response time for onset), and deoxygenation overshoot characteristics. In CHF, deoxygenation kinetics were slower compared with HC (21.3 ± 5.3 s vs. 16.7 ± 4.4 s, P < 0.05, respectively). After priming exercise (i.e., during bout 2), deoxygenation kinetics were accelerated in CHF to values no longer different from HC (16.9 ± 4.6 s vs. 15.4 ± 4.2 s, P = 0.35). However, priming did not speed deoxygenation kinetics in CHF subjects with a deoxygenation overshoot, whereas it did reduce the incidence of the overshoot in this specific group ( P < 0.05). These results provide evidence for heterogeneity with respect to limitations of O2 delivery and utilization during moderate-intensity exercise in patients with CHF, with slowed deoxygenation kinetics indicating a predominant O2 utilization impairment and the presence of a deoxygenation overshoot, with a reduction after priming in a subgroup, indicating an initial O2 delivery to utilization mismatch.


1995 ◽  
Vol 129 (4) ◽  
pp. 690-695 ◽  
Author(s):  
Shinobu Matsui ◽  
Nobuki Tamura ◽  
Tomoyuki Hirakawa ◽  
Saeko Kobayashi ◽  
Noboru Takekoshi ◽  
...  

2012 ◽  
Vol 112 (3) ◽  
pp. 378-387 ◽  
Author(s):  
T. Scott Bowen ◽  
Daniel T. Cannon ◽  
Scott R. Murgatroyd ◽  
Karen M. Birch ◽  
Klaus K. Witte ◽  
...  

The mechanism for slow pulmonary O2 uptake (V̇o2) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O2 utilization or O2 delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2 delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed V̇o2 kinetics during exercise in CHF. Fifteen men with CHF (New York Heart Association I–III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions ( bouts 1 and 2, separated by 6 min of rest) from rest to 90% of lactate threshold on a cycle ergometer. V̇o2 was measured using a turbine and a mass spectrometer, and muscle tissue oxygenation index (TOI) was determined by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3 ± 2.4% ( P = 0.001), attenuated the deoxygenation overshoot (−3.9 ± 3.6 vs. −2.0 ± 1.4%, P = 0.011), and speeded the V̇o2 time constant (τV̇o2; 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τV̇o2 before ( R2 = 0.51, P = 0.014) and after ( R2 = 0.36, P = 0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26 ± 8 vs. 20 ± 8 s) and slowed in the remainder (32 ± 11 vs. 44 ± 16 s), the latter group having worse New York Heart Association scores ( P = 0.042) and slower V̇o2 kinetics ( P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds V̇o2 kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits V̇o2 kinetics during moderate exercise.


2016 ◽  
Vol 86 (1-2) ◽  
Author(s):  
Francesco Giallauria ◽  
Neil Andrew Smart ◽  
Antonio Cittadini ◽  
Carlo Vigorito

Exercise training (ET) is strongly recommended in patients with chronic heart failure (CHF). Moderate-intensity aerobic continuous ET is the best established training modality in CHF patients. In the last decade, however, high-intensity interval exercise training (HIIT) has aroused considerable interest in cardiac rehabilitation community. Basically, HIIT consists of repeated bouts of high-intensity exercise alternated with recovery periods. In CHF patients, HIIT exerts larger improvements in exercise capacity compared to moderate-continuous ET. These results are intriguing, mostly considering that better functional capacity translates into an improvement of symptoms and quality of life. Notably, HIIT did not reveal major safety issues; although CHF patients should be clinically stable, have had recent exposure to at least regular moderate-intensity exercise, and appropriate supervision and monitoring during and after the exercise session are mandatory. The impact of HIIT on cardiac dimensions and function and on endothelial function remains uncertain. HIIT should not replace other training modalities in heart failure but should rather complement them. Combining and tailoring different ET modalities according to each patient’s baseline clinical characteristics (i.e. exercise capacity, personal needs, preferences and goals) seem the most astute approach to exercise prescription.


1999 ◽  
Vol 80 (7) ◽  
pp. 746-750 ◽  
Author(s):  
Barbara Sturm ◽  
Michael Quittan ◽  
Günther F. Wiesinger ◽  
Brigitte Stanek ◽  
Bernhard Frey ◽  
...  

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