Pulmonary oxygen uptake (˙VO2p)
( V ˙ O 2 p )
at exercise onset is severely delayed in heart transplant recipients (HTRs). The role of exercise training to improve ˙VO2p
V ˙ O 2 p
kinetics in HTRs has not been studied. We examined ˙VO2p
V ˙ O 2 p
kinetics before and after 12 weeks of aerobic and strength training (HTR-T; n = 19, mean ± SD age: 57 ± 10 years) or usual care (HTR-UC; n = 16, mean age: 58 ± 12 years). Phase II ˙VO2p
V ˙ O 2 p
kinetics, reflecting the rate of muscle metabolic adaptation, improved 37% after training compared with usual care (HTR-UC, 15 ± 19 vs 2 ± 13 seconds improvement, p = 0.02). The change in rest to steady-state heart rate reserve before and after 12 weeks was not different in HTR-T (−2 ± 9 beats/min) and HTR-UC (−1 ± 7 beats/min; p = 0.78). No significant relation was found between the change in ˙VO2p
V ˙ O 2 p
kinetics and rest to steady-state heart rate reserve. Changes in leg lean tissue mass and ˙VO2p
V ˙ O 2 p
kinetics were significantly related (r = −0.46, p = 0.008). In conclusion, a favorable adaptation in skeletal muscle oxidative function may underpin our finding of faster ˙VO2p
V ˙ O 2 p
kinetics in HTRs after exercise training.
Pulmonary oxygen uptake (˙VO2p)
( V ˙ O 2 p )
kinetics are significantly impaired during a step increase from rest to moderate-intensity exercise (below the gas exchange ventilatory threshold) in heart transplant recipients (HTRs). The persistent impairment in the rate of V ˙ O 2 p
V ˙ O 2 p
adaptation at exercise onset has been attributed to abnormal cardiovascular and skeletal muscle function that result in reduced oxygen delivery to and/or utilization by the working muscles, a finding that also exists in pretransplantation heart failure. The phase II portion of V ˙ O 2 p
V ˙ O 2 p
adaptation at exercise onset is of particular interest because it reflects the rate of exercising muscle O 2 uptake (phase II V ˙ O 2 p
V ˙ O 2 p
illustrated by Tomczak et al). Our group, and others, have shown that exercise training is an effective therapy for improving V ˙ O 2 p
V ˙ O 2 p
at peak exercise in HTRs without altering the cardiovascular function at rest or during exercise. These findings suggest that changes in skeletal muscle oxidative capacity may account for the improvement in peak exercise V ˙ O 2 p
V ˙ O 2 p
with training. Currently, it is unknown whether the impaired V ˙ O 2 p
V ˙ O 2 p
kinetics observed in HTRs are improved with exercise training. Accordingly, we examined the effects of 12 weeks of exercise training (HTR-T) versus usual care (HTR-UC) on V ˙ O 2 p
V ˙ O 2 p
kinetics. We tested the hypothesis that exercise training would significantly improve phase II V ˙ O 2 p
V ˙ O 2 p
kinetics in HTRs.
Methods
The study design, subjects, and inclusion criteria have previously been described. Briefly, HTRs (group mean ± SD age: 57 ± 11 years) were recruited from clinic visits from the University of Alberta heart transplant program and were randomly assigned to 12 weeks of combined aerobic (moderate-intensity continuous and high-intensity interval training) and strength training (HTR-T) versus usual care (HTR-UC). In the first 8 weeks, continuous aerobic (treadmill and cycle ergometer) training was performed for 30 to 45 minutes at a target heart rate equal to 60% to 80% of peak V ˙ O 2 p
V ˙ O 2 p
5 days/week. During the final 4 weeks, continuous aerobic training was performed 3 days/week (45 minutes at heart rate equal to 80% peak V ˙ O 2 p
V ˙ O 2 p
) and high-intensity interval cycle ergometer exercise (30 seconds at 90% to 100% peak power output followed by 60 seconds rest × 25 repetition target) was performed 2 days/week. Strength training (1 to 2 sets) entailed a target of 10 to 15 repetitions for major upper and lower body muscle groups 2 days/week at 50% of maximal strength.
The subjects in this report are a subset of those participants in which gas exchange data were collected for V ˙ O 2 p
V ˙ O 2 p
kinetic modeling. Prerandomization V ˙ O 2 p
V ˙ O 2 p
kinetics have also been reported in a subset of participants. Subjects were excluded if the standard deviation of the V ˙ O 2 p
V ˙ O 2 p
interbreath fluctuations was >0.05 (reflective of a poor signal-to-noise ratio) during 2 minutes of steady state exercise or if there was a significant proportion of aberrant breaths during the transient (nonlinear) phase of V ˙ O 2 p
V ˙ O 2 p
readjustment that precluded a notable exponential profile in V ˙ O 2 p
V ˙ O 2 p
that is typical during square-wave exercise transitions. In total, 19 subjects were HTR-T (age: 57 ± 10 years; 15 men and 4 women) and 16 HTR-UC (age: 58 ± 12 years; 14 men and 2 women), representing 81% of the original cohort who were studied.
All subjects were on standard post-transplant pharmacologic therapy as previously described and included 6 HTR-UC and 5 HTR-T on a steroid regimen. The time from transplant to study commencement was 4.9 ± 4.5 years for the study group. Subjects performed upright cycle ergometry (Corival; Lode, Groningen, The Netherlands) square-wave exercise from rest to the V ˙ O 2 p
V ˙ O 2 p
at 75 ± 12% of the gas exchange ventilatory threshold, as determined from previous maximal exercise testing. The protocol entailed a 5-minute resting baseline followed by 5 minutes of constant work rate exercise that was 27 ± 8 W for the study group (range, 10 to 45 W). This exercise intensity was also used for testing at 12-week follow-up. V ˙ O 2 p
V ˙ O 2 p
was measured by expired gas analysis (TrueOne 2400 Metabolic Measurement System; ParvoMedics, Salt Lake City, Utah).
Data for V ˙ O 2 p
V ˙ O 2 p
kinetic modeling were filtered for aberrant breaths, averaged into 5-second time bins, and smoothed using a 5-point moving average. V ˙ O 2 p
V ˙ O 2 p
kinetics were then determined using a first-order model of the form:
Y ( t ) = Y ( b ) + A · [ 1 − e − ( t − TD ) / τ ]
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