Rehabilitation in Cardiac Patients

Sports Med 2005; 35 (12): 1063-1084 0112-1642/05/0012-1063/$34.95/0 REVIEW ARTICLE  2005 Adis Data Information BV. All rights reserved. Rehabilitation in Cardiac Patients What Do We Know about Training Modalities? Dominique Hansen,1 Paul Dendale,2 Jan Berger2 and Romain Meeusen1 1 2 Department of Human Physiology and Sportsmedicine, Vrije Universiteit Brussel (VUB), Faculty LK, Brussels, Belgium Rehabilitation and Health Centre, Virga Jesse Hospital, Hasselt, Belgium Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1063 1. Description of Collected Reports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1064 2. Effects of Training on Exercise Capacity in Hospital-Based Settings . . . . . . . . . . . . . . . . . . . . . . . . . . . 1064 2.1 General Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1064 2.2 Relationships with Baseline Parameters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1070 2.3 Relationship with Associated Parameters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1072 3. Effects of Training on Exercise Capacity in Partially or Fully Home-Based Settings . . . . . . . . . . . . . . 1073 3.1 General Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1073 3.2 Relationships with Baseline Parameters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1073 3.2.1 Results from Correlation Coefficients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1073 3.2.2 Results from Patient Group Dividing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1073 3.3 Relationship with Associated Parameters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1075 4. Comparison of Training Effect between Hospital- and Home-Based Settings . . . . . . . . . . . . . . . . . . 1076 5. Influence of Training Modalities on Exercise Capacity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1076 5.1 Intensity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1076 5.2 Length of Programme . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1077 5.3 Duration of Training Sessions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1078 5.4 Frequency of Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1078 5.5 Inclusion of Strength Training Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1078 6. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1079 Abstract This article discusses the effects of training in cardiac rehabilitation and describes the influence of various training modalities on the evolution of exercise capacity in cardiac patients. Both home- and hospital-based studies are analysed separately. From the collected studies, a very heterogeneous character of the content of the rehabilitation programmes appears. Direct comparison of the effects of the training programmes on exercise capacity remains difficult. Baseline factors for predicting a better training outcome are: low exercise capacity and peripheral oxygen extraction; presence of hibernating myocardium; high myocardial perfusion; low degree of coronary vessel occlusion; working status; and improved feelings of wellbeing. The increased work capacity as a result of rehabilitation is associated with: an increased volume density of skeletal muscle mitochondria; peripheral muscular vasodilatory capacity; cardiac output and a decreased left ventricular end-diastolic pressure; depletion of muscular phosphocreatine levels; and degree of restenosis. Home- and hospital-based interventions induce comparable training effects. More research is needed concerning the training modalities in cardiac rehabilitation. There is an influence of weekly Hansen et al. 1064 training frequency and programme duration on the training outcome. A higher training frequency and/or duration might induce greater training effects. The evolution of the anaerobic threshold is sensitive to the training intensity and inclusion of strength training, which remains to be established for maximal exercise capacity. However, insufficient information is available on the influence of training session duration on the evolution of exercise capacity. For decades, cardiac patients have been included in rehabilitation programmes. Besides an attempt to decrease cardiovascular morbidity and mortality and improve psychological function, one of the primary goals of this intervention strategy is to increase exercise capacity and functional capacity. A large number of reports on the effects of cardiac rehabilitation on exercise capacity have been published. From this amount of information, it would seem that the training modalities of cardiac rehabilitation are fully understood and optimised. However, in clinical practice, and after a closer look at the collected reports, there is no consensus on the content of the rehabilitation programmes. In analogy, rehabilitation could be approached as a treatment drug with which the physician tries to induce the most optimal effect with a minimal dose. Questions to be addressed relate to what type, duration, frequency and intensity of training induce the greatest training effects with minimal intervention. Therefore, a closer look at the influence of training modalities on exercise capacity in cardiac rehabilitation is needed. The aim of this article is to describe the effects of cardiac rehabilitation on exercise capacity, predictive baseline factors for an altered exercise capacity, and associated factors with an altered exercise capacity as results of training. Furthermore, there will be a description of the influence of training modalities on the evolution of exercise capacity of cardiac rehabilitation patients. 1. Description of Collected Reports Inclusion criteria for the papers were only prospective studies in which the indication for rehabilitation was congestive heart failure (CHF), acute myocardial infarction (AMI), post-percutaneous coronary intervention (PCI) or post-coronary artery bypass grafting (CABG) patients. These patients needed to be involved with an aerobic exercise intervention, with or without inclusion of strength  2005 Adis Data Information BV. All rights reserved. exercises. Controlled and uncontrolled, randomised and non-randomised, and hospital- and home-based studies were included. In order to analyse training effects, a cardiopulmonary exercise test must have been conducted, with analysis of gas exchange to determine oxygen uptake (V̇O2) and/or anaerobic threshold (AT). Trials from January 1980 to present were searched, with the use of MEDLINE, PubMed and ActaMed. The following keywords were used alone or in combination: ‘rehabilitation’, ‘training’, ‘exercise’, ‘heart’, ‘cardiac’, ‘CABG’, ‘PCI’, ‘PTCA’, ‘infarction’ and ‘heart failure’. In total, 252 studies were retrieved and these papers were checked against the aforementioned inclusion criteria. From these criteria, 131 hospitaland 27 home-based clinical trials were reviewed. We chose to make a dissociation between hospitaland home-based trials because it was shown that the level of supervision and training environment were significantly different. 2. Effects of Training on Exercise Capacity in Hospital-Based Settings Most evident was the heterogeneous character of the content of the rehabilitation programmes. The pathology of the patients, training session duration, training intensity, and frequency and programme duration were so different in the collected studies that it was very difficult to compare these programmes and the resulting training outcomes. 2.1 General Effects In general, most studies found an increased maximal oxygen uptake (V̇O2max) or peak oxygen uptake (V̇O2peak), ranging from 7%[1] to 54%[2] (n = 7590, mean = 23 ± 13%, median = 20%) [see table I]. However, eight studies reported no increased exercise capacity as a result of rehabilitation.[3-10] An Sports Med 2005; 35 (12) Study n Age ± SD (y) Session duration (min) Programme duration Frequency/wk 3mo 3mo 3 3 75–85% V̇O2peak 70–85% HRmax 54% ↑a 66% ↑b 3mo 3 13% and 15% ↑a 26% ↑b 21% ↑a 11%, 13%, 8%, 4% ↑a 23% and 30% ↑a 14%, 19% and 20% ↑a 15% ↑a 42% ↑a Intensity Training effect V̇O2a or Wmaxb 40 27 62 ± 9 54 ± 10 Blumenthal et al.[20] 46 52 30–45 30 and extra 45 after 6wk 30–45 Bryniarski et al.[21] Cottin et al.[22] Daub et al.[23] 64 17 57 52 ± 7 52 ± 16 49 60–65 90 40 1mo 2mo 3mo 5 3 3 65–75% V̇O2max 60–80% 75–85% 70–85% DeBusk et al.[24] 61 ? 30–40 2mo or 6mo 3 70–85% HRmax Dressendorfer et al.[3] 38 55 30–35 5wk 1, 2 or 3 70% V̇O2peak Dugmore et al.[25] Ehsani et al.[26] 36 8 51 ± 1 52 ± 3 ? 30–60 1y 1y 3 3–5 Fioretti et al.[27] Goble et al.[28] Gordon et al.[29] Heldal et al.[30] Holmback et al.[5] Ignone et al.[31] 171 124 7 19 34 46 51 53 50 53 55 53 75 30 70 120 45 70 3mo 2mo 4mo 1mo 3mo 1mo 2 3 3 5 2 6 Kalapura et al.[32] Malfatto et al.[33] 50 39 58 52 30–40 60 3mo 2mo 3 5 65–80% V̇O2peak From 50–60% to 70–80% V̇O2max 60–70% HRmax 75–85% HRpeak Ischaemic cardiac threshold 85% HRmax 70–85% HRmax 80–90% ischaemic cardiac threshold 70–85% HRmax 80% HRmax Marra et al.[34] Nordrehaug et al.[35] Pavia et al.[36] 81 27 27 49 ± 8 55 ± 7 ? 70 180–240 25 (2/wk), 4–6km W (5/wk) 2mo 1mo 3mo 4 5 7 80% HRmax 80% HRmax AT Raineri et al.[37] Stahle et al.[38] Stewart et al.[39] Tavazzi and Ignone[40] 70 50 23 95 ? 71 ± 4 ? 53 ± 9 60 50 20–25 or 8 40 4mo 3mo 10wk 1mo 3 3 3 6 ? Music guided 70–80% HRmax 85–95% HRmax ± ± ± ± 10 8 8 9 ±8 V̇O2max or <45% HRmax HRmax HRmax 35% 59% 26% 22% ↔ 36% ↑b ↑a ↑a ↑b 14% 19% ↑a 31% 16% 27% ↑a ↑a and 22% 20% 17% 14% 24% AT ↑b ↑b ↑a and 33% 32% and 42% ↑ ↑a ↑b ↑ and ↔a ↑b Continued next page 1065 Sports Med 2005; 35 (12) Myocardial infarction Arvan[2] Barletta et al.[19] Training Modalities in Cardiac Rehabilitation  2005 Adis Data Information BV. All rights reserved. Table I. Reports on effects of cardiac rehabilitation on exercise capacity in hospital-based settings 1066  2005 Adis Data Information BV. All rights reserved. Table I. Contd Study Teo and Horgan[41] Tomita et al.[42] van Dixhoorn et al.[43] Vanhees et al.[44] Vanhees et al.[45] Velasco et al.[46] n 15 50 156 24 235 48 Age ± SD (y) 56 ± 6 Session duration (min) 20 Programme duration 2mo Frequency/wk Intensity 3 85% HRmax ? 56 51 ± 1 52 ± 8 52 50–90 30 75 75 75 3mo 5wk 3mo 3mo 3mo 3–5 7 3 3 2–3 50–60% HRR 70–80% HRmax 80% max ex cap ? 85% HRmax Training effect V̇O2a or Wmaxb AT 38% and 54% ↑a 8% and 10% ↑a 6% ↑b 42% ↑a 32% ↑a 19% ↑b ± ± ± ± ± ± ± ± ± 60 40 120 120 45 24 55–65 60 20 60 2wk 6mo 1mo 1mo 2mo 2mo 2mo 2wk 3mo 3mo 7 5 7 7 3 3 3 7 3 3 AT 60–70% V̇O2peak ? ? 80–85% V̇O2max 70% HRR 70–85% HRmax 85% HRmax AT 70–85% HRmax 42% ↑a 36% ↑a 9% ↑a 8% ↑a 7% ↑a 20% ↑a 33% ↑a 15% ↑a 33% ↑a 29–35% ↑a 61 62 58 58 53 51 57 59 58 57 Takeyama et al.[54] Vanhees et al.[45] 13 93 59 ± 6 55 ± 7 60 75 2wk 3mo 7 3 AT ? 23% ↑a 32% ↑a Congestive heart failure Belardinelli et al.[55] 36 Belardinelli et al.[56] 18 Belardinelli et al.[57] 50 55 ± 9 56 ± 7 56 ± 7 40 30 40 2.5mo 2mo 14mo 60% V̇O2peak 40% V̇O2peak 60% V̇O2peak 28% ↑a 17% ↑a 27% ↑a Beneke and Meyer[58] Curnier et al.[59] 16 34 52 ± 7 ? 45 (3d), 15 (2d) 30 3wk 1mo 3 3 3 (2m) to 2 (next 12m) 5 (C), 3 (W) 5–6 50% max ex cap AT 17% ↑a 19% and 15% ↑a Delagardelle et al.[60] Demopoulos et al.[61] Dubach et al.[62] Dziekan et al.[63] 14 16 12 10 57 61 ± 2 56 ± 5 56 ± 4 60 60 120 (7d), 45 (4d) 120 (7d), 45 (4d) 6mo 3mo 2mo 2mo 3 4 7 (W), 4 (C) 7 (W), 4 (C) 75% V̇O2peak 50% V̇O2peak 70–80% HRR 60–80% HRR 10% 30% 23% 24% 8 9 6 6 7 4 7 8 6 ↑a ↑a ↑a ↑a 10% ↑ ↔ ↔ 23% ↑ 21–29% ↑ 12% ↑ 31% ↑ 20% ↑ 31% ↑ 25% and 21% ↑ 38% ↑ 39% ↑ 39% ↑ Continued next page Hansen et al. Sports Med 2005; 35 (12) Coronary artery bypass grafting Adachi et al.[47] 34 Arthur et al.[48] 122 Dubach et al.[14] 17 Dubach et al.[15] 22 Froelicher et al.[1] 28 Haennel et al.[49] 8 Hands et al.[50] 10 Iellamo et al.[51] 45 Lan et al.[52] 20 McConnell et al.[53] 101 Study n Goebbels et al.[64] 12 Age ± SD (y) 56 ± 5 Session duration (min) 120 Programme duration 2mo Frequency/wk Intensity 7 70–80% HRR Training effect V̇O2a or Wmaxb 23% ↑a ↔ Gordon et al.[4] 8 62 ± 11 20 2mo 3 60–70% V̇O2peak Gottlieb et al.[65] 11 67 ± 7 45 6mo 3 Borg RPE 12–13 17% ↑a Hertzeanu et al.[66] 11 61 ± 7 30 5y 2 80% ischaemic HR 78% ↑b 7 54 ± 6 75–105 1mo 5 70–80% HRmax 22% ↑a 11 56 ± 6 30 3y 2 90% of subjective maximal work capacity 44% ↑b 14% ↑a Jette et al.[67] Kellerman et al.[68] AT 25% ↑ Keteyian et al.[69] 15 59 30 3mo, 5–6mo 3 80% HRR Keteyian et al.[70] 21 55 ± 12 33 6mo 3 80% HRR 14% ↑a Keteyian et al.[71] 15 52 ± 11 33 6mo 3 80% HRR 16% ↑a 16% ↑ Kiilavuori et al.[7] 12 52 ± 7 30 3mo 3 50–60% V̇O2peak ↔ 21% ↑ Klainman et al.[72] 20 60 ± 6 30–40 6–9mo 2–3 AT 18% ↑a 19% ↑ [73] 13 60 ± 2 40 2mo 3 85% HRpeak 13% ↑a Maiorana et al. Malfatto et al.[74] 30 62 ± 7 60 3mo 5 40–50% V̇O2peak 18% ↑a McConnell et al.[75] 24 64 ± 8 60 3mo 3 70–85% HRmax 8% ↑a 31% ↑ Meyer et al.[76] 18 52 ± 2 25 3wk 3 (C), 5 (W) 50% max ex cap 20% ↑a 24% ↑ Meyer et al.[77] 18 52 ± 2 25 3wk 3 (C), 5 (W) 50% max ex cap 20% ↑a 24% ↑ 35% ↑ Myers et al.[78] 12 56 ± 5 120 (7d), 45 (4d) 2mo 4 (C), 7 (W) 60–70% V̇O2peak 28% ↑a Scalvini et al.[79] 12 56 20–37 5wk 5 70% Wmax 19% ↑a Shephard et al.[17] 21 62 ± 6 ? 4mo 5 60–70% V̇O2peak 14% ↑a ↔ Sturm et al.[18] 13 55 ± 9 20–50 3mo 2–3 50% V̇O2max 18% ↑a ↔ 23% ↑a Sullivan et al.[80] 12 54 ± 10 60 4–6mo 3–5 75% V̇O2peak Sullivan et al.[81] 12 54 ± 10 60 6mo 3–5 75% V̇O2peak Tyni-Lenne et al.[8] 8 62 ± 11 20 2mo 3 60% Wmax ↔ Wielenga et al.[82] 35 ? 30 3mo 3 60% HRR 8% and 11% ↑a 11% and 9% ↑ 20% ↑ Wielenga et al.[11] 35 62 ± 1 30 3mo 3 60% HRR 10% ↑a Willenheimer et al.[9] 22 64 ± 5 15–45 4mo 2–3 80% V̇O2max ↔ 32 51 ± 9 45 3mo 3 60–70% HRmax ↔ 106 52 ± 4 50 3mo 3 70–85% HRmax 10–28% ↑a ? 40 3mo 3 75–85% HRmax 23% and 27% ↑a 61 ± 11 30–45 3mo 3 70–85% HRmax 16% ↑a Wilson et al.[10] Ades and Grunvald[84] Ades et al.[85] 59 303 15% ↑ ↔ Continued next page 1067 Sports Med 2005; 35 (12) Ades et al.[83] Training Modalities in Cardiac Rehabilitation  2005 Adis Data Information BV. All rights reserved. Table I. Contd 1068  2005 Adis Data Information BV. All rights reserved. Table I. Contd Study Ades et al.[86] n 54 Ades et al.[87] Ades et al.[88] Balady et al.[89] 45 50 778 Braun et al.[90] 48 Age ± SD (y) 70 Session duration (min) 50 Programme duration 3mo Frequency/wk Intensity 3 75–90% HRmax 69 ± 6 58 ± 12 60 ± 11 50 40–50 20–40 3mo 3mo 2.5mo 3 3 3 57 30 3mo 3 85–90% HRmax 65–85% HRmax 75–85% HRmax or 60–88% HRR ? Brochu et al.[91] Brubaker et al.[92] Cannistra et al.[93] 82 25 225 61 ± 12 62 ± 8 54 ± 10 40–45 40 30 3mo 1y 3mo 3 3 3 70–85% HRmax 60–80% HRR 75–85% HRmax Cannistra et al.[94] 82 56 ± 11 30 3mo 3 60–85% HRR 42 171 72 59 ± 9 56 ± 10 58 30–40 30–45 30–45 6mo 6mo 6mo 3–5 3 3 60–85% V̇O2max HR at AT HR at AT Dressendorfer et al.[97] Ehsani et al.[98] Fagard et al.[99] 12 12 26 52 52 63 ± 2 40 30–60 75 4mo 1y 3mo 3 3–5 3 HR at ischaemic threshold 50–70% to 70–80% V̇O2max >60% peak ex cap Fragnoli-Munn et al.[100] 45 ? 40 3mo 3 70–85% HRmax Carlson et al.[13] Digenio et al.[95] Digenio et al.[96] 18 58 186 53 ? 54 ± 1 40 50 45 3mo 10wk or 4wk 1y 3 3 or 5 3 70–85% HRmax 60–80% HRmax 50% or 85% V̇O2peak Joughin et al.[104] Keyser et al.[105] Klainman et al.[72] 93 15 32 57 ± 11 ? ? 30 (C) or 5km (W) 30m 30–40 1.5y 3mo 6–9mo 3 3 2–3 AT 70–85% HRR AT 23 237 24 25 ? 58 52 ± 2 65 ± 8 30–40 30–40 35 or 55 30–40 3mo 3mo 2.5mo 3mo 3 3 2 3 70–85% HRmax 70–85% HRmax 60–85% HRmax HR at AT Lavie and Milani[106] Lavie and Milani[107] McCartney et al.[108] Milani and Lavie[109] 27% and 34% ↑a 17% ↑a 28% ↑a 14% and 20% ↑a 18% and 33% ↑a 6% ↑a 15% ↑a 9% and 7% ↑a AT ↔ 11% ↑ 9% and 11% ↑ ↔a 42% ↑a 31% and 40% ↑a 12% and 17% ↑a 20% ↑a 31% ↑a 9% and 13% ↑a ↔ and 11% ↑ 12% ↑a 11% ↑ 9% ↑a ↔ ↔ to 25% ↑a ↔ to 26% ↑ 33% ↑a 26% ↑a 15% ↑ and ↔b 2% ↑a Continued next page Hansen et al. Sports Med 2005; 35 (12) Hartung et al.[101] Hevey et al.[102] Jensen et al.[103] Training effect V̇O2a or Wmaxb 17% and 19% ↑a 16% ↑a 23% ↑a 37%↑a Session duration (min) 30–40 Programme duration 3mo Frequency/wk Intensity 500 Age ± SD (y) 63 ± 11 3 142 57 ? 6mo 3 Study n Milani and Lavie[110] Morris et al.[111] Myers et al. Myers et [12] al.[112] AT HR at AT Training effect V̇O2a or Wmaxb 16% ↑a 70–85% HRmax 15% ↑a 14% ↑ ↑a 48 52 ± 8 45 1y 3 70–80% HRR 9% 12 56 ± 5 45 (C) and 120 (W) 2mo 7 (W), 4 (C) 60–80% HRR 29% ↑a 51% ↑ 35% and 12% ↑ Nieuwland et al.[113] 130 52 65–80 6wk 2 or 10 60–70% HRR 15% and 12% ↑a Nieuwland et al.[114] 38 ? 15 or 35 1.5mo 3 or 5 60–70% HRR 23% and 28% ↑a Oberman et al.[115] 186 54 ± 9 60 1y 3 50 or 85% V̇O2peak 9% and 11% ↑a ↔ Pierson et al.[16] 20 ? 30 6mo 3 65–80% HRmax 18% and 10% ↑a Savage et al.[116] 15 62 ± 10 60–90 4mo 5–7 50–60% V̇O2peak 21% ↑a Szmedra et al.[117] 14 55 ± 2 30 1.5mo 3 70% V̇O2peak 9% and 12% ↑a al.[118] 361 ? 40 3mo 3 70–85% HRmax 46% and 55% ↑a Williams et al.[119] 361 ? 40 3mo 3 70–85% HRmax 48% and 67% ↑a 72 62 ± 11 120 2mo 2 65–85% V̇O2peak 28% ↑a 59 53 ± 11 22 6mo 3 60% V̇O2peak 27% ↑a 27% ↑ ↑a 12% ↑ Williams et Yu et al.[120] Belardinelli et al. [121] [122] ? 20 2wk 7 80% of AT 19% 8 60 ± 8 20 2wk 7 70% V̇O2peak ↔ Lan et al.[123] 16 50 ± 8 20 3mo 3 AT ↔ and 30% ↑a ↔ and 24% ↑ Lan et al.[52] 24 51 ± 10 20 3mo 3 AT 15% ↑a 10% ↑ AT ↑a Fujimoto et al. Kanaya et al.[6] [124] 16 a Percentual evolution of V̇O2. b Percentual evolution of Wmax. 59 ± 7 60 2wk 7 12% AT = anaerobic threshold; C = cycling; HR = heart rate; HRmax = maximum heart rate; HRpeak = peak heart rate; HRR = heart rate reserve; max ex cap = maximal exercise capacity; peak ex cap = peak exercise capacity; RPE = rating of perceived exertion; V̇O2 = oxygen uptake; V̇O2max = maximal oxygen uptake; V̇O2peak = peak oxygen uptake; W = walking; Wmax = maximal cycling resistance; ? indicates unknown; ↑ indicates increased; ↔ indicates no change. 1069 Sports Med 2005; 35 (12) Oya et al. 20 Training Modalities in Cardiac Rehabilitation  2005 Adis Data Information BV. All rights reserved. Table I. Contd 1070 inclusion into a rehabilitation programme did not seem to necessarily enhance the cardiac patients’ exercise capacity. Well defined training duration, intensity, frequency and modality should have been obligatory. The AT increased from 9%[11] to 51%[12] (n = 1876, mean = 15 ± 10%, median = 11%), although an unchanged AT was also reported.[10,13-18] The reported unchanged AT after training might indicate a need for a well defined training modality structure. From the collected reports in which both V̇O2max and AT were assessed before and after training, AT increased to a lesser or greater extent than V̇O2max or V̇O2peak, indicating a discrepancy in the results.[7,12,33,47,52-54,59,62,63,82,105,113,122] Therefore, the danger of assessing V̇O2max or V̇O2peak without considering the AT is to underestimate[12,33,59,62,63,82,113] or overestimate[47,52-54,105,122] the improvement of the patients’ aerobic capacity. 2.2 Relationships with Baseline Parameters First, we will describe correlation coefficients between training outcome and baseline parameters. In this analysis, the evolution of a training outcome parameter (V̇O2max or V̇O2peak) will be plotted against one or various baseline parameters in order to detect a relationship. Several studies showed relationships between baseline exercise capacity and the evolution of exercise capacity. Patients with low initial maximal work capacity seemed to achieve greater training effects,[4,18,46,77,83,89] while patients with a low initial AT attained a bigger increase of AT.[76] As is the case with healthy subjects, cardiac patients with a low exercise capacity realised greater training effects with any training intervention compared with their fitter counterparts. Various cardiac parameters were found to be of predictive value for the evolution of exercise capacity. Belardinelli et al.[55] showed a positive ventricular contractile response to dobutamine, suggesting hibernating myocardium, at the start of the rehabilitation programme to be a strong indicator of capability for increasing the exercise capacity in CHF patients. Those patients with a larger ventricular functional reserve were capable of inducing greater training effects.[55] Ades et al.[83] showed the pres 2005 Adis Data Information BV. All rights reserved. Hansen et al. ence and magnitude of myocardial ischaemia to be of influence on the reachable training effect. In this heterogeneous population of cardiac patients, those with a baseline exercise-induced myocardial ischaemia experienced lesser training effects compared with those without evidence of ischaemia. Also in this study, the magnitude of ST-segment depression had a similar influence on the training effects. Another study by Belardinelli et al.[56] showed a low baseline thallium 1 uptake score index, indicating a higher myocardial perfusion, to be predictive for a greater increase of maximal exercise capacity in CHF patients. The mechanism by which exerciseinduced ischaemia limits exercise conditioning response may be related to its effect on cardiac performance. The presence of myocardial ischaemia correlates with a reduced maximal cardiac output.[96] Indeed, Gordon et al.[4] showed a high cardiac output response index, defined as the ratio between cardiac output increase and V̇O2 increase during incremental exercise, to be a possible factor for greater training effects in CHF patients. Patients with a high baseline cardiac output difference between start and end of an incremental exercise test, corrected for V̇O2, realised greater training effects.[4] In summary, it seems that an impaired myocardial perfusion and cardiac output response during exercise inhibited the enhancement of the exercise capacity. Velasco et al.[46] found the magnitude of the Rwave amplitude change during the baseline incremental exercise test to affect the training effect in myocardial infarction patients. The R-wave amplitude provides information on the left ventricular structure and/or function. Those patients with bigger changes of this wave during increasing workload achieved greater training effects.[46] The clinical implication of these results, however, remains uncertain. van Dixhoorn et al.[43] also identified several psychosocial variables, such as working status, presence of depression, type-A behaviour and feelings of wellbeing, to be of important predictive value for training success in myocardial infarction patients. In summary, various baseline parameters seem to have a determining influence on the training effects in cardiac patients as a result of rehabilitation. The baseline exercise capacity, presence of hibernating Sports Med 2005; 35 (12) Training Modalities in Cardiac Rehabilitation myocardium, degree of myocardial ischaemia and perfusion, cardiac output and R-wave amplitude evolution during incremental exercise and several psychosocial variables were of predictive value to the training outcome. Several studies used group comparisons in order to detect predictive baseline parameters on the training effects as a result of rehabilitation. In these reports, various subgroups, based on one baseline parameter, were compared with regard to training outcome. The danger of this analysis lies in the possibility of influence of other parameters on training outcome that are not controlled or remain unidentified with the formation of two subgroups. Furthermore, even though a baseline parameter might be significantly different between groups, it still remains to be established whether this isolated discrepancy results in differences in the training outcome between groups. Various investigated baseline parameters seem to have no or minor influences on training outcome in cardiac patients. Age did not seem to be of influence on the training effects in cardiac patients.[11,40,84,87,89,100,118,119] Both older and younger cardiac patients attained comparable training results. Also, sex had no influence on the training effect in cardiac patients,[86,87,89,91,93] although Keteyian et al.[69] showed male patients to accomplish greater training effects than female patients. Despite the fact that training compliance was comparable between men and women in the study by Keteyian et al.[69] (70%), it is not stated explicitly whether the duration of the training session was comparable between groups, since only a minimal and not maximal training session duration was mentioned. β-blockade has no influence on the extent of increase in exercise capacity in cardiac patients.[33,36,59,99,118] Therefore, patients who are treated with β-blockers do not have to alter or modify their training modalities in order to induce a similar training outcome, compared with patients treated without β-blockers. Discrepancies were found in the influence of the baseline left ventricular ejection fraction on training outcome. Goebbels et al.[64] and Jette et al.[67] reported patients with a lower left ventricular ejection fraction to experience greater training effects compared with patients with a higher or normal left  2005 Adis Data Information BV. All rights reserved. 1071 ventricular ejection fraction. On the contrary, Digenio et al.[95] and Szmedra et al.[117] found no differences in training effect between patients with a normal or reduced left ventricular ejection fraction. The disparities in results between studies could be explained by the influence of the investigated patients’ cardiac history. In the study by Digenio et al.,[95] there was a difference in the prevalence of AMIs between the low and normal ejection fraction group. The myocardial infarction area size was known to affect the evolution of exercise capacity.[30,83,125] In the study by Szmedra et al.,[117] no data were given concerning cardiac history and type of cardiac events, and/or resultant cardiac interventions were very heterogeneous. In the reports of Jette et al.[67] and Goebbels et al.,[64] on the contrary, the investigated groups were homogeneous; both the low and normal ejection fraction groups showed a similar cardiac history. Wilson et al.[10] suggested that the baseline cardiac output does not influence the training effects in CHF patients, but Tavazzi and Ignone[40] showed myocardial infarction patients with a lower baseline cardiac output to be less able to achieve a sufficient training effect. Also, Gordon et al.[4] showed in a hospital-based setting that the cardiac output was of influence on the attainable training effects in CHF patients; a higher baseline cardiac output index seemed to predict a better training outcome. The differences between analysing methods could possibly explain the contradictory results between Wilson et al.[10] and Gordon et al.[4] In the study by Gordon et al.,[4] not the assessed baseline cardiac output, but the difference of cardiac output between rest and maximal exercise showed a relationship with the evolution of V̇O2peak. This difference was divided by the patients’ V̇O2 difference between rest and maximal exercise. Wilson et al.[10] only measured the baseline cardiac output at rest. The contradictory results between Wilson et al.[10] and Tavazzi and Ignone[40] might be explained by the difference in current cardiac pathology. Despite a correlation between the extent of myocardial ischaemia and the increase of V̇O2peak,[83] and similar results from group comparison in a study by Ades et al.,[83] other studies showed no difference in training effects between high and low levels of baseline myocardial ischaemia[41,70,96] or ST-segSports Med 2005; 35 (12) 1072 ment elevation.[19] A possible explanation for this contradiction will be given later in this review. Results from a study by Klainman et al.[72] showed the number of occluded coronary vessels at baseline to have an influence on the training outcome in patients with coronary artery disease (CAD). Those patients with a larger number of occluded vessels achieved lesser training effects as a result of rehabilitation. Whether performing a dilatation and/or stenting of the occluded coronary vessels before inclusion into a rehabilitation programme indeed results in a faster progression of exercise capacity remains to be established. It is also unclear whether the type of cardiac population has a determining influence on training effects. Lan et al.[52] found a difference in training outcome between post-CABG and post-PCI patients, while Williams et al.[118] did not find a difference between post-CABG and post-AMI patients. However, in the study by Lan et al.,[52] the postCABG patients had a lower baseline exercise capacity compared with the post-PCI patients. In the study by Williams et al.,[118] the baseline exercise capacity was comparable between both groups. As it is known that cardiac surgery results in a more significant decrease in exercise capacity at the start of the rehabilitation programme, training effects are expected to be greater. However, when baseline exercise capacity is well maintained after cardiac surgery, training effects will be comparable with patients undergoing less invasive or non-invasive cardiac procedures. The baseline exercise capacity seems to be of greater importance for the prediction of training effects than the type of cardiac intervention. Cannistra et al.[94] found similar training outcome results between White and Black female cardiac patients. It seems that there was no influence of ethnic origin on the training effect, although this remains to be established in males.[94] McConnell et al.[53] found no difference in training effect between post-CABG patients with high waist-to-hip ratio compared with post-CABG patients with low waist-to-hip ratio. Bryniarski et al.[21] found no differences in training outcome between normotensive and hypertensive myocardial infarction patients.  2005 Adis Data Information BV. All rights reserved. Hansen et al. In summary, at the start of the rehabilitation programme, the degree of coronary vessel occlusion has its influence on training outcome. Age, sex, ethnic origin and β-blockade treatment do not affect the evolution of exercise capacity. It remains to be established whether the left ventricular ejection fraction, cardiac output, degree of myocardial ischaemia and type of cardiac pathology are of influence. 2.3 Relationship with Associated Parameters The information presented in this section was established through correlation by which the evolution of one training outcome parameter during the training period (V̇O2peak or V̇O2max) was plotted against the evolution of other physiological parameters during the rehabilitation period. Whether an improved exercise capacity is primarily related to improved peripheral metabolism or central cardiac adaptation is under discussion. Several studies have tried to correlate peripheral muscular adaptive events with performance parameters. Belardinelli et al.[57] showed an increased V̇O2peak and lactate threshold to be related to an increased volume density of muscular leg mitochondria in CHF patients. Studies by Demopoulos et al.,[61] Dziekan et al.[63] and Sullivan et al.[80] demonstrated an improved calf hyperaemia, pointing at an improved peripheral vasodilatory capacity, to be related to an increased V̇O2peak, also in CHF patients. Cottin et al.[22] showed an increased V̇O2peak to be related to a decreased depletion of peripheral muscular phosphocreatine levels at an identical workload in myocardial infarction patients. Although these studies identified that an altered exercise capacity was mainly related to peripheral muscular adaptations, other reports did find an association between central cardiac adaptations and improved exercise capacity. Sullivan et al.[80] showed an improved cardiac output to be related to an increased V̇O2peak in CHF patients. Importantly, Lan et al.[123] demonstrated restenosis incidence during the rehabilitation period to be related to the V̇O2peak evolution in post-PCI patients. The important finding from this study was that recurrent coronary occlusion had an inhibiting influence on training effects in cardiac patients. Sports Med 2005; 35 (12) Training Modalities in Cardiac Rehabilitation In summary, an increased exercise capacity as a result of training is associated with an increased leg muscular mitochondrial volume density, peripheral vasodilatory muscular capacity, cardiac output and a decreased restenosis incidence. 3. Effects of Training on Exercise Capacity in Partially or Fully Home-Based Settings As in the hospital-based reports, the content of the home-based rehabilitation programmes is very heterogeneous, which makes a direct comparison of the influence of training modalities on the training effect difficult. 3.1 General Effects Table II shows that V̇O2max or V̇O2peak increased from 9%[126] to 87%[127] (n = 1020, mean = 18 ± 13%, median = 16%). Larsen et al.[128] and Adachi et al.[129] reported no change of exercise capacity as a result of rehabilitation. The AT increased from 14%[130] to 23%[131,132] (n = 80, mean = 19 ± 4%, median = 23%). Similar to the hospital-based reports, the AT increased to a lesser[131] or greater[132] extent than V̇O2peak or V̇O2max. Both the AT and maximal exercise capacity should be assessed to fully describe the patients’ progression in work capacity.[131,132] 3.2 Relationships with Baseline Parameters 3.2.1 Results from Correlation Coefficients As in the hospital-based settings, baseline exercise capacity was also an important predictor of the evolution of exercise capacity[125] in home-based settings. Those patients with a low baseline exercise capacity were shown to achieve greater training effects.[125] Peripheral oxygen extraction seemed to have an important influence on training outcome.[135] Myocardial infarction patients with a small increase in peripheral oxygen extraction during the baseline incremental exercise test achieved the best training results.[135] These results show that baseline peripheral muscular metabolism may be of influence on the training outcome as a result of training. In contrast to the results of hospital-based rehabilitation programmes, age[30,125] and sex[30] did have  2005 Adis Data Information BV. All rights reserved. 1073 a determining influence on the training outcome. Younger male patients attained a greater improvement in exercise capacity compared with older female patients.[30,125] The mechanism behind these contradictory results, between hospital- and homebased interventions, remains to be established. Various cardiac parameters were analysed in order to detect a predictive value on the training outcome. The influence of baseline left ventricular ejection fraction on training outcome is under discussion. In a study by Coats et al.,[140] patients with a low baseline left ventricular ejection fraction accomplished greater training effects compared with patients with a normal left ventricular ejection fraction. However, a subsequent study by Coats et al.[139] showed no relationship between baseline ejection fraction and the improvement of exercise capacity. Uchida et al.[135] showed the baseline cardiac output to be of influence on the training effect. Patients with a high baseline cardiac output achieved greater training effects.[135] Heldal et al.[30] discovered a relationship between peak aspartate aminotransferase, which is a determination of infarction size, and training outcome. Patients with a larger myocardial infarct size experienced greater training effects compared with patients with a smaller myocardial infarction size.[30] In summary, there was an influence of baseline age, sex, cardiac output, degree of myocardial ischaemia and peripheral muscular oxygen extraction on training outcome in cardiac patients. The influence of baseline left ventricular ejection fraction on the evolution of exercise capacity in cardiac patients is currently under discussion. 3.2.2 Results from Patient Group Dividing Sakuragi et al.[125] found the baseline infarction size to be of significant influence on training outcome. As in the previously mentioned results of Heldal et al.,[30] patients with a larger baseline infarction area were capable of experiencing greater improvements in exercise capacity. An important contradiction concerning the influence of baseline myocardial ischaemia degree on the training outcome is clear in this review. A larger baseline myocardial ischaemia area predicted in the hospital-based reports results in lesser training effects[83] or no difference in training outcome,[41,70,96] Sports Med 2005; 35 (12) 1074  2005 Adis Data Information BV. All rights reserved. Table II. Reports on effects of cardiac rehabilitation on exercise capacity in partially and fully home-based settings Study n Age ± SD (y) Session duration (min) Programme duration Frequency/wk Intensity Training effect V̇O2a or Wmaxb AT Acute myocardial infarction Adachi et al.[129] 21 ? 15 2mo 5 80 or 120% HR at AT ↔ and 17%a al.[24] 66 ? 20 2 or 6mo 5 70–85% HRmax 27% and 34% ↑a 105 54 ± 9 120 1mo 5 85% HRmax 49% ↑b 102 55 120 1mo 5 85% HRmax 49% ↑b 26 56 ± 1 30–60 (3d), 10–60 (7d) 1.5mo 3 (C), 7 (W) 70% HRmax 10% ↑a 296 61 ± 9 50 3mo 3–5 50–60% HRR 10% and 16% ↑a 12 60 ± 10 60 3mo 5 50–60% HRR 23% ↑a 64 ± 9 40 6mo 5 60–70% V̇O2peak 31% ↑a DeBusk et Heldal et al.[30] Heldal and Leitch et Sire[133] al.[134] Sakuragi et al.[125] Uchida et al.[135] Coronary artery bypass grafting Arthur et al.[48] Foster et al.[127] Goodman et al.[136] Hands et al.[50] Hedback et al.[137] 120 19 56 ± 9 30 1y 5 From 45% to 70% HRR 87% ↑a 31 53 ± 1 45–60 3mo 5 From 50–60% to 75–80% V̇O2max 11% ↑a 8 56 ± 4 ? 2mo 5 Subjective effort 33% ↑a 49 57 ± 7 30–40 1y 3–5 70% HRmax 32% ↑b Congestive heart failure Adamopoulos et al.[138] 12 62 ± 3 20 2mo 5 70–80% HRmax 16% ↑a Coats et al.[139] 17 62 ± 1 20 2mo 5 60–80% HRmax 18% ↑a Coats et al.[140] 11 62 ± 3 20 2mo 5 70–80% HRmax 17% ↑a Davey et al.[126] 22 64 20 2mo 5 70–80% HRmax 9% ↑a Hambrecht et al.[131] 12 50 ± 12 40–60 (7d) and 60 (2d) 6mo 7 (C), 2 (ball games) 70% V̇O2max 33% ↑a 10 54 ± 4 40 6mo 5 70% V̇O2peak 26% ↑a 20 57 50 (3d), 20 (2d) 4mo 5 70–85% HRmax 19% ↑a Kavanagh et al.[130] 21 62 ± 6 ? 1y 5 50–60% V̇O2peak 17% ↑ (at 16wk)a Larsen et al.[128] 30 67 ± 8 25 (3d), 30 (3d) 3mo 6 80% HRmax ↔ McKelvie et al.[143] 90 66 ± 1 30 1y 3 60–70% HRmax 14% ↑a Meyer et al.[144] 12 63 ± 3 25 6wk 5 70–80% Wmax 12% ↑a 23% ↑ 14% ↑ Continued next page Hansen et al. Sports Med 2005; 35 (12) Hambrecht et al.[141] Hoffmann et al.[142] 15% ↑ 7 2mo 100–170 Percentual evolution of V̇O2. Percentual evolution of Wmax. a b 57 ± 10 29 Yoshida et al.[132] Percutaneous coronary intervention  2005 Adis Data Information BV. All rights reserved. AT = anaerobic threshold; C = cycling; HR = heart rate; HRmax = maximum heart rate; HRR = heart rate reserve; V̇O2 = oxygen uptake; V̇O2max = maximal oxygen uptake; V̇O2peak = peak oxygen uptake; W = walking; Wmax = maximal cycling resistance; ? indicates unknown; ↑ indicates increased; ↔ indicates no change. 80–100% HR at AT 17% ↑a 18% ↑a 65–80% HRmax 3–4 45–60 12 Oldridge et al.[146] 51 ± 2 3mo 50–75% HRR 3–5 30–40 16 Brubaker et al.[145] 61 ± 11 1y 18% ↑a 85% HRmax 3 35–40 83 General Ades et al.[88] 56 ± 9 3mo 26% ↑a AT Training effect V̇O2a or Wmaxb Intensity Frequency/wk Programme duration Session duration (min) Age ± SD (y) n Study Table II. Contd 1075 23% ↑ Training Modalities in Cardiac Rehabilitation while in the home-based studies a greater training effect was found in patients with larger myocardial infarction areas.[30,125] It might be suggested that the initial infarction area is not the determining factor in the extent of training effects in post-myocardial infarction patients;[41,70] rather it might be the progression in recovery of this area that is of importance. When a myocardial infarction occurs and reperfusion is established through PCI or thrombolytic therapy, the question arises as to what will happen in this area. Four possibilities are optional: full repair; stunning myocardium; hibernating myocardium; or necrosis.[147] Stunning myocardium is defined as the mechanical myocardial dysfunction that persists after reperfusion, despite the absence of irreversible damage and despite restoration of normal or near-normal blood flow.[148] Hibernating myocardium is defined as a persistent contractile dysfunction that is associated with reduced coronary blood flow but preserved myocardial viability.[148] In the case of stunning or hibernating myocardium, the cardiac muscle cells are alive, not considering whether they are functional or dysfunctional, which is defined as viable myocardium. In cases of necrosis, the myocardial tissue has lost complete function and no repair will occur.[148] It is possible that only a viable myocardium retains the capability to improve function after training and so contribute to an altered exercise capacity.[55] This is illustrated by a study by Belardinelli et al.,[55] in which a hibernating myocardium, detected by dobutamine infusion, was found to be a predictor for an increased exercise capacity as a result of rehabilitation in CHF patients. Patients without the presence of myocardial hibernation showed a lesser or no improvement in exercise capacity. In order to predict the functional outcome of a myocardial infarction patient, the evolution of the cardiomyocyte recovery and viability needs to be determined. This was not conducted in the conflicting studies. To what extent differences in the functional recovery of myocardial ischaemia contribute to exercise capacity gain as a result of rehabilitation remains to be established. 3.3 Relationship with Associated Parameters Hambrecht et al.[131] looked at peripheral parameters by examining the evolution of volume density of cytochrome c-oxidase-positive mitochondria in Sports Med 2005; 35 (12) Hansen et al. 1076 skeletal muscle cells. They found this parameter to be related to the evolution of V̇O2peak and AT. An increased volume density of cytochrome c-oxidasepositive mitochondria as a result of training was associated with an increased exercise capacity.[131] Further evidence of influential peripheral muscular adaptation on training outcome was provided by Hambrecht et al.[141] They found an association between the evolution of exercise capacity and the evolution of acetylcholine-induced leg blood flow. Uchida et al.[135] also reported an association with the evolution of peripheral oxygen extraction. An improved acetylcholine-induced leg blood flow and facilitated increase of peripheral muscular oxygen extraction during incremental exercise was related to an improved exercise capacity.[135,141] However, cardiac adaptation is also related to improved exercise capacity. Uchida et al.[135] found a correlation between evolution of left ventricular end-diastolic pressure, cardiac output and evolution of V̇O2peak in myocardial infarction patients. An increased cardiac output and decreased left ventricular end-diastolic pressure during peak exercise was related to an increased V̇O2peak as a result of training.[135] In summary, an increased exercise capacity was associated with an increased peripheral muscular mitochondrial volume density, peripheral oxygen extraction, vasodilatory muscular capacity, cardiac output and a decreased left ventricular end-diastolic pressure. 4. Comparison of Training Effect between Hospital- and Home-Based Settings From the collected studies, it was difficult to determine whether hospital- or home-based interventions induced the greatest training effects, since the exercise programmes were very heterogeneous. Only a few direct comparisons between the two intervention strategies were reported.[24,48,50,88,145] These comparisons were made in heterogeneous cardiac patients,[88,145] myocardial infarction patients[24] and CABG patients.[48,50] Convincingly, all studies showed similar results. Hospital- and homebased cardiac rehabilitation programmes induced comparable training effects regarding V̇O2 or metabolic equivalent (MET).[24,48,50,88,145] This could be  2005 Adis Data Information BV. All rights reserved. an important message; most cardiac patients are able to exercise in their familiar home environment, with comparable training effects on exercise capacity.[24,48,50,88,145] Whether the conduction of a homebased rehabilitation programme is medically as safe as a hospital-based programme remains to be established.[149] 5. Influence of Training Modalities on Exercise Capacity Despite numerous studies, only a few hospitaland home-based studies have investigated the optimalisation of training modalities in cardiac rehabilitation. This is very surprising considering the large number of patients included in rehabilitation programmes and the great amount of information available on training modalities in healthy subjects.[150] 5.1 Intensity A few studies have assessed the influence of training intensity on exercise capacity in cardiac rehabilitation. Blumenthal et al.[20] investigated 45 myocardial infarction patients who were divided into two subgroups. Both groups trained three times a week, doing 50–65 minutes of aerobic exercise per session, for 3 months. The first group trained at 65–75% of their V̇O2max, while the second group exercised <45% of their V̇O2max. The V̇O2max increased, respectively, by 13% and 15%, with no significant difference in V̇O2max evolution between groups. These results showed no influence of training intensity on the evolution of maximal exercise capacity. Unfortunately, the AT was not determined. Even in the absence of significant differences in evolution of V̇O2max between the groups, there might be a difference in evolution of the AT.[7,103] Jensen et al.[103] compared a group of patients training at 50% of V̇O2peak with a group training at 85% V̇O2peak for 45 minutes per session, three times a week for 1 year. After 6 months of programme participation, V̇O2peak increased to a comparable extent between groups (7.4% vs 7.5%), while after 1 year the V̇O2peak increased to a slightly greater extent in the high-intensity group (with 9% in the low-intensity group compared with 13% in the highSports Med 2005; 35 (12) Training Modalities in Cardiac Rehabilitation intensity group). In a comparable study design by Oberman et al.,[115] during which the patients trained for 60 minutes per session, V̇O2peak increased greater in the low-intensity group after 6 months of training (6.6% vs 5.6%, low intensity vs high intensity, respectively), and lesser after 1 year of training (9% vs 11%, low intensity vs high intensity, respectively) compared with the high-intensity group. So, a clear picture on the effects of training intensity on V̇O2peak could not be given by these investigations. Nonetheless, there is one study that clearly showed effects of training intensity on V̇O2peak change in cardiac patients.[151] In this study, 21 patients with stable CAD were randomised in two groups and trained at 50–60% or 80–90% of their V̇O2peak, three times a week for 10 weeks. After training programme completion, V̇O2peak increased with 17.9% and 7.9% in the high- and low-intensity groups, respectively. Nonetheless, more studies are needed to verify whether high-intensity training produces a greater increase of V̇O2peak. However, a closer look at the evolution of the AT reveals major differences in outcome to the study by Jensen et al.[103] (increased by 2.5% in the lowintensity group compared with 11% in the highintensity group). These results identified the influence of training intensity on the AT, while the maximal exercise capacity showed a comparable enhancement. In a home-based study by Adachi et al.,[129] the high-intensity training group showed an increased V̇O2peak, while no change occurred in the lowintensity training group, which is in contrast with Jensen et al.[103] and Oberman et al.[115] but in accordance with Rognmo et al.[151] Both groups walked for 15 minutes, 5 days a week for 2 months. The high-intensity group trained at 120% of the heart rate at the AT, while the low-intensity group trained at 80% of the heart rate at the AT. However, the baseline age between groups was not comparable (62 ± 7 years vs 51 ± 11 years). Swain and Franklin[152] conducted a meta-analysis in search of a threshold intensity for aerobic training in cardiac patients. After reviewing 23 studies, the authors could not find a threshold intensity for aerobic training. The evolution of V̇O2peak was not influenced by the training intensity in the reviewed studies. The evolution of the aerobic exer 2005 Adis Data Information BV. All rights reserved. 1077 cise capacity was not analysed in this manuscript. The analysis also showed that 45% of V̇O2max currently could be considered as the minimal effective intensity for improving aerobic capacity in cardiac patients. In summary, the influence of training intensity on maximal exercise capacity has not yet been fully determined. However, the evolution of the AT seems to be sensitive to training intensity. 5.2 Length of Programme In most studies, the interventions with the longest training duration have reported the greatest training effects. In a study by Brubaker et al.,[92] 50 cardiac patients were divided into two groups: the first group trained for 3 months, while the second group extended their programme to 12 months. All patients trained three times a week for 60 minutes at 60–80% of their heart rate reserve. Maximum metabolic equivalent (METmax) increased by 9% in the 3-month group and by 23% in the 1-year group. On the other hand, in a study by Hevey et al.,[102] 58 heterogeneous cardiac patients were divided between a 4-week and 10-week rehabilitation programme. All training sessions lasted 50 minutes, with an intensity of 60–80% of their submaximal heart rate. The 4-week rehabilitation group trained five times a week, while the training frequency of the 10-week rehabilitation group was three times. In this study, METmax improved by 31% in both groups. However, the difference in weekly training frequency between groups made it difficult to assess the influence of training duration on training outcome. An important finding from this report was that a manifest training effect, which normally takes 10 weeks to become manifest, can be achieved at 4 weeks. There seems to be a cut-off point during the progression of the rehabilitation programme at which the evolution of exercise capacity becomes less pronounced.[7,24,25,56,61,62,71,87,123,127,130] These cut-off points were established at 1 month,[62] 6 weeks,[61,123] 2 months,[24,56,127] 3 months,[7,71,87] 4 months[25] and 5 months.[130] However, the interval between the exercise tests was minimally 1 month so that the evolution of the patients’ exercise capacity was not followed at high sensitivity. It remains to Sports Med 2005; 35 (12) 1078 be established through weekly evaluation how this point in time can be determined to calculate the minimum programme duration necessary to induce a significant training effect. Nonetheless, in a study of Hamm et al.,[153] 438 male patients with CAD were followed during 52 weeks of rehabilitation, in which V̇O2peak was measured at baseline, 4, 12, 26, 38 and 52 weeks of training. These investigators found that the highest V̇O2peak was established at 38 weeks of rehabilitation, where after no further improvement was noted. It seems that 38 weeks of exercise training is the minimal programme duration for cardiac patients to improve V̇O2peak maximally. One might question whether there is an influence of admission duration on rehabilitation in cardiac patients. Admission duration is defined as the duration between the manifestation of a cardiac event and the start of an ambulatory rehabilitation as a result of this event. In a study by Braun et al.,[90] an early group of cardiac patients, entering within 6 months of the cardiac event, was compared with a late group, entering between 6 and 24 months after the cardiac event. After 3 months of rehabilitation, peak metabolic equivalent (METpeak) increased to a comparable extent in both groups. For this study, early inclusion after a cardiac event was advised, since the health-beneficial effects of an increased exercise capacity were gained after 3 months following the cardiac event rather than keeping the functional capacity low for a longer duration.[90] However, it remains to be established what the influence of the admission duration might be on training outcome when groups entering 3 and 6 months after the cardiac event are compared. 5.3 Duration of Training Sessions Unfortunately, no studies reported the influence of training session duration on the evolution of exercise capacity. From the collected papers, it remains difficult to discern a pattern, since the training intensity, type of cardiac patient and programme duration are too heterogeneous. Further research on this topic is warranted. 5.4 Frequency of Training Dressendorfer et al.[3] investigated 38 myocardial infarction patients who were divided into three sub 2005 Adis Data Information BV. All rights reserved. Hansen et al. groups. All patients trained with 35–45 minutes of aerobic exercise per session, over 5 weeks. The subgroups trained one, two or three times a week. The exercise intensity was determined at 70% of their V̇O2max. The authors found two and three exercise training sessions a week to induce significantly greater training effects than one exercise training session a week (increased V̇O2max of 14%, 19% and 20% in groups training one, two and three sessions a week, respectively). However, there was no difference in training outcome between the groups training two and three exercise sessions a week. Nieuwland et al.[113] divided 130 cardiac patients into two subgroups. The first group trained twice a day, 5 days a week, while the second group trained twice a week. Both groups trained at an intensity of 60–70% of their heart rate reserve over 6 weeks. As a result of the rehabilitation programme, V̇O2peak increased similarly (15% in the high-frequency group vs 12% in the low-frequency group). However, the AT increased to a greater extent in the highfrequency group (with 35%) compared with the lowfrequency group (with 12%). Tygesen et al.[154] investigated 62 cardiac patients in a home-based study. These patients were divided in two subgroups: the first group trained six times a week and the second group trained two times a week. They trained at 70–80% of their maximal cycling strength for 1 hour per session over 3 months. At the conclusion of the training programme, the high-frequency session group increased their maximal cycling resistance (Wmax) by 29W compared with an increased Wmax of 7W in the low-frequency training group. Unfortunately, V̇O2 was not assessed in this study. In summary, there seems to be an influence of weekly training frequency on training outcome. A high training frequency is shown to induce greater training effects compared with a low training frequency. 5.5 Inclusion of Strength Training Exercises Stewart et al.[39] compared two groups of male myocardial infarction patients. The first group cycled for 20–25 minutes per session at 70–80% of the maximal heart rate, while the second group cycled Sports Med 2005; 35 (12) Training Modalities in Cardiac Rehabilitation for 8 minutes per session at an identical intensity. In the second group, a strength training programme was included. As a result of 10 weeks of training with three training sessions a week, the evolution of V̇O2max was significantly different between groups: a 14% increase in the combined training group and no change in the cycle training group. Also, Delagardelle et al.[155] found positive effects of additional strength exercises on V̇O2peak in patients with CHF. In this study, both groups trained in intervals at 50–75% of V̇O2peak, while one group additionally performed strength exercises at 60% of 1RM. No change of V̇O2peak was found after 40 training sessions in the aerobically trained group, while an increase of 8% was found in the combined aerobically/strength-trained group. However, a closer look at the results reveals that the baseline V̇O2peak was significantly lower in the combined aerobic/ strength-training group, compared with the aerobically trained group, which made a comparison between groups and proper conclusions complicated. Contradictory results were reported by Pierson et al.[16] In this study, an aerobic training group was compared with a combined aerobic-strength training group in a 6-month rehabilitation programme. V̇O2max increased by 18% in the aerobic training group, which was significantly different compared with the 10% increased V̇O2max in the combined aerobic-strength training group. However, a possible bias might have occurred in this study. At baseline, the V̇O2max was significantly higher in the combined aerobic-strength training group (24.1 mL/ kg/min) compared with the aerobic training group (16.9 mL/kg/min). As mentioned in section 3.2.1, a lower baseline exercise capacity was reported to be a predictive factor for a higher increase in exercise capacity as a result of training.[4,18,46,77,83,89] Daub et al.[23] have also reported contradictory results. In this study, 57 male post-myocardial infarction patients were randomised into four subgroups. One group only trained aerobically, while the other three groups also participated in strength exercises. The aerobic training programme consisted of cycling and walking for 40 minutes at 70–85% of the maximal heart rate. In addition, the three strength training groups participated in the following programmes: 20 repetitions at 20% of one repetition maximum (1RM); ten repetitions at 40% of  2005 Adis Data Information BV. All rights reserved. 1079 1RM; and seven repetitions at 60% of 1RM, respectively. As a result of 3 months’ programme adherence, the evolution of V̇O2peak was comparable between groups. No significant differences were found in percentual evolution. Unfortunately, the AT was not measured in these studies. This has been achieved in a study of SantaClara et al.,[156] where 12 control subjects without training were compared with 14 subjects in aerobic training and 14 patients in combined aerobic and strength training, all with CAD. The two exercise groups trained for 1 year, three times a week (30 minutes per session), in which one group also performed strength exercises at eight machines (2 × 8–12 repetitions at 50% of 1RM). Also in this study, no differences were found in the evolution of V̇O2max. However, the anaerobic threshold increased significantly greater in the combined exercise and strength training group. The improvement of the anaerobic threshold as a result of additional strength exercises was probably related to an increased muscular strength, so a lower percentage of maximal contraction was required to perform a similar amount of work. A lesser relative muscle contraction would be expected to produce less lactic acid in the blood, decreasing the need for CO2 elimination, and increasing the anaerobic threshold. Even though the anaerobic threshold is influenced by additional strength training, more studies are needed to describe the influence of strength training on peak work capacity in cardiac patients. 6. Conclusions The most striking finding in this review is the heterogeneous character of the content of the rehabilitation programmes, which makes direct comparison of these programmes difficult. Predictive factors for greater training effects have been found to be: a low baseline exercise capacity and peripheral oxygen extraction; presence of hibernating myocardium; high myocardial perfusion; low degree of coronary vessel occlusion; working status; and improved feelings of wellbeing. It remains to be established to what extent age, sex, left ventricular ejection fraction, cardiac output, degree of myocardial ischaemia and cardiac pathology at the start of the rehabilitation programme have an influence on the training outcome. β-blockade treatment and ethnic origin do Sports Med 2005; 35 (12) Hansen et al. 1080 not influence the evolution of exercise capacity as a result of training. An enhanced exercise capacity as a result of training is associated with: an increased volume density of skeletal muscle mitochondria; peripheral vasodilatory capacity; cardiac output and a decreased left ventricular end-diastolic pressure; depletion of muscular phosphocreatine levels; and degree of restenosis. Comparison of the training effects between home- and hospital-based rehabilitation reveals comparable outcomes. A further search for the optimalisation of training modalities in cardiac rehabilitation shows that longer programme duration induces a greater increase in exercise capacity. In addition, a higher number of training sessions per week are more effective than a lower number of training sessions per week in enhancing work capacity. The AT is sensitive to training intensity and strength exercises, which remains to be established for maximal exercise capacity. However, it is unresolved how long a training session should last. 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