Revised: February 19, 2026
Accepted: May 12, 2026
Published online: June 26, 2026
Processing time: 134 Days and 4.2 Hours
Heart failure is a major global health problem resulting in reduced exercise tolerance, functional capacity, and health-related quality of life (HRQoL). In addition to central cardiac dysfunction, peripheral skeletal muscle abnormalities, particularly involving the knee extensors, substantially contribute to physical limitation. This narrative review synthesizes current evidence regarding the ef
Core Tip: In heart failure, exercise intolerance is caused not only by cardiac dysfunction but also by skeletal muscle dysfunction characterized by atrophy, decreased strength, and impaired muscle metabolism. This condition directly contributes to low peripheral muscle fitness, decreased exercise tolerance, and impaired quality of life. Knee extensor resistance training is an important intervention because it specifically targets the key muscle group involved in daily functional activities. Knee extensor resistance training has been shown to increase muscle strength and endurance, improve oxygen utilization efficiency during activity, and reduce fatigue, thus positively impacting functional activities and quality of life in heart failure patients.
- Citation: Nazir A. Isolated knee extension resistance training and functional outcomes in patients with heart failure: A narrative review. World J Cardiol 2026; 18(6): 119751
- URL: https://www.wjgnet.com/1949-8462/full/v18/i6/119751.htm
- DOI: https://dx.doi.org/10.4330/wjc.119751
Heart failure (HF) is a growing global public health challenge, with an estimated 55 million prevalent cases worldwide in 2021[1]. In the United States, approximately 6.7 million adults aged ≥ 20 years currently live with HF, with projections suggesting further increases in the coming decades. The lifetime risk of developing HF is now estimated at 24%, underscoring the substantial and increasing burden of this condition across populations[2]. HF is not only associated with high morbidity and mortality, but is also characterized by exercise intolerance that significantly limits functional capacity and reduces patients’ health-related quality of life (HRQoL)[3]. These functional limitations are not entirely explained by cardiac dysfunction alone, but also by peripheral skeletal muscle dysfunction (SMD), especially in lower extremity muscle groups such as the knee extensors (quadriceps), which play an important role in daily activities[3-5].
Peripheral muscle dysfunction in HF has been identified as a significant factor correlated with decreased exercise capacity and peak oxygen uptake (VO2 peak). HF patients have significantly lower quadriceps muscle endurance capacity and strength than healthy controls, which in turn contributes to their lower aerobic capacity and physical activity ability[3,6-8].
Targeted resistance training (RT) on lower extremity muscles is increasingly being considered in cardiac rehabilitation due to its potential to improve peripheral adaptation without placing excessive central load on the heart. However, most RT programs in HF incorporate whole-body RT or are combined with aerobic training, so the specific effects of RT on knee extensor muscles on clinical outcomes such as muscular fitness, exercise capacity, and HRQoL have not been synthesized[9].
Previous studies have reported that isolated knee-extensor RT (KERT) can improve exercise capacity in HF patients through peripheral muscle adaptations without increasing maximal cardiac output, highlighting the importance of peripheral mechanisms in exercise intolerance in HF. Targeted lower extremity muscle training has also been associated with improvements in functional capacity and VO2 peak[10-12]. However, the heterogeneity of study designs, exercise protocols, and outcomes used has resulted in the absence of a narrative synthesis that specifically evaluates the impact of KERT on muscle fitness, exercise tolerance, and HRQoL in HF patients.
Therefore, this narrative review synthesized the available scientific evidence regarding the effects of isolated KERT in patients with HF. The aim was to assess the effects of this exercise on muscle strength, exercise tolerance/cardiorespiratory fitness (including VO2 peak or other indicators of exercise capacity), and HRQoL in patients with HF.
This study was conducted as a narrative review aimed at synthesizing the available scientific evidence regarding the effects of KERT in patients with HF. A comprehensive but non-systematic literature search was performed using PubMed and Scopus databases, complemented by Google Scholar as a search engine to identify additional relevant studies. Search terms included combinations of keywords related to HF (e.g., “chronic heart failure”, “HFrEF”, “HFpEF”), intervention (e.g., “knee extensor resistance training”, “isolated knee extension”, “single-leg training”, “dynamic knee extensor”, “quadriceps strengthening”, “quadriceps strength training”), and outcomes (e.g., “muscle strength”, “exercise tolerance”, “6-minute walk test”, “VO2 peak”, “exercise capacity”, “functional capacity”, “VO2 max” “cardiorespiratory fitness”, “physical and mental health”, “health-related quality of life”). The search strategy was intentionally broad, and reference lists of selected articles were manually screened to identify additional relevant publications.
Studies were considered eligible if they were published in English, available in full text, involved adult patients with HF, and investigated isolated or predominantly knee extensor-based RT with reported outcomes related to symptoms, muscle fitness, cardiorespiratory fitness, or HRQoL. Original clinical studies constituted the primary evidence base, while review articles and meta-analyses were examined to support mechanistic interpretation and contextual discussion. Studies were excluded if they were case reports, editorials, conference abstracts, did not clearly describe a KERT protocol, or assessed only acute exercise responses without a structured training intervention. Data extraction focused on study characteristics (author, year, population, training intensity, session duration, frequency, and program length) and outcomes.
The extracted data are presented in tabular, graphical, and narrative formats to facilitate structured comparison across studies. Table 1 summarizes key characteristics of KERT protocols, including subject characteristics, training intensity, session structure, frequency, and program duration, highlighting substantial heterogeneity in load prescription and progression models. Table 2 synthesizes functional outcomes, categorizing results into effects on symptoms (e.g., New York Heart Association class), muscle fitness, cardiorespiratory fitness, and HRQoL. In addition, Figure 1 illustrates the proposed pathophysiological framework linking SMD in HF to functional limitations and the potential mechanistic targets of isolated KERT.
| Ref. | Subject | Intensity | Session duration | Frequency, duration of exercise |
| Jankowska et al[26], 2008 | 10 stable CHF patients (NYHA III) with LVEF 30% ± 5% | 35% of maximum strength in the first week, increasing gradually to 60% in the 12th week | ± 30 minutes/session: 10 minutes warm-up, 10-15 minutes KERT, 5-10 minutes cool-down | 3 times per week; program duration 12 weeks (training phase) + 12 weeks detraining |
| Louis et al[48], 2024 | 70 CHF patients (NYHA I-III) who participated in cardiac rehabilitation | 30% 1RM at the start of training, progressively increased by 5%-10% every 4 sessions as tolerated | 30-45 minutes/session: 10-15 minutes warm-up, 15-20 minutes core training (lower-limb resistance with KERT emphasis), 10-15 minutes cool-down | 2 times per week; program duration 12 weeks |
| Jónsdóttir et al[28], 2006 | 43 CHF patients (NYHA II-III) | 0%-25% 1RM in the initial phase, increasing to 35%-40% 1RM at the end of the study (in some patients) | ± 45 minutes/session: 10 minutes warm-up, ± 35 minutes KERT core training, 5 minutes cool-down | 2 times per week; program duration 5 months |
| Esposito et al[10], 2011 | 6 stable male CHF patients (NYHA II-III, VO2 peak Weber class C/B, LVEF 25% ± 3%) and 6 healthy male controls | Intensity varies, progressively increased based on evaluation every 2 weeks during KERT | ± 50 minutes/session per leg: Knee extension exercises, including light warm-up and stretching | 3 times per week; program duration 8 weeks |
| Hearon et al[11], 2022 | 12 HFpEF patients (> 65 years, EF > 50%) + 9 healthy controls | Individual, progressive intensity; initial steady-state, then 8 minutes × 2 minutes and 4 minutes × 4 minutes intervals, kick rate 30-50 kicks/minute | ± 30 minutes/session per leg (total ± 60 minutes/session) | 3 times per week; program duration 8 weeks |
| Magnusson et al[31], 1996 | Eleven patients with chronic CHF (9 men, 2 women), NYHA II-IV, LVEF 5%-39%, some with idiopathic DCM, some post-MI, stable for ≥ 3 months. Randomized to single-leg strength training or single-leg endurance training | Strength training: Single-leg KERT, 80% of maximum. Endurance training: 65%-75% of peak single-leg workload, using a modified ergometer | Strength training: 4 sets of 6-10 repetitions, 2 minutes rest, 3 seconds of up-and-down movement. Endurance training: 15 minutes of dynamic knee extensor exercises | 3 times per week, duration 8 weeks |
| Gordon et al[34], 1996 | 20 patients with stable CHF (NYHA II-III), LVEF 27% ± 3%, aged 43-73 years | 65% of pretraining PWL at baseline, increasing to 75% | ± 15 minutes per session: Two-legged dynamic knee extensor | 3 times per week; program duration 8 weeks |
| Gordon et al[33], 1997 | 21 patients with stable CHF (NYHA II-III), LVEF 28% ± 3%, aged 43-73 years | One-legged KERT: 35% of absolute peak two-legged workload; two-legged KERT: 65%-75% | ± 15 minutes per session: Dynamic knee extensor | 3 times per week; program duration 8 weeks |
| Laoutaris et al[27], 2013 | Stable CHF patients (NYHA II-III) with LVEF ≤ 40%, CHF due to ischemic or dilated cardiomyopathy, hemodynamically stable for ≥ 3 months | AT: 70%-80% maximal HR. RT: Dynamic KERT 50% 1RM, and upper limb resistance exercises using dumbbells of 1-2 kg, progressively every 2 weeks. BMI: 60% SPImax | AT: 20 minutes during the first week, increased by a minimum of 1 minutes in each training session. Combined ARI: AT: 30 minutes; RT: 3 sets of 10-12 repetitions KERT, 2 sets of 10-12 repetitions elbow flexion, shoulder flexion, and abduction; BMI: 20 minutes. Warm up and cooldown: 5 minutes each | 3 times per week; program duration 12 weeks |
| Tyni-Lenné et al[12], 1996 | 16 stable CHF patients (NYHA II-III) with LVEF < 40% | During the first 4 weeks, 65%, and during the last 4 weeks, 75% of the absolute baseline PWL, bilateral dynamic KERT on a knee extensor ergometer | 60 repeats per minute for 15 minutes. Warm-up: 6 minutes of walking and stretching, and a cooldown of 3 minutes of walking and stretching | 3 times per week; program duration 8 weeks |
| Tyni-Lenné et al[36], 1998 | 24 stable CHF patients (NYHA II-III), 12 males & 12 females, LVEF < 40% | 65% baseline PWL (weeks 1-4), 75% (weeks 5-8) | ± 15 minutes/knee-extensor session + 6 minutes warm-up and 3 minutes cool-down | 3 times per week; program duration 8 weeks |
| Ref. | Types of exercise | Effects on symptoms | Muscle fitness | Cardiorespiratory fitness | Health-related quality of life |
| Jankowska et al[26], 2008 | KERT | Improvement in NYHA clinical status, some effects resolved after detraining | Quadriceps strength increased ± 37% right, ± 31% left | 6MWT distance and total exercise time increased, but VO2 peak did not change | Increases after training, does not persist after detraining |
| Jónsdóttir et al[28], 2006 | KERT | No significant NYHA changes | Quadriceps strength increased significantly | 6MWT distance increased significantly, VO2 peak did not change | The exercise capacity subcategory increased significantly, total HRQoL was not significant |
| Gordon et al[34], 1996 | One-legged and two-legged dynamic KERT | There was no significant change in symptoms | Peak workload on both legs increased significantly, and there was no significant increase on one leg | VO2 peak unchanged | Not reported |
| Gordon et al[33], 1997 | Two-legged dynamic KERT | There was no significant change in symptoms | Quadriceps strength increased | VO2 peak unchanged | Training improved the quality of life |
| Magnusson et al[31], 1996 | Strength training (KERT)/endurance training (one-leg dynamic KERT) | There was no significant change in symptoms | Strength: ± 40% increase in isometric and dynamic strength; Endurance: ± 24% increase in isometric strength | Maximal exercise capacity increased by 10%-18%, and VO2 peak remained unchanged | Not reported |
| Esposito et al[10], 2011 | Single-legged KERT | No change in NYHA | Quadriceps strength increased by 15% | Leg VO2 peak increased to control levels | Not reported |
| Hearon et al[11], 2022 | Isolated KERT | PWR increases, and blood pressure during exercise decreases | Not reported | Absolute and relative VO2 peak increased, along with an increase in a-vO2 difference | Not reported |
| Laoutaris et al[27], 2013 | AT/RT/IMT | Improved functional capacity and clinical status | Quadriceps strength increased | VO2 peak increases | Significant increase |
| Tyni-Lenné et al[12], 1996 | Bilateral dynamic KERT | No significant change in symptoms | PWR increased significantly | 6MWT distance increased significantly | Significant increase |
| Tyni-Lenné et al[36], 1998 | KERT | No significant change in symptoms | PWR increased significantly | 6MWT distance increased significantly | Significant increase |
The narrative synthesis is organized into the following subsections: (1) Pathophysiological mechanisms of SMD in HF; (2) Characteristics and safety profile of isolated KERT protocols; and (3) Functional effects of KERT on muscular fitness, submaximal exercise tolerance, maximal aerobic capacity, and HRQoL.
Chronic HF (CHF) is a systemic disease condition often accompanied by decreased physical activity due to symptoms such as dyspnea and fatigue, which ultimately lead to muscle disuse and low-grade systemic inflammation. This combination of inactivity and systemic inflammation plays a key role in skeletal muscle loss by shifting the balance between muscle protein synthesis and degradation, triggering progressive muscle atrophy. Chronic muscle loss activates local inflammatory signaling pathways in skeletal muscle, further amplifying muscle protein degradation and creating a vicious cycle of atrophy and inflammation. This pathological interaction can develop relatively independently of the initial hemodynamic disturbance and is exacerbated by comorbidities such as diabetes mellitus, obesity, hormonal disorders, and sleep-disordered breathing, which are common in HF patients[13].
Patients with HF exhibit higher levels of skeletal muscle fatigability, particularly in lower extremity muscles, which directly contributes to exercise intolerance and limitations in daily activities. The increased fatigability is associated with changes in skeletal muscle metabolism, including increased glycolytic capacity and decreased oxidative capacity, as well as reduced blood perfusion to active muscles during contraction. Most of the mechanisms underlying muscle fatigability in HF are not fully understood, and knowledge gaps remain regarding the relative contributions of peripheral (muscle) and central or neural factors in causing muscle fatigue. Furthermore, the finding of similar skeletal muscle changes in patients with HF with preserved ejection fraction (HFpEF) suggests that the mechanisms of fatigability are not limited to HF with reduced ejection fraction (HFrEF) and may be a general characteristic of the HF syndrome[7].
Abnormalities in skeletal muscle energy metabolism are important determinants of exercise intolerance in HF, as demonstrated by studies using noninvasive approaches to assess muscle energetic fatigue. One study showed that patients with HFrEF who exhibited severe exercise intolerance had more rapid skeletal muscle high-energy phosphate depletion during exercise than patients with similar cardiac function but without exercise intolerance, suggesting impaired peripheral aerobic energy production. Patients with HFpEF exhibited a more severe degree of energetic abnormalities, characterized by rapid phosphocreatine depletion, increased intramuscular lipids, and marked exercise intolerance. Interestingly, all subjects in the study reached fatigue at relatively similar skeletal muscle energetic levels, indicating a common “energetic ceiling” that limits exercise tolerance in HF. These findings confirm that skeletal muscle, which has greater plasticity than cardiac muscle, is a potential target for therapeutic interventions to improve exercise intolerance[14].
Mitochondrial dysfunction is a key feature of SMD in HF and plays a significant role in the reduction of muscle oxidative capacity. Several studies have shown decreased mitochondrial number and function, impaired oxidative phosph
Recent findings in obese HFpEF suggest that extremity muscle weakness is primarily due to muscle atrophy and impaired isotonic mechanics rather than isometric neuromuscular dysfunction. Morphologically, muscle fiber atrophy, a shift to type IIa, and impaired peripheral muscle perfusion limit oxygen extraction. While the diaphragm exhibits slow compartmental adaptation and relatively preserved capillarization, respiratory dysfunction appears to be minimal in early exercise intolerance[16]. Mitochondrial dysfunction is also a central mechanism in HFpEF, with a significant impact on oxidative capacity and exercise tolerance[17].
Skeletal muscle atrophy in patients with HF is primarily due to increased muscle protein breakdown, not simply decreased protein synthesis. This process is closely linked to increased oxidative stress and activation of intracellular inflammatory mechanisms, which collectively accelerate protein degradation and decrease skeletal muscle mass and function. Activation of the neurohormonal system, particularly angiotensin II, plays a key role in exacerbating mito
In HFpEF, particularly in obese patients, exercise intolerance is closely associated with muscle fiber atrophy, impaired isotonic mechanics, and limited skeletal muscle perfusion. Studies have shown that despite relatively preserved isometric neuromuscular function, muscle shortening velocity and mechanical power are significantly reduced, contributing directly to functional activity limitations[16,18]. Impaired skeletal muscle blood flow during exercise, endothelial dysfunction, and decreased nitric oxide bioavailability led to limited peripheral oxygen extraction and are closely associated with low VO2 peak in HFpEF[19].
SMD in HF is the result of a complex interaction between muscle atrophy, mitochondrial dysfunction, fiber type shift, impaired microvascular perfusion, inflammation, and activation of catabolic pathways (Figure 1). This condition significantly contributes to exercise intolerance, reduced HRQoL, and poor prognosis in HF patients, both HFrEF and HFpEF. Therefore, skeletal muscle is now recognized as an important therapeutic target, and interventions aimed at improving muscle metabolism, perfusion, and strength, including targeted RT, have significant potential to improve patient functional capacity[16,17,20].
Only a limited number of studies have specifically investigated isolated quadriceps or KERT in patients with HF, with substantial heterogeneity in training intensity, duration, and progression protocols (Table 1). In addition, important variations are observed in training load prescription [percentage of 1 repetition maximum (1RM) vs percentage of peak workload], total intervention length, session structure, and whether exercises are performed unilaterally or bilaterally. Consequently, variability in training prescription may underlie differences in the magnitude of strength, functional, and cardiorespiratory adaptations reported in the literature.
The exercise protocol is designed to take into account the patient's cardiovascular condition, tolerance to physical activity, and potential risks that may arise during exercise. Based on Table 1, isolated KERT in HF patients is usually performed with an initial light to moderate intensity, between 0%-35% of 1RM or 30%-65% of peak workload, then progressively increased to 60%-80% of maximal strength depending on patient tolerance. The duration of each training session generally ranges from 15-50 minutes per leg, including a warm-up (5-15 minutes), isolated KERT core exercises (10-35 minutes), and a cool-down (3-15 minutes). Exercises can include single- or double-leg dynamic knee extensions, with repetitions or intervals adjusted according to each study protocol.
Notably, unilateral KERT protocol may allow higher relative local muscle loading with reduced central cardiovascular stress, whereas bilateral protocol may induce greater overall metabolic demand. These methodological differences could partly explain variability in functional and cardiorespiratory outcomes reported in the literature.
Evidence comparing unilateral and bilateral RT demonstrates that bilateral lower-limb exercise elicits significantly higher heart rate and rate-pressure product responses than unilateral exercise, indicating greater central hemodynamic stress when a larger muscle mass is recruited[21]. In addition, cardiovascular responses during RT appear to be closely related to the amount of active muscle mass involved. Exercises engaging larger muscle groups are associated with greater increases in blood pressure and overall cardiac workload, further supporting the physiological distinction between unilateral and bilateral protocols[22].
The most commonly used training frequency is 3 times per week, while the program duration ranges from 8 weeks to 12 weeks, although some studies have used durations up to 5 months or included a detraining phase. Intervention length and progression models also differ substantially between studies, which may contribute to inconsistencies in the magnitude of strength gains, submaximal exercise improvements, and changes in VO2 peak. Training adaptations are known to be influenced by exercise intensity, volume, frequency, and progression strategy, following established principles of overload and dose-response relationships in RT[23,24]. Furthermore, variability in program characteristics has been shown to affect functional and cardiorespiratory outcomes in patients with HF[25]. In general, this approach emphasizes progressive intensity, moderate session duration, and individualized training, aimed at improving qua
Previous studies have shown that isolated KERT has been proven safe and effective for HF patients. Cardiac rehabilitation programs with isolated KERT do not increase the risk of acute cardiovascular or musculoskeletal complications when performed appropriately[26-29]. A meta-analysis found no serious adverse events reported in HF patients undergoing an isolated KERT program with progressive loading up to 80% of 1RM[29]. This exercise contributes to increased muscle strength, functional capacity, and HRQoL without causing significant hemodynamic load[26,29].
In a study involving 10 stable HF patients with left ventricular ejection fraction < 40% and New York Heart Association class III, all patients completed 12 weeks of exercise without significant adverse events. During the training and detraining phases, there were no changes in medication, including diuretic use. During the detraining phase, two patients died (one from stroke 3 weeks after exercise, and one from HF progression 3 months after exercise), and one patient developed acute coronary syndrome 2 months after exercise but underwent successful coronary revascularization and survived. All of these events occurred after the exercise program was completed and are therefore not directly related to the exercise program[26].
Another study showed that in the group given a combination of aerobic training, KERT, and inspiratory muscle training, there was an increase in muscular fitness and exercise tolerance without any adverse events during a five-month exercise program. All patients in the intervention group completed the exercise program, and patients who were readmitted 12 months or 28 months after the study did not experience hospitalization due to worsening HF, confirming that supervised exercise is safe for HF patients[28]. Another study reported that of 12 patients, one patient did not complete the post-training test due to illness, but there were no reports of other adverse events related to the training[10].
A prospective randomized study found that of the total 27 patients were able to complete the exercise protocol safely. No adverse events were reported during the rehabilitation program in the study, which used aerobic training, RT, and body mass index to assess the effects on peripheral skeletal muscle function and exercise capacity. Compliance was excellent for both groups, except for one patient in the combination group who failed to complete the exercise program due to long-distance travel[27].
A critical factor in the safety of KERT is selecting the appropriate intensity and volume of training. A program starting at 35% of 1RM and gradually increasing to 60% over 12 weeks has been shown to cause no hemodynamic compromise or left ventricular overload[26]. A study showed that after 12 weeks of exercise, there were no significant changes in cardiac biomarker parameters, indicating that this exercise did not cause additional cardiovascular stress[26]. The RT knee extension program also did not increase resting blood pressure or trigger arrhythmias in stable HF patients[26,30].
Furthermore, no subjects experienced excessive muscle pain, joint injuries, or worsening clinical conditions in patients undergoing KERT in the cardiac rehabilitation program. Monitoring blood pressure, fatigue levels, and exercise progression are key factors in ensuring safe and optimal training[28,29]. With close clinical supervision and tailored progression protocols, KERT can be a safe and effective component of cardiac rehabilitation.
However, it is important to interpret these safety findings with caution. Most available studies include relatively small sample sizes and short to moderate intervention durations (typically 8-12 weeks), which may limit the detection of rare adverse events and restrict conclusions regarding long-term safety and sustainability. In addition, several studies were conducted in clinically stable, carefully selected HF populations under close supervision, which may reduce generalizability to patients with more advanced disease or multiple comorbidities. Therefore, while current evidence supports the short-term safety of supervised isolated KERT in stable HF patients, larger randomized trials with longer follow-up are needed to more definitively establish its long-term safety and efficacy profile.
Isolated KERT has consistently been shown to improve muscle fitness and strength of the lower extremities, particularly the quadriceps, in patients with stable CHF[26,28]. These findings confirm that skeletal muscle weakness in HF is not entirely irreversible, but rather is largely related to deconditioning due to physical inactivity that remains highly responsive to localized RT stimuli[31,32].
Early intervention studies have shown that isolated KERT of relatively low duration and volume, approximately 15 minutes per session, two to three times per week, can produce a 30%-50% increase in quadriceps strength and endurance within a few weeks[31]. This increase is accompanied by improvements in skeletal muscle oxidative capacity, as indicated by increased activity of mitochondrial enzymes such as citrate synthase and increased muscle capillary density[10,31]. The degree of metabolic and functional adaptations has been reported to be comparable to the training response in healthy, untrained individuals, indicating that skeletal muscle plasticity in mild to moderate HF is relatively preserved[31].
The increase in quadriceps muscle strength is primarily mediated by neuromuscular and functional adaptations, not by structurally significant muscle hypertrophy[26]. Muscle strength increases relatively rapidly from the initial phase of training and can be partially maintained during the detraining period, indicating the dominant role of improvements in motor unit recruitment, synchronization of neuromuscular activation, and efficiency of excitation-contraction coupling[26,31]. This explains why strength gains often occur without significant increases in muscle mass in HF patients[26].
Isolated KERT has also been shown to be safe and does not cause significant increases in hemodynamic stress, as it involves only a small muscle mass and produces minimal systemic cardiovascular demands[28,31]. This approach allows patients with limited cardiac reserve to undergo relatively high-intensity RT to the target muscle without triggering a blood pressure response or excessive sympathetic activation[10,31]. Therefore, KERT is highly relevant as an initial rehabilitation strategy for HF patients who are unable to tolerate whole-body exercise[26].
A recent meta-analysis showed that the addition of RT, including isolated KERT, provided significant additional improvements in quadriceps muscle strength compared to aerobic training alone, with effect sizes ranging from moderate to large. This improvement in strength has important clinical implications, given that lower extremity muscle weakness is an independent predictor of decreased functional capacity, limitations in daily activities, and a poorer prognosis in patients with HF[32].
The extent of muscle strength increase resulting from KERT is influenced by several factors, including training intensity, load progression, program duration, and the patient's initial SMD level[26,31]. Protocols with intensities of approximately 40%-60% to 80% of maximal strength, performed progressively with 6-10 repetitions per set for a minimum of 24 sessions, have been reported to increase muscle strength by up to 40% and muscle cross-sectional area by approximately 10% in some patients[31]. In contrast, smaller or non-significant responses are often associated with training loads that are not progressively increased, intervention duration that is too short, or the presence of advanced myopathy and persistent systemic inflammation[26].
Although KERT is effective in increasing maximal strength and muscular endurance, most studies report that these increases occur primarily with slow, controlled contractions[31,32]. These results showed that the effect of KERT on muscle power or the ability to produce force quickly is still limited, so this exercise needs to be combined with other modalities if the rehabilitation goal includes improving explosive function or preventing falls in elderly patients[32].
Although isolated KERT only involves a relatively small muscle mass, various studies have shown that this intervention is able to increase exercise tolerance significantly in patients with CHF[33,34].
Local exercise performance: At the local level, KERT improves quadriceps-specific work capacity, reflected by increased peak workload and endurance during isolated knee extension tests[34]. These improvements are primarily mediated by peripheral skeletal muscle adaptations, including increased oxidative enzyme activity such as citrate synthase (approximately 30% increase), which enhances metabolic efficiency and reduces lactate production at submaximal workloads[33,34]. Reduced lactate accumulation delays peripheral fatigue and improves local muscular endurance[33].
Whole-body functional capacity (submaximal performance): Importantly, these peripheral adaptations translate into improvements in whole-body functional performance. Several studies report increased 6-minute walk test distance and higher peak work rates during submaximal exercise testing following KERT[12,33]. In one study, 8 weeks of bilateral KERT resulted in a 40%-50% increase in 6-minute walk test (distance despite no significant change in VO2 peak[33].
Mechanistically, improved submaximal tolerance is associated with enhanced ventilatory efficiency, reflected by a reduction in VE/VO2 at comparable workloads. KERT has also been shown to attenuate peripheral ergoreflex activation, reducing excessive ventilatory drive and sympathetic activation during exercise. From a neurohumoral perspective, reductions in plasma norepinephrine during submaximal exercise suggest decreased sympathetic stress and improved peripheral hemodynamic efficiency[33]. Collectively, these adaptations improve the ability to sustain daily physical activities, which are predominantly performed at submaximal intensities in HF patients[12].
Maximal aerobic capacity (VO2 peak): In contrast, changes in maximal aerobic capacity are less consistent. Most studies report no significant increase in VO2 peak following isolated KERT, regardless of whether single- or double-limb protocols are used[12,31]. This likely reflects the limited central cardiovascular stimulus associated with training a relatively small muscle mass, as VO2 peak is strongly dependent on maximal cardiac output and total active muscle mass during exercise[10,11,35].
However, small but consistent increases in VO2 peak have been observed in selected subgroups, particularly women with CHF, possibly reflecting greater baseline deconditioning and enhanced peripheral-to-central integration after training[36]. These findings should be interpreted cautiously, as the magnitude of improvement appears to be influenced by patient characteristics, including sex, baseline functional status, and severity of deconditioning. Moreover, meta-analyses evaluating RT as a single intervention demonstrate modest but statistically significant increases in VO2 peak compared with controls, although the effect size is smaller than that observed with aerobic training[29].
Clinically, the improvement in exercise tolerance achieved through KERT is highly relevant, given that daily activities in HF patients are mostly performed at submaximal intensities. Improving the ability to maintain physical activity with milder symptoms has the potential to have a greater functional impact than simply increasing maximal aerobic capacity[12].
HRQoL is a very important clinical outcome in patients with CHF, because it reflects the impact of the disease and therapy on physical function, symptoms, emotional status, and the ability to carry out daily activities[37]. Limited functional capacity, fatigue, and persistent dyspnea are known to contribute significantly to decreased HRQoL, even more so than the degree of left ventricular dysfunction itself[38].
Several studies have shown that isolated KERT can produce significant improvements in HRQoL, although this intervention is local and does not directly increase maximal aerobic capacity[33,36]. Improvements in HRQoL after KERT were primarily reported in the domains of physical function, activity limitations, and perceived fatigue, which were closely related to increased submaximal exercise tolerance[36].
In one study, women with CHF who underwent isolated KERT showed significant improvements in HRQoL scores as measured using disease-specific instruments, along with increased exercise capacity and decreased symptoms during activities of daily living. These findings suggest that improvements in peripheral muscle function can translate directly into improved perceived quality of life, even without significant changes in central heart function[36].
One of the main mechanisms explaining the improvement in HRQoL after KERT is a decrease in peripheral fatigue and dyspnea during daily physical activity. Metabolic adaptations in skeletal muscle, characterized by increased oxidative enzyme activity and decreased lactate production, allow patients to perform activities with less severe symptoms, thereby increasing self-confidence and functional independence[33].
Furthermore, increased knee extensor muscle strength after KERT contributed to improvements in the ability to perform basic functional activities such as standing from a sitting position, walking, and climbing stairs, which are important components of the physical function domain of HRQoL. These functional improvements are highly clinically relevant, given that lower extremity limitations are often a major factor in reducing quality of life in patients with HF[12].
KERT has also been reported to positively impact psychological aspects of HRQoL, including reduced activity-related anxiety and fear of fatigue or dyspnea. By reducing excessive ventilatory responses and sympathetic stress during submaximal exercise, patients tend to experience increased perceptions of control over symptoms, which contributes to emotional well-being[33].
Interestingly, improvements in HRQoL after KERT are often greater than objective changes in physiological parameters such as VO2 peak[36]. This confirms that HRQoL is more sensitive to changes in submaximal functional capacity and the ability to carry out daily activities than maximal cardiorespiratory fitness indicators[39,40].
However, variability in reported HRQoL outcomes across studies may partly reflect differences in assessment instruments and study design. Both generic tools, such as the Short-Form 36 Items, and disease-specific instruments, such as the Minnesota Living with HF Questionnaire, capture distinct domains and may differ in sensitivity to change following exercise interventions[41-46]. In addition, heterogeneity in intervention duration, supervision intensity, patient selection criteria, and baseline functional status may influence the magnitude of HRQoL improvement, limiting direct comparability between studies[47,48].
Findings from a meta-analysis of RT in HF patients also showed that RT, both as a single intervention and in combination, resulted in significant improvements in HRQoL scores compared to standard care. These positive effects are thought to be mediated by improvements in peripheral muscle function, symptom reduction, and increased participation in social and physical activities[29].
From a clinical perspective, KERT has particular advantages in improving HRQoL in patients with severe limitations or intolerance to full-body aerobic exercise. With its relatively low cardiovascular load, KERT allows patients to exercise safely and comfortably, thereby improving exercise adherence and the sustainability of rehabilitation programs, ultimately positively impacting HRQoL[34].
This review highlights the available evidence for isolated KERT as a relevant local training modality for improving muscle fitness, exercise tolerance, and HRQoL in patients with HF. The focus on peripheral adaptations allows for a more specific understanding of the functional benefits of KERT, particularly on submaximal capacity and activities of daily living, despite the lack of consistent improvements in VO2 peak. The main limitations of this review are the limited number of studies, heterogeneity in training protocols and outcomes, and the predominance of designs with small sample sizes. Furthermore, assessment of HRQoL and long-term outcomes was not conducted consistently, and as a narrative review, this article does not include a systematic risk of bias assessment. Future studies are needed to evaluate the effects of KERT with controlled designs, standardized protocols, and long-term follow-up, and to clarify the relationship between peripheral muscle adaptations, increased submaximal exercise tolerance, and improved HRQoL in patients with HF.
Based on the evidence synthesized in this narrative review, isolated KERT appears to be a clinically meaningful non-pharmacological intervention to improve quadriceps strength and submaximal functional capacity in patients with CHF. Peripheral adaptations, including improved metabolic efficiency and reduced symptom burden during daily activities, primarily mediate these benefits. However, substantial heterogeneity exists in training protocols across studies, including differences in intensity prescription, progression models, session structure, unilateral vs bilateral execution, and in
Changes in VO2 peak are inconsistent and appear to depend on baseline conditioning and training characteristics, highlighting the distinction between local muscular adaptations and central cardiovascular responses. Improvements in HRQoL are frequently reported, particularly in domains related to physical function. However, the magnitude of effect varies across studies and may be influenced by differences in assessment instruments and study design.
KERT has demonstrated a favorable safety profile in supervised and clinically stable CHF populations. However, most available studies involve small sample sizes, short intervention durations, and heterogeneous training protocols, which may limit generalizability and long-term interpretation.
Overall, current evidence supports the inclusion of isolated KERT as a complementary component within cardiac rehabilitation programs, particularly when the primary goals are improvement in submaximal functional capacity, HRQoL, and functional independence. Further research is warranted to clarify optimal protocol design and long-term outcomes.
The author would like to thank Universitas Padjadjaran and Dr. Hasan Sadikin General Hospital for database facilitations.
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