Skip to main content
NCBI home page
Sports Medicine - Open logoLink to Sports Medicine - Open
. 2026 Apr 15;12:45. doi: 10.1186/s40798-026-00994-2

Resistance Exercise: A Potential Intervention for Managing Cardiovascular Health in Individuals with a History of Cancer

Alexander M Brooks 1,✉, Abbi D Lane 2, Amy A Kirkham 3,4, Ciaran M Fairman 1
PMCID: PMC13083563  PMID: 41984271

Abstract

Background

Cardiovascular disease (CVD) is a significant long-term health risk for survivors of cancer, particularly those who have received chemotherapy. Mitigation strategies for cancer treatment-related cardiovascular toxicity traditionally include dose reduction, early cessation of cardiotoxic treatments, pharmacological interventions, and lifestyle modifications such as dietary adjustments and increased physical activity. While aerobic exercise is well-documented for its cardioprotective effects, the role of resistance exercise in this context remains inadequately explored.

Main Text

This review examines the potential of resistance exercise to mitigate cardiovascular toxicity in survivors of cancer by addressing key mechanisms such as oxidative stress, mitochondrial dysfunction, chronic inflammation, and ectopic fat accumulation. Additionally, resistance exercise has shown promise in enhancing muscle quality and strength, factors closely linked to CVD risk and mortality. Despite encouraging results from studies in non-cancer populations, evidence within oncology settings remains sparse and inconsistent. The combined application of aerobic and resistance exercise may offer synergistic benefits for cardiovascular health and overall physical function.

Conclusions

Future research should prioritize investigating the independent and combined effects of resistance exercise, optimizing exercise prescriptions to improve cardiovascular outcomes and quality of life in survivors. This review highlights the imperative for further research to elucidate the full cardioprotective potential of resistance exercise in this population.

Keywords: Cardio-Oncology, Toxicity, Strength Training, Supportive Care

Key Points

  • Individuals treated for cancer, particularly with chemotherapy, face a markedly higher risk of developing CVD compared to those without a history of cancer. Therefore, there is a need for effective therapeutic strategies to manage cardiovascular health in this population.

  • Resistance exercise has demonstrated effects in terms of combating several key mechanisms of cardiovascular toxicity in cancer. In addition to this, resistance exercise offers distinct advantages compared to aerobic exercise in improving muscle quality and strength, which are modifiable risk factors for CVD.

  • Although preliminary studies indicate cardiovascular benefits of resistance exercise for survivors of cancer, significant knowledge gaps remain. Further research is essential to understand the effects of resistance exercise, both alone and in combination with aerobic exercise, to better prevent and mitigate the adverse cardiovascular effects commonly experienced by this population.

Background

Cardiovascular disease (CVD) is one of the greatest long-term health concerns for individuals previously treated for cancer [1]. In fact, individuals with a history of cancer can have a 2–6-fold greater risk for CVD compared to cancer-free controls, regardless of cancer site and independent of traditional CVD risk factors [2]. The etiology of this excess risk is partially attributed to cardiac and vascular damage caused by chemotherapy (particularly anthracyclines), thoracic radiation, and other cardiotoxic cancer therapies [3, 4]. This damage can manifest as hypertension, arrhythmias, coronary artery disease, left ventricular dysfunction and ultimately, heart failure, placing individuals treated for cancer at an elevated risk of CVD mortality compared to the general population [2].

Current strategies to attenuate cancer-treatment related cardiovascular toxicity include reducing the dose of cardiotoxic treatments, terminating treatment early, or pharmacological intervention with heart failure treatments [5]. In addition to this, lifestyle behaviors (e.g., physical activity, diet) have also been investigated as potential strategies to mitigate cardiovascular toxicity [6]. Exercise training is a well-documented nonpharmacologic intervention that has demonstrated cardiovascular benefits in non-cancer cardiology settings [7]. Likewise, there is a growing body of evidence suggesting beneficial effects of exercise for those exposed to cardiotoxic cancer treatments [8–12], leading to the development of exercise cardio-oncology referral recommendations and exercise rehabilitation guidelines [13, 14].

Based on the specificity of effects on the heart and vascular system, much of the work in exercise cardio-oncology has focused on aerobic exercise as a countermeasure to cardiovascular injury [15]. However, compared to aerobic exercise, resistance exercise provides greater benefits in terms of improvements in muscle quality and strength [16]. This is notable given the growing body of evidence indicating that impaired muscle quality and dynapenia (muscle weakness) are modifiable risk factors for CVD and are associated with increased CVD related mortality [17, 18]. In addition, evidence supports the independent cardiovascular effects of resistance exercise as demonstrated by improvements in blood pressure and vascular function [19, 20]. Despite the potential benefits, clinical investigations into the use of resistance exercise to offset the cardiotoxic effects of cancer treatments and/or preserve cardiovascular health in survivors are relatively scarce. The broader inclusion of resistance exercise into preventative measures and/or cancer rehabilitation programs could provide synergistic and complementary improvements to cardiovascular health and global wellbeing in cancer. Therefore, the purpose of this review is to discuss the potential role of resistance exercise in (1) mitigating cancer treatment-related cardiovascular injury and (2) improving the overall health and physical function of individuals treated for cancer.

Resistance Exercise as A Potential Countermeasure to Cardiovascular Toxicity in Cancer

The incidence of cardiovascular toxicity in individuals treated for cancer can vary, with estimates ranging from 10% to 40% [21, 22]. This variation is likely due to differences in the definitions of toxicity, patient demographics, treatment modalities and their combinations, and cumulative doses of treatment [23]. The most common method for assessing cardiovascular toxicity in clinical practice and trials involves monitoring changes in left ventricular ejection fraction (LVEF). Typically, this assessment identifies a significant reduction in LVEF, defined as a decrease of more than 10% points to a value below 53% [24]. However, LVEF alone may not capture the full spectrum of cardiovascular damage, as many signs of toxicity can occur without significant LVEF changes. For instance, women treated for breast cancer commonly exhibit characteristics of heart failure with preserved ejection fraction, defined by symptoms such as reduced exercise tolerance, sarcopenia, skeletal muscle dysfunction, diffuse vascular abnormalities, and increased 5- and 10-year mortality rates [25]. Furthermore, cardiovascular toxicity is often evaluated during or shortly after cancer treatment, potentially leading to underestimation of long-term risk and impact. Evidence suggests that the excess risk of cardiovascular mortality persists for at least 10 years after a cancer diagnosis, indicating that many individuals are at risk long after treatment cessation [2].

The underlying pathogenesis of cardiovascular toxicity involves various off-target effects of treatment, including oxidative stress, mitochondrial dysfunction, chronic inflammation, and more recently identified, ectopic fat accumulation [26, 27]. These effects interact synergistically to produce structural and functional damage to the heart and vasculature, resulting in cardiovascular toxicity (Fig. 1). Continued research into novel cardioprotective strategies, particularly those that target the mechanisms of cardiovascular toxicity, is paramount to improve the overall quality of life and long-term outcomes for individuals treated for cancer. Therefore, in the following sections we review the potential for resistance exercise to mitigate the onset and/or severity of the cardiotoxic effects of treatment as well as combat the deterioration of muscle quality and physical function that often accompany them.

Fig. 1.

Fig. 1

Open in a new tab

Mechanisms contributing to the development of cardiovascular toxicity in individuals treated for cancer

Oxidative Stress

Oxidative stress has been implicated in the pathology of a range of adverse cardiovascular side-effects associated with cancer treatments, particularly chemotherapy, radiation, and targeted therapies [28]. For example, alkylating agents induce DNA cross-links, resulting in strand breaks and inhibition of cell division, while antimetabolites resemble cellular precursors, thereby disrupting DNA synthesis [29]. Although these mechanisms effectively target rapidly dividing cancer cells, they can also inadvertently harm healthy cells with high proliferation rates, such as those in the myocardium [3]. When cells are damaged by these treatments, they can release reactive oxygen species (ROS), which are highly reactive molecules containing oxygen atoms, such as superoxide radicals, hydrogen peroxide, and hydroxyl radicals [30]. While ROS are produced naturally as byproducts of various cellular processes (e.g., metabolism or immune responses), an excessive accumulation of ROS can lead to oxidative damage to cellular components like proteins, lipids, and DNA [31]. In turn, this ROS-induced damage can impair the structural integrity and functional capabilities of cardiac cells, leading to cardiomyocyte inflammation, fibrosis, calcium dysregulation, mitochondrial dysfunction as well as vascular dysfunction, contributing to reductions in cardiovascular health [32].

Regular exercise has been demonstrated to reduce oxidative stress in non-cancer populations through an upregulation of the antioxidant defense system, including increased activity of enzymes such as superoxide dismutase, catalase, and glutathione peroxidase [33, 34]. However, a notable gap in our understanding exists, as much of this work has been conducted in otherwise healthy populations performing aerobic exercise [35]. There is a growing body of pre-clinical and clinical work in non-cancer populations suggesting the independent benefits of resistance exercise in terms of reducing cardiac and skeletal muscle related markers of oxidative stress as well as increasing several key antioxidant enzymes [36–46]. Despite positive findings, to our knowledge, there have been no published trials that have investigated the independent effect of resistance exercise on oxidative stress in an oncology setting. However, several studies have found promising results using combined aerobic and resistance exercise interventions [47–49]. Among these, Repka and Hayward conducted a study in which individuals completing chemotherapy and/or radiation were assigned to a 10-week combined aerobic and resistance training intervention or usual care [49]. Compared to usual care, those in the exercise group experienced a significant decrease in markers of oxidative stress as well as a significant within-group increase in antioxidant capacity. Interestingly, a significant association was found between improvements in cancer related fatigue and oxidative stress, indicating a potential causal pathway between the two and a promising area for future investigation.

Collectively, evidence from non-cancer populations suggests that resistance exercise may have the potential to reduce oxidative stress and enhance antioxidant defenses. However, the independent effects of resistance exercise on oxidative stress in oncology settings require further investigation. Although preclinical evidence suggests a potential benefit, there is a need for research in applied settings that investigates the impact of resistance exercise for reducing oxidative stress, and the impact on cardiovascular outcomes.

Mitochondrial Function

Numerous chemotherapy agents such as anthracyclines and cisplatin, as well as targeted therapies like trastuzumab, have been reported to disrupt mitochondria function within skeletal muscle and cardiac cells [50]. This disruption arises from direct treatment induced injury to mitochondria DNA as well as the production of ROS that interfere with mitochondrial enzyme activity and further damage mitochondrial DNA [51]. This presents a vicious cycle in which reductions in mitochondrial function result in oxidative stress, leading to further impairments in energy production and cellular damage [52]. In addition to this, ROS induced mitochondrial damage in cardiac cells alters energy production within the cell via impairments to the electron transport chain and calcium regulating network [53, 54]. These disruptions are associated with the development of arrythmias (e.g., atrial and ventricular fibrillations), and reduced cardiac pumping efficiency, which can ultimately result in heart failure [55].

Several preclinical and clinical studies in non-cancer cardiology settings have found aerobic exercise improves cardiac and skeletal muscle mitochondrial function, including respiration and biogenesis [56, 57]. However, direct evidence from cancer populations is limited. Nilsen and colleagues were among the first to investigate the effects of resistance exercise on skeletal muscle mitochondria function, reporting no significant change following the intervention in men receiving androgen deprivation therapy for prostate cancer [58]. When examining the broader research including otherwise healthy adults and additional clinical populations, studies have produced mixed results, with some reporting increases in markers of mitochondrial biogenesis or oxidative capacity following resistance exercise whereas others report no change [59–61]. Interestingly, this effect appears to be heavily influenced by training status and age, where the impact of resistance exercise on rates of mitochondrial synthesis is greatest in untrained individuals and older adults [62–64]. In line with this, resistance exercise has been found to significantly enhance mitochondrial content and function in older adults and clinical populations such as those with kidney disease and type 2 diabetes [65–68].

Notably, Mijwel and colleagues compared the effects of various exercise programs on mitochondrial content and function in individuals with breast cancer receiving chemotherapy [69]. Participants performed either resistance exercise and high-intensity interval training, aerobic exercise and high-intensity interval training or received usual care for 16 weeks. While usual care led to declines in both mitochondrial content and function, both exercise groups were effective in significantly improving or preserving these markers. In addition to this, the inclusion of resistance exercise resulted in superior improvements to lower body strength compared to aerobic exercise [70]. Although resistance exercise was not studied in isolation, these results suggest that the synergistic effects of resistance exercise and aerobic exercise may have a prominent effect on preserving not only mitochondrial function while receiving chemotherapy, but also improving strength, a finding which warrants further investigation.

In summary, while evidence suggests that resistance exercise may have the potential to positively impact mitochondrial health in non-cancer populations, these results have not yet been replicated in an oncology setting. Furthermore, while the combination of aerobic and resistance exercise may provide a potent countermeasure to mitochondria dysfunction, our current understanding of how changes in skeletal muscle mitochondria may relate to changes in cardiac mitochondria and how these may influence cancer-related cardiovascular toxicity remains limited. As such, further investigation into the effects of resistance exercise on mitochondrial function, both in cardiac and skeletal muscle, represents a promising area for future research.

Chronic Inflammation

Chronic high-grade inflammation is a hallmark feature in many cancer and CVD contexts, particularly those including chemotherapy as part of care [71–73]. Damage-associated molecular patterns are released from injured cells, which activate the immune system and promote a sustained inflammatory response. Chronic inflammation disrupts the cardiovascular system through impairments of endothelial function, reducing the production of vasodilating molecules like nitric oxide, and compromising oxygen delivery to the tissue [74]. This disrupted nitric oxide signaling impedes proper blood vessel dilation, which is linked to elevated blood pressure and more advanced CVD [75]. Further, within arterial walls, persistent inflammation leads to the accumulation of oxidized low-density lipoprotein particles containing cholesterol resulting in atherosclerotic plaques [76]. These plaques can obstruct blood flow, contributing to downstream ischemia, and potentially culminating in myocardial infarction or stroke. In addition, chronic inflammation is associated with the activation of catabolic pathways, inhibition of muscle protein synthesis, and interference with anabolic hormone function, resulting in muscle fatigue, weakness and loss of muscle mass [77]. As such, individuals experiencing chronic inflammation commonly experience decreased exercise tolerance, pain, and slower recovery, further hindering physical function as well as undermining the ability to engage in cardioprotective physical activities [78, 79].

Several clinical trials in individuals with cancer have found combined resistance and aerobic exercise results in significant reductions in pro-inflammatory cytokines [80]. Similarly, evidence from a variety of clinical and non-clinical populations has identified the independent anti-inflammatory effects of resistance exercise [81]. However, findings from trials investigating resistance exercise in isolation in an oncology setting have produced mixed results, with some demonstrating reductions in markers of inflammation [82–84], whereas others have observed no effect [85–87]. The mixed results could be a result of differences in the population studied (i.e., age, disease type, treatment history, and comorbidities), the specific markers of inflammation used, as well as resistance exercise volume, intensity, and duration [88]. Additionally, pro-inflammatory cytokines tend to increase with age and obesity, and have been associated with decreased muscle mass and strength, physical limitations, and poorer metabolic health in older adults [89].

The observation that the most significant reductions in systemic cytokines following resistance exercise are typically seen in older and/or more overweight individuals [90, 91] could clarify why studies have failed to observe a significant reduction in inflammation in cancer survivors who were predominantly normal weight and/or middle-aged [85–87]. For instance, Serra and colleagues reported a significant reduction in several markers of inflammation in older, overweight breast cancer survivors following 16 weeks of resistance exercise, with those with the highest baseline levels experiencing the greatest reduction [92]. This finding suggests that resistance exercise might be particularly effective in managing chronic inflammation, especially in those with more severe inflammatory conditions. The OptiTrain trial also examined the impact of 2 different 16-week exercise interventions on inflammation in women with breast cancer undergoing adjuvant chemotherapy [93]. The exercise intervention involving resistance exercise combined with high-intensity aerobic interval training significantly reduced systemic inflammation compared to usual care yet the exercise intervention involving only aerobic exercise and high-intensity interval training did not affect inflammatory markers [93]. As such, these results would suggest that resistance exercise may confer unique benefits in terms of reducing chemotherapy-induced inflammation.

Overall, a growing body of evidence points to resistance exercise, particularly in combination with aerobic exercise, as a potential intervention to reduce chronic inflammation. Despite these promising early results, further research is warranted to solidify these observations and optimize the implementation of resistance exercise interventions as well as identify the potential cardiovascular health benefits that this may confer.

Ectopic Fat Accumulation

It is well established that the location and distribution of adipose tissue (i.e., fat) is a stronger determinant of CVD risk than the total quantity [94]. For example, subcutaneous fat accounts for 80–95% of total body fat, but essentially acts as storage for positive energy balance and has relatively benign cardiovascular implications [94]. However, when the limit of subcutaneous fat expansion is reached, or in the presence of toxic exposures (e.g., smoking or chemotherapy), fat deposition overflows into ‘ectopic’ sites instead. Although ectopic fat—fat deposited in areas like the viscera, liver cells, around the heart and blood vessels, or within muscle tissue—represents just 5–15% of total body fat, it dramatically raises the risk of coronary artery disease, heart failure, hypertension, and diabetes [95]. Recently, this finding was extended to individuals treated for cancer, where the volumes of visceral and intermuscular fat at the time of a breast cancer diagnosis were linearly related to the risk of cardiovascular events within 6 years of follow-up, even after adjustment for cancer treatment types and pre-existing cardiovascular risk factors [96]. Two different studies have reported that both visceral and intermuscular (thigh and paraspinal) fat accumulates rapidly (within 2–4 months) and persistently (up to 1 year) with receipt of cardiotoxic chemotherapy for early stage breast cancer [97, 98]. Further, accumulation of intermuscular fat within the legs was shown to be significantly inversely correlated with the oxygen extraction within those muscle groups both during and after receipt of chemotherapy [97, 99]. This has major cardiovascular implications as the ability of muscles to extract oxygen from the blood is the key determinant of aerobic capacity beyond cardiac function. Further, the change in visceral fat was found to be inversely correlated with the change in LVEF over the two years after a cancer diagnosis and receipt of cardiotoxic treatment [100].

Each ectopic fat pool has distinct health implications and may respond differently to interventions such as diet and exercise. For example, several trials have demonstrated that resistance exercise significantly reduces visceral fat in individuals with and without obesity [101]. Among individuals treated for cancer, evidence is similar with a meta-analysis of seven resistance exercise intervention studies in prostate cancer survivors finding a significant reduction in visceral fat mass estimated via dual x-ray absorptiometry [102]. However, a meta-analysis of different exercise intervention types among individuals with various chronic diseases found that aerobic exercise and combined aerobic and resistance exercise had larger effect sizes than resistance exercise alone for reductions in intermuscular fat, regardless of intensity [103]. In support of this, Addison et al. reported that weight loss may be a required component of an intervention, whether exercise or dietary, to achieve significant changes in intermuscular fat [104]. Given that weight loss is more difficult to achieve with resistance exercise alone, this may be further evidence to suggest that resistance exercise can be combined with aerobic exercise to have significant effects on intermuscular fat. In a study among older adults with obesity who were pursuing dietary weight loss (via 500–750 kcal deficit), the results indicated that six months of resistance exercise reduced both visceral and intermuscular fat compared to control, but that combined aerobic exercise and resistance exercise had a greater effect than either alone [105].

In summary, the balance of available evidence suggests that combining resistance exercise with aerobic exercise may provide optimal benefits to both visceral and intermuscular fat reduction, which could promote protective effects on overall cardiovascular health. Further work is required to better understand the impact of resistance exercise on ectopic fat in cancer populations, and its subsequent impact on cardiovascular health.

Summary of Resistance Exercise as a Countermeasure to Cardiotoxicity in Cancer

Whilst exercise has garnered a reputation for its cardioprotective effects, the current understanding of the mechanisms through which resistance exercise specifically may contribute to this effect is currently underdeveloped. Preliminary research suggests that resistance exercise may offer benefits in terms of combating select mechanisms of cardiovascular toxicity (Fig. 2). Further, resistance exercise has well-documented benefits in enhancing muscle mass and physical function in individuals treated for cancer, and these effects may be of particular importance for individuals affected by the cardiotoxic effects of treatment. In the following section we discuss the potential of resistance exercise to combat the more global declines in muscle mass and physical function that often accompany impaired cardiovascular health.

Fig. 2.

Fig. 2

Open in a new tab

Preliminary evidence suggests resistance exercise may offset several of the mechanisms contributing to the onset and progression of cardiovascular toxicity in individuals treated for cancer

Resistance Exercise: Combating Physical Decline

Impairments to the cardiovascular system frequently coincide with substantial reductions in skeletal muscle mass and physical function, highlighting the dynamic interplay between the cardiovascular and muscular systems [106, 107]. Among the side effects associated with cancer treatment, unfavorable changes in body composition have received significant attention [108, 109]. Previous studies have reported a 10–15% decline in muscle cross sectional area following 4–6 months of neoadjuvant therapy for breast cancer, a decline comparable to a decade of natural aging in otherwise healthy older adults [110–112]. This presents a significant concern, as diminished muscle mass is a significant risk factor for cardiovascular toxicity and cancer-related mortality [113]. Further, research suggests that nearly 50% of individuals living with and beyond cancer experience physical decline [114], which is not only associated with an increased risk for CVD and mortality, but also negatively impacts their ability to work and carry out activities of daily living [115–119]. Therefore, it is reasonable to suggest that developing interventions to target declines in muscle mass and physical function, could prove to be meaningful in mediating CVD risk in individuals treated for cancer.

Resistance exercise has shown beneficial effects in reducing CVD incidence, cardiovascular-related death, and overall mortality independent of aerobic exercise and after adjusting for physical activity and body mass index in the general population [120]. Evidence from individuals treated for cancer suggests that resistance exercise is not only an effective intervention to improve muscle mass and physical function, but may also provide a more robust stimulus for combating declines in physical function when compared to aerobic exercise [121–125]. By promoting muscle growth and enhancing physical function, resistance exercise may help reduce CVD risk and improve quality of life [126, 127]. Although few studies have investigated the effects of resistance exercise alone on body composition and physical function in CVD populations, several trials have reported significant improvements in body composition (i.e., increased fat-free mass and decreased fat mass) and physical function following combined resistance exercise and aerobic exercise training compared to aerobic exercise alone [128–130]. As such, there is a compelling rationale to further investigate the potential benefits of resistance exercise on cardiovascular health in individuals treated for cancer.

Resistance Exercise: Counteracting Exercise Intolerance

Peak aerobic power (VO2peak) is considered the gold standard for assessing cardiovascular fitness and is a significant independent predictor of overall health and survival in individuals with cancer [131]. Notably, survivors of cancer commonly exhibit a significantly reduced VO2peak compared to non-cancer controls [132]. This observation has been referred to as “exercise intolerance” and reflects the diminished ability to engage in physical activities [133, 134]. The development of exercise intolerance is associated with reduced quality of life and an increased risk for the development of CVD, highlighting the significance of addressing this issue to improve overall prognosis [135, 136].

Exercise intolerance can arise from central (cardiac) and peripheral (skeletal muscle) limitations to oxygen delivery and uptake [137]. For example, skeletal muscle underperfusion (a lack of blood flow to the muscle) is a common cause of exercise intolerance [138]. However, more recent work has suggested that peripheral changes within skeletal muscle may play a more pronounced role in the reduced ability to tolerate physical activity [132, 139]. For example, peripheral changes in skeletal muscle resulting from treatment, including impaired excitation-contraction coupling and substrate oxidation, have been associated with reduced exercise capacity [140, 141]. Additionally, increased intermuscular fat infiltration within thigh skeletal muscle has been identified as a contributing factor to exercise intolerance in individuals treated for cancer [99, 142]. As such, interventions that improve muscle quality may prove advantageous as a treatment strategy. In line with this perspective, resistance exercise alone has demonstrated efficacy in improving VO2peak, particularly in individuals with CVD [143, 144]. Similarly, accumulating evidence indicates that combined training appears to be superior to aerobic exercise for improving VO2peak [145–147].

Although the mechanisms underlying the cardiovascular effects of resistance exercise are currently unclear, it is widely acknowledged that skeletal muscle plays an essential role in facilitating oxidative phosphorylation, metabolic regulation, and the capacity for physical work, all of which appear to be compromised in the context of exercise intolerance [148]. As such, the presence of diminished muscle mass and strength and increased ectopic fat may partially explain why individuals treated for cancer have such difficulties engaging in physical activities, which, in turn, may negatively impact their overall aerobic fitness when compounded over time [149, 150]. Therefore, the augmentation of muscle mass and strength through resistance exercise could serve as a significant connection between impaired VO2peak and exercise intolerance, potentially leading to a reduced risk for the development and progression of CVD (Fig. 3).

Fig. 3.

Fig. 3

Open in a new tab

Resistance exercise has demonstrated benefits in terms of reducing the physical deconditioning that often accompanies cardiovascular and may serve as a potent intervention to offset several key modifiable risk factors such as low muscle mass and physical function

Future Directions

While existing literature provides a strong rationale for incorporating resistance exercise into cardiac rehabilitation programs for older adults and other clinical populations to counteract cardiovascular health decline, direct evidence supporting its efficacy in oncology remains limited. Consequently, several areas remain unexplored (Table 1).

Table 1.

Research questions and considerations for future studies

Future Research Questions Considerations
What independent effects does resistance exercise have in offsetting cardiovascular toxicity resulting from cancer treatments?

− Cancer type and treatment regimen

− Age and presence of comorbid conditions

− Mechanism of effect
Does resistance exercise provide complimentary and/or synergistic effects to aerobic exercise for reducing toxicity and improving well-being? − Outcome measures of interest: left ventricular ejection fraction, arterial stiffness, arterial calcification, circulating biomarkers, physical function, quality of life.
How can the timing, dose, intensity, setting, and combination of resistance exercise and aerobic exercise be manipulated to optimize outcomes?

− Timing within treatment timeline

− Duration of exercise sessions, length of intervention, intensity of exercise sessions, setting of intervention.

− Tailoring exercise interventions to specific cancer/treatment types and populations.
How can resistance exercise and/or aerobic exercise be most effectively disseminated and implemented in oncology settings?

− Strategies for widespread uptake and adherence

− Integration into standard clinical practice
Open in a new tab

In 2019, the American Heart Association introduced Cardio-Oncology Rehabilitation (CORE), a multidisciplinary framework designed to support the cardiovascular health of cancer survivors by adapting principles from traditional cardiac rehabilitation programs used in patients without cancer [151]. CORE places strong emphasis on aerobic and resistance exercise and is broadly aligned with public health and American College of Sports Medicine guidance that recommends accumulating ~ 150 min per week of moderate intensity or ~ 75 min per week of vigorous intensity aerobic activity, together with resistance exercise on at least two days per week [152]. While these recommendations provide a useful starting point, the specificity of resistance exercise guidance remains limited, as current guidelines suggest twice-weekly sessions without specifying duration or volume. Observational data suggest a potential J-shaped relationship, with lower cardiovascular risk observed with up to 60 min per week of resistance exercise, but risk reduction plateauing or even increasing at ≥ 130 min per week [153]. Though intriguing, these findings remain speculative and the dose-response relationship between resistance exercise and cardiovascular risk is relatively unexplored compared to that for cardiovascular exercise. This highlights the need for further research to inform more detailed resistance exercise prescriptions, including session duration, number of sets and repetitions, and exercise intensity, and how these might impact long term cardiovascular health.

There is a need for future research to investigate the role and mechanisms of resistance exercise in offsetting cardiotoxicity, both in isolation and in combination with aerobic exercise. There is also a considerable need to better understand the efficacy and tolerability of different timings, doses, and combinations of exercise modalities to best optimize improvements in cardiovascular health, whole body conditioning, and quality of life in individuals treated for cancer. Continued research in this area may lead to improvements in exercise prescriptions, potentially supporting improved CVD related outcomes for individuals treated for cancer.

Conclusion

The cardiotoxic effects of cancer treatment are amongst the most common and debilitating side effects and increase the risk of CVD incidence and mortality after surviving cancer. In terms of lifestyle interventions to reduce this risk, much of the literature to date has primarily focused on the role of aerobic exercise, with preliminary evidence showing promise. In this review, we have highlighted the potential role of resistance exercise in targeting several of the mechanisms of cardiotoxicity, along with the potential added benefits for muscle health, body composition and physical function in combatting whole body deconditioning that persistently burdens individuals treated for cancer. However, considerable gaps remain in our understanding of the effects of resistance exercise alone or in combination with aerobic exercise to target cardiotoxicity in cancer and these warrant further investigation.

Acknowledgements

Not applicable.

Abbreviations

CVD

Cardiovascular disease

LVEF

Left ventricular ejection fraction

ROS

Reactive oxygen species

Author Contributions

AMB and CMF conceived the idea for the article. AMB conducted the literature search and synthesis. All authors were involved in the critical revision of the work, contributing to the final manuscript.

Funding

No sources of funding were used to assist in the preparation of this article.

Data Availability

Not applicable.

Declarations

Ethics Approval and Consent to Participate

Not applicable.

Consent for Publication

Not applicable.

Competing Interests

The authors declare that they have no competing interests.

Footnotes

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

References

  • 1.Cheng E, Lee DH, Tamimi RM, Hankinson SE, Willett WC, Giovannucci EL, et al. Long-Term Survival and Causes of Death After Diagnoses of Common Cancers in 3 Cohorts of US Health Professionals. JNCI Cancer Spectr. 2022;6(2):pkac021. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Sturgeon KM, Deng L, Bluethmann SM, Zhou S, Trifiletti DM, Jiang C, et al. A population-based study of cardiovascular disease mortality risk in US cancer patients. Eur Heart J. 2019;40(48):3889–97. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Herrmann J. Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia. Nat Rev Cardiol. 2020;17(8):474–502. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Herrmann J. Vascular toxic effects of cancer therapies. Nat Rev Cardiol. 2020;17(8):503–22. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Kourek C, Touloupaki M, Rempakos A, Loritis K, Tsougkos E, Paraskevaidis I, et al. Cardioprotective Strategies from Cardiotoxicity in Cancer Patients: a Comprehensive Review. J Cardiovasc Dev Dis. 2022;9(8):259. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Kirkham AA, Mackey JR, Thompson RB, Haykowsky MJ, Oudit GY, McNeely M, et al. TITAN trial: a randomized controlled trial of a cardiac rehabilitation care model in breast cancer. JACC: Adv. 2023;2(6):100424. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Smith SC Jr, Benjamin EJ, Bonow RO, Braun LT, Creager MA, Franklin BA, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011;124(22):2458–73. [DOI] [PubMed] [Google Scholar]
  • 8.Kirkham AA, Eves ND, Shave RE, Bland KA, Bovard J, Gelmon KA, et al. The effect of an aerobic exercise bout 24 h prior to each doxorubicin treatment for breast cancer on markers of cardiotoxicity and treatment symptoms: a RCT. Breast Cancer Res Treat. 2018;167(3):719–29. [DOI] [PubMed] [Google Scholar]
  • 9.Hojan K, Procyk D, Horyńska-Kęstowicz D, Leporowska E, Litwiniuk M. The Preventive role of Regular Physical Training in Ventricular Remodeling, Serum Cardiac Markers, and Exercise Performance Changes in Breast Cancer in Women Undergoing Trastuzumab Therapy-An REH-HER Study. J Clin Med. 2020;9(5):1379. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Chung WP, Yang HL, Hsu YT, Hung CH, Liu PY, Liu YW, et al. Real-time exercise reduces impaired cardiac function in breast cancer patients undergoing chemotherapy: a randomized controlled trial. Ann Phys Rehabil Med. 2022;65(2):101485. [DOI] [PubMed] [Google Scholar]
  • 11.Foulkes SJ, Howden EJ, Haykowsky MJ, Antill Y, Salim A, Nightingale SS, et al. Exercise for the Prevention of Anthracycline-Induced Functional Disability and Cardiac Dysfunction: the BREXIT Study. Circulation. 2023;147(7):532–45. [DOI] [PubMed] [Google Scholar]
  • 12.Kerrigan DJ, Reddy M, Walker EM, Cook B, McCord J, Loutfi R, et al. Cardiac Rehabilitation Improves Fitness in Patients With Subclinical Markers of Cardiotoxicity While Receiving Chemotherapy: a Randomized Controlled Study. J Cardiopulm Rehabil Prev. 2023;43(2):129–34. [DOI] [PubMed] [Google Scholar]
  • 13.Wilson RL, Christopher CN, Yang EH, Barac A, Adams SC, Scott JM, et al. Incorporating Exercise Training into Cardio-Oncology Care: current Evidence and Opportunities: JACC: cardioOncology State-of-the-Art Review. Cardio Oncol. 2023;5(5):553–69. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Scott JM, Nilsen TS, Gupta D, Jones LW. Exercise therapy and cardiovascular toxicity in cancer. Circulation. 2018;137(11):1176–91. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Kang DW, Wilson RL, Christopher CN, Normann AJ, Barnes O, Lesansee JD, et al. Exercise Cardio-Oncology: exercise as a Potential Therapeutic Modality in the Management of Anthracycline-Induced Cardiotoxicity. Front Cardiovasc Med. 2021;8:805735. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Lee D-c, Brellenthin AG, Lanningham-Foster LM, Kohut ML, Li Y. Aerobic, resistance, or combined exercise training and cardiovascular risk profile in overweight or obese adults: the CardioRACE trial. Eur Heart J. 2024;45(13):1127–42. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Damigou E, Kouvari M, Panagiotakos D. The role of skeletal muscle mass on cardiovascular disease risk: an emerging role on modulating lipid profile. Curr Opin Cardiol. 2023;38(4):352–7. [DOI] [PubMed] [Google Scholar]
  • 18.Artero EG, Lee DC, Lavie CJ, España-Romero V, Sui X, Church TS, et al. Effects of muscular strength on cardiovascular risk factors and prognosis. J Cardiopulm Rehabil Prev. 2012;32(6):351–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Paluch AE, Boyer WR, Franklin BA, Laddu D, Lobelo F, Lee D-C, et al. Resistance exercise training in individuals with and without cardiovascular disease: 2023 update: a scientific statement from the American Heart Association. Circulation. 2024;149(3):e217–31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Liu Y, Lee DC, Li Y, Zhu W, Zhang R, Sui X, et al. Associations of Resistance Exercise with Cardiovascular Disease Morbidity and Mortality. Med Sci Sports Exerc. 2019;51(3):499–508. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.López-Sendón J, Álvarez-Ortega C, Zamora Auñon P, Buño Soto A, Lyon AR, Farmakis D, et al. Classification, prevalence, and outcomes of anticancer therapy-induced cardiotoxicity: the CARDIOTOX registry. Eur Heart J. 2020;41(18):1720–9. [DOI] [PubMed] [Google Scholar]
  • 22.Lima MAC, Brito HRA, Mitidieri GG, de Souza EP, Sobral ACG, Melo H, et al. Cardiotoxicity in cancer patients treated with chemotherapy: a systematic review. Int J Health Sci (Qassim). 2022;16(6):39–46. [PMC free article] [PubMed] [Google Scholar]
  • 23.Curigliano G, Cardinale D, Suter T, Plataniotis G, De Azambuja E, Sandri MT, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23:vii155–66. [DOI] [PubMed] [Google Scholar]
  • 24.Plana JC, Galderisi M, Barac A, Ewer MS, Ky B, Scherrer-Crosbie M, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart Journal–Cardiovascular Imaging. 2014;15(10):1063–93. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Haykowsky MJ, Kirkham AA, Li T, Pituskin E, Thompson RB, Paterson DI, et al. Determinants of oxygen utilization in breast cancer: similarities between heart failure with preserved ejection fraction. Prog Cardiovasc Dis. 2022;74:45–52. [DOI] [PubMed] [Google Scholar]
  • 26.Han X, Zhou Y, Liu W. Precision cardio-oncology: understanding the cardiotoxicity of cancer therapy. NPJ precision Oncol. 2017;1(1):31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Britton KA, Fox CS. Ectopic fat depots and cardiovascular disease. Circulation. 2011;124(24):e837–41. [DOI] [PubMed] [Google Scholar]
  • 28.Deavall DG, Martin EA, Horner JM, Roberts R. Drug-induced oxidative stress and toxicity. J Toxicol. 2012;2012:645460. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Chu E, Sartorelli A. Cancer chemotherapy. Lange’s Basic and Clinical Pharmacology. 2018:948 – 76.
  • 30.Snezhkina AV, Kudryavtseva AV, Kardymon OL, Savvateeva MV, Melnikova NV, Krasnov GS, et al. ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells. Oxid Med Cell Longev. 2019;2019:6175804. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Chen Y, Jungsuwadee P, Vore M, Butterfield DA, St Clair DK. Collateral damage in cancer chemotherapy: oxidative stress in nontargeted tissues. Mol Interv. 2007;7(3):147. [DOI] [PubMed] [Google Scholar]
  • 32.Tsutsui H, Kinugawa S, Matsushima S. Oxidative stress and heart failure. Am J Physiol Heart Circ Physiol. 2011;301(6):H2181–90. [DOI] [PubMed] [Google Scholar]
  • 33.Zhou Z, Chen C, Teo E-C, Zhang Y, Huang J, Xu Y, et al. Intracellular oxidative stress induced by physical exercise in adults: systematic review and meta-analysis. Antioxidants. 2022;11(9):1751. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Ye Y, Lin H, Wan M, Qiu P, Xia R, He J, et al. The effects of aerobic exercise on oxidative stress in older adults: a systematic review and meta-analysis. Front Physiol. 2021;12:701151. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Wang Y, Luo D, Jiang H, Song Y, Wang Z, Shao L, et al. Effects of physical exercise on biomarkers of oxidative stress in healthy subjects: a meta-analysis of randomized controlled trials. Open Life Sci. 2023;18(1):20220668. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Chicco AJ, McCarty H, Reed AH, Story RR, Westerlind KC, Turner RT, et al. Resistance exercise training attenuates alcohol-induced cardiac oxidative stress. Eur J Cardiovasc Prev rehabilitation. 2006;13(1):74–9. [DOI] [PubMed] [Google Scholar]
  • 37.Soufi FG, Saber MM, Ghiassie R, Alipour M. Role of 12-week resistance training in preserving the heart against ischemia-reperfusion-induced injury. Cardiol J. 2011;18(2):140–5. [PubMed] [Google Scholar]
  • 38.Rodrigues EA, Lima ARR, Gomes MJ, Souza LM, Pontes THD, Pagan LU, et al. Influence of Isolated Resistance Exercise on Cardiac Remodeling, Myocardial Oxidative Stress, and Metabolism in Infarcted Rats. Antioxidants. 2023;12(4):896. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Effting PS, Brescianini S, Sorato HR, Fernandes BB, Fidelis GSP, Silva PRLd, et al. Resistance exercise modulates oxidative stress parameters and TNF-α content in the heart of mice with diet-induced obesity. Arquivos brasileiros de cardiologia. 2019;112:545–52. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Mesquita PH, Lamb DA, Godwin JS, Osburn SC, Ruple BA, Moore JH, et al. Effects of resistance training on the redox status of skeletal muscle in older adults. Antioxidants. 2021;10(3):350. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Vincent HK, Bourguignon C, Vincent KR. Resistance training lowers exercise-induced oxidative stress and homocysteine levels in overweight and obese older adults. Obesity. 2006;14(11):1921–30. [DOI] [PubMed] [Google Scholar]
  • 42.Vincent KR, Vincent HK, Braith RW, Lennon SL, Lowenthal DT. Resistance exercise training attenuates exercise-induced lipid peroxidation in the elderly. Eur J Appl Physiol. 2002;87:416–23. [DOI] [PubMed] [Google Scholar]
  • 43.Gambassi BB, Coelho-Junior HJ, Paixão dos Santos C, de Oliveira Gonçalves I, Mostarda CT, Marzetti E, et al. Dynamic resistance training improves cardiac autonomic modulation and oxidative stress parameters in chronic stroke survivors: a randomized controlled trial. Oxidative Med Cell Longev. 2019;2019:5382843. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Alikhani S, Sheikholeslami-Vatani D. Oxidative stress and anti‐oxidant responses to regular resistance training in young and older adult women. Geriatr Gerontol Int. 2019;19(5):419–22. [DOI] [PubMed] [Google Scholar]
  • 45.Padilha CS, Ribeiro AS, Fleck SJ, Nascimento MA, Pina FLC, Okino AM, et al. Effect of resistance training with different frequencies and detraining on muscular strength and oxidative stress biomarkers in older women. AGE. 2015;37(5):104. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Parise G, Brose AN, Tarnopolsky MA. Resistance exercise training decreases oxidative damage to DNA and increases cytochrome oxidase activity in older adults. Exp Gerontol. 2005;40(3):173–80. [DOI] [PubMed] [Google Scholar]
  • 47.Repka CP, Hayward R. Oxidative stress and fitness changes in cancer patients after exercise training. Med Sci Sports Exerc. 2016;48(4):607–14. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.Yen C-J, Hung C-H, Tsai W-M, Cheng H-C, Yang H-L, Lu Y-J, et al. Effect of exercise training on exercise tolerance and level of oxidative stress for head and neck cancer patients following chemotherapy. Front Oncol. 2020;10:1536. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Repka CP, Hayward R. Effects of an exercise intervention on cancer-related fatigue and its relationship to markers of oxidative stress. Integr cancer Ther. 2018;17(2):503–10. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 50.Varga ZV, Ferdinandy P, Liaudet L, Pacher P. Drug-induced mitochondrial dysfunction and cardiotoxicity. Am J Physiol Heart Circ Physiol. 2015;309(9):H1453–67. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51.Gorini S, De Angelis A, Berrino L, Malara N, Rosano G, Ferraro E. Chemotherapeutic Drugs and Mitochondrial Dysfunction: focus on Doxorubicin, Trastuzumab, and Sunitinib. Oxid Med Cell Longev. 2018;2018:7582730. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 52.Chen Q, Vazquez EJ, Moghaddas S, Hoppel CL, Lesnefsky EJ. Production of reactive oxygen species by mitochondria: central role of complex III. J Biol Chem. 2003;278(38):36027–31. [DOI] [PubMed] [Google Scholar]
  • 53.Zhou B, Tian R. Mitochondrial dysfunction in pathophysiology of heart failure. J Clin Investig. 2018;128(9):3716–26. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Dedkova EN, Blatter LA. Calcium signaling in cardiac mitochondria. J Mol Cell Cardiol. 2013;58:125–33. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Brown DA, O’Rourke B. Cardiac mitochondria and arrhythmias. Cardiovascular Res. 2010;88(2):241–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 56.Viloria MAD, Li Q, Lu W, Nhu NT, Liu Y, Cui ZY, et al. Effect of exercise training on cardiac mitochondrial respiration, biogenesis, dynamics, and mitophagy in ischemic heart disease. Front Cardiovasc Med. 2022;9:949744. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Lim AY, Chen YC, Hsu CC, Fu TC, Wang JS. The Effects of Exercise Training on Mitochondrial Function in Cardiovascular Diseases: a Systematic Review and Meta-Analysis. Int J Mol Sci. 2022;23(20):12559. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58.Nilsen TS, Thorsen L, Kirkegaard C, Ugelstad I, Fosså SD, Raastad T. The effect of strength training on muscle cellular stress in prostate cancer patients on ADT. Endocr Connect. 2016;5(2):74–82. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 59.Groennebaek T, Vissing K. Impact of Resistance Training on Skeletal Muscle Mitochondrial Biogenesis, Content, and Function. Front Physiol. 2017;8:713. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60.Parry HA, Roberts MD, Kavazis AN. Human Skeletal Muscle Mitochondrial Adaptations Following Resistance Exercise Training. Int J Sports Med. 2020;41(6):349–59. [DOI] [PubMed] [Google Scholar]
  • 61.Ruegsegger GN, Pataky MW, Simha S, Robinson MM, Klaus KA, Nair KS. High-intensity aerobic, but not resistance or combined, exercise training improves both cardiometabolic health and skeletal muscle mitochondrial dynamics. J Appl Physiol. 2023;135(4):763–74. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62.Donges CE, Burd NA, Duffield R, Smith GC, West DW, Short MJ, et al. Concurrent resistance and aerobic exercise stimulates both myofibrillar and mitochondrial protein synthesis in sedentary middle-aged men. J Appl Physiol. 2012;112(12):1992–2001. [DOI] [PubMed] [Google Scholar]
  • 63.Robinson MM, Dasari S, Konopka AR, Johnson ML, Manjunatha S, Esponda RR, et al. Enhanced protein translation underlies improved metabolic and physical adaptations to different exercise training modes in young and old humans. Cell Metabol. 2017;25(3):581–92. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 64.Wilkinson SB, Phillips SM, Atherton PJ, Patel R, Yarasheski KE, Tarnopolsky MA, et al. Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle. J Physiol. 2008;586(15):3701–17. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65.Melov S, Tarnopolsky MA, Beckman K, Felkey K, Hubbard A. Resistance exercise reverses aging in human skeletal muscle. PLoS ONE. 2007;2(5):e465. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 66.Jubrias SA, Esselman PC, Price LB, Cress ME, Conley KE. Large energetic adaptations of elderly muscle to resistance and endurance training. J Appl Physiol. 2001;90(5):1663–70. [DOI] [PubMed] [Google Scholar]
  • 67.Balakrishnan VS, Rao M, Menon V, Gordon PL, Pilichowska M, Castaneda F, et al. Resistance training increases muscle mitochondrial biogenesis in patients with chronic kidney disease. Clin J Am Soc Nephrology: CJASN. 2010;5(6):996. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68.Sparks LM, Johannsen NM, Church TS, Earnest CP, Moonen-Kornips E, Moro C, et al. Nine months of combined training improves ex vivo skeletal muscle metabolism in individuals with type 2 diabetes. J Clin Endocrinol Metabolism. 2013;98(4):1694–702. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 69.Mijwel S, Cardinale DA, Norrbom J, Chapman M, Ivarsson N, Wengström Y, et al. Exercise training during chemotherapy preserves skeletal muscle fiber area, capillarization, and mitochondrial content in patients with breast cancer. FASEB J. 2018;32(10):5495–505. [DOI] [PubMed] [Google Scholar]
  • 70.Mijwel S, Backman M, Bolam KA, Olofsson E, Norrbom J, Bergh J, et al. Highly favorable physiological responses to concurrent resistance and high-intensity interval training during chemotherapy: the OptiTrain breast cancer trial. Breast Cancer Res Treat. 2018;169:93–103. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71.Chai EZP, Siveen KS, Shanmugam MK, Arfuso F, Sethi G. Analysis of the intricate relationship between chronic inflammation and cancer. Biochem J. 2015;468(1):1–15. [DOI] [PubMed] [Google Scholar]
  • 72.Wang L, Chen Q, Qi H, Wang C, Wang C, Zhang J, et al. Doxorubicin-induced systemic inflammation is driven by upregulation of toll-like receptor TLR4 and endotoxin leakage. Cancer Res. 2016;76(22):6631–42. [DOI] [PubMed] [Google Scholar]
  • 73.Pusztai L, Mendoza TR, Reuben JM, Martinez MM, Willey JS, Lara J, et al. Changes in plasma levels of inflammatory cytokines in response to paclitaxel chemotherapy. Cytokine. 2004;25(3):94–102. [DOI] [PubMed] [Google Scholar]
  • 74.Steyers CM III, Miller FJ Jr. Endothelial dysfunction in chronic inflammatory diseases. Int J Mol Sci. 2014;15(7):11324–49. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 75.Terwoord JD, Beyer AM, Gutterman DD. Endothelial dysfunction as a complication of anti-cancer therapy. Pharmacol Ther. 2022;237:108116. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 76.Hulthe J, Fagerberg Br. Circulating oxidized LDL is associated with subclinical atherosclerosis development and inflammatory cytokines (AIR Study). Arteriosc Thromb Vasc Biol. 2002;22(7):1162–7. [DOI] [PubMed]
  • 77.Draganidis D, Jamurtas AZ, Chondrogianni N, Mastorakos G, Jung T, Grune T, et al. Low-Grade Systemic Inflammation Interferes with Anabolic and Catabolic Characteristics of the Aged Human Skeletal Muscle. Oxid Med Cell Longev. 2021;2021:8376915. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 78.Bower JE. Cancer-related fatigue: links with inflammation in cancer patients and survivors. Brain Behav Immun. 2007;21(7):863–71. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 79.Louati K, Berenbaum F. Fatigue in chronic inflammation-a link to pain pathways. Arthritis Res therapy. 2015;17(1):1–10. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 80.Khosravi N, Stoner L, Farajivafa V, Hanson ED. Exercise training, circulating cytokine levels and immune function in cancer survivors: a meta-analysis. Brain Behav Immun. 2019;81:92–104. [DOI] [PubMed] [Google Scholar]
  • 81.Rose GL, Mielke GI, Durr M, Schaumberg MA. Effect of resistance training on chronic inflammation: a systematic review and meta-analysis. Translational Sports Med. 2021;4(6):900–13. [Google Scholar]
  • 82.Schmidt ME, Meynköhn A, Habermann N, Wiskemann J, Oelmann J, Hof H, et al. Resistance Exercise and Inflammation in Breast Cancer Patients Undergoing Adjuvant Radiation Therapy: mediation Analysis From a Randomized, Controlled Intervention Trial. Int J Radiation Oncology*Biology*Physics. 2016;94(2):329–37. [DOI] [PubMed] [Google Scholar]
  • 83.Hagstrom A, Marshall P, Lonsdale C, Papalia S, Cheema B, Toben C, et al. The effect of resistance training on markers of immune function and inflammation in previously sedentary women recovering from breast cancer: a randomized controlled trial. Breast Cancer Res Treat. 2016;155(3):471–82. [DOI] [PubMed] [Google Scholar]
  • 84.Serra MC, Ryan AS, Ortmeyer HK, Addison O, Goldberg AP. Resistance training reduces inflammation and fatigue and improves physical function in older breast cancer survivors. Menopause (New York NY). 2018;25(2):211–6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 85.Christensen JF, Tolver A, Andersen JL, Rørth M, Daugaard G, Hojman P. Resistance Training Does Not Protect Against Increases in Plasma Cytokine Levels Among Germ Cell Cancer Patients During and After Chemotherapy. J Clin Endocrinol Metabolism. 2014;99(8):2967–76. [DOI] [PubMed] [Google Scholar]
  • 86.Madzima TA, Ormsbee MJ, Schleicher EA, Moffatt RJ, Panton LB. Effects of Resistance Training and Protein Supplementation in Breast Cancer Survivors. Med Sci Sports Exerc. 2017;49(7):1283–92. [DOI] [PubMed] [Google Scholar]
  • 87.Simonavice E, Liu P-Y, Ilich JZ, Kim J-S, Arjmandi B, Panton LB. The effects of a 6-month resistance training and dried plum consumption intervention on strength, body composition, blood markers of bone turnover, and inflammation in breast cancer survivors. Appl Physiol Nutr Metab. 2014;39(6):730–9. [DOI] [PubMed] [Google Scholar]
  • 88.Sardeli AV, Tomeleri CM, Cyrino ES, Fernhall B, Cavaglieri CR, Chacon-Mikahil MPT. Effect of resistance training on inflammatory markers of older adults: a meta-analysis. Exp Gerontol. 2018;111:188–96. [DOI] [PubMed] [Google Scholar]
  • 89.Cesari M, Penninx BW, Pahor M, Lauretani F, Corsi AM, Williams GR, et al. Inflammatory markers and physical performance in older persons: the InCHIANTI study. Journals Gerontol Ser A: Biol Sci Med Sci. 2004;59(3):M242–8. [DOI] [PubMed] [Google Scholar]
  • 90.Greiwe JS, Cheng B, Rubin DC, Yarasheski KE, Semenkovich CF. Resistance exercise decreases skeletal muscle tumor necrosis factor α in frail elderly humans. FASEB J. 2001;15(2):475–82. [DOI] [PubMed] [Google Scholar]
  • 91.Phillips MD, Patrizi RM, Cheek DJ, Wooten JS, Barbee JJ, Mitchell JB. Resistance training reduces subclinical inflammation in obese, postmenopausal women. Med Sci Sports Exerc. 2012;44(11):2099–110. [DOI] [PubMed] [Google Scholar]
  • 92.Serra MC, Ryan AS, Ortmeyer HK, Addison O, Goldberg AP. Resistance training reduces inflammation and fatigue and improves physical function in older breast cancer survivors. Menopause. 2018;25(2):211–6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 93.Hiensch AE, Mijwel S, Bargiela D, Wengström Y, May AM, Rundqvist H. Inflammation Mediates Exercise Effects on Fatigue in Patients with Breast Cancer. Med Sci Sports Exerc. 2021;53(3):496–504. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 94.Després J-P. Body fat distribution and risk of cardiovascular disease: an update. Circulation. 2012;126(10):1301–13. [DOI] [PubMed] [Google Scholar]
  • 95.Zhang P, Konja D, Wang Y. Adipose tissue secretory profile and cardiometabolic risk in obesity. Endocr Metabolic Sci. 2020;1(3–4):100061. [Google Scholar]
  • 96.Cespedes Feliciano EM, Chen WY, Bradshaw PT, Prado CM, Alexeeff S, Albers KB, et al. Adipose tissue distribution and cardiovascular disease risk among breast cancer survivors. J Clin Oncol. 2019;37(28):2528–36. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 97.Kirkham AA, Pituskin E, Mackey JR, Grenier JG, Ian Paterson D, Haykowsky MJ, et al. Longitudinal changes in skeletal muscle metabolism, oxygen uptake, and myosteatosis during cardiotoxic treatment for early-stage breast cancer. Oncologist. 2022;27(9):e748–54. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 98.Kirkham AA, Pituskin E, Thompson RB, Mackey JR, Koshman SL, Jassal D, et al. Cardiac and cardiometabolic phenotyping of trastuzumab-mediated cardiotoxicity: a secondary analysis of the MANTICORE trial. Eur Heart Journal-Cardiovascular Pharmacotherapy. 2022;8(2):130–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 99.Kirkham AA, Haykowsky MJ, Beaudry RI, Grenier JG, Mackey JR, Pituskin E, et al. Cardiac and skeletal muscle predictors of impaired cardiorespiratory fitness post-anthracycline chemotherapy for breast cancer. Sci Rep. 2021;11(1):14005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 100.Reding KW, Ghemigian K, Carbone S, D’Agostino R Jr, Jordan JH, Meléndez G, et al. The relationship between abdominal fat and change in left ventricular ejection fraction in cancer patients. Obes Sci Pract. 2021;7(1):82–90. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 101.Khalafi M, Malandish A, Rosenkranz SK, Ravasi AA. Effect of resistance training with and without caloric restriction on visceral fat: a systemic review and meta-analysis. Obes Rev. 2021;22(9):e13275. [DOI] [PubMed] [Google Scholar]
  • 102.Keilani M, Hasenoehrl T, Baumann L, Ristl R, Schwarz M, Marhold M, et al. Effects of resistance exercise in prostate cancer patients: a meta-analysis. Support Care Cancer. 2017;25:2953–68. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 103.Tuñón-Suárez M, Reyes-Ponce A, Godoy-Órdenes R, Quezada N, Flores-Opazo M. Exercise training to decrease ectopic intermuscular adipose tissue in individuals with chronic diseases: a systematic review and meta-analysis. Phys Ther. 2021;101(10):pzab162. [DOI] [PubMed] [Google Scholar]
  • 104.Addison O, Marcus RL, Lastayo PC, Ryan AS. Intermuscular fat: a review of the consequences and causes. Int J Endocrinol. 2014;2014:309570. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 105.Waters DL, Aguirre L, Gurney B, Sinacore DR, Fowler K, Gregori G, et al. Effect of aerobic or resistance exercise, or both, on intermuscular and visceral fat and physical and metabolic function in older adults with obesity while dieting. Journals Gerontology: Ser A. 2022;77(1):131–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 106.Tyrovolas S, Panagiotakos D, Georgousopoulou E, Chrysohoou C, Tousoulis D, Haro JM, et al. Skeletal muscle mass in relation to 10 year cardiovascular disease incidence among middle aged and older adults: the ATTICA study. J Epidemiol Community Health. 2020;74(1):26–31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 107.Carbone S, Kirkman DL, Garten RS, Rodriguez-Miguelez P, Artero EG, Lee D-c, et al. Muscular strength and cardiovascular disease: an updated state-of-the-art narrative review. J Cardiopulm Rehabil Prev. 2020;40(5):302–9. [DOI] [PubMed] [Google Scholar]
  • 108.Rier HN, Jager A, Sleijfer S, Maier AB, Levin MD. The Prevalence and Prognostic Value of Low Muscle Mass in Cancer Patients: a Review of the Literature. Oncologist. 2016;21(11):1396–409. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 109.Mallard J, Hucteau E, Hureau TJ, Pagano AF. Skeletal muscle deconditioning in breast cancer patients undergoing chemotherapy: current knowledge and insights from other cancers. Front Cell Dev Biology. 2021;9:719643. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 110.Rossi F, Torri L, Lambertini M, De Giorgis S, Calabrese M, Tagliafico AS. Muscle mass loss after neoadjuvant chemotherapy in breast cancer: estimation on breast magnetic resonance imaging using pectoralis muscle area. Eur Radiol. 2020;30(8):4234–41. [DOI] [PubMed] [Google Scholar]
  • 111.Wiederin J, Gu C, Jewett P, Blaes AH. Pectoralis muscle wasting during chemotherapy. Am Soc Clin Oncol. 2020.
  • 112.Volpi E, Nazemi R, Fujita S. Muscle tissue changes with aging. Curr Opin Clin Nutr Metab Care. 2004;7(4):405–10. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 113.van den Berg M, Kok DE, Posthuma L, Kamps L, Kelfkens CS, Buist N, et al. Body composition is associated with risk of toxicity-induced modifications of treatment in women with stage I-IIIB breast cancer receiving chemotherapy. Breast Cancer Res Treat. 2019;173(2):475–81. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 114.Ness KK, Wall MM, Oakes JM, Robison LL, Gurney JG. Physical performance limitations and participation restrictions among cancer survivors: a population-based study. Ann Epidemiol. 2006;16(3):197–205. [DOI] [PubMed] [Google Scholar]
  • 115.Stergiou-Kita M, Grigorovich A, Tseung V, Milosevic E, Hebert D, Phan S, et al. Qualitative meta-synthesis of survivors’ work experiences and the development of strategies to facilitate return to work. J Cancer Surviv. 2014;8(4):657–70. [DOI] [PubMed] [Google Scholar]
  • 116.Pergolotti M, Deal AM, Williams GR, Bryant AL, Bensen JT, Muss HB, et al. Activities, function, and health-related quality of life (HRQOL) of older adults with cancer. J geriatric Oncol. 2017;8(4):249–54. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 117.Neo J, Fettes L, Gao W, Higginson IJ, Maddocks M. Disability in activities of daily living among adults with cancer: a systematic review and meta-analysis. Cancer Treat Rev. 2017;61:94–106. [DOI] [PubMed] [Google Scholar]
  • 118.Nakano J, Fukushima T, Tanaka T, Fu JB, Morishita S. Physical function predicts mortality in patients with cancer: a systematic review and meta-analysis of observational studies. Support Care Cancer. 2021;29(10):5623–34. [DOI] [PubMed] [Google Scholar]
  • 119.Zhang D, Spiropoulos KA, Wijayabahu A, Christou DD, Karanth SD, Anton SD, et al. Low muscle mass is associated with a higher risk of all–cause and cardiovascular disease–specific mortality in cancer survivors. Nutrition. 2023;107:111934. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 120.Saeidifard F, Medina-Inojosa JR, West CP, Olson TP, Somers VK, Bonikowske AR, et al. The association of resistance training with mortality: a systematic review and meta-analysis. Eur J Prev Cardiol. 2019;26(15):1647–65. [DOI] [PubMed] [Google Scholar]
  • 121.Clifford B, Koizumi S, Wewege MA, Leake HB, Ha L, Macdonald E, et al. The effect of resistance training on body composition during and after cancer treatment: a systematic review and meta-analysis. Sports Med. 2021;51:1–20. [DOI] [PubMed] [Google Scholar]
  • 122.Buffart LM, Kalter J, Sweegers MG, Courneya KS, Newton RU, Aaronson NK, et al. Effects and moderators of exercise on quality of life and physical function in patients with cancer: an individual patient data meta-analysis of 34 RCTs. Cancer Treat Rev. 2017;52:91–104. [DOI] [PubMed] [Google Scholar]
  • 123.Sweegers MG, Altenburg TM, Chinapaw MJ, Kalter J, Verdonck-de Leeuw IM, Courneya KS, et al. Which exercise prescriptions improve quality of life and physical function in patients with cancer during and following treatment? A systematic review and meta-analysis of randomised controlled trials. Br J Sports Med. 2018;52(8):505–13. [DOI] [PubMed] [Google Scholar]
  • 124.Winters-Stone KM, Torgrimson-Ojerio B, Dieckmann NF, Stoyles S, Mitri Z, Luoh S-W. A randomized-controlled trial comparing supervised aerobic training to resistance training followed by unsupervised exercise on physical functioning in older breast cancer survivors. J Geriatric Oncol. 2022;13(2):152–60. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 125.Courneya KS, Segal RJ, Mackey JR, Gelmon K, Reid RD, Friedenreich CM, et al. Effects of aerobic and resistance exercise in breast cancer patients receiving adjuvant chemotherapy: a multicenter randomized controlled trial. J Clin Oncol. 2007;25(28):4396–404. [DOI] [PubMed] [Google Scholar]
  • 126.Lee SJ, Park YJ, Cartmell KB. Sarcopenia in cancer survivors is associated with increased cardiovascular disease risk. Support Care Cancer. 2018;26:2313–21. [DOI] [PubMed] [Google Scholar]
  • 127.Damluji AA, Alfaraidhy M, AlHajri N, Rohant NN, Kumar M, Al Malouf C, et al. Sarcopenia and Cardiovascular Diseases. Circulation. 2023;147(20):1534–53. [DOI] [PMC free article] [PubMed]
  • 128.Pierson LM, Herbert WG, Norton HJ, Kiebzak GM, Griffith P, Fedor JM, et al. Effects of combined aerobic and resistance training versus aerobic training alone in cardiac rehabilitation. J Cardiopulm Rehabil Prev. 2001;21(2):101–10. [DOI] [PubMed] [Google Scholar]
  • 129.Marzolini S, Thomas SG, Goodman JM. Aerobic and resistance training in coronary disease: single versus multiple sets. Med Sci Sports Exerc. 2008;40(9):1557–64. [DOI] [PubMed] [Google Scholar]
  • 130.Beniamini Y, Rubenstein JJ, Faigenbaum AD, Lichtenstein AH, Crim MC. High-intensity strength training of patients enrolled in an outpatient cardiac rehabilitation program. J Cardiopulm Rehabil Prev. 1999;19(1):8–17. [DOI] [PubMed] [Google Scholar]
  • 131.Groarke JD, Payne DL, Claggett B, Mehra MR, Gong J, Caron J, et al. Association of post-diagnosis cardiorespiratory fitness with cause-specific mortality in cancer. Eur Heart J Qual Care Clin Outcomes. 2020;6(4):315–22. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 132.Haykowsky MJ, Beaudry R, Brothers RM, Nelson MD, Sarma S, La Gerche A. Pathophysiology of exercise intolerance in breast cancer survivors with preserved left ventricular ejection fraction. Clin Sci. 2016;130(24):2239–44. [DOI] [PubMed] [Google Scholar]
  • 133.Jones LW, Eves ND, Haykowsky M, Freedland SJ, Mackey JR. Exercise intolerance in cancer and the role of exercise therapy to reverse dysfunction. Lancet Oncol. 2009;10(6):598–605. [DOI] [PubMed] [Google Scholar]
  • 134.Bonsignore A, Warburton D. The mechanisms responsible for exercise intolerance in early-stage breast cancer: What role does chemotherapy play? Hong Kong Physiotherapy J. 2013;31(1):2–11. [Google Scholar]
  • 135.Hayek S, Brinkman TM, Plana JC, Joshi VM, Leupker RV, Durand JB, et al. Association of Exercise Intolerance With Emotional Distress, Attainment of Social Roles, and Health-Related Quality of Life Among Adult Survivors of Childhood Cancer. JAMA Oncol. 2020;6(8):1194–202. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 136.Ness KK, Plana JC, Joshi VM, Luepker RV, Durand JB, Green DM, et al. Exercise Intolerance, Mortality, and Organ System Impairment in Adult Survivors of Childhood Cancer. J Clin Oncol. 2020;38(1):29–42. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 137.Dillon HT, Foulkes SJ, Baik AH, Scott JM, Touyz RM, Herrmann J, et al. Cancer Therapy and Exercise Intolerance: the Heart Is But a Part. JACC CardioOncology. 2024;6(4):496–513. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 138.Jones LW, Haykowsky M, Pituskin EN, Jendzjowsky NG, Tomczak CR, Haennel RG, et al. Cardiovascular Reserve and Risk Profile of Postmenopausal Women After Chemoendocrine Therapy for Hormone Receptor–Positive Operable Breast Cancer. Oncologist. 2007;12(10):1156–64. [DOI] [PubMed] [Google Scholar]
  • 139.Beaudry RI, Kirkham AA, Thompson RB, Grenier JG, Mackey JR, Haykowsky MJ. Exercise Intolerance in Anthracycline-Treated Breast Cancer Survivors: the Role of Skeletal Muscle Bioenergetics, Oxygenation, and Composition. Oncologist. 2020;25(5):e852–60. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 140.Kunz HE, Port JD, Kaufman KR, Jatoi A, Hart CR, Gries KJ, et al. Skeletal muscle mitochondrial dysfunction and muscle and whole body functional deficits in cancer patients with weight loss. J Appl Physiol. 2022;132(2):388–401. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 141.Haykowsky MJ, Kouba EJ, Brubaker PH, Nicklas BJ, Eggebeen J, Kitzman DW. Skeletal muscle composition and its relation to exercise intolerance in older patients with heart failure and preserved ejection fraction. Am J Cardiol. 2014;113(7):1211–6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 142.Reding KW, Brubaker P, D’Agostino R, Kitzman DW, Nicklas B, Langford D, et al. Increased skeletal intermuscular fat is associated with reduced exercise capacity in cancer survivors: a cross-sectional study. Cardio-Oncology. 2019;5(1):3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 143.Smart TFF, Doleman B, Hatt J, Paul M, Toft S, Lund JN, et al. The role of resistance exercise training for improving cardiorespiratory fitness in healthy older adults: a systematic review and meta-analysis. Age Ageing. 2022;51(6):afac143. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 144.Hollings M, Mavros Y, Freeston J, Fiatarone Singh M. The effect of progressive resistance training on aerobic fitness and strength in adults with coronary heart disease: a systematic review and meta-analysis of randomised controlled trials. Eur J Prev Cardiol. 2020;24(12):1242–59. [DOI] [PubMed] [Google Scholar]
  • 145.Marzolini S, Oh PI, Brooks D. Effect of combined aerobic and resistance training versus aerobic training alone in individuals with coronary artery disease: a meta-analysis. Eur J Prev Cardiol. 2012;19(1):81–94. [DOI] [PubMed] [Google Scholar]
  • 146.Xanthos PD, Gordon BA, Kingsley MI. Implementing resistance training in the rehabilitation of coronary heart disease: a systematic review and meta-analysis. Int J Cardiol. 2017;230:493–508. [DOI] [PubMed] [Google Scholar]
  • 147.Wang Z, Peng X, Li K, Wu CJJ. Effects of combined aerobic and resistance training in patients with heart failure: a meta-analysis of randomized, controlled trials. Nurs Health Sci. 2019;21(2):148–56. [DOI] [PubMed] [Google Scholar]
  • 148.Argilés JM, Campos N, Lopez-Pedrosa JM, Rueda R, Rodriguez-Mañas L. Skeletal Muscle Regulates Metabolism via Interorgan Crosstalk: roles in Health and Disease. J Am Med Dir Assoc. 2016;17(9):789–96. [DOI] [PubMed] [Google Scholar]
  • 149.Prado CM, Purcell SA, Alish C, Pereira SL, Deutz NE, Heyland DK, et al. Implications of low muscle mass across the continuum of care: a narrative review. Ann Med. 2018;50(8):675–93. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 150.Wang DXM, Yao J, Zirek Y, Reijnierse EM, Maier AB. Muscle mass, strength, and physical performance predicting activities of daily living: a meta-analysis. J Cachexia Sarcopenia Muscle. 2020;11(1):3–25. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 151.Gilchrist SC, Barac A, Ades PA, Alfano CM, Franklin BA, Jones LW, et al. Cardio-oncology rehabilitation to manage cardiovascular outcomes in cancer patients and survivors: a scientific statement from the American Heart Association. Circulation. 2019;139(21):e997–1012. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 152.Piercy KL, Troiano RP, Ballard RM, Carlson SA, Fulton JE, Galuska DA, et al. The physical activity guidelines for Americans. JAMA. 2018;320(19):2020–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 153.Momma H, Kawakami R, Honda T, Sawada SS. Muscle-strengthening activities are associated with lower risk and mortality in major non-communicable diseases: a systematic review and meta-analysis of cohort studies. Br J Sports Med. 2022;56(13):755. [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Not applicable.

Articles from Sports Medicine - Open are provided here courtesy of Springer

RESOURCES