Cardio-sarcopenia: A syndrome of concern in aging

Loh, De Rong; Tan, Ru San; Lim, Wee Shiong; Koh, Angela S.

doi:10.3389/fmed.2022.1027466

Cited by 12 publications

(10 citation statements)

References 91 publications

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“…The discovery that musclin is upregulated after DUSP22 targeting may also warrant further investigation, because this myokine has been shown to be critical for cardiac conditioning [52]. Cardiac hypertrophy and skeletal muscle wasting are known to share similar molecular mechanisms, and cardio-sarcopenia has recently been described as a syndrome of concern in aging [53, 54]. In addition, skeletal muscle-secreted musculin has recently been shown to alleviate depression in animal models [55, 56].…”

Section: Discussionmentioning

confidence: 99%

Targeting phosphatase DUSP22 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression

Lee,

Kim,

Kim

et al. 2024

Preprint

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Skeletal muscle wasting results from numerous conditions, such as sarcopenia, glucocorticoid therapy or intensive care. It prevents independent living in the elderly, predisposes to secondary diseases, and ultimately reduces lifespan. There is no approved drug therapy and the major causative mechanisms are not fully understood. Dual specificity phosphatase 22 (DUSP22) is a pleiotropic signaling molecule that plays important roles in immunity and cancer. However, the role of DUSP22 in skeletal muscle wasting is unknown. In this study, DUSP22 was found to be upregulated in sarcopenia patients and models of skeletal muscle wasting. DUSP22 knockdown or pharmacological inhibition prevented multiple forms of muscle wasting. Mechanistically, targeting DUSP22 suppressed FOXO3a, a master regulator of skeletal muscle wasting, via downregulation of the stress-activated kinase JNK, which occurred independently of aberrant Akt activation. DUSP22 targeting was also effective in human skeletal muscle cells undergoing atrophy. In conclusion, phosphatase DUSP22 is a novel target for preventing skeletal muscle wasting. The DUSP22-JNK-FOXO3a axis could be exploited to treat sarcopenia or related aging disorders.

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Section: Discussionmentioning

confidence: 99%

Targeting phosphatase DUSP22 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression

Lee,

Kim,

Kim

et al. 2024

Preprint

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“…It is here that the influences of sarcopenia on the heart muscle might act. Cardio-sarcopenia is a relatively novel concept [ 42 ], especially as traditionally hypertrophy rather than wasting of the heart is seen with ageing. However, a small number of studies have shown reductions in the left ventricular mass in sarcopenia [ 43 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic Parameters Underlying the Relationship between Sarcopenia and Blood Pressure Recovery on Standing

Duggan,

Knight,

Xue

et al. 2023

JCM

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Background: Sarcopenia, delayed blood pressure (BP) recovery following standing, and orthostatic hypotension (OH) pose significant clinical challenges associated with ageing. While prior studies have established a link between sarcopenia and impaired BP recovery and OH, the underlying haemodynamic mechanisms remain unclear. Methods: We enrolled 107 participants aged 50 and above from a falls and syncope clinic, conducting an active stand test with continuous non-invasive haemodynamic measurements. Hand grip strength and five-chair stand time were evaluated, and muscle mass was estimated using bioelectrical impedance analysis. Participants were categorised as non-sarcopenic or sarcopenic. Employing mixed-effects linear regression, we modelled the effect of sarcopenia on mean arterial pressure and heart rate after standing, as well as Modelflow®-derived parameters such as cardiac output, total peripheral resistance, and stroke volume, while adjusting for potential confounders. Results: Sarcopenia was associated with diminished recovery of mean arterial pressure during the 10–20 s period post-standing (β −0.67, p < 0.001). It also resulted in a reduced ascent to peak (0–10 s) and recovery from peak (10–20 s) of cardiac output (β −0.05, p < 0.001; β 0.06, p < 0.001). Furthermore, sarcopenia was associated with attenuated recovery (10–20 s) of total peripheral resistance from nadir (β −0.02, p < 0.001) and diminished recovery from peak (10–20 s) of stroke volume (β 0.54, p < 0.001). Notably, heart rate did not exhibit a significant association with sarcopenia status at any time interval post-standing. Conclusion: The compromised BP recovery observed in sarcopenia appears to be driven by an initial reduction in the peak of cardiac output, followed by attenuated recovery of cardiac output from its peak and total peripheral resistance from its nadir. This cardiac output finding seems to be influenced by stroke volume rather than heart rate. Possible mechanisms for these findings include cardio-sarcopenia, the impact of sarcopenia on the autonomic nervous system, and/or the skeletal muscle pump.

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“…Changes in cardiac function and structure trigger a series of negative effects on skeletal muscle, resulting in decreased strength, endurance and functional capacity. This skeletal muscle dysfunction can, in turn, contribute to a vicious cycle, where muscle weakness resulting from HF leads to a sedentary lifestyle, further aggravating sarcopenia (5). Among the most common symptoms of HF are dyspnea, a feeling of fatigue and exercise intolerance (6).…”

Section: Introductionmentioning

confidence: 99%

Impact of inspiratory muscle training on respiratory muscle function and functional capacity in patients with heart failure: a scoping review

Cavegn,

Rodrigues Junior

2024

HVT

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Heart failure (HF) is one of the most prevalent diseases in the world and is characterized as a complex clinical syndrome. It is a disease that affects both the peripheral muscles and the respiratory muscles, causing damage such as reduced strength and endurance. One of the main symptoms is fatigue and exercise intolerance. The aim of this review article is to assess whether the use of inspiratory muscle training (IMT) associated with conventional training enhances inspiratory muscle strength (PImax) and inspiratory muscle endurance (SPImax) and functional capacity in patients with HF. Methods: A literature review was carried out on the use of IMT in patients, including 6 randomized clinical trials, searched in the PubMed, PEDro and Lilacs databases. Results: There is evidence showing an increase in PImax and SPImax with the addition of IMT to training; in addition, an improvement in VO2 peak, circulatory power and ventilatory efficiency. Conclusion:The use of IMT associated with conventional training is an interesting strategy for boosting gains in strength and inspiratory muscle endurance, increasing exercise tolerance and consequently improving patients' quality of life. However, more studies are needed in order to more clearly define the selection criteria and methodology for applying IMT.

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Cardio-sarcopenia: A syndrome of concern in aging

Cited by 12 publications

References 91 publications

Targeting phosphatase DUSP22 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression

Targeting phosphatase DUSP22 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression

Haemodynamic Parameters Underlying the Relationship between Sarcopenia and Blood Pressure Recovery on Standing

Impact of inspiratory muscle training on respiratory muscle function and functional capacity in patients with heart failure: a scoping review

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