Reduced muscle strength in patients with long-COVID-19 syndrome is mediated by limb muscle mass

Abstract

Understanding the impact of COVID-19 on muscle strength may help to elucidate the organ systems that contribute to acute and chronic COVID-19 sequelae. We questioned whether patients with postdischarge symptoms after COVID-19 had compromised muscle strength compared with a control group, and if this potential relationship was mediated by the lower appendicular lean mass index (ALMI). A total of 99 patients with long-COVID-19 and 97 control participants were screened. Maximal grip strength was assessed with a TKK 5101 digital dynamometer, and leg extension 1RM was measured using EGYM Smart Strength machines. Body composition (fat mass percentage, lean mass, visceral fat and appendicular lean mass index) was determined using a whole-body dual-energy X-ray densitometer. Results showed that grip strength and leg extension strength were significantly higher in controls than in COVID-19 survivors (mean [SD], 32.82 [10.01] vs. 26.94 [10.33] kg; difference, 5.87 kg; P < 0.001) and (mean [SD], 93.98 [33.73] vs. 71.59 [33.70] kg; difference, 22.38 kg; P < 0.001), respectively). The relationship between long-COVID syndrome and grip/leg strength levels was partly mediated by ALMI, which explained 52% of the association for grip strength and 39% for leg extension. Our findings provide novel insights into the mechanisms underlying the relationship between long-COVID syndrome and grip/leg strength levels, supporting the negative effects of long-COVID syndrome on muscle function.

Mechanisms underlying exercise intolerance in Long COVID: an accumulation of multi-system dysfunction

“…Support for a skeletal muscle deficit more generally was also evidenced by the reduced knee extension/flexion force in 62% of Long COVID cases enrolled here. This may be explained by the reduced lean mass in our study group, as was described by Ramirez-Velez and colleagues [35]. Only 7% of individuals with Long COVID had a hand-grip strength outside the normal range [35], which may suggest a detraining effect on the lower limbs in line with the increase in sedentary time that we observed objectively.…”

“…This may be explained by the reduced lean mass in our study group, as was described by Ramirez-Velez and colleagues [35]. Only 7% of individuals with Long COVID had a hand-grip strength outside the normal range [35], which may suggest a detraining effect on the lower limbs in line with the increase in sedentary time that we observed objectively. However, we also report similar self-reported and objectively measured levels of physical activity between groups which would argue against detraining.…”

Mechanisms underlying exercise intolerance in long COVID: An accumulation of multisystem dysfunction

“…Support for a skeletal muscle deficit more generally was also evidenced by the reduced knee extension/flexion force in 62% of long COVID cases enrolled here. This may be explained by the reduced lean mass in our study group, as was described by Ramirez-Velez and colleagues (Ramírez-Vélez et al, 2023). Only 7% of individuals with long COVID had a hand-grip strength outside the normal range (Ramírez-Vélez et al, 2023), which may suggest a detraining effect on the lower limbs in line with the increase in sedentary time that we observed objectively.…”

“…This may be explained by the reduced lean mass in our study group, as was described by Ramirez-Velez and colleagues (Ramírez-Vélez et al, 2023). Only 7% of individuals with long COVID had a hand-grip strength outside the normal range (Ramírez-Vélez et al, 2023), which may suggest a detraining effect on the lower limbs in line with the increase in sedentary time that we observed objectively. However, we also report similar self-reported and objectively measured levels of physical activity between groups which would argue against detraining.…”

https://actascientific.com/ASOR/pdf/ASOR-06-0704.pdf

“…Yet, even here, challenges in establishing their severity and mortality risk persist [61][62][63][64][65], as well what its rheumatologic disease features denote [63,66], what variations in neurological symptoms from mild to severe in the central as well as the peripheral nervous system imply, if one or more of these emergent sequels to COVID-19 recovery are found to have little correlation with any objective pathology or established pathophysiological mechanisms [67,68]. The role of muscle mass losses and strength capacity, and an hypothesis that at least some long COVID cases may have brainstem dysfunction or subnormal impacts' that account for their diverse complications, and possible decreases in cortical grey matter volume also adds another challenge to deciphering the approach needed to limit a possible bout of secondary infections, as well as declines in health and how to assess these and intervene effectively [69][70][71]. As well, multiple post-acute neurophenotypes of long COVID, with different etiological pathways and recovery trajectories may prevail that will require phenotype-specific approaches to treatment, once identified [72].…”