You hit the gym. You try to eat right. Maybe you’ve even convinced yourself that feeling a little more tired, a little weaker, or a little slower is just part of getting older.
But what if it’s not?
What if something deeper—something you can’t see—was quietly wrecking your endurance, draining your energy, and making every workout feel harder than it should?
Science is finally exposing a brutal truth: your muscles might be deteriorating long before you ever notice. And waiting to address it could make regaining that strength an uphill battle.
Let’s break it down—because ignoring this could cost you more than just your next PR.
Reduced exercise capacity, reflected in lower peak oxygen uptake (VO₂ peak), is a defining characteristic of heart failure and is linked to poorer quality of life, as well as a higher risk of hospitalization and mortality. The decline in VO₂ peak in heart failure is driven by multiple factors, traditionally attributed to impaired cardiac function. However, non-cardiac peripheral factors— such as reduced lean mass, oxidative muscle fibers, and capillary density—may also play a role.
Due to individual variability and differences in
physical activity levels between heart failure patients and healthy age-matched controls, the extent of lean mass loss and skeletal muscle changes in heart failure, as well as their impact on VO₂ peak, remains unclear. To clarify this, a recent systematic review and meta-analysis was conducted to assess how whole-body and skeletal muscle composition differences contribute to reduced VO₂peak in heart failure compared to controls(1).
A search of the PubMed database was conducted from 1975 to May 2024 to identify relevant studies. Cross-sectional studies assessing VO₂peak, body composition, or muscle biopsies in heart failure and controls were considered. Of the 709 articles reviewed, 27 met the inclusion criteria for this analysis(1).
Key Themes and Findings
Significantly Reduced VO2peak in Heart Failure
Heart failure patients exhibit a significant and marked reduction in VO2peak (∼10 mL/min/kg) compared with control group. The average VO2peak in heart failure patients was 16 mL/kg/min, which is well below the 18 mL/kg/min VO2 threshold required for full and independent living(2).
This highlights the functional significance of the observed reduction.
Muscle Atrophy as a Major Component of Heart Failure Syndrome
Individuals with heart failure have reduced total and lower body lean mass and skeletal muscle area relative to control. This finding supports the concept of muscle atrophy as a major contributing factor to heart failure pathology.
A significant association between total body and leg lean mass with absolute VO2peak was observed. This reinforces the direct link between
muscle mass and exercise capacity.
Each kilogram increase in lean mass is associated with a concomitant increase in absolute VO2peak of about 145 mL/min(3).
The analysis reinforces the clinical relevance by aligning to data showing high prevalence of sarcopenia in heart failure and how heart failure patients with sarcopenia have decreased VO2peak, reduced physical performance, and lower quality of life(4).
Figure: The absolute VO2peak (mL/min) was significantly associated with total body lean mass (adapted from Schmid et al, 2024(1))
Alterations in Skeletal Muscle Fiber Composition
Heart failure patients have a reduced proportion of highly oxidative Type I muscle fibers and an increased proportion of Type IIx (glycolytic) fibers compared to controls. Results of this analysis indicate that individuals with heart failure have a lower capillary-to-fiber ratio and a significant association with VO2peak in patients with heart failure. These alterations impair muscle oxygen diffusive conductance and
oxygen utilization by skeletal muscles which limit aerobic performance.
Muscle Function and Biochemical Changes
Heart failure patients exhibit a diminished succinate dehydrogenase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase indicating decreased aerobic oxidative enzyme activity. Conversely, there is a tendency for glycolytic enzyme content and activity to increase in patients with heart failure(5).
Research indicates a reduction in mitochondrial oxidative metabolism, coupled with increased glycolytic metabolism and up-regulation of catabolic gene expression within skeletal muscle in patients with heart failure, potentially contributing to decreased VO2peak and functional limitations.
Sarcopenic Obesity Phenotype
Total body and leg fat were 3.3 and 1.4 kg higher, respectively, in heart failure vs. control, highlighting not only a transition towards sarcopenia but also a sarcopenic obesity phenotype, which is associated with a poorer prognosis and increased functional limitations.
While fat mass may not directly reduce VO2peak, it contributes to metabolic inefficiencies, increasing the oxygen demand for basic movements.
Implications and Recommendations
The findings support the development and implementation of interventions targeting skeletal muscle health in heart failure patients. This includes both increasing muscle mass and improving muscle quality.
Interventions targeting
increases in muscle and decreases in fat mass, such as combined dietary (e.g. caloric restriction + increased dietary protein intake) and resistance-based exercise interventions” should be considered.
Caution is advised when prescribing medically induced weight loss with bariatric surgery or medications such as glucagon-like peptide-1 agonists, which have the potential to cause marked reductions in lean body mass in addition to their effects on fat mass.
Further research is needed to fully understand the complex interplay between skeletal muscle function, inflammation, and exercise intolerance in heart failure, particularly considering differences in heart failure phenotypes and the role of comorbidities.
Summary
This systematic review and meta-analysis offer compelling evidence that skeletal muscle dysfunction, characterized by reduced lean mass, altered fiber composition, and impaired oxidative capacity, plays a significant role in the exercise intolerance observed in heart failure.
These findings highlight the importance of considering and targeting skeletal muscle health in the management of heart failure patients.
The takeaway? Never stop exercising.
Building and preserving muscle isn’t just about looking strong—it’s about keeping your body functioning at its best, especially when your heart is under stress. Resistance training and proper nutrition are key, but there’s another powerful tool you can add to your arsenal:
CoQ10 is a vital compound that supports heart health(6,7), energy production, and muscle endurance at the cellular level.
And in its liposomal form, it’s absorbed more efficiently, delivering
maximum benefits where your body needs it most.
Give your heart and muscles the extra support they deserve—because staying strong starts from the inside out.
References:
1. Schmid V, Foulkes SJ, Walesiak D, et al: Impact of whole-body and skeletal muscle composition on peak oxygen uptake in heart failure: a systematic review and meta-analysis. Eur Heart J Open 4:oeae082, 2024
2. Paterson DH, Cunningham DA, Koval JJ, et al: Aerobic fitness in a population of independently living men and women aged 55-86 years. Med Sci Sports Exerc 31:1813-20, 1999
3. Jubrias SA, Esselman PC, Price LB, et al: Large energetic adaptations of elderly muscle to resistance and endurance training. J Appl Physiol (1985) 90:1663-70, 2001
4. Emami A, Saitoh M, Valentova M, et al: Comparison of sarcopenia and cachexia in men with chronic heart failure: results from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF). Eur J Heart Fail 20:1580-1587, 2018
5. Sullivan MJ, Green HJ, Cobb FR: Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. Circulation 81:518-27, 1996
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3742297/
7. https://www.jacc.org/doi/10.1016/j.jacc.2020.12.009
