Well your doctor should have been doing something like this from May 2017 already to prevent your muscle atrophy. Has your doctor initiated human research?
'Exercise-in-a-pill' boosts athletic endurance by 70 percent May 2017
Or this?
A replacement for exercise? January 2020
The latest here:
An electrical stimulation intervention protocol to prevent disuse atrophy and muscle strength decline: an experimental study in rat
Journal of NeuroEngineering and Rehabilitation volume 20, Article number: 84 (2023)
Abstract
Background
Skeletal muscle is negatively impacted by conditions such as spaceflight or prolonged bed rest, resulting in a dramatic decline in muscle mass, maximum contractile force, and muscular endurance. Electrical stimulation (ES) is an essential tool in neurophysiotherapy and an effective means of preventing skeletal muscle atrophy and dysfunction. Historically, ES treatment protocols have used either low or high frequency electrical stimulation (LFES/HFES). However, our study tests the use of a combination of different frequencies in a single electrical stimulation intervention in order to determine a more effective protocol for improving both skeletal muscle strength and endurance.
Methods
An adult male SD rat model of muscle atrophy was established through 4 weeks of tail suspension (TS). To investigate the effects of different frequency combinations, the experimental animals were treated with low (20 Hz) or high (100 Hz) frequency before TS for 6 weeks, and during TS for 4weeks. The maximum contraction force and fatigue resistance of skeletal muscle were then assessed before the animals were sacrificed. The muscle mass, fiber cross-sectional area (CSA), fiber type and related protein expression were examined and analyzed to gain insights into the mechanisms by which the ES intervention protocol used in this study regulates muscle strength and endurance.
Results
After 4 weeks of unloading, the soleus muscle mass and fiber CSA decreased by 39% and 58% respectively, while the number of glycolytic muscle fibers increased by 21%. The gastrocnemius muscle fibers showed a 51% decrease in CSA, with a 44% decrease in single contractility and a 39% decrease in fatigue resistance. The number of glycolytic muscle fibers in the gastrocnemius also increased by 29%. However, the application of HFES either prior to or during unloading showed an improvement in muscle mass, fiber CSA, and oxidative muscle fibers. In the pre-unloading group, the soleus muscle mass increased by 62%, while the number of oxidative muscle fibers increased by 18%. In the during unloading group, the soleus muscle mass increased by 29% and the number of oxidative muscle fibers increased by 15%. In the gastrocnemius, the pre-unloading group showed a 38% increase in single contractile force and a 19% increase in fatigue resistance, while in the during unloading group, a 21% increase in single contractile force and a 29% increase in fatigue resistance was observed, along with a 37% and 26% increase in the number of oxidative muscle fibers, respectively. The combination of HFES before unloading and LFES during unloading resulted in a significant elevation of the soleus mass by 49% and CSA by 90%, with a 40% increase in the number of oxidative muscle fibers in the gastrocnemius. This combination also resulted in a 66% increase in single contractility and a 38% increase in fatigue resistance.
Conclusion
Our results indicated that using HFES before unloading can reduce the harmful effects of muscle unloading on the soleus and gastrocnemius muscles. Furthermore, we found that combining HFES before unloading with LFES during unloading was more effective in preventing muscle atrophy in the soleus and preserving the contractile function of the gastrocnemius muscle.
Background
Skeletal muscle atrophy is commonly associated with aging, malnutrition, fasting and disuse conditions such as bed rest, inactivity, and microgravity [1, 2], resulting in a decrease in muscle mass and fiber cross-sectional area (CSA). Muscle atrophy is also frequently accompanied by changes in muscle fiber type and declining contractile function [3,4,5], leading to impaired mobility and inconvenience [6], increased risk of injury, and slower recovery [7, 8]. The imbalance between skeletal muscle protein synthesis and degradation, and the shift in muscle fiber types are the main causes of skeletal muscle atrophy [9,10,11,12,13]. Exercise is a proven and effective method of treating skeletal muscle atrophy by promoting protein synthesis through the PI3K/AKT/mTOR pathway and reducing protein degradation through the downregulation of MuRF1 expression [14,15,16,17,18]. However, exercise may not be feasible for individuals with trauma or post-surgery, making alternative methods of muscle contraction necessary.
In the 1960s, the field of physical medicine introduced physiological electrical stimulation (ES), a technique that simulates muscle contraction. This led to the development of a functional electrical stimulation system for clinical use, designed to trigger useful muscle contraction and maintain muscle quality and function [19, 20]. Today, ES is not only used as a rehabilitation treatment [21,22,23], but also as an effective training tool for people with physical weakness and for the general population to improve their sports performance [24]. Studies have shown that different electrical stimulation frequencies have varying effects on skeletal muscles. High frequency electrical stimulation (HFES, > 40 Hz in general) mimics resistance training to promote skeletal muscle protein synthesis and increase muscle mass, helping to prevent the decline of muscle mass and contractility that often occurs with aging and denervation [25,26,27]. Low frequency electrical stimulation (LFES, 5 to 30 Hz in general) mimics aerobic exercise and promotes the biological activity of mitochondria [23, 28,29,30,31]. Noteworthy, frequencies under 16 Hz were not strong enough to produce a significant contraction [32]. Although the contraction force generated by LFES (10-30 Hz) is low, the duration of the contraction force can last 24 h or longer, an effect not seen with higher frequency stimulation [19]. Despite the extensive research on the effects of single-frequency electrical stimulation on skeletal muscles, there have been relatively fewer studies exploring the impact of combining high and low frequency electrical stimulation on skeletal muscle mass and contractile function. This remains an area of active research, as researchers aim to better integrate electrical stimulation protocols with specific treatment goals and develop effective stimulation treatment plans to improve the contractility and fatigue resistance of skeletal muscles.
In this study, various treatment regiments combining high frequency or low frequency electrical stimulation at different stages of muscle atrophy were used to evaluate their effects. The maximum contractile and fatigue resistance of skeletal muscle, skeletal muscle weight, fiber CSA were measured to determine the most effective treatment regimen. Our results showed that a pretreatment with HFES can mitigate the negative impact of muscle unloading on the soleus and gastrocnemius muscles. Additionally, LFES treatment during unloading, following HFES pretreatment, was found to be more effective in resisting soleus muscle atrophy and preventing a decline in the contractile function of gastrocnemius muscle. The protein expression of nuclear factor of activated T cell (NFAT) and calcium/calmodulin-dependent phosphatase calcineurin (CaN), which can impact the fiber type of skeletal muscle [33, 34], were also detected using Western Blot analysis.
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