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Does carbohydrate ingestion affect exercise performance and fatigue?

This is an excerpt from Biochemistry Primer for Exercise Science-5th Edition by A. Russell Tupling,Peter M. Tiidus & Michael E. Houston.

Carbohydrate, Exercise Performance, and Fatigue
At various points in this chapter, we have noted the correlation of muscle glycogen depletion with the onset of fatigue, as well as the ability of glucose ingestion to delay the onset of fatigue during exercise. These relationships have been well documented by exercise scientists for more than 50 years. As well as improvements in duration of endurance exercise and total work, carbohydrate ingestion may also enhance repeated high-power work output as well as performance in multiple bouts of resistance exercise (Karelis et al. 2010). Recent research, however, has demonstrated the effects of carbohydrate supplementation on improving maximal endurance performance of at least 45 min (Spriet 2021).

Despite these established associations, the exact mechanisms by which carbohydrate ingestion delays muscle fatigue are still not fully established. As we have previously noted, fatigue is a complex and multifaceted occurrence that is influenced by a myriad of events during different intensities and durations of exercise. The maintenance of blood glucose levels and muscle carbohydrate oxidation, or glycogen stores by carbohydrate administration, may influence a number of these factors. Carbohydrate administration during exercise may influence at least three important factors that result in delayed fatigue and enhanced work capacity: (1) enhanced neural drive and attenuation of central fatigue, (2) protection from disruption of muscle cell homeostasis and integrity, and (3) maintenance of sodium–potassium pump ATPase activity (Cheng et al. 2021; Karelis et al. 2010).

Although experimental evidence of the effects of hypoglycemia on exercise performance is conflicting, maintenance of carbohydrate availability to the brain and central nervous system, which, as we have noted earlier, are highly reliant on carbohydrate metabolism, could enhance and maintain the central nervous system’s function and ability to continue to fully activate muscle contraction. In support of this, several studies have found when assessing the total amount of work accomplished by elite athletes over a 1 h period that performance when fasted is improved by both carbohydrate ingestion and the sipping and spitting out of a carbohydrate beverage. This suggests that sensors in the mouth can detect carbohydrate and signal its imminent arrival to the brain. The brain, which would be starting to invoke fatigue mechanisms to prevent the imminent depletion of carbohydrate and blood glucose levels, delays this intervention in the expectation of more carbohydrate; therefore, it allows exercise to continue for a period of time at a high intensity, delaying “central fatigue” (Karelis et al. 2010). These findings suggest that in some cases, actual depletion of carbohydrate and glycogen stores is not the primary cause of fatigue but that central fatigue can occur to prevent their imminent depletion. Subsequent studies have also confirmed the performance-enhancing benefits of carbohydrate sensing by its ability to actually enhance muscle power production in prolonged exercise as well as high-power sprint performance. This again suggests that sensing the presence of carbohydrate in the mouth will stimulate the central nervous system in ways that enhance performance beyond the metabolic effects of carbohydrate alone (Jensen et al. 2018; Beaven et al. 2013).

Studies also suggest that carbohydrate ingestion may be effective in attenuation of exercise-induced immune suppression, synthesis of heat shock proteins, oxidative stress, and positive regulators of inflammation (e.g., inflammatory cytokines and cortisol) (Karelis et al. 2010). These effects may delay fatigue by attenuating some of the acute negative effects of inflammation-associated muscle disruption. Other studies have suggested that the sodium–potassium ATPase, which hydrolyzes ATP to maintain muscle membrane polarization during muscle contraction and relaxation, may be inhibited when the ability to maintain ATP homeostasis during exercise is compromised. Carbohydrate administration may be able to delay this by providing a source for muscle metabolism when muscle and liver glycogen levels are being depleted (Karelis et al. 2010). Other possible mechanisms that may delay fatigue onset during endurance exercise in association with carbohydrate administration include the maintenance of calcium homeostasis and SERCA ATPase activity, maintenance of the rate of ATP production via glycolysis and carbohydrate oxidation that may not be matched by aerobic metabolism of fatty acids, and maintenance of appropriate levels of other high–energy-related metabolic intermediates, including Cr phosphate, IMP, and Pi levels (Karelis et al. 2010; Cheng et al. 2021).

It is well recognized that one of the main purposes of muscle fatigue during exercise is to downregulate muscular contraction and metabolic demand for ATP in order to preserve muscle ATP levels and energy status before they can drop to catastrophic levels. Enhanced carbohydrate availability during endurance exercise may be able, in a number of ways, to prolong ATP synthesis rates for a period of time, thus delaying the need for muscle contraction to be attenuated by fatigue mechanisms. The reviews by Karelis and colleagues (2010) and Cheng and colleagues (2021) highlighted the myriad of possible factors involved in maintaining and limiting muscular activity and physical performance during endurance exercise, as well as the extent to which current research findings support or refute some of these mechanisms as being critically
influenced by carbohydrate administration.

NEXT STAGE
Type 1 Diabetes, Muscle Health, and Exercise
Approximately 1.5 million North Americans are living with T1DM. Control of blood glucose for those with T1DM is critical for their health since glycemic dysregulation can accelerate the occurrence of a number of health complications as noted previously in this chapter. An article by Monaco and colleagues (2019) has highlighted additional issues associated with skeletal muscle health that appear to be accelerated by T1DM that also may be related to glycemic dysregulation and other complications. These issues link muscle function, health, and age-related muscle loss, which are discussed in more detail in chapter 8, with mechanisms that regulate blood glucose uptake and use as discussed in this chapter, and they highlight the complex interrelationships in biochemistry of health and exercise. In the commentary accompanying the Monaco et al. (2019) article, Alway (2019) notes that the hypothesis proposed by Monaco and colleagues (2019) is that the accelerated loss of muscle mass and function associated with T1DM is really a form of accelerated muscle aging, is a metabolic disease, and involves disruption of mitochondrial function. Monaco and colleagues (2019) note a number of similarities between muscle of aged and T1DM individuals. These include loss of muscle mass, which occurs after age 50 in normal individuals but starts much earlier in T1DM. They suggest that this may be partially attributable to the lack of tight insulin regulation (even if relatively well controlled) in those with T1DM, resulting in an overall disruption in insulin’s ability to suppress protein degradation as well as related disruption of growth hormone-IGF-1 function as it ultimately relates to glycemic dysregulation. Similar to older individuals, younger people with T1DM also experience a reduction in muscle satellite cell content, which could contribute to impaired muscle repair following exercise or damage and, hence, cumulatively to a reduced muscle size over time. Muscle strength and power are also compromised earlier in T1DM populations than normal adults.

Impairments in muscle metabolism, including dysregulation of glucose, lipid, and protein metabolism, are also characteristics of aging that occur earlier in individuals with T1DM (Monaco et al. 2019). The development of insulin insensitivity in those with T1DM is also common and may be related to poor glycemic control and the accumulation of intramyocellular lipids consequent to reduced mitochondrial oxidative capacity, which may also accelerate the production of oxygen radicals. In fact, mitochondrial dysfunction and reduction of mitochondrial oxidative capacity are consequences of T1DM and the primary factors in more rapid deterioration of muscle function and health in T1DM populations. This includes the more rapid loss of muscle mass and muscle strength, a reduction in muscle glycolytic and oxidative capacities, impaired mitochondrial Ca2+ handling, and increased production of oxygen radicals and resultant oxidative stress. Although the physiological links between T1DM and the deterioration of muscle and mitochondrial function are not well known, Monaco and colleagues (2019) have suggested that this may be a function of the hyperglycemic and low-insulin environment associated with T1DM, which results in both glucose and lipid overload exposure to muscles consequent to regular insulin injections that bypass the “liver-first” canonical pathway. It is suggested that this altered metabolic environment may promote posttranslational modifications of muscle and mitochondrial proteins, leading to functional impairments noted earlier.

Monaco and colleagues (2019) further propose that as with aging adults, muscle mitochondrial function may be improved by regular exercise in those with T1DM. Both aerobic and resistance exercise have been shown to improve muscle mitochondrial content as well as mitochondrial turnover and regeneration. The latter is particularly important in maintaining a healthy mitochondrial population. An earlier study by Monaco and colleagues (2018) demonstrated that even in a young, active T1DM population, significant mitochondrial metabolic and structural deficits were present. This highlights the complexities in managing blood glucose levels during and after exercise in individuals with T1DM. While current guidelines suggest at least a cumulative 150 min of moderate to vigorous exercise per week spread over at least 3 days, individual response differences, as well as exercise, type, intensity, duration, and insulin delivery mode and location, all will influence exercise and postexercise blood glucose response in those with T1DM (Scott et al. 2021). Hence, personalized monitoring of exercise insulin administration on blood glucose levels is critical in optimizing individual exercise and blood glucose responses to enhance health in those with T1DM (Scott et al. 2021).

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