This is dedicated to all my cycling buddies who have noticed that if we are away from the bike for a couple of weeks that our endurance begins to suffer. What’s going on here? Is it anything serious? Is there some point at which all of our previous conditioning goes for naught?
I’m referring here to the effects of complete inactivity on endurance, when a once well-conditioned athlete goes “cold turkey” and does not engage in any type of physical training for a particular time period, regardless of the reason.
Physiologists have studied the effects of training cessation on well-conditioned endurance athletes. The term they’ve coined for this type of inactivity is “detraining.” Detraining is different from either tapering or maintenance, both of which involve purposeful physical activity which guards against performance decline when athletes are not engaged in their normal training routines. Detraining is also different from the type of recovery in which a cyclist may be inactive for a few days following a long, multi-day ride, for example.
Detraining can result in the loss of physiological gains that have accrued in some cases from years of endurance training. Some of the declines begin to occur in as little as two weeks of inactivity. In one particular study that I use as a reference and whose results I report here, most declines begin to plateau at about 56 days of detraining. However, even the fully detrained athlete has greater endurance than a sedentary control who never trained.
What follows is a brief summary of some of the physiological declines affecting performance in endurance athletes and their timeline. Caution should be exercised in generalizing these findings to individual circumstances. As our riding buddy, Lin, so aptly puts it, “Your mileage may vary.”
12 Days of Detraining
In as little as 12 days of detraining, there are perceptible physiological changes affecting performance.
Most notable to athletes themselves is an increase in perceived exertion during sub-maximal exercise accompanied by an increased heart rate.
What’s happening? At the cellular level, there is a decline in the activity of muscle mitochondrial enzymes. These enzymes convert fuel in the presence of oxygen to the high-energy molecule—ATP—which powers muscles. With a decrease in enzyme activity, muscles cannot work as hard, since there is less ATP. The mitochondrial enzymes rather than oxygen have become the limiting factor. It is easy to understand why VO2 max, which is a measure of the peak volume of oxygen the body consumes during a given time period for a given body weight, declines. VO2max is sometimes taken as an indicator of endurance potential.
During this same time period, there are metabolic changes. Muscles begin to shift away from using fat to using carbohydrate for energy. Ironically, however, a muscle’s ability to store carbohydrate—in the form of glycogen—begins to decline with detraining and, unfortunately, returns to baseline levels within just a few weeks of detraining. Moreover, because carbohydrates provide less energy than fats, the athlete who is detraining pays double. One particular study notes the abrupt onset of these latter changes with detraining:
These metabolic changes may take place within 10 d[ays] of training cessation.
21 Days of Detraining
At 21 days of detraining, the aforementioned declines continue, while others become noticeable.
The reduction in fat metabolism has decreased now from 24% of energy utilization to 7%.
The rate of decline in muscle mitochondrial enzyme activity, which was first noticeable after just 10-12 days of detraining, has accelerated.
Ventilation (breathing) has increased significantly from day 12 of detraining.
Other noticeable changes at this time include declines in blood volume (mostly plasma); stroke volume; and VO2max. Meanwhile, peripheral resistance in blood vessels has increased.
What does all this mean? An increase in peripheral resistance means that the heart must pump harder to get blood to the tissues. Because stroke volume (the amount of blood the heart pumps with each contraction) has decreased, heart rate must increase to compensate.
In contrast, well-conditioned athletes possess the opposite cardiovasculature: low peripheral resistance, low pulse, and high stroke volume. Moreover, conditioned athletes store more glycogen (while burning it more efficiently) and metabolize fat better than detrained athletes.
56 Days of Detraining
At 56 days of detraining, many of the aforementioned declines begin to plateau.
VO2max appears to stabilize as does the activity of mitochondrial enzymes, with values still 50% above those of sedentary controls.
Moreover, there is no reduction in muscle capillarization, the amount of small blood vessels serving the muscles. However, stroke volume and mitochondrial enzyme activity have declined to control, or baseline, levels.
By this time, there is a noticeable change in the type of skeletal muscle fibers (cells) brought about by inactivity. Broadly speaking, skeletal muscles are made up of type I and type II fibers, type I being preferred by endurance athletes due to their resistance to fatigue during aerobic exercise. There are also two types of type II muscle fibers—type IIa and type IIb. Type IIa is preferred over type IIb for the same reason that type I is preferred over type II. While there is no loss of type I muscle fibers, detraining results in the conversion of a percentage of type IIa fibers to the less-preferred type IIb fibers. In fact there was an increase in type IIb fibers from 5% to 19% as a result of detraining
60 Days of Detraining
At 60 days of detraining, there is measurable atrophy (decrease in thickness) of the heart’s muscle wall and, consequently, its ability to pump. This corresponds to the decrease in stroke volume noted earlier, necessitating a faster pulse.
84 Days of Detraining
At 84 days of detraining, the once highly conditioned endurance athlete still has 50% more mitochondrial enzyme activity than the sedentary individual who has never trained.
Additionally, the former still enjoys 22% better lactate dehydrogenase (LDH) enzyme activity over controls.
The more LDH activity an individual has the greater is his or her lactate threshold. An athlete with a high lactate threshold is able to exercise at a higher level aerobically than an athlete with a lower lactate threshold. The lactate threshold is the point at which an athlete begins metabolizing anaerobically. (Anaerobic respiration is incompatible with endurance cycling.) This occurs because lactate, which is a by-product of anaerobic respiration, interferes with other metabolic pathways. LDH removes lactate (or what some refer to as lactic acid). It follows from this that an athlete’s LDH enzyme activity is a good indicator of aerobic or endurance conditioning (capacity).
Summary
It is true that an endurance athlete’s performance begins to suffer as a direct result of inactivity even in the space of ten days. The good news is that performance decline is not progressively linear as a function of time of inactivity. While we may lose our competitive edge quickly, the physiological declines of inactivity begin to plateau at about 56 days with the exceptions of stroke volume and glycogen storage capacity both of which continue to decline to baseline, or control, levels. Consequently, the detrained athlete will still be able to outperform the sedentary individual who has never trained. Even the pumping action of the heart of a fully detrained fifty-year-old male is as strong as that of a much younger male who has never trained.
There are ways that endurance athletes with limited time to condition can stave off the adverse effects of detraining, that is, if they can manage short, intense workouts known as interval training. One possibility for cyclists who wish to maintain their present conditioning level is speed training. According to some:
[S]peed endurance training can maintain muscle oxidative capacity, capillarization, and endurance performance in already trained individuals despite reduction in the amount of training.
Another group maintains that athletes who are able to train as little as once per week at 70% VO2 max are still able to maintain their aerobic conditioning level.
Summary of Physiological Effects of Detraining
Heart rate increases as well as total peripheral resistance
Blood volume decreases (mostly the plasma portion)
Stroke volume decreases to baseline levels
Cardiac output decreases
VO2max decreases
Conversion of some type IIa skeletal muscle fibers to type IIb muscle fibers
Lactate threshold decreases
Ventilatory efficiency decreases while rate increases
Fat metabolism decreases while carbohydrate metabolism increases
Resting muscle glycogen levels decrease
Mitochondrial enzyme activity decreases
Let’s ride!
I’m referring here to the effects of complete inactivity on endurance, when a once well-conditioned athlete goes “cold turkey” and does not engage in any type of physical training for a particular time period, regardless of the reason.
Physiologists have studied the effects of training cessation on well-conditioned endurance athletes. The term they’ve coined for this type of inactivity is “detraining.” Detraining is different from either tapering or maintenance, both of which involve purposeful physical activity which guards against performance decline when athletes are not engaged in their normal training routines. Detraining is also different from the type of recovery in which a cyclist may be inactive for a few days following a long, multi-day ride, for example.
Detraining can result in the loss of physiological gains that have accrued in some cases from years of endurance training. Some of the declines begin to occur in as little as two weeks of inactivity. In one particular study that I use as a reference and whose results I report here, most declines begin to plateau at about 56 days of detraining. However, even the fully detrained athlete has greater endurance than a sedentary control who never trained.
What follows is a brief summary of some of the physiological declines affecting performance in endurance athletes and their timeline. Caution should be exercised in generalizing these findings to individual circumstances. As our riding buddy, Lin, so aptly puts it, “Your mileage may vary.”
12 Days of Detraining
In as little as 12 days of detraining, there are perceptible physiological changes affecting performance.
Most notable to athletes themselves is an increase in perceived exertion during sub-maximal exercise accompanied by an increased heart rate.
What’s happening? At the cellular level, there is a decline in the activity of muscle mitochondrial enzymes. These enzymes convert fuel in the presence of oxygen to the high-energy molecule—ATP—which powers muscles. With a decrease in enzyme activity, muscles cannot work as hard, since there is less ATP. The mitochondrial enzymes rather than oxygen have become the limiting factor. It is easy to understand why VO2 max, which is a measure of the peak volume of oxygen the body consumes during a given time period for a given body weight, declines. VO2max is sometimes taken as an indicator of endurance potential.
During this same time period, there are metabolic changes. Muscles begin to shift away from using fat to using carbohydrate for energy. Ironically, however, a muscle’s ability to store carbohydrate—in the form of glycogen—begins to decline with detraining and, unfortunately, returns to baseline levels within just a few weeks of detraining. Moreover, because carbohydrates provide less energy than fats, the athlete who is detraining pays double. One particular study notes the abrupt onset of these latter changes with detraining:
These metabolic changes may take place within 10 d[ays] of training cessation.
21 Days of Detraining
At 21 days of detraining, the aforementioned declines continue, while others become noticeable.
The reduction in fat metabolism has decreased now from 24% of energy utilization to 7%.
The rate of decline in muscle mitochondrial enzyme activity, which was first noticeable after just 10-12 days of detraining, has accelerated.
Ventilation (breathing) has increased significantly from day 12 of detraining.
Other noticeable changes at this time include declines in blood volume (mostly plasma); stroke volume; and VO2max. Meanwhile, peripheral resistance in blood vessels has increased.
What does all this mean? An increase in peripheral resistance means that the heart must pump harder to get blood to the tissues. Because stroke volume (the amount of blood the heart pumps with each contraction) has decreased, heart rate must increase to compensate.
In contrast, well-conditioned athletes possess the opposite cardiovasculature: low peripheral resistance, low pulse, and high stroke volume. Moreover, conditioned athletes store more glycogen (while burning it more efficiently) and metabolize fat better than detrained athletes.
56 Days of Detraining
At 56 days of detraining, many of the aforementioned declines begin to plateau.
VO2max appears to stabilize as does the activity of mitochondrial enzymes, with values still 50% above those of sedentary controls.
Moreover, there is no reduction in muscle capillarization, the amount of small blood vessels serving the muscles. However, stroke volume and mitochondrial enzyme activity have declined to control, or baseline, levels.
By this time, there is a noticeable change in the type of skeletal muscle fibers (cells) brought about by inactivity. Broadly speaking, skeletal muscles are made up of type I and type II fibers, type I being preferred by endurance athletes due to their resistance to fatigue during aerobic exercise. There are also two types of type II muscle fibers—type IIa and type IIb. Type IIa is preferred over type IIb for the same reason that type I is preferred over type II. While there is no loss of type I muscle fibers, detraining results in the conversion of a percentage of type IIa fibers to the less-preferred type IIb fibers. In fact there was an increase in type IIb fibers from 5% to 19% as a result of detraining
60 Days of Detraining
At 60 days of detraining, there is measurable atrophy (decrease in thickness) of the heart’s muscle wall and, consequently, its ability to pump. This corresponds to the decrease in stroke volume noted earlier, necessitating a faster pulse.
84 Days of Detraining
At 84 days of detraining, the once highly conditioned endurance athlete still has 50% more mitochondrial enzyme activity than the sedentary individual who has never trained.
Additionally, the former still enjoys 22% better lactate dehydrogenase (LDH) enzyme activity over controls.
The more LDH activity an individual has the greater is his or her lactate threshold. An athlete with a high lactate threshold is able to exercise at a higher level aerobically than an athlete with a lower lactate threshold. The lactate threshold is the point at which an athlete begins metabolizing anaerobically. (Anaerobic respiration is incompatible with endurance cycling.) This occurs because lactate, which is a by-product of anaerobic respiration, interferes with other metabolic pathways. LDH removes lactate (or what some refer to as lactic acid). It follows from this that an athlete’s LDH enzyme activity is a good indicator of aerobic or endurance conditioning (capacity).
Summary
It is true that an endurance athlete’s performance begins to suffer as a direct result of inactivity even in the space of ten days. The good news is that performance decline is not progressively linear as a function of time of inactivity. While we may lose our competitive edge quickly, the physiological declines of inactivity begin to plateau at about 56 days with the exceptions of stroke volume and glycogen storage capacity both of which continue to decline to baseline, or control, levels. Consequently, the detrained athlete will still be able to outperform the sedentary individual who has never trained. Even the pumping action of the heart of a fully detrained fifty-year-old male is as strong as that of a much younger male who has never trained.
There are ways that endurance athletes with limited time to condition can stave off the adverse effects of detraining, that is, if they can manage short, intense workouts known as interval training. One possibility for cyclists who wish to maintain their present conditioning level is speed training. According to some:
[S]peed endurance training can maintain muscle oxidative capacity, capillarization, and endurance performance in already trained individuals despite reduction in the amount of training.
Another group maintains that athletes who are able to train as little as once per week at 70% VO2 max are still able to maintain their aerobic conditioning level.
Summary of Physiological Effects of Detraining
Heart rate increases as well as total peripheral resistance
Blood volume decreases (mostly the plasma portion)
Stroke volume decreases to baseline levels
Cardiac output decreases
VO2max decreases
Conversion of some type IIa skeletal muscle fibers to type IIb muscle fibers
Lactate threshold decreases
Ventilatory efficiency decreases while rate increases
Fat metabolism decreases while carbohydrate metabolism increases
Resting muscle glycogen levels decrease
Mitochondrial enzyme activity decreases
Let’s ride!
