What Happens to Your Body When You Stop Training?
Understanding how detraining impacts your VO2 max, endurance, and key body systems, along with actionable ways to protect your athletic gains.
Unfortunately, turning 30 last October wasn't just another birthday for me. Within the previous seven years I'd embraced high-volume training, a commitment often met by peers with the cautionary advice: "wait until you're 30 – you won't be able to sustain so much training". It turns out, there was some truth to that advice. Within these last few months I've faced a series of minor injuries, and one more persistent setback, that have significantly disrupted my routine.
This forced downtime, while frustrating, led me to a critical question: what happens to an athlete's body when regular training stops? How quickly do those hard-earned adaptations fade? And more importantly, can we do anything to lessen the impact?
Fortunately, scientific research offers some insights. Recent comprehensive reviews, such as those by Barbieri et al., Petek et al., and Zheng et al., provide a solid foundation for understanding the phenomenon of "detraining."
The consistent finding across these studies is that detraining is a tangible process. Just as consistent training leads to physiological improvements, a reduction or complete cessation of that training results in a loss of those adaptations.
However, the question of how quickly these changes occur and which aspects of our fitness are most affected is one which merits a closer look? This article will explore the physiological changes that occur when training is reduced, including the impact on the heart, muscles, and metabolic system. We will then delve into metrics more specific to runners, such as changes in VO2 max and running endurance. Finally, we'll discuss practical strategies that can help minimize the effects of detraining, allowing athletes to preserve their fitness even during periods of reduced activity.
Understanding the Detraining Effect on the Cardiac System
After considering the unexpected shifts that can occur when training is reduced, as noted in the introduction, understanding the specific physiological changes becomes crucial. Given the heart's central role in athletic performance, especially in movement-based sports, it serves as a logical starting point for our exploration of detraining's effects.
To appreciate these changes, a basic understanding of the heart's function is helpful. The heart, though often thought of as a single muscle, is essentially divided into two main sides: a right chamber and a left chamber. De-oxygenated blood from the body first enters the right chamber, flowing into the right atrium and then the right ventricle. From there, this blood is pumped a short distance to the lungs, where red blood cells pick up oxygen. The now oxygen-rich blood returns to the heart's left chamber, entering the left atrium and then the left ventricle. The left ventricle, a powerful pump, then sends this oxygenated blood out to the rest of the body, delivering it to muscles and other tissues. Once the oxygen is used, the de-oxygenated blood cycles back to the right chamber of the heart, restarting the process.
While the heart functions as a coordinated unit, the demands on its different chambers are not equal. The left ventricle typically performs more work because it must pump blood across the entire body, reaching even the farthest extremities. In contrast, the right ventricle only pumps blood to the nearby lungs. For this reason, the left ventricle is a key component in endurance activities like running, cycling, and swimming, which demand a continuous supply of oxygenated blood to the working muscles. Regular exercise leads to adaptations in the left ventricle, causing it to become thicker and stronger, enabling it to pump blood more efficiently.
However, the right ventricle experiences increased stress under certain conditions that affect breathing or blood flow within the lungs. Examples include exercising at high altitudes, where less oxygen is available; engaging in high-intensity interval sports, which cause rapid changes in blood pressure and breathing; or participating in breath-hold activities like free diving, where changes in chest pressure can significantly impact blood flow to the lungs.
What Changes During Detraining
Given that cardiac adaptations are influenced by the type and intensity of exercise performed, precisely quantifying how quickly and extensively the heart de-adapts can be complex. Nevertheless, observations indicate that changes in the heart's structure begin to occur relatively quickly during periods of reduced training.
Specifically, the mass of the left ventricle has been observed to start decreasing after just a few weeks of detraining. While there is some ongoing discussion about whether the overall size of the left chamber also reduces, studies consistently show that the reduction in mass is linked to a thinning of the left ventricle wall. This thinning can commence within 1 to 4 weeks of prolonged inactivity. It is worth noting that while long-term studies are limited, initial research suggests that some of the positive left ventricle adaptations, particularly chamber size, may remain for many years, resisting even more than a decade of reduced training.
Studies focusing on the right ventricle are less numerous however, initial findings in marathon runners suggest that reductions in its size can occur after approximately 8 weeks of no training, which is a slower rate compared to the changes seen in the left ventricle. Conversely, other studies involving athletes from various sports have reported no significant alterations in right ventricle dimensions, possibly due to the diverse training adaptations fostered by different athletic disciplines.
Beyond these structural alterations, more noticeable functional changes can also emerge. Within 28 days of detraining, the maximal heart rate can increase by 2 to 9 beats per minute. Over longer periods of inactivity, the resting heart rate may rise by approximately 13%, translating to an average increase of about 7 beats per minute compared to pre-detraining levels. Blood pressure also shows changes; during submaximal upright exercises, it can increase by 7% in the short term, and prolonged detraining can lead to an 11% increase in blood pressure during activities like swimming and cycling.
One additional research found that older athletes experienced a decline in blood flow to the brain after just 10 days of inactivity however, this did not appear to immediately impair their cognitive function.
Reversal of Musclar Adaptations During Rest
While the effects of detraining on muscles have been less extensively researched compared to other physiological systems, and sometimes with varying outcomes, existing studies, many dating from the late 1990s and early 2000s, offer valuable insights into what happens when training ceases.
Even after just a few days of reduced activity, observations suggest that muscle size can begin to decrease. This is often accompanied by a reduction in the rate at which new muscle proteins are generated, a process essential for muscle growth and repair.
Additionally, a noticeable shift can occur in the types of muscle fibers. Muscles are composed of different types of fibers, each suited for different tasks. Slow-twitch (Type I) fibers are efficient for endurance activities and resist fatigue, while fast-twitch fibers are responsible for powerful, explosive movements but fatigue more quickly. Fast-twitch fibers can be further categorized into Type IIa (which have a mix of endurance and power characteristics) and Type IIx (or IIb, the fastest and most powerful, but also the most easily fatigued). During detraining, there can be a transition from Type IIa muscle fibers towards Type IIx fibers. This means that while the muscle might retain its potential for bursts of high power, it becomes less efficient for sustained efforts and more prone to rapid fatigue, affecting overall endurance performance.
Another observed change is a reduction in the production of Adenosine Triphosphate (ATP). ATP serves as the primary energy currency for all cells, including muscle cells. It is created through a complex process that converts energy from the food we eat (carbohydrates, fats, and proteins) into a usable form that powers cellular activities. A decrease in ATP production means muscles have less immediate fuel, which can lead to them fatiguing more quickly.
Furthermore, some studies indicate a reduction in muscle capillarization. Capillaries are tiny blood vessels that form a dense network around muscle fibers, playing a crucial role in delivering oxygen and nutrients to the muscles, and removing waste products. A reduction in this network means oxygen and nutrients don't reach the muscle as quickly or efficiently, and waste removal is slower. This impaired delivery also contributes to muscles fatiguing more rapidly. This decrease in oxygen supply to the muscles is also considered one of the factors contributing to the decline in VO2 max, a topic we will explore in greater detail later.
How Your Body's Fuel System Changes
Beyond the heart and muscles, detraining also significantly impacts the body's metabolism - the complex set of chemical processes that convert food into energy and support all bodily functions. A trained metabolism is highly efficient at using different fuel sources, but this efficiency can diminish rapidly with reduced activity.
One notable change observed within 90 days of no training is a shift in the body's fuel-burning preference, indicated by a change in the 'fuel burning' rate from 0.93 to 1.0. For trained individuals, the body becomes highly adept at burning a mix of carbohydrates and fat for energy, especially during sustained efforts. This fat-burning efficiency is beneficial because it spares the body's limited carbohydrate stores, which are crucial for higher intensity activities. However, with detraining, the body tends to rely more heavily on carbohydrates as its primary fuel, even at intensities where it previously used a greater amount of fat. This means the body loses some of its fuel versatility and may deplete its carbohydrate reserves more quickly.
Additionally, a drop in lactate threshold is observed within a few weeks of reduced training. The lactate threshold is the exercise intensity at which lactate, a byproduct of energy production, begins to accumulate rapidly in the blood. In trained individuals, this threshold is higher, meaning they can sustain higher intensities before lactate build-up causes fatigue. With detraining, the body starts producing more lactate at the same intensity, and lactate accumulation begins even at lower intensity levels. This accelerated lactate accumulation contributes to quicker fatigue at intensities that were previously manageable.
Similarly, within a few weeks, your muscles' ability to create and store glycogen reduces. Glycogen is the stored form of carbohydrates in your muscles, serving as the body's primary and most readily available fuel source particularly for high-intensity exercise. A reduced capacity to store glycogen means muscles have less immediate fuel readily available, leading to quicker exhaustion during physical activity.
When it comes to metabolic detraining, one of the most visible effects can be seen in body weight and body composition. Research indicates that body weight and composition tend to remain relatively stable for about 4 weeks after training cessation however, beyond this period, a noticeable increase in body weight is common, typically characterized by an increase in body fat and a reduction in muscle mass.
Measuring Detraining Through Key Performance Metrics
For runners, VO2 max is often considered a gold standard measure of aerobic fitness. It represents the maximum amount of oxygen your body can effectively use during intense or maximal exercise. While VO2 max itself is a single measurable value, its decline during detraining is influenced by a combination of all the physiological changes we've discussed so far, including adaptations in the heart, muscles, and metabolic system.
Studies on the effects of detraining on VO2 max are abundant and reveal clear patterns. In the short term, typically defined as up to 28 days of reduced or no training, a reduction of at least 4% in VO2 max has been consistently observed. This decline can increase to 10% when detraining periods extend between 28 and 90 days. Interestingly, for highly trained athletes, the rate of decrease in VO2 max tends to stabilize, with no significant additional decline typically observed beyond the 90-day mark.
However, it is important to recognize that the reduction in VO2 max is not uniform across all individuals; factors such as age, prior training status, and the type of detraining (whether it's a complete cessation or partial reduction in activity) can lead to significantly different outcomes. For instance, a more pronounced initial decrease in VO2 max has been noted in highly trained athletes who start with higher baseline values. Despite this steeper initial decline, these athletes often retain a portion of their gains over longer detraining periods, whereas less trained individuals may experience a complete loss of their acquired fitness over extended periods of inactivity.
Age also plays a role in how VO2 max is affected by detraining. Younger athletes tend to show a greater reduction in VO2 max over long periods of inactivity compared to older athletes, suggesting older individuals might exhibit a degree of resistance to detraining's effects in this regard. The precise reasons for this age-related difference, such as the influence of accumulated training over a lifetime, are not yet fully understood. In a related observation, younger athletes also demonstrated a smaller decline in maximal cycling power output tests compared to their older counterparts, further illustrating that different age groups may respond distinctly to detraining.
Beyond VO2 max, detraining also impacts practical running performance metrics. While running economy, how efficiently a runner uses oxygen at a given speed, generally shows no significant changes during detraining, overall endurance performance is compromised relatively quickly. Evidence from time to exhaustion tests shows a reduction of approximately 9% after just two weeks of reduced training. This reduction in the ability to sustain effort is largely attributed to the increased levels of blood lactate, a phenomenon we discussed in the previous section on metabolism.
This section highlights how the internal physiological changes in the heart, muscles, and metabolism manifest as observable declines in key performance indicators like VO2 max and running endurance. This reinforces the core principle established at the outset of this article: just as consistent training leads to positive physical adaptations, those very adaptations will reverse once training is reduced or ceases.
Strategies to Preserve Fitness
The prospect of losing hard-earned adaptations, which often take years to develop and can diminish in a matter of days or weeks, might seem discouraging. However, the scientific literature also offers practical strategies to significantly reduce these detraining effects.
The most straightforward approach to minimize detraining is to adopt a partial reduction in training, rather than a complete cessation. Studies indicate that VO2 max, a key indicator of aerobic fitness, can be largely maintained for up to 15 weeks if athletes sustain a program with reduced frequency and duration, provided they maintain a sufficient intensity. For instance, engaging in a 40-minute training session at approximately 80% of maximum heart rate twice a week has been shown to significantly slow the decrease in VO2 max. Similarly, for longer-term maintenance, jogging at 50-60% of VO2 max for 20-30 minutes, two to three times a week, can help offset many negative effects of detraining, though higher intensity efforts would still be needed to maintain VO2 max.
This evidence suggests that a total reduction in training load and intensity is generally not advisable for periods longer than one or two weeks. Even a minimal training dose appears sufficient to offset a portion of the observed detraining effects.
For athletes entering an off-season, the recommendation is to continue with a few weekly workouts, ideally including two high-intensity sessions, to help preserve fitness.
For athletes recovering from musculoskeletal injuries, rehabilitation efforts should incorporate cross-training. This involves activities that allow the athlete to achieve similar intensities and cardiac output to their main sport, without putting undue stress on the injured area. Such interventions can play a crucial role in reducing the negative effects of detraining, ensuring the athlete is well-prepared to resume progression shortly after returning to their regular training.
In conclusion, while the body's adaptations to training are indeed reversible, a principle evident across the cardiac, muscular, and metabolic systems, as well as in critical performance metrics like VO2 max and running endurance, this reversal is not an uncontrollable process. By understanding how the body de-adapts, athletes can implement targeted strategies, even with a reduced training volume or alternative activities. This proactive approach allows for the preservation of a substantial portion of hard-earned fitness, ensuring that periods of reduced training become manageable plateaus rather than complete setbacks, and enabling a smoother, quicker return to peak performance.