Resting Heart Rate Changes in Overtrained Athletes: What Your Morning Pulse Is (and Isn’t) Telling You
Table of Contents
Introduction
In clinical practice, I often see disruptions in heart rate regulation in overtrained patients. Many describe a noticeable increase in their resting heart rate, sometimes confirmed by wearable devices. Others present with reduced heart rate variability (HRV). In my experience, however, an elevated resting heart rate is often one of the most obvious and intuitive signals for the athlete, and the one that most commonly raises concern about inadequate recovery.
Overtraining is associated with widespread physiological changes across multiple systems. In clinical practice, I often observe alterations in resting heart rate (RHR), alongside broader physiological changes reflected in heart rate variability (HRV) and laboratory markers such as cortisol, testosterone, and their ratios—although these findings are variable and not consistently reliable as diagnostic markers.
Resting heart rate (RHR) changes in response to overtraining. Resting heart rate changes in overtrained athletes do not always occur in the direction athletes expect, not always with the magnitude coaches assume, and not always through mechanisms that a single morning measurement can reliably capture. In this article I will examine what peer-reviewed evidence actually shows about how RHR behaves across the overtraining continuum, why both elevations and reductions can be clinically meaningful, what limits the utility of morning RHR as a standalone marker, and how to build a monitoring approach that uses heart rate data more intelligently— particularly when interpreting resting heart rate changes in overtrained athletes.
The Overtraining Continuum: Where Heart Rate Fits
Before examining RHR specifically, it is necessary to understand where it sits within the broader overtraining framework. The joint consensus statement of the European College of Sport Science and the American College of Sports Medicine defines three distinct states along a training-recovery spectrum [7]:
Functional overreaching (FOR) involves a temporary performance decrement that resolves within days to weeks after appropriate rest, often yielding a supercompensatory performance gain.
Non-functional overreaching (NFOR) represents a more prolonged performance decrement — weeks to months — accompanied by psychological and neuroendocrinological symptoms.
Overtraining syndrome (OTS) is defined by a performance decrement lasting more than two months, more severe systemic maladaptation, and the exclusion of other medical diagnoses.
The distinction between NFOR and OTS matters clinically but is often only made in retrospect, based on how long recovery takes [7]. Research into RHR changes spans all three states, which contributes to some of the contradictions in the literature.
Epidemiologically, the burden of these conditions is substantial. Survey-based career prevalence estimates have reached approximately 60–64% in elite runners and 34.6% in age-group competitive swimmers, though these figures are derived from retrospective self-report rather than prospective clinical diagnosis and are vulnerable to recall bias and inconsistent case definitions [1][7]. They nonetheless reflect the genuine frequency with which athletes encounter this spectrum of conditions.
Many of the elite athletes I see in clinical practice go through at least a phase of non-functional overreaching at some point in their careers, and in some cases this progresses to true OTS. In my own athletic career, I deliberately pursued functional overreaching as part of structured training, aiming for supercompensation and peak performance, although periods of non-functional overreaching likely occurred as well. In reality, this exists on a continuum, where the boundary between adaptive and maladaptive states is not always clear.
How the Autonomic Nervous System Drives RHR Changes
The heart rate at rest is not determined by the heart alone — it is actively regulated by the autonomic nervous system (ANS). Understanding this regulation is the key to interpreting heart rate changes during overtraining, because the direction of those changes depends critically on which branch of the ANS predominates [2].
Under normal training conditions, endurance training progressively increases parasympathetic (vagal) tone and reduces sympathetic drive at rest, producing the well-known training bradycardia of well-conditioned athletes — resting heart rates of 40–50 bpm are common in highly trained endurance athletes [1].
When training load exceeds the athlete’s adaptive capacity, this ANS equilibrium is disrupted. The literature describes two commonly observed patterns — though it is important to note that real-world presentations are often mixed, shifting, or intermediate rather than cleanly binary [2]:
Sympathetic overtraining — more common in athletes training at high intensity in anaerobic sports (sprinting, jumping, throwing) — involves sympathetic dominance at rest. The hallmarks include elevated resting heart rate, restlessness, insomnia, irritability, elevated blood pressure, and agitation. This pattern is sometimes considered an early-stage response to excessive load, representing the body’s attempt to maintain homeostasis through upregulation of stress system activity [2].
Interestingly, I recognized my own period of overtraining partly from a consistent pattern of waking at night to urinate. It became a near-nightly occurrence, and in retrospect, it likely reflected disrupted sleep and increased autonomic arousal rather than a specific physiological marker of overtraining itself.
Parasympathetic overtraining — more prevalent in high-volume endurance athletes (distance runners, cyclists, swimmers) — involves progressive parasympathetic dominance and sympathetic suppression. Paradoxically, this pattern may present with decreased or unchanged resting heart rate alongside symptoms of fatigue, depression, apathy, and loss of motivation [1][2]. Not every case shows overt bradycardia; some athletes present with normal RHR but markedly impaired HRV and subjective deterioration. The body, having exhausted its capacity to sustain sympathetic overactivation, shifts into what might be characterized as a physiological withdrawal state.
This classical model explains a persistent source of confusion in both the research literature and clinical practice: overtrained athletes may have either higher or lower resting heart rates than their baseline depending on where they sit on the overtraining continuum, what sport they train for, and how far the process has progressed. Newer research suggests the division between these phenotypes is not always sharp, and some athletes exhibit dysregulated ANS function that does not map neatly onto either category [2].
Most of my athletic patients are familiar with the concept of sympathetic overtraining, and it is often easier to recognize due to its more classic and overt symptoms. In contrast, the parasympathetic form is often new to them. Many athletes already have a low resting heart rate, which is commonly attributed to good fitness or “athlete’s heart,” making this presentation more difficult to recognize clinically. In my experience, it can also resemble fatigue syndromes or burnout, which further complicates interpretation.
Resting Heart Rate Changes in Overtrained Athletes: What the Meta-Analysis Actually Shows
The most rigorous quantitative evaluation of heart rate as an overreaching marker comes from a meta-analysis published in the British Journal of Sports Medicine, which pooled data from studies using competitive athletes subjected to controlled overload training protocols [3].
For short-term interventions (less than two weeks of overload), the analysis found a moderate increase in resting heart rate (standardized mean difference = 0.55; p = 0.01) alongside a moderate decrease in maximal exercise heart rate (SMD = -0.75; p = 0.01). This concurrent elevation in resting HR and suppression of maximal HR represents a characteristic autonomic signature of short-term overload: resting sympathetic tone is increased while the cardiovascular response to maximal effort is blunted [3].
For long-term interventions (more than two weeks), the picture changed. Resting heart rate was no longer meaningfully altered, while submaximal and maximal exercise heart rate showed small but significant decreases [3].
The authors were careful to note a critical limitation: the amplitude of resting HR changes — particularly the moderate effect size of 0.55 — means that expected differences may fall within the day-to-day biological variability of the measurement itself [3]. A resting heart rate that fluctuates by 3–5 bpm day to day due to sleep quality, hydration, ambient temperature, or caffeine may mask or mimic overtraining-related changes of comparable magnitude.
This finding does not render RHR monitoring useless. It means that single-point morning measurements cannot be interpreted in isolation, and that the magnitude of deviation required to be meaningful exceeds what many coaches and athletes assume.
In my clinical practice, the diagnosis of overtraining syndrome is always a holistic assessment and, importantly, a diagnosis of exclusion—it cannot be based on any single measurement parameter. I consider the broader clinical picture, including performance changes, symptoms, and recovery patterns. That said, patients often use resting heart rate as an early clue that they can monitor and recognize themselves. At the same time, I emphasize that the absence of changes in resting heart rate does not exclude the diagnosis—normal RHR does not rule out overtraining syndrome. I also frequently see elevated resting heart rate associated with psychological stress, burnout, or anxiety, which often coexist and can present with overlapping symptoms, making them clinically difficult to distinguish from one another.
The Sleeping Heart Rate Advantage
One of the more practically important nuances in the literature concerns the difference between morning waking RHR and heart rate measured during sleep.
A review of intensified training research summarizes a study of well-trained cyclists who increased their weekly training duration by 45% and high-intensity training volume by 350% over two weeks [5]. All subjects developed overtraining symptoms with measurable performance decrements. Maximal heart rate fell significantly. Time trial performance deteriorated. And notably, sleeping heart rate increased while the heart rate pattern during the night became less regular, with higher peaks compared with the normal training state [5].
This finding points to an important consideration: nocturnal heart rate monitoring, particularly when averaged over multiple hours of sleep, may provide a more stable and sensitive signal than a brief pre-waking measurement taken under conditions that are difficult to fully standardize (time spent awake before measurement, body position, ambient noise, bladder fullness). A 2024 study in 24 recreational runners found that while nocturnal and morning HR and HRV correlated moderately to highly during baseline training, their responses to intensified training were not similarly aligned — nocturnal recordings appeared sensitive to acute physical loading and were associated with performance-related training responses, suggesting they provide complementary rather than interchangeable information to morning measurements [8].
Modern wearable devices — including chest straps, wrist-worn monitors, and ring-based sensors — now make continuous nocturnal HR recording accessible to most athletes, representing a practical upgrade from the traditional morning finger-on-wrist count.
Many of my patients use smart rings that continuously track heart rate throughout the day and night. As a result, they often have access to nocturnal resting heart rate data, whereas those using wrist-worn devices frequently need to charge them overnight and may lack this information. In that sense, smart rings can be among the most practical tools for monitoring nocturnal heart rate in everyday settings. These devices often also provide additional metrics, such as sleep quality and heart rate variability (HRV), which together can offer a fairly comprehensive picture of recovery and physiological state. At the same time, it is important to recognize that these consumer devices lack full standardization, and their findings should be seen as supportive rather than definitive—they can inform clinical reasoning but should not be used in isolation to make clinical conclusions.
HRV: The Mechanistically Richer Signal
Heart rate variability (HRV) — the beat-to-beat variation in the intervals between heartbeats — reflects autonomic regulation with considerably more nuance than heart rate alone. Where RHR provides a single number, HRV captures the dynamic interplay between sympathetic and parasympathetic drives and can detect autonomic dysfunction before it becomes large enough to shift RHR by a clinically detectable margin. Many of my patients are increasingly familiar with HRV; it is increasingly becoming common knowledge among athletes, particularly with the growing use of smart rings and other wearable devices.
A study examining 12 severely overtrained athletes (6 men, 6 women) and 12 matched control athletes found no significant differences in HRV during night sleep itself [4]. However, after awakening, overtrained athletes showed meaningfully lower standard deviation of RR intervals (84 ± 31 ms versus 116 ± 41 ms; p < 0.05) and reduced low-frequency HRV power (2153 ± 2232 vs 4286 ± 2904 ms²; p < 0.05) [4]. The transition from sleep to waking normally involves an upregulation of sympathetic activity; in overtrained athletes, this transition was blunted, suggesting a reduced capacity for normal ANS responsiveness [4].
Research in athletes with confirmed NFOR and OTS found lower HRV and reduced vagal influence alongside increased sympathetic cardiovascular control compared with well-trained athletes without overtraining [2]. HRV findings across studies are not entirely uniform — some cohorts show sympathetic dominance, others show reduced overall autonomic activity — which reflects the heterogeneity of the overtraining spectrum itself. In athletes with the most advanced OTS, a state of “total autonomic dystonia” — representing depression of both branches of the ANS — has been reported in some cohorts in up to approximately 67% of cases, reflecting the most severe degree of regulatory failure [2]. This category is not yet universally standardized and should be understood as a descriptive framework rather than a replicated diagnostic threshold.
This is why HRV, particularly when measured in the morning after awakening, is increasingly considered a mechanistically richer signal than RHR alone. It is worth noting that ANS dysregulation is not the only physiological driver of OTS — concurrent disruption of the hypothalamic-pituitary-adrenal axis, with alterations in cortisol and ACTH responses to exercise stress, and changes in central neurotransmitter dynamics (particularly serotonergic and dopaminergic pathways) contribute to the syndrome’s full symptom profile [1][2]. Heart rate monitoring captures the autonomic dimension of this broader systemic disruption.
At the same time, neither physiological metrics nor laboratory findings alone are sufficient to establish the diagnosis—accurate assessment requires a thorough clinical anamnesis and the judgment of an experienced clinician, integrating these findings into the overall clinical context. In Finland, we have sports medicine specialists who are specifically trained in diagnosing overtraining syndrome. In many cases, the diagnosis is only confirmed after assessment by such a specialist; prior to that, it often remains a clinical suspicion rather than a definitive diagnosis.
If my patient has access to a wearable device, heart rate variability (HRV) often provides more nuanced insight into recovery than resting heart rate alone. However, in patients without such devices, an increase in resting heart rate is often the first change they notice themselves, and can serve as a simple, low-threshold indicator of inadequate recovery.
Summary
In summary, resting heart rate is a useful but inherently limited marker in the assessment of overtraining. While an elevated RHR can serve as an early and intuitive signal of inadequate recovery—often first noticed by the athlete themselves—it does not behave consistently across the overtraining continuum and cannot be interpreted in isolation. Both increases and decreases in resting heart rate may be clinically meaningful, depending on the underlying autonomic state, which contributes to confusion in both research and practice.
Heart rate variability and nocturnal heart rate measurements can add important depth to this picture. HRV, in particular, reflects autonomic regulation in a more nuanced way and may reveal changes that are not yet visible in resting heart rate. Similarly, nocturnal measurements provide a more stable signal that is less affected by measurement conditions. When combined—especially through wearable devices that track sleep, HRV, and heart rate continuously—these metrics can offer a more comprehensive view of recovery and physiological stress. At the same time, it is important to recognize that consumer devices lack full standardization, and their outputs should be interpreted as supportive rather than definitive.
Ultimately, overtraining syndrome is a complex, multi-system condition involving not only autonomic dysregulation, but also endocrine, central nervous system, and psychological components. No single metric—whether RHR, HRV, or laboratory values—is sufficient to establish the diagnosis. In clinical practice, OTS remains a diagnosis of exclusion that requires a careful anamnesis, evaluation of performance trends, and consideration of overlapping conditions such as stress, burnout, and anxiety. Objective measurements can provide useful clues and help guide clinical reasoning, but they do not replace it. The diagnosis is made by integrating multiple signals into a coherent clinical picture, guided by experience and clinical judgment.
References
1 https://pmc.ncbi.nlm.nih.gov/articles/PMC3435910/
2 https://pmc.ncbi.nlm.nih.gov/articles/PMC10013019/
3 https://pubmed.ncbi.nlm.nih.gov/18308872/
4 https://pubmed.ncbi.nlm.nih.gov/16531900/
5 https://pmc.ncbi.nlm.nih.gov/articles/PMC3963240/
