How Long Does It Take for Your Body Too Recover From 2 Days of Continuous Strenuous Activity
J Appl Physiol (1985). 2017 Apr 1; 122(4): 925–932.
Recovery from Exercise
The cardiovascular system after exercise
Steven A. Romero
1University of Texas Southwestern Medical Center, Dallas, Texas;
2Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, Texas; and
Christopher T. Minson
3Department of Human Physiology, University of Oregon, Eugene, Oregon
John R. Halliwill
3Department of Human Physiology, University of Oregon, Eugene, Oregon
Received 2016 Sep 9; Revised 2017 Jan 10; Accepted 2017 Jan 12.
Abstract
Recovery from exercise refers to the time period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It also refers to specific physiological processes or states occurring after exercise that are distinct from the physiology of either the exercising or the resting states. In this context, recovery of the cardiovascular system after exercise occurs across a period of minutes to hours, during which many characteristics of the system, even how it is controlled, change over time. Some of these changes may be necessary for long-term adaptation to exercise training, yet some can lead to cardiovascular instability during recovery. Furthermore, some of these changes may provide insight into when the cardiovascular system has recovered from prior training and is physiologically ready for additional training stress. This review focuses on the most consistently observed hemodynamic adjustments and the underlying causes that drive cardiovascular recovery and will highlight how they differ following resistance and aerobic exercise. Primary emphasis will be placed on the hypotensive effect of aerobic and resistance exercise and associated mechanisms that have clinical relevance, but if left unchecked, can progress to symptomatic hypotension and syncope. Finally, we focus on the practical application of this information to strategies to maximize the benefits of cardiovascular recovery, or minimize the vulnerabilities of this state. We will explore appropriate field measures, and discuss to what extent these can guide an athlete's training.
Keywords: blood pressure, heart rate, blood flow, recovery, athletic performance
recovery from exercise refers to the time period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It also refers to specific physiological processes or states occurring after exercise that are distinct from the physiology of either the exercising state or the resting state (44). In this context, recovery of the cardiovascular system after exercise occurs across a period of minutes to hours, recognized early on in Hill's initial observations (35) on blood pressure responses following aerobic exercise.
What is the importance of studying the cardiovascular system during recovery from exercise? Recovery of the cardiovascular system following exercise is not simply a return to preexercise; rather, it is a dynamic period in which many physiological changes occur. Although exercise is a critical stress that drives the beneficial cardiovascular adaptations associated with routine physical activity, it is during the recovery period in which these adaptations take place. Some of these changes observed in recovery may be necessary for long-term adaptation to exercise training, yet some can lead to cardiovascular instability during recovery. Thus, it could be argued that the recovery period is equally important as the exercise stimulus. Furthermore, some of these changes during recovery from exercise may provide insight into when the cardiovascular system has recovered from prior training and is physiologically ready for additional training stress.
Over the latter part of the last century, our understanding of the cardiovascular system in recovery from exercise grew modestly. However, over the last two decades, many intricacies of recovery have been uncovered through mechanistic studies, often performed in humans, and the growth of knowledge in this area has been strong (24). This work has focused largely on measurable and clinically relevant outcomes (e.g., blood pressure), the mechanisms that control and regulate these outcomes, and the situations and conditions in which the measurable outcomes differ (due to competing or mitigating influences).
Given the depth and breadth of current information on this topic and results of several recent reviews (23, 24, 38, 45, 47), this review will focus on the hemodynamic adjustments and underlying mechanisms that occur in response to acute bouts of aerobic versus resistance exercise, with most attention on those adjustments that are sustained for more than 20 min after exercise. We will explore the potential for practical application of this information to strategies that maximize the benefits of cardiovascular recovery, or minimize the vulnerabilities of this state (27), and discuss appropriate field measures and the extent that these can guide an athlete's training.
Arterial Pressure as a Key Outcome Variable
Arterial blood pressure is one of the most extensively studied hemodynamic variables following exercise, and much of the literature on cardiovascular recovery following exercise has focused on postexercise hypotension. Arterial pressure is arguably the most highly regulated cardiovascular variable, yet there is a sustained reduction in arterial pressure following whole body aerobic exercise of moderate duration and intensity. This hemodynamic change has been referred to as postexercise hypotension (23, 24, 38, 47), and has been observed following both aerobic and resistance exercise.
This is not to suggest that both modes of exercise produce the same cardiovascular response, but to recognize that some aspects, such as reduced pressure, may be common in recovery from many forms of exercise. In its simplest model, arterial pressure is the product of arterial inflow (cardiac output) divided by ease of outflow (systemic vascular conductance, the inverse of total peripheral resistance). Thus, the mechanisms mediating the reduction in arterial pressure following exercise can be dissected by examining the terms in this equation, which can be further reduced to their determinants (e.g., cardiac output can be reduced to heart rate and stroke volume, and venous return can be considered to be a determinant of stroke volume, etc.). Systemic vascular conductance is determined by the extent of vasoconstriction or vasodilation of individual vascular beds.
Although arterial pressure is a clinically meaningful measurement and the hallmark of postexercise hypotension, it is important to note that the reduction in arterial pressure reflects sustained complex adjustments in cardiovascular control, and that some of the responses to exercise appear to be obligatory (consistently observed primary responses to exercise; for example, arterial baroreflex resetting, histamine release, and receptor activation), but others appear to be situational (e.g., reduced preload on the heart can be secondary to fluid loss, elevated body core temperature, or changes in body position) (8, 24, 27). Thus, the integration of obligatory components and situational influences can result in minimal (or absent), modest, or severe (symptomatic) hypotension.
Cardiovascular Function Following Aerobic Exercise
For the purpose of this review, aerobic exercise will be considered as large or small muscle mass exercise (e.g., cycling, dynamic knee extension) performed for at least 20 min. In general, there is a dose-dependent effect of intensity and duration on the cardiovascular changes following exercise, although there are some inconsistencies in the literature, and postexercise hypotension may be similar across a broad range of intensities and durations (8, 47). These cardiovascular changes also appear following continuous and intermittent exercise, assuming total work is comparable. In general, following whole body dynamic exercise of moderate duration and intensity, the magnitude of the increase in vascular conductance (or reduction in vascular resistance) is larger than the elevations in cardiac output, meaning that a vasodilation is the driver of the pressure reductions (23). However, in situations such as passive recovery in the upright position, the loss of the muscle pump in the face of gravitational pooling of blood in the dependent limbs can reduce venous return, central venous pressure, and cardiac preload, resulting in severe hypotension and syncope (26).
The persistent vasodilation that underlies postexercise hypotension lasts several hours, and is known as sustained postexercise vasodilation. It occurs largely within the vascular beds of previously active skeletal muscle (28) with a lesser contribution from nonactive skeletal muscle (15, 30). Notably, vascular conductance in the splanchnic (65), cutaneous (80), and cerebral (81) vascular beds remains unchanged relative to preexercise. Halliwill and colleagues (28) were the first to demonstrate that sustained postexercise vasodilation is mediated by combined central neural mechanisms (arterial baroreflex resetting) and local vasodilatory mechanisms. The arterial baroreflex is shifted downward and to the left, such that that sympathetic activity is reduced despite operating at a lower pressure. This is associated with changes in recovery of heart rate and its beat-to-beat fluctuation (i.e., heart rate variability). Although the immediate recovery of heart rate (fast phase) following aerobic exercise is due solely to parasympathetic reactivation, the slow phase of recovery is thought to be due to withdrawal of sympathetic outflow lasting upward of 90 min after exercise (61, 75).
Vasodilation within nonactive skeletal muscle probably occurs via resetting of the arterial baroreflex and resulting reductions in sympathetic vasoconstrictor tone. Conversely, vasodilation within previously active skeletal muscle results from combined arterial baroreflex resetting, blunted vascular transduction, and release of local vasodilatory substances. For a thorough review of the specific brain regions, pathways, neurotransmitters, and receptors involved in mediating the resetting of the arterial baroreflex and associated sympathoinhibition, readers are referred to the excellent work by Chen and Bonham (13).
Our understanding of the local dilatory mechanisms of sustained postexercise vasodilation have been greatly advanced within the last decade by the work of Halliwill and colleagues. Their studies demonstrate that the vasodilation is not dependent on nitric oxide (26), prostanoids (41), or changes in α-adrenergic receptor sensitivity (25), but that histamine (as shown via the use of combined high-dose histamine H1 and H2 receptor antagonists) has an obligatory role as a primary mediator of sustained postexercise vasodilation (42, 50, 51). Sustained postexercise vasodilation following 60 min of moderate-intensity cycling is inhibited by 80% when histamine receptors are blocked. The remaining 20% that is not affected by histamine blockade is presumed to be the result of resetting of the baroreflex and sympathetic withdrawal, because it is not apparent following unilateral dynamic knee-extension exercise (3), a model that lacks the baroreflex resetting observed after cycling (10).
More recently, Romero and colleagues (74) demonstrated that histamine is elevated in previously active skeletal muscle in humans, which is consistent with indirect evidence in rodent models (2, 19, 59, 83). In addition, Romero et al. (74), using skeletal muscle microdialysis, were able to determine that mast cell degranulation and de novo formation via histidine decarboxylase (the enzyme responsible for the conversion of histidine to histamine) contribute to histamine formation and sustained postexercise vasodilation, a model represented in Fig. 1.
Sources of histamine in skeletal muscle after exercise. Mast cell degranulation and de novo formation via histidine decarboxylase (HDC, the enzyme responsible for the conversion of histidine to histamine) contribute to histamine formation and sustained postexercise vasodilation by activation of histamine H1 and H2 receptors. In addition to vasodilation, histamine has broad effects on the exercise transcriptome (45, 73, 74). [Modified with permission from (24).]
It is now clear that histamine, formed and released within active skeletal muscle tissue, and subsequent activation of histamine H1 and H2 receptors, mediates sustained postexercise vasodilation. However, the upstream exercise related factor(s) governing this process remain unidentified. Given the dynamic environment within active skeletal muscle, a number of mechanisms have been postulated as the upstream trigger for this pathway to sustained postexercise vasodilation, including increased temperature, vibration, shear stress, cytokines, and oxidative stress (24). Along these lines, Romero et al. (72) examined whether exercise-induced oxidative stress was a necessary contributing factor. They found that the systemic infusion of a high-dose antioxidant had no effect on sustained postexercise vasodilation, suggesting that exercise-induced oxidative stress is not obligatory. To date, the exercise-related trigger for histamine release remains elusive.
Cardiovascular Function Following Resistance Exercise
For the purpose of this review, we will restrict the discussion of resistance exercise to an acute bout of multiple, whole body strength exercises (e.g., circuit training). Importantly, the sustained changes in cardiovascular function and underlying mechanisms following these types of whole body strength routines are distinct from those immediately following a single set of resistance exercise performed by an isolated muscle group (i.e., more muscle groups must be involved to evoke many of the changes to be discussed below).
At face value, resistance and aerobic exercise are quite distinct from one another. These differences underlie several unique cardiovascular adjustments that occur during resistance exercise that may explain some of the divergent responses following exercise, when compared with aerobic exercise. Resistance exercise is characterized by intermittent, mostly dynamic exercise that is accompanied by large and rapid swings in arterial blood pressure accompanied by a progressive rise in heart rate (49). In contrast, changes in arterial pressure during aerobic exercise tend to be slight to moderate, and relatively stable.
Compared with the wealth of studies investigating hemodynamic adjustments following aerobic exercise, studies investigating cardiovascular function and associated control mechanisms following resistance exercise are fairly limited. However, as highlighted recently by Casonotto et al. (11) the literature is rich with studies investigating the hypotensive effect of resistance exercise and its various permutations. Despite the broad possibilities for what is considered resistance exercise in studies (i.e., the many variations on movements, repetitions, sets), in general, arterial blood pressure is reduced for up to several hours following resistance exercise, although this is not a universal finding (11, 20, 21, 58). In 1994, Brown et al. (9) provided initial observations on the hypotensive effect of resistance exercise; those findings were later confirmed by MacDougal et al. using intra-arterial measures of blood pressure (49). Rezk et al. (67a) further characterized the hemodynamic adjustments mediating postresistance exercise hypotension. However, in contrast to aerobic exercise, postexercise hypotension with resistance exercise is largely due to attenuated cardiac output resulting from reduced stroke volume. Additionally, systemic vascular conductance is reduced, further supporting the notion that hypotension after resistance exercise is due to central (i.e., cardiac hemodynamics), and not peripheral vasodilation, in contrast to hypotension after aerobic exercise. It is unclear why the mechanisms differ following resistance and aerobic exercise. The divergent cardiac output response following resistance exercise may be related to changes in cardiac sympathetic activation and/or arterial baroreflex sensitivity, whereas attenuated systematic vascular conductance may be related to changes in local vasodilator mechanisms within previously active skeletal muscle. For example, knee-extension exercise that replicates classical resistance training (i.e., three sets of eight repetitions at 80% of maximum) does not generate a sustained histaminergic vasodilation, whereas knee-extension exercise that replicates aerobic training does (3). However, there is likely some overlap in central mechanisms, because combined aerobic and resistance exercise does not further reduce arterial pressure compared with aerobic exercise alone (77). Finally, we note that sex may influence the hemodynamic balance that underlies hypotension after resistance exercise, because it may be more dependent on vasodilation in women (67). It is unclear why this sex-dependent difference exists, but it may be related to sex-based differences in cardiac morphology and/or variations in sex hormone levels (22, 32). In the one study to report differences, phase of menstrual cycle was not considered (67).
The underlying mechanisms, hemodynamic adjustments (e.g., regional vascular changes), and autonomic contributions (e.g., baroreflex resetting) are not as well documented following resistance exercise as they are for aerobic exercise, as summarized in Table 1. However, drawing from studies that used noninvasive measures of cardiac vagal tone (i.e., heart rate variability), we can gain some insight into the possible neural/autonomic mechanisms that are attenuating the rise in cardiac output and contributing to the reduced arterial blood pressure following resistance exercise. The pattern of heart rate variability after resistance exercise is consistent with a withdrawal of cardiac vagal tone (39). However, these reductions in cardiac vagal tone and increases in heart rate are insufficient to offset the reduction in stroke volume following resistance exercise (34). Additionally, the ability of the arterial baroreflex to buffer reductions in blood pressure is inhibited due to attenuated cardiovagal baroreflex sensitivity (33, 58). To our knowledge, more direct measures of these autonomic adjustments, such as direct recordings of sympathetic nerve activity and assessment of baroreflex resetting, have not been made in humans following resistance exercise. Taken together, these existing data suggest that the mechanisms underlying the hemodynamic adjustments following resistance exercise are due, in part, to central neural adjustments.
Table 1.
Hemodynamic adjustments during the recovery from aerobic and resistance exercise
| Hemodynamic Parameter | Postaerobic | Postresistance |
|---|---|---|
| Mean arterial pressure | ↓ | ↓ |
| Cardiac output | ↑ | ↓ |
| Systemic vascular conductance | ↑↑ | ↓ |
| Skeletal muscle conductance | ↑↑ | ? |
| Splanchnic and renal conductances | ∼ | ? |
| Cutaneous conductance | ∼ | ? |
| Cerebral conductance | ∼ | ? |
Translation from the Laboratory to the Field: What Matters?
As highlighted recently by Luttrell and Halliwill (44), recovery from exercise can be viewed as a vulnerable period in which individuals are at heightened risk for adverse events, or a window of opportunity in which the positive adaptations to training can be manipulated and potentially augmented. Furthermore, it may provide insight into when the cardiovascular system has recovered from prior training and is physiologically ready for additional training stress. Some of these research perspectives are readily translated to coaches and athletes, but others have yet to reach their translational potential.
Limiting the vulnerability to symptomatic hypotension and syncope.
Cardiovascular vulnerability following exercise often presents as postexercise syncope; the development of presyncopal signs and symptoms such as lightheadedness, tunnel vision, blurred vision, etc.; or loss of consciousness following either aerobic and resistance exercise (16, 27, 40, 56, 71, 76). Generally, postexercise syncope is neurogenically mediated and is related to an exaggerated expression of the processes discussed above for postexercise hypotension, such as sustained peripheral vasodilation and reduced cardiac preload, which can be made worse by the loss of the muscle pump, upright posture, and hot environmental conditions (27).
Several strategies exist that can prevent postexercise syncope (27); however, some common medical strategies for treating recurrent syncope (e.g., use of beta-adrenergic blockers and implantable pacemakers) are ill-advised for postexercise syncope, especially in sport or competitive settings. One pharmacological approach that is worth exploring in individuals with recurrent postexercise syncope is the use of antihistamines (52).
Active recovery is arguably the most easily implemented and most effective recovery strategy that can prevent postexercise syncope. Active recovery prevents postexercise syncope by enhancing venous return in augmenting cardiac preload through rhythmic contractions of skeletal muscle (i.e., the muscle pump). This may be the best justification for performing a cool-down after intense exercise. There are also several effective physical countermeasures, such as squatting and muscle tensing (79), that can be easily implemented after various sport or athletic events, even those in which active recovery may be difficult [e.g., stuck at a finish line with no room to move (84)]. Leg compression, implemented by compression garments or pneumatic systems can potentially be of help (66).
In addition, fluid replacement, particularly in hot and humid conditions, can be considered a basic step to reduce vulnerability to postexercise syncope. In one case report, ingesting 1 liter of water 15 min before exercise has been shown to be effective in preventing postexercise syncope (78), but this volume of fluid ingestion may not be well tolerated by athletes. Water consumption during exercise that approximates sweat loss may be more practical, and increases blood pressure and cardiac output (46) during the recovery from exercise. Postexercise fluid replacement, particularly the type designed to target electrolyte deficits, may mitigate postexercise syncope and also prepare athletes for subsequent exercise bouts or athletic events (14).
There is some potential to augment the respiratory pump to reduce the likelihood of postexercise syncope. Inspiratory resistance breathing was originally developed as a resuscitation method. By augmenting intrathoracic negative pressure, it increases venous return and cardiac preload. Along these lines, Lacewell and colleagues (40) demonstrated that inspiratory resistance improves orthostatic tolerance following a modified Wingate test. Although inspiratory resistance breathing shows promise, it has yet to be translated to the field.
Body cooling (i.e., cryotherapy, cold water immersion), which has gained widespread attention as a strategy to enhance exercise recovery, could also serve as a preventive strategy for postexercise syncope, particularly in hot and humid conditions. Indeed, Wilson et al. (82) demonstrated that skin surface cooling improved orthostatic tolerance in heat-stressed humans. Notably, this benefit occurred despite elevated body core temperature, suggesting that local cold-induced vasoconstriction mediated improved orthostatic tolerance. There is currently a bit of controversy over whether postexercise cold water immersion is beneficial or counterproductive to training adaptations, but that is beyond the scope of this review (60, 68–70).
Exploiting the window of opportunity.
Some features of the cardiovascular system after exercise may lend themselves to beneficial manipulation. For example, our group explored the role that sustained postexercise vasodilation can play in delivering glucose to the previously exercised muscle, at a time when glucose is taken up for glycogen replacement (18, 62, 63). A similar role can be imagined for amino acid delivery during recovery from resistance exercise. Others have suggested that postexercise hypotension facilitates the restoration of plasma volume after aerobic exercise (31), even in the absence of fluid replacement. To date, these concepts have yet to be translated into novel training interventions, but the potential seems high.
We recently found that the histamine signal associated with exercise has a profound effect on the transcriptome response to exercise (73), suggesting that manipulation of when and for how long this signal is active may potentiate some of the positive training adaptations associated with exercise. That said, we are only beginning to understand the breadth of the transcriptome response, including which aspects are necessary, which are counterproductive, and what to target for intervention. More is not always better. Along these lines, we found that histamine blockade before muscle-damaging exercise (downhill running) increased serum creatine kinase (a marker of muscle damage), and yet resulted in less muscle soreness and more retention of muscle strength during the period of delayed onset muscle soreness (17). To some, the risk of greater muscle damage may be worth the advantages of reduced discomfort and preservation from loss of strength.
Readiness for additional training stress.
What can assessment of the cardiovascular system after exercise tell us about recovery from prior training and physiological readiness for additional training stress? Perhaps a more important question, which we think is seldom considered, is whether the cardiovascular system needs a recovery period after aerobic or resistance exercise, or whether we are more limited by the recovery time needed by skeletal muscle to adapt, or energy stores to be replaced. Aside from the fluid losses from the vascular space that need to be replaced following exercise, does the human heart fatigue and need recovery time?
Several studies have now reported that after marathon and ultramarathon running events, evidence of cardiac fatigue in the form of diastolic dysfunction is present in some runners (more often men than women) (12, 36, 37, 43, 54, 55, 57). However, this does not appear to be the case following most forms of aerobic exercise, and it seems fair to say there is no deficit in cardiovascular function for most exercisers after a single bout of aerobic or resistance exercise. Thus, we shift the question to whether assessment of the cardiovascular system after exercise tells us about recovery of other systems from prior training, and physiological readiness of those other systems for additional training stress. Along these lines, resting heart rate and heart rate variability are often promoted to athletes and coaches as useful biomarkers of recovery and preparedness.
Measuring heart rate is arguably the easiest and most widely used tool to assess recovery following exercise. Typically, heart rate is measured using a heart rate sensor embedded in a chest strap, but wrist-based sensors are becoming common. Heart rate is usually displayed on a wristwatch, or more recently, sent to cell phones or tablets using wireless technology. Measurement of heart rate in this fashion is fairly accurate, inexpensive (price range, $50–250), and easily implemented.
Certain portable heart rate monitors have the capability to assess heart rate variability, which reflects the beat-to-beat fluctuation in heart rate and/or the duration of R-wave intervals (5). Heart variability metrics are thought to reflect cardiac autonomic regulation, specifically parasympathetic and to a lesser extent sympathetic cardiac control, or some combination thereof (i.e., sympatho-vagal balance) (1, 6). The use of heart rate variability metrics within the context of exercise or sport has dramatically increased since its mainstream inception, probably owing to its low cost and ease of use. In general, heart rate variability follows the same temporal pattern as heart rate during recovery from exercise (29, 64).
In theory, these cardiac measures could serve as "the canary in the coal mine" for overreaching and overtraining, because they represent the integration of autonomic pathways that are sensitive to a wide range of homeostatic processes. But in general, the research on heart rate and heart rate variability as biomarkers of recovery during long-term training stress suggests that they fail to live up to this promise (4, 7, 53). Away from the confines of a controlled laboratory environment and strict experimental guidelines, caution should be used when using heart rate or its variability to assess cardiac autonomic control or recovery from exercise or sport. Rather, an integrated approach should be used beyond the immediate recovery period and include other markers of overreaching or overtraining, such as generalized fatigue, performance that has reached a plateau or is declining, sleeplessness, irritability, an inability to attain higher heart rates during training, etc.
Conclusions
The cardiovascular system after exercise exists in a physiologic state that differs from both rest and exercise. It has a physiology of its own, including the phenomena of postexercise hypotension, sustained postexercise vasodilation, and activation of a histamine signaling pathway of undefined consequence. The hemodynamic adjustments that occur during the recovery from aerobic and resistance exercise are driven by highly coordinated and controlled mechanisms. However, if left unchecked, these adjustments can progress to cardiovascular instability. The future likely will include training methods that take advantage of the processes present in the cardiovascular system after exercise, and it may yet provide a window into recovery and readiness for training stress.
GRANTS
Support for this work was provide by National Institutes of Health Grants HL-115027 and GM-117693.
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the authors.
AUTHOR CONTRIBUTIONS
S.A.R. drafted manuscript; S.A.R., C.T.M., and J.R.H. edited and revised manuscript; S.A.R., C.T.M., and J.R.H. approved final version of manuscript.
ACKNOWLEDGMENTS
We thank those who have contributed to our work on exercise recovery over the last decade.
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