Loss of Consciousness During Intense Exercise

Abstract

Background

An 18-year-old female middle-distance runner was referred for loss of consciousness (LOC) during races.

Case Summary

A treadmill exercise test was completed with direct, continuous measures of arterial blood pressure. We were able to elicit LOC during maximal exertion on 2 occasions. Beat-by-beat arterial pressure demonstrated that the LOC occurred despite having normal exercising blood pressure.

Discussion

We demonstrate an instructive case in which LOC during maximal exertion may be a consequence of an athlete exercising outside of their physiological limits in the absence of hypotension, causing cerebral hypoperfusion and subsequent syncope.

Take-Home Message

In highly motivated athletes, LOC may occur during maximal exercise in the absence of hypotension.

Visual Summary

History of Presentation

An 18-year-old female National Collegiate Athletic Association Division I middle-distance runner (personal record, 800 m: 2:25.17 minutes, 1600 m: 5:15.15 minutes) was referred for evaluation given episodes of loss of consciousness (LOC) while racing. She reported experiencing spotted and clouded vision before LOC, both during races and near the finish line. These events only occurred during competitions and never during practice, even during high-intensity sessions mimicking race pace. A comprehensive evaluation by her pediatric cardiologist showed normal cardiac structure and function, and excluded the presence of an arrhythmia during these clinical events. Multiple empiric trials of medications targeting hypotension or neurally mediated syncope failed to prevent LOC.

Take-Home Messages

• •Loss of consciousness during maximal exercise in highly motivated athletes can occur in the absence of hypotension.
• •Loss of consciousness may be attributable to athletes exercising outside their physiological limits rather than true hypotension leading to cerebral hypoperfusion and syncope.

Indirect measures of blood pressure (ie, brachial cuff pressure) do not have the accuracy or temporal resolution to capture true hypotension during all-out running efforts. As the documentation of hypotension is critical to clarifying the pathophysiology and directing therapy, the patient was referred to the Sports Cardiology Clinic at the Institute for Exercise and Environmental Medicine for invasive investigation into the LOC episodes.

Past Medical History

The patient's medical history was unremarkable, with normal body composition (height: 181.5 cm, weight: 63.9 kg, body mass index: 19.4 kg/m²). Resting electrocardiography showed sinus bradycardia with normal intervals, and without pre-excitation or ST-T wave changes. Prolonged patch monitoring showed no arrhythmias or periods of bradycardia including during at least 1 clinical event. Previous treadmill stress tests and stress echocardiogram were normal without arrhythmia or provocable ischemia. Echocardiogram showed normal right and left ventricular wall thickness, normal wall motion, and normal ventricular outflow (2.0 m/s). The patient had a history of iron deficiency, which was acutely corrected with intravenous infusion, and she remained adherent to oral supplementation. Despite supplementation, ferritin (41.7 ng/mL) and iron saturation (40%) levels remained on the low end of normal for an endurance athlete at the time of referral. She reported no history of disordered eating or amenorrhea. The patient had no family history of unexpected or unexplained death, syncope, or frequent collapse. Her father had a history of performance anxiety treated with propranolol.

Differential Diagnosis

Given the absence of arrhythmia during the episodes, most of the life-threatening causes of LOC (such as hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, catecholaminergic polymorphic ventricular tachycardia) were unlikely. Coronary ischemia from an anomalous coronary artery or myocardial bridge was not excluded by coronary computed tomography angiography; however, coronary origins appeared normal by high-quality pediatric echocardiography, and the patient was a young, elite female athlete with no detectable arrythmias or signs/symptoms of ischemia. It is possible that microvascular dysfunction could cause ischemia and a resultant Bezold-Jarisch reflex with sympathetic withdrawal and vasodilation,¹ and if she had developed hypotension or any evidence of ischemia during our high-resolution testing, the benefit of a coronary computed tomography angiogram would have exceeded the risk and would have been performed. However, our bias is to avoid radiating the chest of a young woman without a compelling reason to suspect ischemia, especially when all other testing points away from an ischemic etiology. Rarely, athletes can develop such profound skeletal muscle vasodilation combined with inadequate vasoconstriction in nonexercising vascular beds that it overwhelms cardiac output, leading to hypotension.² Finally, exercise-associated collapse, with or without hypotension (including “nonsyncopal fainting”³), was also considered.

Investigations

Rest and steady-state exercise

Resting measures were completed with the patient standing. Steady-state exercise was completed at 8 miles per hour (mph) (7:30 min/mile), 9 mph (6:40 min/mile), and 10 mph (6:00 min/mile), which are standard paces for elite female runners in our clinic. Heart rate and rhythm were continuously monitored and recorded with 12-lead electrocardiography. Blood pressure was continuously monitored and recorded via an intra-arterial catheter in the radial artery, leveled at the height of the right atrium as determined by fluoroscopy. The arterial catheter allowed arterial blood gas sampling and direct, beat-by-beat blood pressure monitoring. Throughout exercise, breath-by-breath measures of minute ventilation, oxygen uptake, and carbon dioxide production were recorded. During steady-state exercise, cardiac output was measured using the foreign gas rebreathing technique.⁴ As such, stroke volume could be calculated.

Standing blood pressure was normal (Table 1). The patient's response to steady-state exercise was largely unremarkable (Table 1), with a normal hemodynamic response and no arrythmias detected. Notably, the intensity of 10 mph proved to be above the threshold of a steady-state intensity, as the patient struggled to maintain pace, complained of lightheadedness during gas-exchange collection, and had substantial blood lactate accumulation (12.4 mmol/L), more consistent with a near-maximal effort. Despite the relatively high intensity, the patient's cardiorespiratory response to the exercise was normal, with no signs of dysfunctional blood pressure regulation (Figure 1). From rest to steady-state exercise, arterial blood gases showed a moderate decline in arterial oxygen partial pressure (−18 mm Hg) and an increase in alveolar-to-arterial oxygen partial pressure difference (+28 mm Hg), with a maintained arterial saturation (Table 1). There were no obvious signs of disordered ventilatory pattern from rest to exercise; however, a slight increase in arterial carbon dioxide partial pressure would suggest minor hypoventilation (Table 1).

Table 1.

Exercise Response

	At Rest	Running Speed
		8 mph	9 mph	10 mph
V̇o2, L/min	0.37	2.88	3.19	3.30
V̇o2, mL/kg/min	5.7	45.1	49.7	51.7
RER	0.77	0.93	1.06	1.17
Q̇C, L/min	5	17	18	—
SV, mL	86	99	101	—
HR, beats/min	58	168	182	185
Systolic pressure, mm Hg	124	154	150	170
Diastolic pressure, mm Hg	62	60	58	65
V̇E, L/min	15	84	100	112
Bf, breaths/min	16	40	47	53
V̇E/V̇co2	39	28	27	26
V̇D/V̇T	0.36	0.17	0.14	0.20
Lactate, mmol/L	0.8	2.5	5.1	12.4
pH	7.39	7.36	7.31	7.16
Paco2, mm Hg	35	37	38	42
PAo2, mm Hg	106	112	116	116
Pao2, mm Hg	101	92	83	86
PA-ao2, mm Hg	5	20	33	30
Sao2, %	99	98	97	95

B_f = breathing frequency; HR = heart rate; P_aco₂ = partial pressure of arterial carbon dioxide; P_Ao₂ = partial pressure of alveolar oxygen; P_ao₂ = partial pressure of arterial oxygen; P_A-ao₂ = partial pressure difference of alveolar-to-arterial oxygen; Q̇_C = cardiac output; RER = respiratory exchange ratio; S_ao₂ = saturation of arterial oxygen; SV = stroke volume; V̇_E = minute ventilation; V̇co₂ = carbon dioxide production; V̇_D = dead space; V̇o₂ = oxygen uptake; V̇_T = tidal volume.

Figure 1.

Arterial Pressure During Staged Exercise at 8, 9, and 10 mph

Points represent a 10-second average of arterial pressure. Also presented are raw pressure traces collected via the radial artery. MAP = mean arterial pressure; mph = miles per hour.

Maximal exercise

The patient then completed a series of running bouts to exhaustion near race pace while secured with a safety tether. To capture race-like symptoms and preserve the integrity of the arterial pressure recording while maintaining the safety of the patient, the maximal exercise bouts were completed without breath-by-breath recordings of oxygen uptake or ventilation. Based on recent training and race history, maximal efforts were run at 11.0 mph (5:27 min/mile pace) and 11.5 mph (5:13 min/mile pace).

LOC occurred during the 2 maximal efforts, with the patient collapsing into the harness. The clearest representation of the LOC during maximal running is presented in Figure 2. At 20 seconds and 5 seconds before LOC, the patient reported clouded and spotted vision. During both symptoms, mean arterial pressure was completely normal (89 and 93 mm Hg, respectively), with clear beat-by-beat pressure waveforms to the moment of LOC. After LOC, the patient (as well as pressure transducers) was lowered to the ground within 10 seconds, during which time the mean arterial pressure had fallen (to 53 mm Hg). The acute decline in mean arterial pressure was unsurprising after intense exercise with LOC and rapid maneuvering into a supine position. Arterial pressure recovered normally in the supine position. The LOC lasted for less than 1 minute, and there was no incontinence or myoclonic jerking observed after either episode. The patient reported no chest pain or palpitations at any point.

Figure 2.

Arterial Pressure During Maximal Running (5:13 min/mile) to the Moment of Loss of Consciousness

The arrows indicate major events, and raw traces present the radial artery pressure at the associated time points. Numerical values across the top present the average (range) systolic and diastolic pressures associated with the raw pressure tracings. ∗Moment of loss of consciousness. DBP = diastolic blood pressure; LOC = loss of consciousness; MAP = mean arterial pressure; SBP = systolic blood pressure.

Outcome and Follow-Up

The spotting of vision and LOC experienced during maximal exercise were not associated with systemic hypotension. Cerebral hypotension can likely be ruled out, although brain magnetic resonance imaging/magnetic resonance angiography was recommended to ensure no anatomic cerebrovascular anomaly (ultimately completed with normal findings). Therapies aimed at raising the patient's blood pressure, such as the alpha-adrenergic vasoconstrictor midodrine, would likely not be successful in eliminating her symptoms nor would avoid future incidents of unconsciousness. To address the patient's recurring LOC, tools such as shortening intervals in practice to ensure sustained competitive velocities, and inspiratory muscle training to reduce symptoms of dyspnea during high-velocity running were recommended.

Discussion

We elicited a patient's real-world symptoms of LOC during maximal running with direct, invasive intra-arterial blood pressure monitoring. Distinctively, LOC occurred midstride in the final steps of maximal running efforts. The evidence, to the heartbeat, clearly demonstrated normal exercising blood pressure (Figure 2). A final diagnosis cannot be made regarding the causes of LOC in this particular case, but many specific causes can be ruled out.

The response to steady-state exercise provided a key perspective. The patient is a competitive middle-distance runner at the collegiate level. However, her response to 10-mph steady-state exercise (6:00 min/mile), which she struggled to complete with a blood lactate level of 12.4 mmol/L, is indicative of lower aerobic fitness than necessary for success at this level of competition. She did demonstrate mild exercise-induced arterial hypoxemia, which is not uncommon among female endurance athletes,⁵ but this was not severe enough to cause LOC.

Our patient may be experiencing what is colloquially referred to as “exercise swoon syndrome.”⁶ The LOC could be the consequence of a conflict between the patient's physiological (ie, aerobic fitness) limitations and an incredible motivation to perform. One other case of exercise swoon has been described, although it was attributed to possible overtraining.⁷ Our patient only reported LOC near the finish line of a race, and never during training where effort can be intrinsically modulated. The clinical exercise testing on the treadmill was therefore a fitting environment to elicit the LOC. As in a race, the high treadmill speed during the patient's effort was outside of the capacity that her current fitness level could support. She could not slow down, and thus any such conflict between expectation and internal sensations could not be reduced. Indeed, even running at 10 mph proved to be near maximal for the patient, with an estimated maximal oxygen uptake of 54 mL/kg/min. The patient is able to taper effort during training, but during a race (or in the laboratory with 10 clinical staff observing) it is all or nothing. Eventually, the central nervous system chooses swoon.

The discordance also highlights the possibility of a psychological component, whereby the patient may be experiencing fear and anticipation of a repeated LOC. The patient was previously referred to a sports psychologist to no effect. It is possible she may benefit from cognitive behavioral therapy with expertise in exercise-associated collapse. The recommendation of modifying high-intensity training intervals such that she can accumulate greater exposure to race pace and manage internal conflict can potentially minimize the likelihood of future events. Additionally, inspiratory muscle training may alleviate any potential feelings of breathlessness that may perpetuate LOC.

Conclusions

This case challenges the traditional assumption regarding LOC during maximal running that is due to hypotension and highlights how advanced methods and testing infrastructure can aid in ruling out hypotension. Without direct and continuous measures of arterial pressure during maximal exercise, it was assumed the patient had some form of autonomic dysfunction causing systemic hypotension and cerebral hypoperfusion. In contrast, we demonstrate LOC during maximal running with completely normal arterial pressure. The cause of LOC in the current case or similar instances may never be directly identifiable, but it highlights a potential interplay between psychological and physiological stressors that may be experienced by some highly driven athletes.

Visual Summary.

A Normotensive Arterial Pressure Trace Before and After Loss of Consciousness in a Female Middle-Distance Runner Elicited at a 5:13 min/mile Pace

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.