Discussion

The main findings of this study indicate that both prerace and postrace orthostatic challenges induced a gravitational decrease in SV, leading to a marked reduction in blood pressure, which was corrected by a significant increase in HR in the prerace condition only. In the postrace period blood pressure remained below baseline despite a significantly greater increase in HR.

Immediately postrace, the participants were not hypotensive in the supine position despite a significant reduction in body mass (2.1 (2.7) kg), presumably due to fluid loss. This apparent dehydration was not associated with hypotension or a decline in CO, since HR was elevated. Indeed, in the supine position postrace CO was elevated. This data suggests that, in the supine posture postmarathon, there is no evidence to indicate heightened cardiovascular strain despite an almost 3% loss in body mass. The lack of postexercise hypotension is contrary to previous studies that have documented a fall in blood pressure in normotensive individuals in the supine posture that may last for up to 60 minutes4; however, these studies were concerned with the effect of shorter (<60 minutes) and much higher exercise intensities on recovery blood pressure.3,–,5 Given that the degree of postexercise hypotension is intensity and duration-dependent,14 this may explain this contrasting finding.

Postrace standing responses demonstrated a trend towards an orthostatic reduction in SBP, resulting in operative values significantly lower than prerace stand values. Nonetheless, defence of BP regulation was adequate, enabling each subject to complete the entire standing challenge. Throughout the 3 minutes of standing postrace, heart rate was elevated further (101 (8) beats/min, p<0.05) to compensate for the displacement of blood to the periphery and active muscles causing a reduction in central blood volume and therefore filling of the heart. Postrace, significant elevations in resting HR, in combination with larger relative (prerace: 20 vs postrace: 23%) and absolute (prerace: Δ13 (7) vs postrace: Δ19 (6) beats/min) increases in heart rate during the stand, may contribute to the maintenance of systolic blood pressure at a level sufficient to prevent OI subsequent to completion of the challenges.

Stroke volume postrace did not distinctly differ from prerace supine values (prerace: 92 (20) vs postrace: 81 (16) ml, p = 0.08). Postrace, however, there was a decrease in TPR and a trend displaying a reduction in stroke volume in the supine position in comparison to baseline values. At such a time, peripheral capacitance may be amplified, increasing circulatory stress postexercise, despite retaining a recumbent position. Upon completion of the postrace challenge, SV had significantly reduced to 55 (7) ml (p<0.05). This alteration in SV was greater than that observed during prerace orthostasis in absolute (prerace: Δ−16 (9) vs postrace: Δ−26 (14) ml) and relative (prerace: −17% vs postrace: −32%) terms, and relates to a redistribution of blood to the lower limbs causing greater reduction in central blood volume following the race. Due to gravitational stress during the standing phase, the volume of blood in the lower limbs is increased, causing blood flow “transit time” to be increased. Increases in transit time may be more evident during the orthostatic challenge due to decreased TPR relative to baseline prior to the postrace challenge. The reduction in central blood volume will ultimately lead to a reduced venous return and a consequent reduction in SV.

The reported reductions in SV were lower than those seen amongst asymptomatic high-fit, mid-fit and low-fit groups respectively, in response to −40 mm Hg LBNP (−39.6 (5.7)%, −23.1 (5.6)%, −34.7 (2.7)%).15 These values are in excess of the reduction noted here and likely reflect the more aggressive stimulus of LBNP. In the present study the reductions in SV did not reduce blood pressure to levels leading to presyncope.

Arterial hypotension is recognised as an imbalance in CO and TPR. In the current study, CO was significantly increased during the postrace challenge; however, TPR remained unchanged, inferring that, in the presence of a falling SV, HR is solely responsible for the maintenance of blood pressure. Subjects did not display alterations in CO or TPR as a result of the prerace challenge, suggesting that the current group of subjects regulate BP via an increased cardiac sympathetic drive. The finding that TPR does not increase in response to orthostasis postrace is consistent with the observation of decreased vascular responsiveness to sympathetic stimulation in recovery from exercise.16 Indeed, at this time, as well as the lack of responsiveness to sympathetic vasoconstriction, it is likely that there is increased vasodilator activity due to the accumulation of metabolites from the preceding exercise. If the orthostatic challenge were of longer duration, it is likely that the lack of vasoconstrictor responsiveness and background dilator activity would reduce TPR further, leading to a greater fall in pressure and causing the onset of syncope. Translocation of the blood from the periphery via circulatory reflexes including recovery of vasoconstrictor tone at onset of orthostasis would be reflected by increased calculated TPR. It is apparent that the current study demonstrates a suppression of vascular resistance, vasodepressor reflex, during increased gravitational stress. Nevertheless, alternative central sympathetic reflexes are adequate for the maintenance of BP and orthostatic tolerance throughout the study.

The clinical implications for exercise-induced orthostatic intolerance may include accurate diagnosis, notably to differentiate from syncope which occurs during exercise. Analysis of physiological responses of individuals who experience presyncope and/or syncope despite presenting without a history of syncope can determine those susceptible to instances in situational circumstances (prolonged standing in queues). All 10 athletes remained orthostatically tolerant to the standing challenge postrace despite trends suggesting greater reductions in SBP (p = 0.06). The Δ−15 (20) mm Hg reduction in SBP as a result of the 3 minute stand would appear to be inadequate to facilitate the development of presyncope amongst the athletes, with the exception of one athlete who reported blurred vision and nausea (SBP Δ−30 mm Hg, HR Δ18 beats/min, SV Δ−41 ml (−53%)). Individuals who develop such symptoms, but do not progress to syncope, can be classified to have an “orthostatic weakness”.17 Susceptibility to the onset of presyncope and syncope has previously been proposed to be related to the development of postural hypotension18; however, asymptomatic postural hypotension postexercise has previously been reported.19

One limitation to the generalisation of the current results was that the study recruited runners with no history of exercise-associated presyncope or syncope. Evaluation of this population would have important clinical implications and should be the focus of future research. The period of the standing challenge (3 min) may not have been sufficient to induce reductions in SV. This response is thought to be associated with pre-exercise and/or postexercise orthostatic alterations in individuals with recurrent presyncope and a history of syncope postexercise, although this is not seen in the current study. If the orthostatic period is prolonged, the potentially continuous reduction in SV, in combination with reduced vasoconstrictor responsiveness, may exacerbate the pooling effect, which may in principle lead to presyncopal symptoms. However, for the purpose of the present study a 3 min period was selected to ensure that each athlete was assessed without delay upon presentation to the testing area.

Furthermore, the indirect measurement of BP at a peripheral assessment location, and the estimation of consequential haemodynamic variables, may not be as accurate as invasive measurement, but these measures have been shown to provide a reliable index of change during interventions.10,–,13 Methods such as echocardiography are preferable to ensure more accurate measurement of SV and subsequent CO. However, in this field situation, the PortAPres was more appropriate for the assessment of athletes and recorded stable BP responses during the supine and orthostatic periods.