Effects of dynamic exercise and its intensity on ocular blood flow in humans

Institute of Health Science and Graduate School of Human-Environment Studies, Kyushu University, Kasuga, Fukuoka, Japan.
Arbeitsphysiologie (Impact Factor: 2.19). 03/2011; 111(10):2601-6. DOI: 10.1007/s00421-011-1880-9
Source: PubMed

ABSTRACT Visual performance is impaired when the ocular blood flow decreases, indicating that ocular blood flow plays a role in maintaining visual performance during exercise. We examined the ocular blood flow response to incremental cycling exercise to test the hypothesis that ocular blood flow is relatively stable during dynamic exercise because of its autoregulatory nature. The blood flow in the inferior and superior temporal retinal arterioles (ITRA and STRA, respectively) and retinal and choroidal vessels (RCV), mean arterial pressure, and heart rate (HR) were measured at rest and during leg cycling in nine young and healthy subjects (26 ± 5 years, mean ± SD). Ocular blood flow was measured by laser speckle flowmetry. The exercise intensity was incremented by 30 W every 3 min until the subject was unable to maintain a position appropriate for measuring ocular blood flow. Blood flow data obtained during cycling exercise were categorized based on HR as follows: <100, 100-120, and >120 bpm. Blood flow in the RCV increased with the exercise intensity: by 16 ± 8, 32 ± 13, and 40 ± 19% from baseline, respectively. However, blood flow and vascular conductance in the ITRA and STRA did not change significantly with exercise. These findings demonstrate for the first time that ocular blood flow increases in the retina and choroid, but not in the arterioles, with increasing exercise intensity during dynamic exercise.

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Available from: Naoyuki Hayashi, Nov 05, 2014
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    • "In response to the increase in perfusion pressure, a vasoconstriction of retinal arteries and veins occurs, inducing an increase in vascular resistance. This compensatory autoregulation, also known as myogenic response, is responsible for the maintenance of normal blood flow in central retinal arteries and veins during dynamic exercise (Harris et al. 1996; Iester et al. 2007; Hayashi et al. 2011). In seniors, the retinal arterial myogenic response induced by a systemic blood pressure increase during isometric resistance training has been shown to be decreased compared to younger adults (Jeppesen et al. 2004). "
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    ABSTRACT: Alterations of retinal vessel diameters are associated with increased cardiovascular risk. We aimed to investigate changes in retinal vessel diameters in response to acute dynamic exercise of different intensities and whether these changes are age dependent. Seventeen healthy seniors (median (IQR) age 68 (65, 69) years) and 15 healthy young adults (median (IQR) age 26 (25, 28) years) first performed a maximal treadmill test (MTT) followed by a submaximal treadmill test (SMTT) and a resting control condition in randomised order. Central retinal arteriolar (CRAE) and central retinal venular (CRVE) diameter equivalents were measured before as well as 5 (t5) and 40 (t40) minutes after exercise cessation using a static retinal vessel analyser. Both exercise intensities induced a significant dilatation in CRAE and CRVE at t5 compared to the control condition (P < 0.001). At t40, the mean increase in CRAE and CRVE was greater for MTT compared to that for SMTT (CRAE 1.7 μm (95 % confidence interval (CI) −0.1, 3.6; P = 0.061); CRVE 2.2 μm (95 % CI 0.4, 4.1; P = 0.019)). However, the estimated difference at t5 between seniors and young adults in their response to MTT compared to SMTT was 5.3 μm (95 % CI 2.0, 8.5; P = 0.002) for CRAE and 4.1 μm (95 % CI −0.4, 8.6; P = 0.076) for CRVE. Wider arteries and veins after maximal versus submaximal exercise for seniors compared to young adults suggest that myogenic vasoconstriction in response to exhaustive exercise may be reduced in seniors. Age-related loss of vascular reactivity has clinical implications since the arteriolar vasoconstriction protects the retinal capillary bed from intraluminal pressure peaks. Electronic supplementary material The online version of this article (doi:10.1007/s11357-014-9650-3) contains supplementary material, which is available to authorized users.
    Age 04/2014; 36(3). DOI:10.1007/s11357-014-9650-3 · 3.45 Impact Factor
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    • "The blood Xow velocity in the RCV increased with increasing MAP without a change in CI at 6 min of exercise . This result indicated that autoregulation in RCV did not overwhelm the change in MAP during submaximal dynamic exercise, similarly to our previous study (Hayashi et al. 2011a). However, the ratio of relative change in the RCV blood Xow velocity against the change in MAP was 1.1% per 1 mmHg change in MAP at 6 min in the present study. "
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    ABSTRACT: It is unclear whether exhaustive dynamic exercise increases ocular blood flow, although we have reported that submaximal exercise increases ocular blood flow. We hypothesized that ocular blood flow decreases at exhaustion, since exhaustion causes hyperventilation, which induces a reduction in PaCO(2). To test this hypothesis, ocular blood flow, blood pressure, and respiratory measurements were made in 12 healthy male subjects during cycle ergometer exercise at 75% of maximal heart rate, until exhaustion. Blood flows in the retinal and choroidal vasculature (RCV), the superior temporal retinal arteriole (STRA), and the superior nasal retinal arteriole (SNRA) were measured with the aid of laser-speckle flowgraphy every 3 min during the exercise. The conductance index (CI) in the ocular vasculature was calculated by dividing the blood flow by the mean arterial pressure (MAP). The mean arterial partial pressure of CO(2) (PaCO(2)) was estimated from tidal volume and end-tidal CO(2) partial pressure. MAP significantly increased from the resting baseline throughout the exercise, while PaCO(2) was significantly decreased at exhaustion and during the recovery period. By 6 min after the onset of exercise, blood flow velocity in the RCV significantly increased by 32 ± 6% (mean ± SD) from the resting baseline value. At exhaustion, blood flow velocity in the RCV did not differ significantly from the resting baseline value, and the STRA blood flow was significantly decreased by 13 ± 4%. The CIs in the RCV, STRA, and SNRA were significantly decreased compared to baseline at exhaustion. These findings suggest that ocular blood flow is increased by submaximal exercise, whereas it is suppressed by the hypocapnia associated with exhaustion.
    Arbeitsphysiologie 01/2012; 112(9):3313-8. DOI:10.1007/s00421-012-2313-0 · 2.19 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether autoregulation exerts similar effects in the ocular and cerebral vessels, which are both branches of the internal carotid artery. Ocular blood flow velocities, cerebral blood flow velocity and blood pressure were measured in 11 subjects during a 2-min resting period, static handgrip exercise (HG) and a cold pressor test (CPT). Blood velocity data for the superior and inferior temporal retinal arterioles (STRA and ITRA, respectively) and the retinal and choroidal vasculature (RCV) were obtained for 4 s during the measurement using laser speckle flowmetry. Mean blood flow velocity in the middle cerebral artery (MCAVmean) was measured by transcranial Doppler ultrasound. The conductance index (CI) of each vessel was calculated by dividing blood flow by mean arterial pressure. Blood flow velocity in the RCV increased by 19 ± 9% from resting baseline level during the CPT (P < 0.05), while blood flow in the STRA, ITRA and MCAVmean did not. The CI of the MCA decreased. The RCV blood flow velocity, ITRA blood flow and MCAVmean increased by 8 ± 1, 9 ± 3 and 11 ± 4%, respectively, during the HG (P < 0.05). Conversely, STRA blood flow remained unchanged. The HG did not significantly change the CI in any of the vessels measured. These findings suggest that cerebral blood flow velocity was maintained during the CPT, but autoregulation does not work well in the RCV during the CPT and HG.
    Arbeitsphysiologie 06/2011; 112(2):641-6. DOI:10.1007/s00421-011-2016-y · 2.19 Impact Factor
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