4 research outputs found
The aetiology of Spaceflight‐Associated Neuro‐ocular Syndrome (SANS) might be explained by a neural mechanism regulating intraocular pressure
Hypercapnia augments resistive exercise‐induced elevations in intraocular pressure in older individuals
The present study assessed the effect of 6° head down (establishing the cephalad displacement noted in astronauts in microgravity) prone (simulating the effect on the eye) tilt during rest and exercise (simulating exercise performed by astronauts to mitigate the sarcopenia induced by unloading of weight‐bearing limbs), in normocapnic and hypercapnic conditions (the latter simulating conditions on the International Space Station) on IOP.Volunteers (average age = 57.8 ± 6 yrs.; N = 10) participated in two experimental sessions, each comprising: i) 10‐min rest, ii) 3‐min handgrip dynamometry (30% max), and iii) 2‐min recovery, inspiring either room air (NCAP), or a hypercapnic mixture (1% CO2, HCAP). We measured IOP in the right eye, cardiac output (CO), stroke volume (SV), heart rate (HR) and mean arterial pressure (MAP) at regular intervals. Baseline IOP in the upright seated position while breathing room air was 14.1 ± 2.9 mmHg. Prone 6° HDT significantly (p < 0.01) elevated IOP in all three phases of the NCAP (rest: 27.9 ± 3.7 mmHg; exercise: 32.3 ± 4.9 mmHg; recovery: 29.1 ± 5.8 mmHg) and HCAP (rest: 27.3 ± 4.3 mmHg; exercise: 34.2 ± 6.0 mmHg; recovery: 29.1) trials, with hypercapnia augmenting the exercise‐induced elevation in IOP (p < 0.01). CO, SV, HR and MAP were significantly increased during handgrip dynamometry, but there was no effect of hypercapnia. The observed IOP measured during prone 6°HDT in all phases of the NCAP and HCAP trials exceeded the threshold pressure defining ocular hypertension. The exercise‐induced increase in IOP is exacerbated by hypercapnia
Heat acclimation enhances the cold-induced vasodilation response
Purpose It has been reported that the cold-induced vasodilation (CIVD)
response can be trained using either regular local cold stimulation or
exercise training. The present study investigated whether repeated
exposure to environmental stressors, known to improve aerobic
performance (heat and/or hypoxia), could also provide benefit to the
CIVD response.
Methods Forty male participants undertook three 10-day acclimation
protocols including daily exercise training: heat acclimation (HeA;
daily exercise training at an ambient temperature, T-a = 35 degrees C),
combined heat and hypoxic acclimation (HeA/HypA; daily exercise training
at T-a = 35 degrees C, while confined to a simulated altitude of similar
to 4000 m) and exercise training in normoxic thermoneutral conditions
(NorEx; no environmental stressors). To observe potential effects of the
local acclimation on the CIVD response, participants additionally
immersed their hand in warm water (35 degrees C) daily during the
HeA/HypA and NorEx. Before and after the acclimation protocols,
participants completed hand immersions in cold water (8 degrees C) for
30 min, followed by 15-min recovery phases. The temperature was measured
in each finger.
Results Following the HeA protocol, the average temperature of all five
fingers was higher during immersion (from 13.9 +/- 2.4 to 15.5 +/- 2.5
degrees C; p = 0.04) and recovery (from 22.2 +/- 4.0 to 25.9 +/- 4.9
degrees C; p = 0.02). The HeA/HypA and NorEx protocols did not enhance
the CIVD response.
Conclusion Whole-body heat acclimation increased the finger vasodilatory
response during cold-water immersion, and enhanced the rewarming rate of
the hand, thus potentially contributing to improved local cold
tolerance. Daily hand immersion in warm water for 10 days during HeA/Hyp
and NorEx, did not contribute to any changes in the CIVD response