PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) microvascular function (laser Doppler flowmetry), as well as endothelial-dependent (flow-mediated dilation) and endothelial-independent (nitroglycerin-mediated dilation) function. Bubble grades were monitored with Doppler according to the Spencer grade.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 μM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10(-5) M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension.

INTRODUCTION: Hyperoxia causes oxidative stress. Breath-hold diving is associated with transient hyperoxia followed by hypoxia and a build-up of carbon dioxide (CO₂), chest-wall compression and significant haemodynamic changes. This study analyses variations in plasma oxidative stress markers after a series of repetitive breath-hold dives. METHODS: Thirteen breath-hold divers were asked to perform repetitive breath-hold dives to 20 metres' depth to a cumulative breath-hold time of approximately 20 minutes over an hour in the open sea. Plasma nitric oxide (NO), peroxinitrites (ONOO⁻) and thiols (R-SH) were measured before and after the dive sequence. RESULTS: Circulating NO significantly increased after successive breath-hold dives (169.1 ± 58.26% of pre-dive values; P = 0.0002). Peroxinitrites doubled after the dives (207.2 ± 78.31% of pre-dive values; P = 0.0012). Thiols were significantly reduced (69.88 ± 19.23% of pre-dive values; P = 0.0002). CONCLUSION: NO may be produced by physical effort during breath-hold diving. Physical exercise, the transient hyperoxia followed by hypoxia and CO₂ accumulation would all contribute to the increased levels of superoxide anions (O₂²⁻). Since interaction of O₂²⁻ with NO forms ONOO⁻, this reaction is favoured and the production of thiol groups is reduced. Oxidative stress is, thus, present in breath-hold diving.

AIM: Our study's aim is to show how a five-week stretch training protocol, based on passive stretching, can change muscle performance during a drop jump (stretch shortening cycle). METHODS: This study observes in 8 healthy subjects (four males and four females), the effect of a 5-week passive stretch training protocol on the stretch shortening cycle (SSC) during the performance of a drop jump, and identify the architectural changes in the muscle. Subjects underwent measurements of their drop jump performance 3 times before, and 3 times after, the stretch training protocol. For the muscle tendon unit (MTU), changes were measured using the Hawkins and Hull's model. In order to calculate the length changes in the MTU, we measured the ankle and knee angles. For changes in the fascicle, the pennation angle and the thickness of the gastrocnemius medialis (GM) muscle were measured.

Bubbles are known to form in the body after scuba dives, even those done well within the decompression model limits. These can sometimes trigger decompression sickness and the dive protocols should therefore aim to limit bubble formation and growth from hyperbaric decompression. Understanding these processes physiologically has been a challenge for decades and there are a number of questions still unanswered. The physics and historical background of this field of study is presented and the latest studies and current developments reviewed. Heterogeneous nucleation is shown to remain the prime candidate for bubble formation in this context. The two main theories to account for micronuclei stability are then to consider hydrophobicity of surfaces or tissue elasticity, both of which could also explain some physiological observations. Finally the modeling relevance of the bubble formation process is discussed, together with that of bubble growth as well as multiple bubble behavior.