Vascular occlusion training as an alternate method of gaining muscle

Training whilst under the effects of vascular occlusion has become increasingly popular due to the resultant muscle gain associated with this training technique. However, when exercising with the use of a tourniquet type device, it is possible for the pressure being applied to be inconsistent, due the constantly changing cross sectional area of the limb being occluded. This Paper describes the design of a device capable of causing vascular occlusion, but also being able to maintain a stable pressure required to create the blood flow restriction, this being able to be utilized in a sports science environment

Altered responsiveness of the kidney to activation of the renal nerves in fat-fed rabbits

We tested whether mild adiposity alters responsiveness of the kidney to activation of the renal sympathetic nerves. After rabbits were fed a high-fat or control diet for 9 wk, responses to reflex activation of renal sympathetic nerve activity (RSNA) with hypoxia and electrical stimulation of the renal nerves (RNS) were examined under pentobarbital anesthesia. Fat pad mass and body weight were, respectively, 74% and 6% greater in fat-fed rabbits than controls. RNS produced frequency-dependent reductions in renal blood flow, cortical and medullary perfusion, glomerular filtration rate, urine flow, and sodium excretion and increased renal plasma renin activity (PRA) overflow. Responses of sodium excretion and medullary perfusion were significantly enhanced by fat feeding. For example, 1 Hz RNS reduced sodium excretion by 79 ± 4% in fat-fed rabbits and 46 ± 13% in controls. RNS (2 Hz) reduced medullary perfusion by 38 ± 11% in fat-fed rabbits and 9 ± 4% in controls. Hypoxia doubled RSNA, increased renal PRA overflow and medullary perfusion, and reduced urine flow and sodium excretion, without significantly altering mean arterial pressure (MAP) or cortical perfusion. These effects were indistinguishable in fat-fed and control rabbits. Neither MAP nor PRA were significantly greater in conscious fat-fed than control rabbits. These observations suggest that mild excess adiposity can augment the antinatriuretic response to renal nerve activation by RNS, possibly through altered neural control of medullary perfusion. Thus, sodium retention in obesity might be driven not only by increased RSNA, but also by increased responsiveness of the kidney to RSNA.

Chronic intraocular pressure elevation impairs autoregulatory capacity in streptozotocin-induced diabetic rat retina

Purpose: To assess ocular blood flow responses to acute IOP stress following 4 weeks of chronic IOP elevation in streptozotocin (STZ)-induced diabetic and control rats. We hypothesise that chronic IOP elevation for 4 weeks will further impair blood flow regulation in STZ-induced diabetic rats eyes. Methods: Two weeks following citrate buffer or STZ-injections chronic IOP elevation was induced in Long Evans rats via fortnightly intracameral injections of microspheres (15 μm) suspended in 5% polyethylene glycol. IOP was monitored daily. Electroretinography (ERG, -6.79-2.07 log cd s m-2) was undertaken at Week 4 to compare photoreceptor (RmPIII), ON-bipolar cell (Vmax) and ganglion cell dominant ERG [scotopic threshold response (STR)] components. 4 weeks post-chronic IOP induction, ocular blood flow (laser Doppler flowmetry) was measured in response to acute IOP challenge (10-100 mmHg, in 5 mmHg steps, each 3 min). Results: Four weeks of chronic IOP (mean ± S.E.M., citrate: 24.0 ± 0.3 to 30.7 ± 1.3 and STZ-diabetes: 24.2 ± 0.2 to 31.1 ± 1.2 mmHg) was associated with reduced photoreceptor amplitude in both groups (-25.3 ± 2.2% and -17.2 ± 3.0%, respectively). STZ-diabetic eyes showed reduced photoreceptor sensitivity (citrate: 0.5 ± 1.8%, STZ-diabetic: -8.1 ± 2.4%). Paradoxically ON-bipolar cell sensitivity was increased, particularly in citrate control eyes (citrate: 166.8 ± 25.9%, STZ-diabetic: 64.8 ± 18.7%). The ganglion cell dominant STR was not significantly reduced in STZ-diabetic rats. Using acute IOP elevation to probe autoregulation, we show that STZ-diabetes impaired autoregulation compared with citrate control animals. The combination of STZ-diabetes and chronic IOP elevation further impaired autoregulation. Conclusions: STZ-diabetes and chronic IOP elevation appear to be additive risk factors for impairment of ocular blood flow autoregulation.

Switching to a 10-day Mediterranean-style diet improves mood and cardiovascular function in a controlled crossover study

OBJECTIVES: Even short-term adherence to a Mediterranean-style diet may benefit aspects of psychological functioning. The aim of the present study was to assess the effects of switching to a 10-d Mediterranean-style diet on mood, cognition, and cardiovascular measures. METHODS: Using a crossover design, 24 women were randomly assigned to either the diet change (where they switched to a Mediterranean-style diet) or no diet change (normal diet) condition for 10 days before switching to the other condition for the same duration. Mood, cognition, and cardiovascular measures of blood pressure, blood flow velocity, and arterial stiffness were assessed at baseline and at the completion of the two diets (days 11 and 22). RESULTS: Independent of whether the Mediterranean-style diet was undertaken before or after the crossover, it was associated with significantly elevated contentment and alertness, and significantly reduced confusion. Additionally, aspects of cognition, such as memory recall, improved significantly as a result of switching to the Mediterranean-style diet. Regarding cardiovascular measures, there was a significant reduction in augmentation pressure associated with the Mediterranean-style diet intervention, but blood flow velocity through the common carotid artery did not change. CONCLUSIONS: This Mediterranean-style diet has the potential to enhance aspects of mood, cognition, and cardiovascular function in a young, healthy adult sample.

Modulating exercise-induced hormesis: does less equal more?

Hormesis encompasses the notion that low levels of stress stimulate or upregulate existing cellular and molecular pathways that improve the capacity of cells and organisms to withstand greater stress. This notion underlies much of what we know about how exercise conditions the body and induces long-term adaptations. During exercise, the body is exposed to various forms of stress, including thermal, metabolic, hypoxic, oxidative, and mechanical stress. These stressors activate biochemical messengers, which in turn activate various signaling pathways that regulate gene expression and adaptive responses. Historically, antioxidant supplements, nonsteroidal anti-inflammatory drugs, and cryotherapy have been favored to attenuate or counteract exercise-induced oxidative stress and inflammation. However, reactive oxygen species and inflammatory mediators are key signaling molecules in muscle, and such strategies may mitigate adaptations to exercise. Conversely, withholding dietary carbohydrate and restricting muscle blood flow during exercise may augment adaptations to exercise. In this review article, we combine, integrate, and apply knowledge about the fundamental mechanisms of exercise adaptation. We also critically evaluate the rationale for using interventions that target these mechanisms under the overarching concept of hormesis. There is currently insufficient evidence to establish whether these treatments exert dose-dependent effects on muscle adaptation. However, there appears to be some dissociation between the biochemical/molecular effects and functional/performance outcomes of some of these treatments. Although several of these treatments influence common kinases, transcription factors, and proteins, it remains to be determined if these interventions complement or negate each other, and whether such effects are strong enough to influence adaptations to exercise.

Effect of retinal image defocus on the thickness of the human choroid

PURPOSE: To describe the time-course and amplitude of changes to sub-foveal choroidal thickness (SFCT) induced by imposed hyperopic and myopic retinal defocus and to compare the responses in emmetropic and myopic subjects. METHODS: Twelve East Asian subjects (age: 18-34 years; six were emmetropic and six had myopia between -2.00 and -5.00 dioptres (D)) viewed a distant target (video movie at 6 m) for 60 min on two separate occasions while optical coherence tomography (OCT) images of the choroid were taken in both eyes every 5 min to monitor SFCT. On each occasion, one eye was optimally corrected for distance with a contact lens while the other eye wore a contact lens imposing either 2.00 D hyperopic or 2.00 D myopic retinal defocus. RESULTS: Baseline SFCT in myopic eyes (mean ± S.D.): 256 ± 42 μm was significantly less than in emmetropic eyes (423 ± 62 μm; p < 0.01) and was correlated with magnitude of myopia (-39 μm per dioptre of myopia, R(2) = 0.67: p < 0.01). Repeated measures anova (General Linear Model) analysis revealed that in both subject groups, 2.00 D of myopic defocus caused a rapid increase in SFCT in the defocussed eye (significant by 10 min, increasing to approximately 20 μm within 60 min: p < 0.01), with little change in the control eye. In contrast, 2.00 D of hyperopic defocus caused a decrease in SFCT in the experimental eye (significant by 20-35 min. SFCT decreased by approximately 20 μm within 60 min: p < 0.01) with little change in the control eye. CONCLUSIONS: Small but significant changes in SFCT (5-8%) were caused by retinal defocus. SFCT increased within 10 min of exposure to 2.00 D of monocular myopic defocus, but decreased more slowly in response to 2.00 D of monocular hyperopic defocus. In our relatively small sample we could detect no difference in the magnitude of changes to SFCT caused by defocus in myopic eyes compared to emmetropic eyes.

Resistive exercise versus resistive vibration exercise to counteract vascular adaptations to bed rest

Bed rest results in marked vascular adaptations, and resistive vibration exercise (RVE) has been shown to be an effective countermeasure. As vibration exercise has practical and logistical limitations, the use of resistive exercise (RES) alone has the preference under specific circumstances. However, it is unknown if RES is sufficient to prevent vascular adaptations to bed rest. Therefore, the purpose of the present study was to examine the impact of RES and RVE on the vascular function and structure of the superficial femoral artery in young men exposed to 60 days of bed rest. Eighteen healthy men (age: 31 +/- 8 yr) were assigned to bed rest and randomly allocated to control, RES, or RVE groups. Exercise was applied 3 times/wk for 5-7 min/session. Resting diameter, blood flow, flow-mediated dilation (FMD), and dilator capacity of the superficial femoral artery were measured using echo-Doppler ultrasound. Bed rest decreased superficial femoral artery diameter and dilator capacity (P < 0.001), which were significantly attenuated in the RVE group (P < 0.01 and P < 0.05, respectively) but not in the RES group (P = 0.202 and P = 0.696, respectively). Bed rest significantly increased FMD (P < 0.001), an effect that was abolished by RVE (P < 0.005) but not RES (P = 0.078). Resting and hyperemic blood flow did not change in any of the groups. Thus, RVE abolished the marked increase in FMD and decrease in baseline diameter and dilator capacity normally associated with prolonged bed rest. However, the stimulus provided by RES alone was insufficient to counteract the vascular adaptations to bed rest.

Impact of bed rest on conduit artery remodeling: effect of exercise countermeasures

Physical inactivity is a potent stimulus for vascular remodeling, leading to a marked decrease in conduit artery diameter. However, little is known about the impact of physical inactivity on artery wall thickness or wall:lumen ratio or the potential of exercise countermeasures to modify artery wall thickness. The purpose of the study was to examine the impact of 60 days of bed rest, with or without exercise countermeasures, on carotid and superficial femoral artery wall thickness. Eighteen men were assigned to bed rest (second Berlin Bed Rest Study) and randomly allocated to control, resistive exercise, or resistive vibration exercise. Both exercise countermeasures were applied 3 times per week while the subjects were in the supine position on the bed. Sonography was used to examine baseline diameter and wall thickness of the carotid and femoral arteries. Bed rest decreased diameter of the superficial femoral artery (P=0.001) but not the carotid artery (P=0.29). Bed rest induced a significant increase in carotid and superficial femoral artery wall thickness (P=0.007 and 0.03) and wall:lumen ratio (P=0.009 and 0.001). Exercise prevented the increase in wall thickness of the carotid artery. In addition, exercise partly prevented the increased wall:lumen ratio in the superficial femoral artery. In conclusion, 8 weeks of bed rest resulted in approximately 20% increase in conduit artery wall thickness. Exercise countermeasures completely (carotid artery) or partly (superficial femoral artery) abolished the increase in wall thickness. These findings suggest that conduit artery wall thickness, a vascular characteristic associated previously with atherosclerosis, can rapidly adapt to physical inactivity and exercise in humans.