The role of angiotensin II in the development of hypertension and in the maintenance of glomerular filtration rate during 48 hours of renal artery stenosis in conscious dogs.

The responses to 48 h of renal artery stenosis were compared in uninephrectomized, chronically-instrumented dogs with or without inhibition of angiotensin II (AII) formation by enalapril. Mean arterial pressure rose by an average of 29.9 mmHg (s.e.m. 3.5) in untreated dogs and by 14.5 mmHg (s.e.m. 2.8) in enalapril-treated dogs over the two days of stenosis. Renal artery stenosis reduced glomerular filtration rate (GFR) by 49% (s.e.m. 9) in untreated dogs and by 86% (s.e.m. 8) in enalapril-treated dogs. Compared to untreated dogs, enalapril-treated dogs also had lower renal artery pressure distal to the stenosis, drank less water and had larger rises in plasma K+ following renal artery stenosis. There were no differences in renal blood flow or urinary Na+ excretion in the two groups of dogs. Thus blockade of AII production did not prevent hypertension occurring in response to renal artery stenosis, but the rise in blood pressure was only about half that which occurred in normal dogs and GFR was much more severely reduced.

Resistance exercise training increases muscle strength, endurance, and blood flow in patients with chronic heart failure.

Resistance exercise training was well tolerated in patients with stable, chronic heart failure, resulting in increased strength and endurance, and lower oxygen consumption at submaximum workloads but no improvement in VO2peak. There was also a significant increase in basal forearm blood flow following this form of exercise training.

Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance.

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 x (5 g Cr-H(2)O + 5 g dextrose)/day)] or a placebo (6 x 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased (P < 0.05) at 0 [by 22.9 +/- 4.2, 8.9 +/- 1.9, and 14.0 +/- 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.

Effect of creatine supplementation on sprint exercise performance and muscle metabolism.

The aim of the present study was to examine the effect of creatine supplementation (CrS) on sprint exercise performance and skeletal muscle anaerobic metabolism during and after sprint exercise. Eight active, untrained men performed a 20-s maximal sprint on an air-braked cycle ergometer after 5 days of CrS [30 g creatine (Cr) + 30 g dextrose per day] or placebo (30 g dextrose per day). The trials were separated by 4 wk, and a double-blind crossover design was used. Muscle and blood samples were obtained at rest, immediately after exercise, and after 2 min of passive recovery. CrS increased the muscle total Cr content (9.5 +/- 2.0%, P < 0.05, mean +/- SE); however, 20-s sprint performance was not improved by CrS. Similarly, the magnitude of the degradation or accumulation of muscle (e.g., adenine nucleotides, phosphocreatine, inosine 5'-monophosphate, lactate, and glycogen) and plasma metabolites (e.g. , lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did not induce an improved sprint exercise performance or alterations in anaerobic muscle metabolism.

Effect of CHO ingestion on exercise metabolism and performance in different ambient temperatures.

Two series of experiments were conducted to examine the effect of ingesting beverages with differing carbohydrate (CHO) concentrations and osmolalities on metabolism and performance during prolonged exercise in different environmental conditions. In series 1, 12 subjects performed three cycling exercise trials to fatigue at 70% VO2peak in either 33 degrees C (N = 6) (HT1) or 5 degrees C (N = 6) (CT). Subjects ingested either a 14% CHO solution (osmolality = 390 mosmol.1(-1) (HCHO); a 7% CHO solution (330 mosmol.1(-1) (NCHO) or a placebo (90 mosmol.1(-1) (CON1). In series 2, six subjects performed the same three trials at 33 degrees C (HT2), while ingesting either NCHO, a 4.2% CHO solution (240 mosmol.1(-1) (LCHO) or a placebo) (240 mosmol.1(-1) (CON2). Plasma glucose was higher (P < 0.05) in HCHO than NCHO, which in turn was higher (P < 0.05) than CON1 in both CT and HT1. Plasma glucose was lower (P < 0.05) in CON2 compared with NCHO and LCHO in HT2. The fall in plasma volume was greater (P < 0.05) in HCHO than other trials in both CT and HT1 but was not different when comparing the three trials in HT2. Exercise time was not different when comparing the trials in either HT1 or HT2 but was longer (P < 0.05) in NCHO compared with HCHO, which, in turn, was longer (P < 0.05) than CON1 in CT. These data demonstrate that, during prolonged exercise in the heat, fatigue is related to factors other than CHO availability. In addition, during exercise in 5 degrees C a 7% CHO solution is more beneficial for exercise performance than a 14% CHO solution.

Role of angiotensin II in the hypertension induced by renal artery stenosis.

Identical degrees of renal artery stenosis were induced in 5 dogs on two separate occasions; once during continuous inhibition of angiotensin I converting enzyme with enalapril, and once with the dogs untreated. Arterial pressure rose about 25 mm Hg during 3 days of stenosis in untreated dogs, due to increased total peripheral resistance. When the dogs were treated with enalapril, blood pressure had risen 14.5 +/- 3.4 mm Hg 24 hours after stenosis due to a 35% increase in cardiac output while total peripheral resistance fell by 16%. By the third day, blood pressure had returned to pre-stenosis levels, cardiac output was close to normal and total peripheral resistance had increased. The stenosis on the renal artery increased the resistance to blood flow of the kidneys in both untreated and enalapril treated dogs. This increase in kidney resistance in the untreated dogs accounted for about 30% of the change in total peripheral resistance. In the enalapril treated dogs, the increased kidney resistance helped offset the vasodilatation in the rest of the vasculature. These results suggest that angiotensin II mediated vasoconstriction of nonrenal vascular beds was responsible for about 2/3 of the hypertension following renal artery stenosis, and the resistance of the stenosis responsible for about 1/3.

Mechanisms involved in the renal responses to intravenous and renal artery infusions of noradrenaline in conscious dogs.

1. The renal haemodynamic and glomerular filtration rate (G.F.R.) responses to intravenous and intrarenal infusions of noradrenaline were studied in conscious dogs, either with or without prior blockade of angiotensin II formation with teprotide. 2. Infusion noradrenaline by either route resulted in dose-related rises in plasma renin activity. 3. Pretreatment with teprotide reduced the rise in mean arterial pressure and abolished the rise in G.F.R. seen during intravenous infusions of noradrenaline (0.1, 0.2 and 0.4 microgram/kg . min). Noradrenaline also reduced filtration fraction more after teprotide pretreatment. 4. Renal blood flow rose and renal vascular resistance fell in response to I.V. noradrenaline infusions. This renal vasodilatation was unaffected by pretreatment of the dogs with teprotide, indomethacin or DL-propranolol. However after pentolinium pretreatment, I.V. noradrenaline infusion caused a dose-related renal vasoconstriction. 5. Infusion of noradrenaline into the renal artery (0.02, 0.05 and 0.1 microgram/kg . min) resulted in rises in mean arterial pressure and G.F.R. which were abolished by teprotide pretreatment. Filtration fraction rose when noradrenaline was administered alone but fell when it was infused after teprotide treatment. 6. Thus angiotensin II formed as the result of increased renin release acted to maintain G.F.R. and filtration fraction during noradrenaline infusion. In addition, I.V. noradrenaline infusions in conscious dogs caused reflex vasodilatation of the renal vasculature.

Psychophysiological stress in elite golfers during practice and competition.

This study examined self-reported state anxiety (cognitive anxiety, somatic anxiety and self-confidence) measured by the Competitive State Anxiety Inventory-2 (CSAI-2; Martens, Vealey, Bump, & Smith, 1990) and physiological responses (salivary cortisol concentration and heart rate) in elite golfers prior to, during and on completion of a tournament and practice round. The relationships between psychophysiological variables were investigated by comparing physiological and psychological responses during competition and practice to each other, and to performance. Performance was determined for each player as the difference between 18 hole score and handicap. Fifteen male Professional Golfing Association (PGA) trainees (aged 21-25 years) competed in a PGA sanctioned tournament and a practice round on the same, or similar golf course. Players completed the CSAI-2 and collected saliva for cortisol analysis on four occasions: prior to tee off, and after completing holes 6, 12 and 18. Cortisol concentration was corrected for circadian variations in cortisol secretion, using baseline cortisol measures. Within-subject analysis revealed elite golfers experienced elevated cortisol, heart rate, cognitive and somatic anxiety, and lower self-confidence during competition compared to practice. For both game conditions, the highest cortisol response was measured prior to the commencement of play, whilst state anxiety measures did not change significantly during the golf rounds. Univariate and multivariate analyses failed to reveal significant correlations between the psychophysiological variables and golf performance. In conclusion, competition and practice were clearly discriminated by the psychophysiological variables, but none of these predicted performance.

Renal responses to angiotensin II in conscious dogs: effects of aspirin and indomethacin.

1. Angiotensin II was infused into the renal artery of unanaesthetized dogs at 0.4 and 2.0 ng/kg per min for 40 min each. 2. Indomethacin (3 mg/kg, and 1 mg/kg per h infusion i.v.) accentuated the angiotensin II-induced falls in glomerular filtration rate, renal blood flow and urine flow rate. Indomethacin did not alter the effects of angiotensin II on Na+ or K+ excretions. 3. Aspirin (35 mg/kg p.o. 2.5 h and 0.5 h prior to experiment) did not significantly change the renal effects of angiotensin II. 4. Both aspirin and indomethacin accentuated renal vasoconstriction during briefer (5 min) angiotensin II infusion. 5. Thus indomethacin and aspirin had markedly different effects on the actions of angiotensin II in the kidney. This suggests that at least one of these drugs has actions which affect angiotensin II-mediated vasoconstriction other than via cyclooxygenase inhibition.

Comparison of aspirin and indomethacin pre-treatments on the responses to reduced renal artery pressure in conscious dogs.

To examine the role of prostaglandins in physiologically induced renin release, we reduced renal artery pressure within the autoregulatory range in chronically instrumented conscious dogs with aspirin, indomethacin or no pre-treatment. In untreated dogs, reduction of renal artery pressure to 60 mmHg for 90 min produced rises in plasma renin activity (+ 5.4 +/- 1.0 ng ml.-1 hr-1) and mean arterial pressure (+ 17 +/- 2 mmHg) without significant effect on renal blood flow (n = 13). Aspirin pre-treatment (2 X 25-40 mg kg-1 orally) had no effect on the renin, arterial pressure or renal blood flow responses to renal artery pressure reduction (n = 7). In contrast, indomethacin pre-treatment (2 X 2-3 mg kg-1 orally) significantly lessened the increase in plasma renin activity during reduced renal artery pressure (+ 2.0 +/- 0.3 ng ml.-1 hr-1, n = 11). The relative effectiveness of aspirin and indomethacin in inhibiting prostaglandin production in the kidney was then tested in separate experiments by measuring the renal blood flow responses to renal artery injections of arachidonate (5-200 micrograms kg-1). In the doses used above, aspirin markedly attenuated the blood flow response to arachidonate but indomethacin had almost no effect. Both aspirin and indomethacin abolished the hypotensive effect of intravenous arachidonate (0.5 mg kg-1). These results tentatively suggest that indomethacin may not effectively inhibit renal prostaglandin production in conscious dogs at the doses used in these experiments. Thus the reduced renin release in response to lowered renal artery pressure in indomethacin pre-treated dogs may have been due to another, non-prostaglandin action of indomethacin. The results from the aspirin pre-treated dogs suggest that prostaglandins are not involved in the release of renin in response to reduced renal artery pressure in conscious dogs.

Accumulated oxygen deficit measurements during and after high-intensity exercise in trained male and female adolescents.

The purpose of this study was to compare accumulated oxygen deficits and markers of anaerobic metabolism [plasma ammonia (NH3) and lactate (La-) concentrations] in anaerobically trained male [n = 8, age 14.8 (0.5) years; maximal oxygen consumption VO2max 61.74 (2.23) ml x kg(-1) x min(-1)] and female [n = 8, age 14.5 (0.2) years; VO2max 49.62 (3.52) ml x kg(-1) x min(-1)] adolescents. The exercise protocol consisted of runs to exhaustion at speeds predicted to represent 120% and 130% of VO2max. Arterialised blood samples were obtained from a pre-warmed hand via a catheter inserted into a forearm vein. Samples were taken at rest and after 1, 3, 5, 7, 10, 15 and 20 min of recovery. The high-intensity exercise resulted in mean accumulated oxygen deficits that were less (P < 0.05) in females (52.3 ml x kg(-1)) than in males (68.6 ml x kg(-1)). Lower (P < 0.05) plasma concentrations of NH3 and La(-1), and a higher pH were evident in females compared with males during various stages of the 20-min recovery period. The increase in anaerobic performance in the male adolescent athletes when compared with their female counterparts was associated with an increased plasma concentration of selected plasma and blood metabolites. The observed results may reflect well-established differences between the sexes in the morphology and metabolic power of muscle.