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BACKGROUND: Tart cherry supplementation has been shown to enhance recovery from strenuous exercise due to its antioxidant properties. The majority of these studies used tart cherry juice, with a significant calorie content. The primary purpose of this study was to assess whether powdered tart cherry extract with minimal calorie content reduces oxidative stress and enhances recovery following intense resistance exercise. METHODS: Thirteen men (mean age: 26.2 ± 5.3 years; height: 184.3 ± 8.2 cm; weight: 92.9 ± 15.6 kg) performed a demanding resistance exercise protocol consisting of 6 sets of 10 repetitions of barbell back squat with 80% 1RM. The protocol was performed once following 7 days of 500 mg of tart cherry extract and once following placebo. Serum protein carbonyl (PC) content, creatine kinase activity (CK) and creatine kinase myocardial band content (CK-MB) were used to assess oxidative stress, skeletal and cardiac muscle damage respectively. Muscle soreness was assessed by visual analog scale. Physical performance was measured by countermovement jump power and handgrip dynamometer strength. RESULTS: There was a significant increase in PC in the placebo (PL) condition when compared to the Tart Cherry (TC) condition at Immediate Post (IP) (PL: 0.4 ± 0.3 vs. TC: - 0.4 ± 0.2 nmol∙mg- 1; p < 0.001), 1 h (PL: 0.3 ± 0.3 vs. TC: - 0.7 ± 0.3 nmol∙mg- 1; p < 0.001) and 24 h (PL: 0.1 ± 0.4 vs. TC: - 0.3 ± 0.5 nmol∙mg- 1; p = 0.010). There was a significant increase in CK activity in PL when compared to the TC at IP (PL: 491.1 ± 280 vs. TC: 296.3 ± 178 U∙L- 1; p = 0.008) and 3 h (PL: - 87 ± 123 vs. TC: 43.1 ± 105.3 U∙L- 1; p = 0.006). There was a significant (p = 0.003) increase in CKMB concentration in PL when compared to the TC (PL: 21.6 ± 12.4 vs. TC: - 0.3 ± 11.8 ng∙ml- 1; p = 0.006) at 1 h post. There was a significant increase in handgrip strength in TC when compared to PL (PL: - 2 ± 5.1 vs. TC: 1.7 ± 3 kg; p = 0.017) at 24 h post. CONCLUSIONS: This study demonstrated that tart cherry extract reduced oxidative stress and markers of muscle and cardiac damage following intense resistance exercise. This occurred along with a prevention of the decrease in handgrip strength seen following the intense exercise protocol, indicating a potential reduction in central fatigue. These benefits were seen with minimal energy intake.

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PURPOSE: Our intent was to (a) characterize weekly changes in resting testosterone (T), cortisol (C), and the T:C ratio in males during an intensive endurance training program, and (b) determine if clinical androgen deficiency (AD) based upon T-level criteria developed. METHODS: An 18-week training program in which individual training volume (km/week) increased at 25% increments over baseline (BL) levels observed prior to the study beginning at 4-week intervals throughout the first 12 weeks. After 12 weeks, the volume was reduced to that of the first 4 weeks until the study end (week 18). Competitive performance running tests were assessed at BL and every 4 weeks, while blood T and C were assessed weekly. RESULTS: Performance improved from BL at weeks 4-16 (p < 0.01). T was reduced (p < 0.01) from BL at weeks 3, and 5-18. The greatest reduction from BL was at week 13, subsequently T returned toward BL at week 18. C was highly variable, and no significant changes from BL were noted. The T:C ratio at weeks 5, 6, and 8-16 was significantly less than at BL (p < 0.01), the greatest reduction at week 13. The T:C ratio values also returned toward BL by week 18. Finally, ∼50% of the subjects reached T levels to be classified as AD. CONCLUSIONS: Sports scientists should recognize decreases in T or T:C ratio is not always indicative of compromised competitive performance potential. Clinicians should be aware increased training loads can lead to AD in men.

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Tyrosine hydroxylase (TH) mRNA and activity and concentrations of 3,4-dihydroxyphenylalanine (DOPA) and catecholamines were examined as markers of sympathetic innervation and catecholamine synthesis in peripheral tissues of sympathectomized and intact rats. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) markedly decreased norepinephrine and to a generally lesser extent TH activities and dopamine in most peripheral tissues (stomach, lung, testis, duodenum, pancreas, salivary gland, spleen, heart, kidney, thymus). Superior cervical ganglia, adrenals and descending aorta were unaffected and vas deferens showed a large 92% decrease in norepinephrine, but only a small 38% decrease in TH activity after 6-OHDA. Presence of chromaffin cells or neuronal cell bodies in these latter tissues, indicated by consistent expression of TH mRNA, explained the relative resistance of these tissues to 6-OHDA. Stomach also showed consistent expression of TH mRNA before, but not after 6-OHDA, suggesting that catecholamine synthesizing cells in gastric tissue are sensitive to the toxic effects of 6-OHDA. Tissue concentrations of DOPA were mainly unaffected by 6-OHDA, indicating that much of the DOPA in peripheral tissues is synthesized independently of local TH or sympathetic innervation. The differential effects of chemical sympathectomy on tissue catecholamines, DOPA, TH mRNA and TH activity demonstrate that these variables are not simple markers of sympathetic innervation or catecholamine synthesis. Other factors, including presence of neuronal cell bodies, parenchymal chromaffin cells, non-neuronal sites of catecholamine synthesis and alternative sources of tissue DOPA, must also be considered when tissue catecholamines, DOPA and TH are examined as markers of sympathetic innervation and local catecholamine synthesis.

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Increased plasma adrenalin (A) levels following arecoline in normal subjects and patients with multiple system atrophy (MSA) may result from nicotinic adrenal stimulation. Lack of this response in patients with pure autonomic failure (PAF) is consistent with peripheral sympathetic dysfunction. The mechanisms underlying diminished plasma corticotropin (ACTH) responses to arecoline may differ in patients with autonomic failure. Hypothalamic, cholinergic degeneration could prevent the response in MSA whereas patients with PAF do not manifest the normal increase in A which may be required to elicit an ACTH response. The appearance and exacerbation of tremor, vertigo, and pathological affect in the MSA group suggest that some central cholinergic receptors remain functional.

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We examined the cardiovascular, plasma norepinephrine (NE), and plasma renin (PRA) responses to isoproterenol infusion in patients with autonomic failure and in normal subjects. Slopes of the blood pressure response/dose relationships were more negative in patients with multiple system atrophy and pure autonomic failure (PAF) than in normal subjects, consistent with impaired baroreflex modulation. A shift to the left in patients with PAF suggests beta-adrenergic receptor supersensitivity. In normal subjects, the increase in plasma NE and PRA was proportional to the log of the plasma isoproterenol level. Isoproterenol infusion did not increase plasma NE or PRA in either patient group despite a reduction in mean blood pressure. Reflexive cardiovascular and renal mechanisms appear to play a role in eliciting the plasma NE and PRA responses to isoproterenol infusion in normal subjects.

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A prospective, randomized double-blind trial of doxycycline prophylaxis for traveler's diarrhea was conducted on 145 volunteers during a 2.5-day visit to Mexico. Traveler's diarrhea occurred in 15 (21%) of the placebo group and in 3 (4%) of the doxycycline group (p = 0.002). There was no rebound increase in the incidence of acute diarrhea after departure from the high risk area in the doxycycline-treated group. A variety of bacterial pathogens were isolated from individuals symptomatic with traveler's diarrhea. Nausea alone (8%) or nausea with vomiting (4%) occurred in the doxycycline-treated group only and were the only side effects observed (p = 0.003). We conclude that doxycycline is safe and efficacious for the prophylaxis of traveler's diarrhea for short-term exposure in a high risk area.

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