Strength prior to endurance intra-session exercise sequence optimizes neuromuscular and cardiovascular gains in elderly men

Abstract

This study investigated the effects of different intra-session exercise sequences in the cardiovascular and neuromuscular adaptations induced by concurrent training in elderly. Twenty-six healthy elderly men (64.7±4.1years), were randomly placed into two concurrent training groups: strength training prior to (SE, n=13) or after (ES, n=13) endurance training. Subjects trained strength and endurance training 3 times per week performing both exercise types in the same training session. The peak oxygen uptake (VO(2peak)), maximum aerobic workload (W(máx)), absolute (VT(1) and VT(2)) and relative (VT(1)% and VT(2)%) ventilatory thresholds, as well as workloads at VT(1) and VT(2) (W(VT1) and W(VT2)) were evaluated during a maximal incremental test on a cycle ergometer before and after the training. In addition, muscle quality (MQ) was evaluated by the quotient between maximal dynamic strength (one repetition maximum test) of the knee extensors and the quadriceps femoris muscle thickness determined by ultrasonography. There were no modifications after training in the VT(1), VT(2), VT(1)%, and VT(2)%. There was significant increase in the W(VT1) only in SE (P<0.05), as well as significant increase in the W(VT2) in both groups (P<0.001). There was significant increase in the VO(2peak), with both groups showing increases (P<0.001), with no difference between groups; as well significant increase in the W(máx) (P<0.001) with no difference between SE and ES. The force per unit of muscle mass of knee extensors increased in both groups (P<0.001), but the increase was significantly higher in SE than in ES (27.5±12.7 vs. 15.2±10.3%, P<0.02). Hence, the intra-session exercise sequence had no influence in the maximal endurance power adaptations to concurrent training, but had influence in the magnitude of the muscle quality enhancements.

Copyright © 2011. Published by Elsevier Inc.

The protective effect of prolyl-hydroxylase inhibition against renal ischaemia requires application prior to ischaemia but is superior to EPO treatment

Abstract

BACKGROUND:

Inhibition of the HIF regulating prolyl hydroxylation domain (PHDs) proteins prior to renal injury (preconditioning) has been shown to protect the kidney via activation of hypoxia-inducible transcription factors (HIF). Application of erythropoietin (EPO), one of the HIF target genes, has also been shown to be nephroprotective, and it remains unclear to what extent the effect of HIF induction is mediated by EPO. It is also unknown whether HIF activation after the onset of ischaemia (postconditioning) is still able to protect the kidney.

METHODS:

Using a rat model of renal ischaemia-reperfusion injury, animals were treated with the PHD inhibitor (PHD-I) 2-(1-chloro-4-hydroxyisoquinoline-3-carboxamido) acetate (ICA), vehicle (Veh) or recombinant human EPO (300 IU/kg) 6 h (ICA or Veh) or 30 min (EPO) prior to ischaemia (preconditioning) or with ICA prior to reperfusion (postconditioning). Renal function was assessed at baseline, 24 h and 72 h. After 72 h, kidneys were processed for histology and morphometric analysis. HIF immunohistochemistry and real-time polymerase chain reaction for HIF target genes, including EPO, were performed to evaluate ICA effects.

RESULTS:

ICA treatment resulted in stabilization of HIF-1α and -2α and up-regulation of HIF target genes in a dose-dependent manner. Preconditional activation of HIF by ICA significantly improved serum creatinine levels and renal morphology in comparison to Veh (P < 0.05), while postconditional ICA treatment was ineffective. EPO therapy improved tissue morphology but had no impact on the course of serum creatinine.

CONCLUSION:

These findings are in line with the concept that PHD-Is exert their protective effects through accumulation of HIF target gene products, with time requirements for increased transcription and translation of HIF-dependent genes, and suggest that their renoprotective effect is not predominately mediated by EPO.

Positive effects of pentoxifylline (Trental) on blood, oxygen uptake, oxidative stress, diabetes…

The effect of pentoxifylline on the flow properties of human blood

Ehrly AM.

Abstract

Recent investigations have revealed that erythrocytes from patients with chronic arterial occlusive disease are significantly less deformable than red blood cells from healthy subjects. The influence of pentoxifylline on red blood cell fluidity was measured by a standard filtration technique using 8 micron membrane filters. Impaired deformability of erythrocytes was significantly improved in patients suffering from peripheral vascular disorders following intravenous injection of 200 mg pentoxifylline. Studies on reduced red cell deformability induced by hyperosmolarity in vitro showed that pentoxifylline (4 and 20 microgram/ml) produced a dose-dependent improvement both in blood from healthy subjects and from patients with peripheral arterial occlusive disease. The results suggest that the positive therapeutic effect of pentoxifylline in peripheral arterial occlusive disease is mediated by improving red cell fluidity in the microcirculation.

PMID: 710175

[PubMed – indexed for MEDLINE]

Effect of pentoxiphylline on oxygen transport during hypothermia.

Hershenson MB, Schena JA, Lozano PA, Jacobson MJ, Crone RK.

Source

Department of Anaesthesia, Harvard Medical School, Children’s Hospital, Boston, Massachusetts 02115.

Abstract

At least two investigators have demonstrated a reduction in O2 extraction during induced hypothermia (Cain and Bradley, J. Appl. Physiol. 55: 1713-1717, 1983; Schumacker et al., J. Appl. Physiol. 63: 1246-1252, 1987). We hypothesized that administration of pentoxiphylline (PTX), a theobromine that lowers blood viscosity and has vasodilator effects, would increase O2 extraction during hypothermia. To test this hypothesis, we studied O2 transport in anesthetized, paralyzed, mechanically ventilated beagles exposed to hypoxic hypoxia during either 1) normothermia (38 degrees C), 2) hypothermia (30 degrees C), or 3) hypothermia + PTX (30 degrees C and PTX, 20 mg.kg-1.h-1). Measurements included arterial and mixed venous PO2, hemoglobin concentration and saturation, cardiac output, systemic vascular resistance (SVR), blood viscosity, and O2 consumption (VO2). Critical levels of O2 delivery (DO2, the product of arterial O2 content and cardiac output) were determined by a system of linear regression. Hypothermia significantly decreased base line cardiac output (-35%), DO2 (-37%), and VO2 (-45%), while increasing SVR and blood viscosity. Addition of PTX increased cardiac output (35%) and VO2 (14%), and returned SVR and blood viscosity to normothermic levels. Hypothermia alone failed to significantly reduce the critical level of DO2, but addition of PTX did [normothermia, 11.4 +/- 4.2 (SD) ml.kg-1.min-1; hypothermia, 9.3 +/- 3.6; hypothermia + PTX, 6.6 +/- 1.3; P less than 0.05, analysis of variance]. The O2 extraction ratio (VO2/DO2) at the critical level of DO2 was decreased during hypothermia alone (normothermia, 0.60 +/- 0.13; hypothermia, 0.42 +/- 0.16; hypothermia + PTX, 0.62 +/- 0.19; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2917962 [PubMed – indexed for MEDLINE]

Pentoxifylline improves haemoglobin and interleukin-6 levels in chronic kidney disease.

Ferrari P, Mallon D, Trinder D, Olynyk JK.

Source

Department of Nephrology, Fremantle Hospital, Alma Street, Perth, WA 6160, Australia. paolo.ferrari@health.wa.gov.au

Abstract

AIM:

To assess whether pentoxifylline improves anaemia of chronic kidney disease (CKD) via suppression of interleukin-6 (IL-6) and improved iron mobilization.

BACKGROUND:

CKD patients may have elevated IL-6 and tumour necrosis factor alpha levels. These cytokines can increase hepcidin production, which in turn reduces iron release from macrophages resulting in reduced availability of iron for erythropoiesis. In experimental models, pentoxifylline was shown to reduce IL-6 expression.

METHODS:

We studied 14 patients with stages 4-5 CKD (glomerular filtration rate <30mL/min per 1.73 m(2)) due to non-inflammatory renal diseases. None of the patients had received immunosuppressive or erythropoietin-stimulating agents or parenteral iron. Patients had weekly blood tests for iron studies and cytokines during a control run-in period of 3 weeks and during 4 weeks of pentoxifylline treatment.

RESULTS:

Ten patients (eGFR 23 + or – 6 mL/min) completed the study. At the end of the run-in period average haemoglobin was 111 + or – 5 g/L, ferritin 92 + or – 26 microg/L, transferrin saturation 15 + or – 3% and circulating IL-6 10.6 + or – 3.8 pg/mL. Tumour necrosis factor alpha values were below threshold for detection. Treatment with pentoxifylline reduced circulating IL-6 (6.6 + or – 1.6 pg/mL, P < 0.01), increased transferrin saturation (20 + or – 5%, P < 0.003) and decreased serum ferritin (81 + or – 25 microg/L, P = NS). Haemoglobin increased after the second week of pentoxifylline, reaching 123 + or – 6 g/L by week 4 (P < 0.001).

CONCLUSIONS:

Pentoxifylline reduces circulating IL-6 and improves haemoglobin in non-inflammatory moderate to severe CKD. These changes are associated with changes in circulating transferrin saturation and ferritin, suggesting improved iron release. It is hypothesized that pentoxifylline improves iron disposition possibly through modulation of hepcidin.

PMID:

20470305

[PubMed – indexed for MEDLINE]

Effects of pentoxifylline on oxidative stress and levels of EGF and NO in blood of diabetic type-2 patients; a randomized, double-blind placebo-controlled clinical trial.

Radfar M, Larijani B, Hadjibabaie M, Rajabipour B, Mojtahedi A, Abdollahi M.

Source

Faculty of Pharmacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, PO Box 14155-6451, Tehran, Iran.

Abstract

BACKGROUND:

As oxidative stress contributes to both progression and pathologic complications of diabetes and effective therapeutic strategies to prevent or delay the damage remain limited, the aim of the present study was to assess the efficacy of pentoxifylline in reducing of oxidative stress. Since there is a relationship between nitric oxide (NO), epidermal growth factor (EGF) and oxidative stress, we measured the effect of this drug on these parameters in comparison to placebo.

METHODS:

Thirty-nine patients with type-2 diabetes mellitus were randomized in a double blind, placebo-controlled clinical trial to receive either pentoxifylline 400 mg four times a day or placebo for 14 days. Blood samples were obtained at baseline and at the end of the study. Samples were analyzed for thiobarbituric reactive substances (TBARS) as a marker of lipid peroxidation, ferric reducing ability (total antioxidant power, TAP), EGF and NO levels.

RESULTS:

Pentoxifylline in comparison to placebo was effective (P < 0.05) in reduction of lipid peroxidation in plasma of the patients without significant effects on TAP, levels of EGF and NO in plasma.

CONCLUSION:

Adding of pentoxifylline to drug regimen of diabetic type-2 patients can be helpful. Exact mechanism of action of pentoxifylline in reduction of blood lipid peroxidation remains to be elucidated.

PMID:

            15932791 begin_of_the_skype_highlighting            15932791      end_of_the_skype_highlighting      

[PubMed – indexed for MEDLINE]