British Dietetic Association evidence-based guidelines for the protein requirements of adults undergoing maintenance haemodialysis or peritoneal dialysis.

BACKGROUND: Existing nutritional guidelines suggest that protein requirements of adults with stage five chronic kidney disease undergoing haemodialysis (HD) or peritoneal dialysis (PD) are increased as a result of protein losses during dialysis. The present review aimed to update previous guidance and develop evidence-based practice guidelines on the protein requirements of adults undergoing maintenance dialysis. METHODS: Following a PICO approach (Participants or Population, Intervention or Exposure, Comparison and Outcome), four research questions were formulated to investigate the total protein requirement and protein quality required by adults undergoing HD and PD. A comprehensive, systematic review was undertaken using the databases Medline, EMBASE and the Cochrane Library from 2005 to September 2009 for HD studies and from 1997 to September 2009 for PD studies. RESULTS: The literature search yielded 2931 studies, which were assessed for inclusion. Following appraisal, 19 studies in HD and 18 studies in PD met the inclusion criteria and were systematically reviewed. Limited good quality evidence supports the recommendations that: (i) adults undergoing maintenance HD require a minimum protein intake of 1.1 g kg(-1) ideal body weight (IBW) per day; and (ii) adults undergoing maintenance PD require a minimum protein intake of 1.0-1.2 kg(-1) IBW per day, in conjunction with an adequate energy intake. There were no studies that addressed the quality of protein for either HD or PD. CONCLUSIONS: Evidence suggests that nutritional status may be maintained with lower protein intakes than previously recommended. However, the evidence base is limited and further randomised controlled trials are required to establish the optimal protein intake for dialysis patients.

Reduced oxygen uptake during steady state exercise after 21-day mountain climbing expedition to 6,194 m.

We investigated the effect of a 21-day climbing expedition to 6,194 m on the oxygen uptake (V022) and leg blood flow (LBF) responses to submaximal exercise in five healthy, fit men during two-leg kicking exercise a 0-W and 50-W. Tests were completed 1 week before and 3 days after altitued acclimatization. The adaptation of VO2 at exercise onset was described by the time to 63% of the new steady state. Steady state VO2 during 50-W exercise was less post-climb (1290+/- 29 mL/min, mean +/- SE) than pre-climb (1413+/- 63 mL/min, P <.05). VO2 adapted more slowly at the onset of 50-W exercise post climb. There were no differences in the steady state LBF during the 50-W exercise, the increase above baseline, or the adaptation post-climb. Respiratory exchange ratio was greater at 50-W post-climb compared to pre-climb. Reduced steady state V02 during exercise after exposure to high altitude is consistent with an increase in metabolic efficiency.

Peripheral circulatory factors limit rate of increase in muscle O(2) uptake at onset of heavy exercise.

We used an exercise paradigm with repeated bouts of heavy forearm exercise to test the hypothesis that alterations in local acid-base environment that remain after the first exercise result in greater blood flow and O(2) delivery at the onset of the second bout of exercise. Two bouts of handgrip exercise at 75% peak workload were performed for 5 min, separated by 5 min of recovery. We continuously measured blood flow using Doppler ultrasound and sampled venous blood for O(2) content, PCO(2), pH, and lactate and potassium concentrations, and we calculated muscle O(2) uptake (VO(2)). Forearm blood flow was elevated before the second exercise compared with the first and remained higher during the first 30 s of exercise (234 +/- 18 vs. 187 +/- 4 ml/min, P < 0.05). Flow was not different at 5 min. Arteriovenous O(2) content difference was lower before the second bout (4.6 +/- 0.9 vs. 7.2 +/- 0.7 ml O(2)/dl) and higher by 30 s of exercise (11.2 +/- 0.7 vs. 10.8 +/- 0.7 ml O(2)/dl, P < 0. 05). Muscle VO(2) was unchanged before the start of exercise but was elevated during the first 30 s of the transition to the second exercise bout (26.0 +/- 2.1 vs. 20.0 +/- 0.9 ml/min, P < 0.05). Changes in venous blood PCO(2), pH, and lactate concentration were consistent with reduced reliance on anaerobic glycolysis at the onset of the second exercise bout. These data show that limitations of muscle blood flow can restrict the adaptation of oxidative metabolism at the onset of heavy muscular exertion.

Blood flow dynamics in heart failure.

BACKGROUND: Exercise intolerance in heart failure (HF) may be due to inadequate vasodilation, augmented vasoconstriction, and/or altered muscle metabolic responses that lead to fatigue. METHODS AND RESULTS: Vascular and metabolic responses to rhythmic forearm exercise were tested in 9 HF patients and 9 control subjects (CTL) during 2 protocols designed to examine the effect of HF on the time course of oxygen delivery versus uptake (protocol 1) and on vasoconstriction during exercise with 50 mm Hg pressure about the forearm to evoke a metaboreflex (protocol 2). In protocol 1, venous lactate and H+ were greater at 4 minutes of exercise in HF versus CTL (P<0.05) despite similar blood flow and oxygen uptake responses. In protocol 2, mean arterial pressure increased similarly in each group during ischemic exercise. In CTL, forearm blood flow and vascular conductance were similar at the end of ischemic and ambient exercise. In HF, forearm blood flow and vascular conductance were reduced during ischemic exercise compared with the ambient trial. CONCLUSIONS: Intrinsic differences in skeletal muscle metabolism, not vasodilatory dynamics, must account for the augmented glycolytic metabolic responses to moderate-intensity exercise in class II and III HF. The inability to increase forearm vascular conductance during ischemic handgrip exercise, despite a normal pressor response, suggests that enhanced vasoconstriction of strenuously exercising skeletal muscle contributes to exertional fatigue in HF.

Prostaglandin inhibition causes an increase in reactive hyperaemia after ischaemic exercise in human forearm.

The hypothesis that prostaglandins contribute to the reactive hyperaemia after 5 min of ischaemia or 5 min of ischaemic exercise was investigated in six men by inhibiting prostaglandin production with ibuprofen (1800 mg) and indomethacin (225 mg) over 24 h before testing. Blood flow was measured continuously in the baseline and after ischaemia by combined pulsed and echo Doppler as the product of velocity and cross-sectional area. After 5 min of ischaemia, there were no differences in blood flow between placebo and the two drug conditions, except at 5 and 10 s when flow with indomethacin was greater than both placebo and ibuprofen. After 5 min of ischaemic exercise, blood flow was significantly greater as a consequence of increased vascular conductance in each of ibuprofen and indomethacin than placebo from 5 until 90 s of recovery. We conclude that prostaglandin inhibition had little or no effect on reactive hyperaemia after 5 min of circulatory occlusion alone, but that blood flow after ischaemic exercise was elevated due to increased vascular conductance when prostaglandin synthesis was inhibited.

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans.

The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (gamma = 8.MBV/D), and forearm blood flow (FBF = MBV.pi r2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (approximately 10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and gamma was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 +/- 3 beats/min) compared with placebo (57 +/- 3 beats/min) (P < 0.05) without change to MPP. With placebo, D increased in both arm positions from approximately 4.3 mm at rest to approximately 4.5 mm at 5 min of exercise (P < 0.05). This response was not altered with Ibu (P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow (P > 0.05) in either arm position. The gamma was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise (P < 0.05). Because PG inhibition altered the time course of gamma at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.