Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimise performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimise performance is to heat acclimatise. Heat acclimatisation should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimise dehydration during exercise. Following the development of commercial cooling systems (eg, cooling-vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organisers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimising the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events, for hydration and body cooling opportunities, when competitions are held in the heat.

Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

Exercise intensity prescription during heat stress: A brief review.

Exercise intensity can be prescribed using a variety of indices, such as rating of perceived exertion, heart rate, levels of absolute intensity (e.g., metabolic equivalents), and levels of relative intensity [e.g., percentage of maximal aerobic capacity (% V ˙ O 2 m a x ) or percentage of oxygen uptake reserve (% V ˙ O 2 R )]. Heart rate has a linear relationship with oxygen uptake, is easy to measure, and requires relatively inexpensive monitoring equipment, so it is commonly used to monitor exercise intensity. During heat stress, however, cardiovascular adjustments - including a rise in heart rate that is disproportionate to absolute intensity - result in diminished aerobic capacity and performance. These adjustments include cardiovascular drift, the progressive rise in heart rate and fall in stroke volume over time during prolonged, constant-rate exercise. A variety of factors have been shown to modulate the magnitude of cardiovascular drift, e.g., hyperthermia, dehydration, exercise intensity, and ambient temperature. Regardless of the mode of manipulation, decreases in stroke volume with cardiovascular drift are associated with proportionally similar decreases in V ˙ O 2 m a x , which affects the relationship between heart rate and relative metabolic intensity (% V ˙ O 2 m a x or % V ˙ O 2 R ). This review summarizes the current state of knowledge regarding the influence of cardiovascular drift and reduced V ˙ O 2 m a x on exercise intensity prescription in hot conditions.

Caloric restriction alters the feeding response of key metabolic enzyme genes.

Differential 'fuel usage' has been proposed as a mechanism for life-span extension by caloric restriction (CR). Here, we report the effects of CR, initiated after weaning, on metabolic enzyme gene expression 0, 1.5, 5, and 12 h after feeding of 24-month-old mice. Plasma glucose and insulin were reduced by approximately 20 and 80%. Therefore, apparent insulin sensitivity, as judged by the glucose to insulin ratio, increased 3.3-fold in CR mice. Phosphoenolpyruvate carboxykinase mRNA and activity were transiently reduced 1.5 h after feeding, but were 20-100% higher in CR mice at other times. Glucose-6-phosphatase mRNA was induced in CR mice and repressed in control mice before, and for 5 h following feeding. Feeding transiently induced glucokinase mRNA fourfold in control mice, but only slightly in CR mice. Pyruvate kinase and pyruvate dehydrogenase activities were reduced approximately 50% in CR mice at most times. Feeding induced glutaminase mRNA, and carbamyl phosphate synthetase I and glutamine synthase activity (and mRNA). They were each approximately twofold or higher in CR mice. These results indicate that in mice, CR maintains higher rates of gluconeogenesis and protein catabolism, even in the hours after feeding. The data are consistent with the idea that CR continuously promotes the turnover and replacement of extrahepatic proteins.

Calories and aging alter gene expression for gluconeogenic, glycolytic, and nitrogen-metabolizing enzymes.

We characterized the effects of calorie restriction (CR) on the expression of key glycolytic, gluconeogenic, and nitrogen-metabolizing enzymes in mice. Of the gluconeogenic enzymes investigated, liver glucose-6-phosphatase mRNA increased 1.7- and 2. 3-fold in young and old CR mice. Phosphoenolpyruvate carboxykinase mRNA and activity increased 2.5- and 1.7-fold in old CR mice. Of the key glycolytic enzymes, pyruvate kinase mRNA and activity decreased approximately 60% in CR mice. Hepatic phosphofructokinase-1 and pyruvate dehydrogenase mRNA decreased 10-20% in CR mice. Of the genes that detoxify ammonia generated from protein catabolism, hepatic glutaminase, carbamyl phosphate synthase I, and tyrosine aminotransferase mRNAs increased 2.4-, 1.8-, and 1.8-fold with CR, respectively. Muscle glutamine synthetase mRNA increased 1.3- and 2. 1-fold in young and old CR mice. Hepatic glutamine synthetase mRNA and activity each decreased 38% in CR mice. These CR-induced changes are consistent with other studies suggesting that CR may decrease enzymatic capacity for glycolysis and increase the enzymatic capacity for hepatic gluconeogenesis and the disposal of byproducts of muscle protein catabolism.

Reaction of ozone with enzymes of erythrocyte membranes.

Ozone is a widespread component of polluted air. It is the cause of many adverse effects on the lung such as decreased athletic performance and exacerbation of asthma. Ozone inactivated acetylcholine esterase (AChE) both in intact washed human erythrocytes and in ghosts prepared from the erythrocytes. This is consistent (a) with the location of AChE on the outer face of the membrane and (b) with the change in structure of AChE when amino acids were oxidized. The glyceraldehyde-3-phosphate dehydrogenase (G3PDH) of intact washed erythrocytes was unaffected by ozone. However, ozone severely inactivated G3PDH of ghosts, much more severely than AChE in ghosts. This result raised questions about the relative permeability of intact erythrocytes and ghosts and also about the inherent susceptibility of the two enzymes. Inhibition of the ozone-treated erythrocyte AChE with the competitive inhibitor trimethyl-(p-aminophenyl) ammonium chloride was measured. The inhibited enzyme had a higher K(M) and slightly lower Vmax than the control. Ozone did not affect the K(M) of the uninhibited enzyme but decreased the K(M) of the inhibited enzyme. Ozone decreased the Vmax of both the inhibited and the uninhibited enzyme. The K(I) was unchanged by the treatment with ozone. This suggested that the active site of the enzyme was not affected by ozone, but other features of the protein were changed by ozone. The effects of products of lipid ozonolysis [hydrogen peroxide, nonanal, and 1-palmitoyl-2-(9-oxononanyl)-sn-3-glycerophosphorylcholine (PN1PC)] were tested on the ghost preparations. The ozonolysis products were tested at concentrations equivalent to calculated amounts that could have been produced by ozone. Hydrogen peroxide had no effect on the G3PDH and AChE. Nonanal slightly increased the permeability of the ghost membrane, as judged by the increase in rate of G3PDH in the absence of Triton X-100, but did not inhibit enzyme activity. PN1PC increased the permeability of the ghosts, as judged by the increase in rate of G3PDH in the absence of Triton X-100. There was also an increase in the activity of G3PDH in the presence of Triton X-100. AChE was not inhibited by ozone in the presence or absence of Triton X-100.

Late results of suprarenal Greenfield vena cava filter placement.

Placement of the Greenfield filter above the renal veins was necessary in 71 (9%) of 821 total patients in the filter registries of two institutions. The status of 60 patients (85%) could be verified, with follow-up data ranging from 18 months to 16 years (average, 53 months). Of 24 deaths (34%), none was from recurrent embolism or renal failure; death was most commonly associated with a malignant neoplasm. The recurrent embolism rate was 4%, identical to the infrarenal experience. Duplex evaluation of the filters in 22 patients, representing the majority (61%) of living patients, showed that all the filters were patent. Sixteen patients (41%) had lower-extremity edema that predated filter insertion, and in no patient did the results of noninvasive venous studies worsen. Filter fracture (two patients) or distal migration (two patients) had no clinical sequelae, and there was no evidence of renal dysfunction. For thrombus extending to the level of the renal veins or within them and for pregnant patients or women of childbearing age, suprarenal placement of the Greenfield filter is safe and effective, with no filter obstruction seen in follow-up extending to 16 years.

Recurrent versus residual carotid stenosis. Incidence detected by Doppler ultrasound.

A sterile Doppler probe was used for intraoperative monitoring of the integrity of carotid endarterectomy of 125 vessels of 107 patients. Our objective was to reduce the contribution of residual carotid lesions to recurrent stenosis, which was evaluated by Doppler spectrum analysis in the early (less than 3 months, 66 arteries) and late (3-77 months, mean 32 months, 47 arteries) postoperative period. Intraoperative Doppler monitoring detected residual occlusion in six (4.8%) external carotid arteries and stenosis in ten (8.0%) internal carotid arteries permitting selected arteriography and correction of all significant lesions. Follow-up revealed one (1.5%) asymptomatic common carotid occlusion at 6 weeks and three (6.4%) asymptomatic internal carotid stenoses at 6, 10 and 25 months after operation. When compared to previous published experience, these results suggest that intraoperative correction of residual carotid obstruction detected by Doppler ultrasound may reduce the incidence of postoperative "recurrent" carotid stenosis.

The blue toe syndrome: hemodynamics and therapeutic correlates of outcome.

We reviewed the limb and digit hemodynamics of 67 extremities of 48 patients evaluated for blue toe syndrome in our vascular laboratory during 7 years. These patients represented 1.4% of the arterial examinations during this period. Abnormal ankle/arm pressure indices (less than 0.9), signifying proximal arterial obstruction, were present in 31 limbs (47%). Toe/ankle indices were abnormal (less than 0.6) in 57 extremities (85%), indicating pedal or digital artery obstruction. Arteriograms were obtained in 40 of 64 extremities (63%) available for follow-up, which revealed atherosclerotic disease in 90% (aortoiliac 20%, femoropopliteotibial 30%, and combined 40%), aneurysm in 7.5%, and no disease in only one extremity (2.5%). Of 64 extremities followed for 1 to 84 months (mean, 26 months), only 28 (44%) manifested an uncomplicated outcome. Tissue loss was noted in 24 (38%), recurrent digital ischemia occurred in nine (14%), and 14 limbs (22%) required amputation of toe(s) (seven), forefeet (three) or legs (four). Nine patients (20%) died in the follow-up period. Outcomes did not correlate with limb or digit hemodynamics or with therapy (surgical in 31, medical in 11, or none in 22) except that tissue necrosis was more common in patients undergoing operation. The blue toe syndrome deserves recognition as an important sign of potential limb-threatening arterial disease, but the optimal therapy remains to be established.