Strenuous endurance training in humans reduces oxidative stress following exhausting exercise

The aim of this study was to evaluate whether high-intensity endurance training would alleviate exercise-induced oxidative stress. Nine untrained male subjects (aged 19–21 years) participated in a 12-week training programme, and performed an acute period of exhausting exercise on a cycle ergometer before and after training. The training programme consisted of running at 80% maximal exercise heart rate for 60 min · day⁻¹, 5 days · week⁻¹ for 12 weeks. Blood samples were collected at rest and immediately after exhausting exercise for measurements of indices of oxidative stress, and antioxidant enzyme activities [superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT)] in the erythrocytes. Maximal oxygen uptake (V˙O_2max) increased significantly (P < 0.001) after training, indicating an improvement in aerobic capacity. A period of exhausting exercise caused an increase (P < 0.01) in the ability to produce neutrophil superoxide anion (O₂ ^•−) both before and after endurance training, but the magnitude of the increase was smaller after training (P < 0.05). There was a significant increase in lipid peroxidation in the erythrocyte membrane, but not in oxidative protein, after exhausting exercise, however training attenuated this effect. At rest, SOD and GPX activities were increased after training. However, there was no evidence that exhausting exercise enhanced the levels of any antioxidant enzyme activity. The CAT activity was unchanged either by training or by exhausting exercise. These results indicate that high-intensity endurance training can elevate antioxidant enzyme activities in erythrocytes, and decrease neutrophil O₂ ^•− production in response to exhausting exercise. Furthermore, this up-regulation in antioxidant defences was accompanied by a reduction in exercise-induced lipid peroxidation in erythrocyte membrane. Accepted: 26 September 2000     

Change in post-exercise vagal reactivation with exercise training and detraining in young men

We studied the effects of aerobic exercise training and detraining in humans on post-exercise vagal reactivation. Ten healthy untrained men trained for 8 weeks using a cycle ergometer [70% of initial maximal oxygen uptake ( ) for 1 h, 3–4 days·week^–1] and then did not exercise for the next 4 weeks. Post-exercise vagal reactivation was evaluated as the time constant of the beat-by-beat decrease in heart rate during the 30 s (t₃₀) immediately following 4 min exercise at 80% of ventilatory threshold (VT). The and the oxygen uptake at VT had significantly increased after the 8 weeks training programme (P<0.0001, P<0.001, respectively). The t₃₀ had shortened after training, and values after 4 weeks and 8 weeks of training were significantly shorter than the initial t₃₀ (P<0.05, P<0.01, respectively). The change in the t₃₀ after 8 weeks of training closely and inversely correlated with the initial t₃₀ (r=–0.965, P<0.0001). The reduced t₃₀ was prolonged significantly after 2 weeks of detraining, and had returned almost to the baseline level after a further 2 weeks of detraining. These results suggest that aerobic exercise training of moderate intensity accelerates post-exercise vagal reactivation, but that the accelerated function regresses within a few weeks of detraining. Electronic Publication     

Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise

This study investigated the influence of environmental heat stress on ammonia (NH₃) accumulation in relation to nucleotide metabolism and fatigue during intermittent exercise. Eight males performed 40 min of intermittent exercise (15 s at 306±22 W alternating with 15 s of unloaded cycling) followed by five 15 s all-out sprints. Control trials were conducted in a 20°C environment while heat stress trials were performed at an ambient temperature of 40°C. Muscle biopsies and venous blood samples were obtained at rest, after 40 min of exercise and following the maximal sprints. Following exercise with heat stress, the core and muscle temperatures peaked at 39.5±0.2 and 40.2±0.2°C to be ~ 1°C higher (P<0.05) than the corresponding control values. Mean power output during the five maximal sprints was reduced from 618±12 W in control to 558±14 W during the heat stress trial (P<0.05). During the hot trial, plasma NH₃ increased from 31±2 μM at rest to 93±6 at 40 min and 151±15 μM after the maximal sprints to be 34% higher than control (P<0.05). In contrast, plasma K⁺ and muscle H⁺ accumulation were lower (P<0.05) following the maximal sprints with heat stress compared to control, while muscle glycogen, CP, ATP and IMP levels were similar across trials. In conclusion, altered levels of “classical peripheral fatiguing agents” does apparently not explain the reduced capacity for performing repeated sprints following intermittent exercise in the heat, whereas the augmented systemic NH₃ response may be a factor influencing fatigue during exercise with superimposed heat stress.     

Urinary excretion of prostaglandin F2α and 6-keto-prostaglandin F1α during volume expansion in man

Renal function and the urinary excretion of immunoreactive prostaglandin F_2α (PGF_2α) and 6-keto-prostaglandin F_1α (6-keto-PGF_1α) were investigated during volume expansion (VE) in 9 healthy young adults. The studies were started after at least 17 h of food and fluid deprivation. Volume expansion (3% of body weight) was achieved by a continuous infusion of Ringer's solution (0.22 ml/kg/min). This increased the urinary excretion of sodium from 195±25 to 714±55 μmol/min/1.73 m²(mean ± S.E.) and decreased the excretion of potassium by 24% and plasma renin activity by 60% (P<0.01). The clearance of inulin increased slightly (from 102.4±3.7 to 114.5±6.2 ml/min/1.73 m², P<0.025), whüe clearance of PAH did not change. The excretion of immunoreactive PGF_2α decreased in 8 out of 9 individuals during VE, from 1.58±0.15 to 0.97±0.10 ng/min/1.73 m²(P<0.01). In contrast, excretion of immunoreactive 6-keto-PGF_1α increased in 8 out of 9 subjects, from 2.32±0.20 to 3.47±0.48 ng/min/1.73 m²(P<0.05). Urinary excretion of PGF_2α and 6-keto-PGF_1α may reflect renal synthesis of prostaglandins (PGs) and prostacyclin (PGI₂), respectively. The results indicate that synthesis of PGs is decreased and that of PGI₂ is increased during VE in man. However, no simple relationship could be found between the prostaglandins and the renal functional parameters.     

Contraction-induced changes in skeletal muscle Na+,K+ pump mRNA expression – importance of exercise intensity and Ca2+-mediated signalling

Aim: To investigate if exercise intensity and Ca²⁺ signalling regulate Na⁺,K⁺ pump mRNA expression in skeletal muscle. Methods: The importance of exercise intensity was evaluated by having trained and untrained humans perform intense intermittent and prolonged exercise. The importance of Ca²⁺ signalling was investigated by electrical stimulation of rat soleus and extensor digitorum longus (EDL) muscles in combination with studies of cell cultures. Results: Intermittent cycling exercise at ∼85% of VO_2peak increased (P < 0.05) α1 and β1 mRNA expression ∼2-fold in untrained and trained subjects. In trained subjects, intermittent exercise at ∼70% of VO_2peak resulted in a less (P < 0.05) pronounced increase (∼1.4-fold; P < 0.05) for α1 and no change in β1 mRNA. Prolonged low intensity exercise increased (P < 0.05) mRNA expression of α1 ∼3.0-fold and α2 ∼1.8-fold in untrained but not in trained subjects. Electrical stimulation of rat soleus, but not EDL, muscle increased (P < 0.05) α1 mRNA expression, but not when combined with KN62 and cyclosporin A incubation. Ionomycin incubation of cultured primary rat skeletal muscle cells increased (P < 0.05) α1 and reduced (P < 0.001) α2 mRNA expression and these responses were abolished (P < 0.05) by co-incubation with cyclosporin A or KN62. Conclusion: (1) Exercise-induced increases in Na⁺,K⁺ pump α1 and β1 mRNA expression in trained subjects are more pronounced after high- than after moderate- and low-intensity exercise. (2) Both prolonged low and short-duration high-intensity exercise increase α1 mRNA expression in untrained subjects. (3) Ca²⁺_i regulates α1 mRNA expression in oxidative muscles via Ca²⁺/calmodulin-dependent protein kinase (CaMK) and calcineurin signalling pathways.     

Muscle triacylglycerol and hormone-sensitive lipase activity in untrained and trained human muscles

During exercise, triacylglycerol (TG) is recruited in skeletal muscles. We hypothesized that both muscle hormone-sensitive lipase (HSL) activity and TG recruitment would be higher in trained than in untrained subjects in response to prolonged exercise. Healthy male subjects (26 ± 1 years, body moss index 23.3 ± 0.5 kg m⁻²), either untrained (N = 8, VO_2max 3.8 ± 0.2 l min⁻¹) or trained (N = 8, VO_2max 5.1 ± 0.1 l min⁻¹), were studied. Before and after 3-h exercise (58 ± 1% VO_2max), a biopsy was taken. Muscle citrate synthase (32 ± 2 vs. 47 ± 6 μmol g⁻¹ min⁻¹ d.w.) and β-hydroxy-acyl-CoA-dehydrogenase (38 ± 3 vs. 52 ± 5 μmol g⁻¹ min⁻¹ d.w.) activities were lower in untrained than in trained subjects (p < 0.05). Throughout the exercise, fat oxidation was higher in trained than in untrained subjects (p < 0.05). Muscle HSL activity was similar at rest (0.72 ± 0.08 and 0.74 ± 0.03 mU mg⁻¹ protein) and after exercise (0.71 ± 0.1 and 0.68 ± 0.03 mU mg⁻¹ protein) in untrained and trained subjects. At rest, the chemically determined muscle TG content (37 ± 8 and 26 ± 5 mmol g⁻¹ d.w.) was similar (p > 0.05), and after exercise it was unchanged in untrained and lower (p < 0.05) in trained subjects (41 ± 9 and 10 ± 2 mmol g⁽¹ d.w.). Determined histochemically, TG was decreased (p < 0.05) after exercise in type I and II fibres. Depletion of TG was not different between fibre types in untrained, but tended to be higher (p = 0.07) in type I compared with type II fibres in trained muscles. In conclusion, HSL activity is similar in untrained and trained skeletal muscles both before and after prolonged exercise. However, the tendency to higher muscle TG recruitment during exercise in the trained subjects suggests a difference in the regulation of HSL or other lipases during exercise in trained compared with untrained subjects.     

Leptin response to acute prolonged exercise after training in rowers

The aim of this study was to determine if there is a training effect on leptin levels at rest or after prolonged exercise during an 8-month training season of rowers. Eleven trained rowers were evaluated at three sessions (control, early and late) during the season. At the early and late sessions, leptin and insulin concentrations were measured before and after 90 min of rowing exercise (70–75% maximal oxygen consumption, O₂max), 120 min and 24 h afterwards. Anthropometrics data were collected at each session. Energy balance was determined on the days of exercise sessions. Resting leptin levels were not modified over the season and were in correlation with weight and body fat (P<0.05). At exercise sessions, a delayed reducing effect of acute exercise on leptin levels appeared (P<0.01 compared to pre-exercise). After 24 h of recovery, leptin levels remained lower at early (P<0.001) but not at late sessions, and a training effect appeared between early and late sessions (P<0.001). Leptin levels were correlated with energy balance at early and late sessions (P<0.05). At the two training sessions, insulin levels were decreased immediately post-exercise and at 120 min of recovery compared to pre-exercise (P<0.01 and P<0.001 respectively for the two sessions). A training effect on insulin levels appeared at 24 h of recovery (P<0.05 between early and late sessions). We concluded that rowing training over a season did not alter resting leptin levels but it attenuated the exercise-induced reduction in leptin. This could be attributed to an alteration in energy balance, although an influence of training on insulin may also be involved in the leptin response to acute exercise.An erratum to this article can be found at     

Regional distribution of prostanoids in rat brain: effect of insulin and 2-deoxyglucose

Summary Prostaglandin synthesis in the brain has been suggested as a component in the control mechanism of the cerebral circulation. During insulininduced hypoglycemia there is a significant increase in local cerebral blood flow in various brain regions, however, regional loss of autoregulation occurs under these conditions. In the present study the regional distribution of PGE₂, TXB₂ (the stable metabolite of thromboxane) and 6-keto-PGF₁ (the stable metabolite of prostacyclin) was determined in rat brain following decapitation. Three groups of rats were treated with either saline, insulin or 2-deoxyglucose and their brains were rapidly removed one hour later. Samples from the cortex hypothalamus, hippocampus, striatum, nucleus accumbens and cerebellum were assayed by RIA for the content of PGE₂, TXB₂ and 6-keto-PGF₁ The levels of all three compounds in control rats were the lowest in the striatum and cerebellum, while in the cortex and hippocampus their levels were 4–6 times higher. Insulin had selective effect on the post decapitation levels of prostanoids. It increased PGE₂ in the n. accumbens and TXB₂ in the hippocampus, and reduced 6-keto-PGF₁ and TXB₂ in the cortex. 2-DG reduced all PGs in the cortex and 6-keto-PGF₁ in the hypothalamus and hippocampus. The results demonstrate that discrete brain areas have a differential capacity to accumulate PGs following decapitation. This capacity is selectively affected by insulin and 2-DG.     

Substrate use and biochemical response to a 3,211-km bicycle tour in trained cyclists

The purpose of this study was to assess the physiological adaptations in physically fit individuals to a period of intensified training. Ten trained males cycled outdoors ~170 km day⁻¹ on 19 out of 21 days. Expired gas was collected on days 1 and 21 during maximal graded exercise and used for the determination of gross efficiency and whole body substrate use. Muscle biopsies were obtained before and after exercise on days 2 and 22 for the determination of mtDNA/gDNA ratio, gene expression, metabolic enzyme activity and glycogen use. Muscle glycogen before and after exercise, fat oxidation, and gross efficiency increased, carbohydrate oxidation decreased (p < 0.05), and VO_2max did not change over the 21 days of training. Citrate synthase (CS), β-hydroxyacyl CoA dehydrogenase (β-HAD) and cytochrome c oxidase (COX) enzyme activity did not change with training. CS and β-HAD mRNA did not change with acute exercise or training. COX (subunit IV) mRNA increased with acute exercise (p < 0.05) but did not change over the 21 days. PGC-1α mRNA increased with acute exercise, but did not increase to the same degree on day 22 as it did on day 2 (p < 0.05). UCP3 mRNA decreased with training (p < 0.05). Acute exercise caused an increase in mitofusin2 (MFN2) mRNA (p < 0.05) and a trend for an increase in mtDNA/gDNA ratio (p = 0.057). However, training did not affect MFN2 mRNA or mtDNA/gDNA ratio. In response to 3,211 km of cycling, changes in substrate use and gross efficiency appear to be more profound than mitochondrial adaptations in trained individuals.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

The effect of high-intensity training on purine metabolism in man

The effect of intermittent high-intensity training on the activity of enzymes involved in purine metabolism and on the concentration of plasma purines following acute short-term intense exercise was investigated. Eleven subjects performed sprint training three times per week for 6 weeks. Muscle biopsies for determination of enzyme activities were obtained prior to and 24 h after the training period. After training, the activity of adenosine 5′-phosphate (AMP) deaminase was lower (P < 0.001) whereas the activities of hypoxanthine phosphoribosyl transferase (HPRT) and phosphofructokinase were significantly higher compared with pre-training levels. The higher activity of HPRT with training suggests an improved potential for rephosphorylation of intracellular hypoxanthine to inosine monophosphate (IMP) in the trained muscle. Before and after the training period the subjects performed four independent 2-min tests at intensities from a mean of 106 to 135 % of Vo_max. Venous blood was drawn prior to and after each test. The accumulation of plasma hypoxanthine following the four tests was lower following training compared with prior to training (P < 0.05). The accumulation of uric acid was significantly lower (46% of pre-training value) after the test performed at 135% of Fo_2mM (P < 0.05). Based on the observed alterations in muscle enzyme activities and plasma purine accumulation, it is suggested that high intensity intermittent training leads to a lower release of purines from muscle to plasma following intense exercise and, thus, a reduced loss of muscle nucleotides.     

Determination oi 6-keto-prostaglandin Flα in rabbit kidney and urine and its relation to sodium balance

The occurrence of 6-keto-prostaglandin F_lα (6-keto-PGF_1α) was demonstrated in rabbit kidney medulla and cortex by mass-spectrometry. The post-mortem accumulation of 6-keto-PGF_1α was studied by mass-fragmentography in regions of the rabbit kidney using (3,3,4,4,-²H₄) 6-keto-PGF_lα as an internal standard. The cortex contained 1.4 + 0.3 μMg/g, the medulla 2.1 ± 0.6 μg/g and the papilla 3.7 ± 0.7 (S.E.) μg/g. The accumulation of 6-keto-PGF_1α is thus about 5 fold higher in the cortex than reported for PGE₂ and PGF_2α, whereas accumulation of PGE₂ and PGF_2α dominates over 6-keto-PGF_lα in the medulla and the papilla. The occurrence of 6-keto-PGF_lα in rabbit urine was demonstrated by mass-fragmentography. On a low salt diet unanesthetized, female rabbits (n = 6) excreted Na⁺ 0.09 ± 0.01 (S.E.) mmol/day, 6-keto-PGF_lα 11.8 ± 2.2 μg/day and immunoreactive PGF_2α (iPGF_2α) 2.0 ± 0.6 μg/day. Two days treatment with acetylsalicylic acid (30 mg/kgx 2) reduced urinary excretion of 6-keto-PGF_lα and iPGF_2α by 71 and 85%, respectively (both p < 0.05), but sodium excretion was unchanged. On the same diet supplemented with NaCl, the rabbits excreted Na⁺ 27.5 ± 3.4 mmol/day (p < 0,05), 6-keto-PGF_lα 13.3 ± 4.6 μg/day (p > 0.05) and iPGF_2α 0.63 ± 0.10 μg/day (p < 0.05). 6-keto-PGF_lα is a major metabolite of prostacyclin (PGI₂). The occurrence of 6-keto-PGF_lα in kidney and urine indicates a considerable synthesis of PGI₂ in the kidney. The data on urinary PG excretion indicate that intrarenal synthesis of PGI₂, in contrast to PGF_2α, is not influenced by dietary variations in NaCl.     

Converting enzyme inhibitor ramipril stimulates prostacyclin synthesis by isolated rat aorta: Evidence for a kinin-dependent mechanism

Summary The present study was performed to investigate the effect of the angiotensin I-converting enzyme inhibitor ramipril on vascular synthesis of prostacyclin (PGI₂). Administration of ramipril (Hoe 498) to rats significantly stimulated prostacyclin (PGI₂) synthesis, quantified by radioimmunoassay of its stable hydrolysis product 6-keto-PGF₁, by portions of the animals' isolated aorta. This effect was maximal at a dose range of 10^–7 mol/kg ramipril. The addition of the active ramipril metabolite ramipril diacid directly into the incubation buffer at final concentrations of 10^–9, 10^–6, and 10^–4 M resulted in a dose-dependent stimulation of 6-keto-PGF₁ released by isolated aortic tissue. Pretreatment of rats with aprotinin (40,000 U s.c. 60 min before the incubations) attenuated the ramipril-induced effect on aortic 6-keto-PGF₁ synthesis. Our results show that the angiotensin I-converting enzyme inhibitor ramipril stimulates PGI₂ synthesis in vascular tissue and that this effect may be secondary to changes in the activity of the kinin system.Abbreviations ACE angiotensin I-converting-enzyme - PG prostaglandin - PGI₂ prostacyclin Dedicated to Prof. Dr. F. Krück on the occasion of his 65th birthday     

Experimental diabetes: No effects on prostacyclin release from the vessel wall and renal cortex

Diabetes is commonly complicated by thrombosis and atherosclerosis. In humans, diabetes mellitus has been associated with a decreased synthesis of prostacyclin, which could partly explain the prothrombotic state. Experimental diabetes has been diverging in this aspect, and endothelial damage has been proposed to be an early event. To analyse whether the effect of inducing diabetes had any influence on prostacyclin release from diabetic tissue, streptozotocin-induced diabetic rat aortas and renal tissue were incubated in Hank's balanced salt solution. The stable degradation product for prostacyclin 6-keto-PGF₁ was determined by radioimmunoassay. There was no difference in the release of 6-keto-PGF₁ from aorta and renal tissue in diabetic animals compared to controls, and insulin given to diabetic animals also had no effect.In order to study only the intraluminal release of prostacyclin, aortas and caval veins from alloxan-diabetic rabbits were perfused for five 15 min periods. Diabetic animals had the same release of 6-keto-PGF₁ from the aorta and caval vein as control animals.Scanning electron microscopy of the luminal side of the perfused vessels revealed the same degree of endothelial coverage with approximately 75% coverage after perfusion.It is concluded that experimental diabetes of 6 months' duration does not alter the vascular and renal prostacyclin release in response to exogenous trauma like incubation or perfusion.     

Prostacyclin aerosol and inhaled nitric oxide fail to reverse pulmonary vasoconstriction induced by thromboxane analogue in dogs

Inhalation of either prostacyclin (PGI₂) as an aerosol or nitric oxide (NO) has been shown to elicit selective pulmonary vasodilation during hypoxic pulmonary vasoconstriction in dogs. Hypoxia may produce cardiovascular changes confounding interpretation of drug effects. Therefore, we investigated the effects of PGI₂-aerosol and inhaled NO (50 p.p.m.) on pulmonary pressure-flow relationships (P/Q_ plots) during thromboxane analogue (U46619) induced pulmonary vasoconstriction. In eight anaesthetized dogs infusion of U46619 (0.33 ± 0.18 μg kg_¹ min^-1) increased the slope (3.5 ± 1.1 to 8.4 ± 1.7 mmHg L^-1 min^-1, P < 0.001) and the intercept (4.4±2.3 to 10.2 ± 4.6 mmHg, P < 0.01) of P/Q plots indicating pulmonary vasoconstriction. Inhalation of both aerosolized PGI₂ solution (10μgmL^-1) and NO (50 p.p.m.) reduced neither the slope nor the intercept of the P/Q_ plots. Increasing the concentration of the aerosolized PGI₂ solution to 50 μg mL^-1: (n= 3) did not enhance the effect on pulmonary circulation but systemic vascular resistance fell by 23%. Oxygenation and intrapulmonary shunt remained unchanged during both PGI₂-aerosol and inhaled NO. The failure of PGI₂-aerosol to induce pulmonary vasodilation indicates that during aerosolization PGI₂-concentrations at receptor sites on pulmonary vessels were insufficient to surmount U46619 induced vasoconstriction; this notion is supported by unchanged arterial plasma concentrations of the PGI₂ degradation product 6-keto-PGF_lα. Considering that NO inhaled at comparable concentrations in sheep reversed U46619 induced pulmonary vasoconstriction, species differences may account for the failure of both PGI₂-aerosol and NO to dilate pulmonary vessels in dogs.     

Muscle morphology and performance in master athletes: A systematic review and meta-analyses

IntroductionThe extent to which chronic exercise training preserves age-related decrements in physical function, muscle strength, mass and morphology is unclear. Our aim was to conduct a systematic review of the literature to determine to what extent chronically trained master athletes (strength/power and endurance) preserve levels of physical function, muscle strength, muscle mass and morphology in older age, compared with older and younger controls and young trained individuals.MethodsThe systematic data search included Medline, EMBASE, SPORTDiscus, CINAHL and Web of Science databases.Inclusion criteriai) master athletes mean exercise training duration ≥20 years ii) master athletes mean age of cohort >59 years) iii) at least one measurement of muscle mass/volume/fibre-type morphology and/or strength/physical function.ResultsFifty-five eligible studies were identified. Meta-analyses were carried out on maximal aerobic capacity, maximal voluntary contraction and body composition. Master endurance athletes (42.0 ± 6.6 ml kg⁻¹ min⁻1) exhibited VO_2max values comparable with young healthy controls (43.1 ± 6.8 ml kg⁻¹ min⁻¹, P = .84), greater than older controls (27.1 ± 4.3 ml kg⁻¹ min⁻¹, P < 0.01) and master strength/power athletes (26.5 ± 2.3 mlkg⁻¹ min⁻¹, P < 0.01), and lower than young endurance trained individuals (60.0 ± 5.4 ml kg⁻¹ min⁻¹, P < 0.01). Master strength/power athletes (0.60 (0.28–0.93) P < 0.01) and young controls (0.71 (0.06–1.36) P < 0.05) were significantly stronger compared with the other groups. Body fat% was greater in master endurance athletes than young endurance trained (−4.44% (−8.44 to −0.43) P < 0.05) but lower compared with older controls (7.11% (5.70–8.52) P < 0.01).ConclusionDespite advancing age, this review suggests that chronic exercise training preserves physical function, muscular strength and body fat levels similar to that of young, healthy individuals in an exercise mode-specific manner.     

Muscle activation of the knee extensors following high intensity endurance exercise in cyclists

This study was conducted to assess the effects in trained cyclists of exhausting endurance cycle exercise (CE) on maximal isometric force production, surface electromyogram (EMG) and activation deficit (AD) of the knee extensors. Ten male subjects made four isometric maximal voluntary contractions (MVC) of the knee extensor muscles immediately prior (pre), 10 min after (post) and 6 h after completion of CE. The CE consisted of 30 min of exercise on a stationary cycle ergometer at an intensity corresponding to 80% of maximal oxygen uptake (V˙O_2max) followed by four × 60-s periods at 120% of V˙O_2max. Two MVC were performed with recording of surface EMG from the knee extensors, whilst an additional two MVC were completed with percutaneous electrical muscle stimulation (EMS; 25 pulses at 100 Hz with the maximal tolerable current) superimposed over the maximal voluntary contraction force (MVF) but without EMG (to avoid interference). The MVF, integrated EMG (iEMG), and AD [calculated as the difference between MVF and the electrically stimulated force (ESF) during the EMS contractions] were statistically analysed. The MVF was significantly reduced (P < 0.05) post and 6-h post compared to pre-CE level. The iEMG was significantly reduced (P < 0.05) post and 6 h post CE. The ESF was also reduced, whilst AD was significantly increased (P < 0.05) post and 6-h post CE compared to the pre CE. These results suggest that the level of exercise stress administered in this study was sufficient to impair the central and peripheral mechanisms of force generation in knee extensors for a period of 6-h. Athletes engaged in concurrent training (strength and endurance) should consider this effect in exercise programming. Accepted: 22 September 1999     

Interspersed normoxia during live high, train low interventions reverses an early reduction in muscle Na+, K+ATPase activity in well-trained athletes

Hypoxia and exercise each modulate muscle Na⁺, K⁺ATPase activity. We investigated the effects on muscle Na⁺, K⁺ATPase activity of only 5 nights of live high, train low hypoxia (LHTL), 20 nights consecutive (LHTLc) versus intermittent LHTL (LHTLi), and acute sprint exercise. Thirty-three athletes were assigned to control (CON, n = 11), 20-nights LHTLc (n = 12) or 20-nights LHTLi (4 × 5-nights LHTL interspersed with 2-nights CON, n = 10) groups. LHTLc and LHTLi slept at a simulated altitude of 2,650 m (F_IO₂ 0.1627) and lived and trained by day under normoxic conditions; CON lived, trained, and slept in normoxia. A quadriceps muscle biopsy was taken at rest and immediately after standardised sprint exercise, before (Pre) and after 5-nights (d5) and 20-nights (Post) LHTL interventions and analysed for Na⁺, K⁺ATPase maximal activity (3-O-MFPase) and content ([³H]-ouabain binding). After only 5-nights LHTLc, muscle 3-O-MFPase activity declined by 2% (P < 0.05). In LHTLc, 3-O-MFPase activity remained below Pre after 20 nights. In contrast, in LHTLi, this small initial decrease was reversed after 20 nights, with restoration of 3-O-MFPase activity to Pre-intervention levels. Plasma [K⁺] was unaltered by any LHTL. After acute sprint exercise 3-O-MFPase activity was reduced (12.9 ± 4.0%, P < 0.05), but [³H]-ouabain binding was unchanged. In conclusion, maximal Na⁺, K⁺ATPase activity declined after only 5-nights LHTL, but the inclusion of additional interspersed normoxic nights reversed this effect, despite athletes receiving the same amount of hypoxic exposure. There were no effects of consecutive or intermittent nightly LHTL on the acute decrease in Na⁺, K⁺ATPase activity with sprint exercise effects or on plasma [K⁺] during exercise.     

The effects of mild one-legged isometric or dynamic training

Summary Four men isometrically trained their stronger leg for 19 weeks (attempted knee extension against a restraining strap incrementally increasing to 30 brief maximal contractions x 6 wk⁻¹). Five others similarly trained dynamically (repeated knee extension against a 63 N resistance force, incrementally increasing to 300 extensions x 6 wk⁻¹). Before, at regular intervals during training and after de-training (between 7–11 weeks) measurements were made using trained and control legs of: Maximum Voluntary Isometric Contraction (M.V.C.), Endurance at 60% M.V.C., Knee Extension Performance Test (K.E.P.T.) and One-legged Work Test. Isometric training produced a 30% (p<0.01) increase in M.V.C. with a 15% (p<0.05) increase in the control leg. These changes persisted with some deterioration after the de-training period. Endurance at 60% M.V.C. remained unchanged, even though M.V.C. was increasing in both trained and control legs. There was some evidence that isometric training improved the cardio-vascular response to one-legged exercise. Dynamic training did not result in changes in M.V.C, Endurance at 60% M.V.C. or the One-legged work Test, but K.E.P.T. (time taken for 50 knee extensions at a comfortable pace against 63 N resistance) improved by 33% (p<0.01) and 28% (p<0.01) in the trained and control legs respectively. Isometric training resulted in similar improvements in performance of K.E.P.T. (28%, p<0.05, trained leg; 18%, p<0.05 control leg). For similar time spent in training, isometric work appeared more effective than dynamic work in improving the parameters of muscle function, these improvements appeared to be both centrally (C.N.S.) and locally mediated.     

The effects of resistance training on functional outcomes in patients with chronic obstructive pulmonary disease

Aerobic exercise training is used for rehabilitation in patients with chronic obstructive pulmonary disease (COPD), although it has little effect on muscle weakness and atrophy. Resistance training may be a useful addition to aerobic programs for these patients. The purpose of the present study was to investigate the effects of resistance training in addition to aerobic training on functional outcomes in patients with COPD. Seventeen COPD patients enrolled in an aerobic-based program that met twice a week were assigned to a 12-week control/aerobic [CON: n=8; 63 (8) years; mean (SD)] or a resistance/aerobic group [RES: n=9; 61 (7) years]. RES trained an additional twice a week on 12 resistance machines, performing three sets of 8–12 repetitions at 32–64% of their one-repetition maximum (1-RM) lifts. RES (P<0.05) increased upper (36%) and lower (36%) body strength, as well as lean body mass (5%), while CON showed little to no change. The 12-min walk distance increased (P<0.05) in only the RES [676 (219) to 875 (172) m]. Measurements of three of the eight tasks of activities of daily living improved in RES (P<0.05) compared to CON. This study demonstrated that progressive resistance training was well tolerated and improved functional outcomes in COPD patients that were currently involved in an aerobic training program.