Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Oxidative stress, inflammation and recovery of muscle function after damaging exercise: effect of 6-week mixed antioxidant supplementation

There is no consensus regarding the effects of mixed antioxidant vitamin C and/or vitamin E supplementation on oxidative stress responses to exercise and restoration of muscle function. Thirty-eight men were randomly assigned to receive either placebo group (n = 18) or mixed antioxidant (primarily vitamin C & E) supplements (n = 20) in a double-blind manner. After 6 weeks, participants performed 90 min of intermittent shuttle-running. Peak isometric torque of the knee flexors/extensors and range of motion at this joint were determined before and after exercise, with recovery of these variables tracked for up to 168 h post-exercise. Antioxidant supplementation elevated pre-exercise plasma vitamin C (93 ± 8 μmol l⁻¹) and vitamin E (11 ± 3 μmol l⁻¹) concentrations relative to baseline (P < 0.001) and the placebo group (P ≤ 0.02). Exercise reduced peak isometric torque (i.e. 9–19% relative to baseline; P ≤ 0.001), which persisted for the first 48 h of recovery with no difference between treatment groups. In contrast, changes in the urine concentration of F₂-isoprostanes responded differently to each treatment (P = 0.04), with a tendency for higher concentrations after 48 h of recovery in the supplemented group (6.2 ± 6.1 vs. 3.7 ± 3.4 ng ml⁻¹). Vitamin C & E supplementation also affected serum cortisol concentrations, with an attenuated increase from baseline to the peak values reached after 1 h of recovery compared with the placebo group (P = 0.02) and serum interleukin-6 concentrations were higher after 1 h of recovery in the antioxidant group (11.3 ± 3.4 pg ml⁻¹) than the placebo group (6.2 ± 3.8 pg ml⁻¹; P = 0.05). Combined vitamin C & E supplementation neither reduced markers of oxidative stress or inflammation nor did it facilitate recovery of muscle function after exercise-induced muscle damage.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

The effects of whole body vibration and exercise on fibrinolysis in men

Whole body vibration (WBV) is a novel modality that has been demonstrated to enhance muscular and cardiovascular functions reported to increase fibrinolytic activity. The purpose of this study was to examine the fibrinolytic response to WBV and exercise in men. Twenty healthy males (23.8 ± 0.9 years, 25.6 ± 0.2 kg m⁻²) participated in the study. Each subject performed three trials in randomized order separated by 1 week: exercise (X), vibration (V) and vibration + exercise (VX). Exercise sessions consisted of 15 min of unloaded squatting at a rate of 20 per minute. Vibration sessions were conducted on a WBV platform vibrating for 15 min. Tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI-1) were assessed at baseline and immediately after each condition. The increase in tPA activity was significantly greater in VX (0.87 ± 0.35 to 3.21 ± 1.06 IU ml⁻¹) compared to X (0.71 ± 0.36 to 2.4 ± 1.13 IU ml⁻¹) or V (0.83 ± 0.25 to 1.00 ± 0.37 IU ml⁻¹) conditions, and greater in the X condition compared to the V condition. PAI-1 activity decreased significantly more in the VX (6.54 ± 5.53 to 4.89 ± 4.13 IU ml⁻¹) and X (9.76 ± 8.19 to 7.48 ± 7.11 IU ml⁻¹) conditions compared to the V (5.68 ± 3.53 to 5.84 ± 3.52 IU ml⁻¹) condition. WBV does not augment fibrinolytic activity in healthy men. However, WBV combined with squatting exercise increases fibrinolytic activity more than exercise alone.     

The impact of exercise intensity on the release of cardiac biomarkers in marathon runners

We sought to determine the influence of exercise intensity on the release of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in amateur marathon runners. Fourteen runners completed three exercise trials of the same duration but at exercise intensities corresponding to: (a) a competitive marathon [mean ± SD: heart rate 159 ± 7 beat min⁻¹, finish time 202 ± 14 min]; (b) 95% of individual anaerobic threshold [heart rate 144 ± 6 beat min⁻¹] and; (c) 85% of individual anaerobic threshold [heart rate 129 ± 5 beat min⁻¹]. cTnI and NT-proBNP were assayed from blood samples collected before, 30 min and 3 h post-exercise for each trial. cTnI and NT-proBNP were not different at baseline before each trial. After exercise at 85% of individual anaerobic threshold cTnI was not significantly elevated. Conversely, cTnI was elevated after exercise at 95% of individual anaerobic threshold (0.016 μg L⁻¹) and to an even greater extent after exercise at competition intensity (0.054 μg L⁻¹). Peak post-exercise values of NT-proBNP were elevated to a similar extent after all exercise trials (P < 0.05). The upper reference limit for cTnI (0.04 μg L⁻¹) was exceeded in six subjects at competition intensity. No data for NT-proBNP surpassed its upper reference limit. Peak post-exercise values for cTnI and NT-proBNP were correlated with their respective baseline values. These data suggest exercise intensity influences the release of cTnI, but not NT-proBNP, and that competitive marathon running intensity is required for cTnI to be elevated over its upper reference limit.     

Plasma IL-6 concentration during ultra-endurance exercise

Interleukin 6 (IL-6) response was studied during two ultra endurance events—one laboratory 24 h protocol (9 men) with exercise intensity set to 60% of VO_2max and one Adventure Race over 6 days (12 men/6 women) with a self-selected race pace, including rests, of about 38% of VO_2max. In the 24-h protocol IL-6 level was elevated from 0.76 ± 0.48 pg mL⁻¹ at rest to 7.16 ± 2.70 pg mL⁻¹ at 6 h, and increased further to 10.58 ± 1.04 pg mL⁻¹ at 12 h, but remained thereafter unchanged at 24 h, (10.89 ± 0.36 pg mL⁻¹). All participants had nearly identical values at 12 and 24 h, supporting intensity as main determinant in the IL-6 response during prolonged exercise since exercise duration did not increase IL-6 level after 12 h. Possible confounding factors do not seem to influence the IL-6 concentration during the longer races (>12 h), but might very well do so during shorter exercise bouts. In the 6-day race IL-6 increased from rest to 24 h, but thereafter there was no change in plasma IL-6 value until the end of the race (mean 143.5 h). There was no elevation of TNF-α in any of the protocols, suggesting that the competitors were free from systemic inflammation. We conclude that during endurance exercise lasting >12 h intensity, and not duration, is the main determinant of the IL-6 response, while during shorter exercise bouts both intensity and duration contribute to the accumulation of IL-6 in plasma.     

Levels of serum creatine kinase and myoglobin in women after two isometric exercise conditions

Summary The purpose of this study was to measure serum creatine kinase (CK) activity and serum myoglobin (MG) concentrations in women after two unilateral isometric knee extension exercises. Forty maximal voluntary contractions (MVC) were held for 10 s, with either a 5 s (10∶5) or 20 s 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h and MG values were measured pre, 0, 3, 6, and 18 h post exercise. For CK, the highest post exercise values were observed at 6 h following the 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h following the 10∶5 exercise (194.1±18.6 mU · ml⁻¹). For MG, the highest values were found 3 h after the 10∶20 exercise (148.9±61.7 ng · ml⁻¹) and 6 h after the 10∶5 exercise (67.3±10.9 ng · ml⁻¹). Serum CK and MG levels were significantly greater (p<0.01) after the 10∶20 exercise bout. The data demonstrate that CK and MG values for women increase significantly after isometric exercise. Since greater tension levels were maintained during the 10∶20 exercise it is hypothesized that increased serum CK and MG values after isometric exercise may be related to the tension generated by the contracting muscle.     

The intraocular pressure response to dehydration: a pilot study

The aim of this study was to determine the intraocular pressure response to differing levels of dehydration. Seven males participated in 90 min of treadmill walking (5 km h⁻¹ and 1% grade) in both temperate (22°C) and hot (43°C) conditions. At baseline and 30 min intervals intraocular pressure, nude body mass, body temperature and heart rate were recorded. Statistically significant interactions (p < 0.05) were observed for intraocular pressure (hot condition: baseline 17.0 ± 2.9, 30 min 15.6 ± 3.5, 60 min 14.5 ± 3.7 and 90 min 13.6 ± 2.9 mmHg; temperate condition: baseline 16.8 ± 2.7, 30 min 16.5 ± 2.6, 60 min 15.8 ± 2.5 and 90 min 15.7 ± 1.8 mmHg) and body mass loss (hot condition: 30 min −1.07 ± 0.35, 60 min −2.17 ± 0.55 and 90 min −3.13 ± 0.74%; temperate condition: 30 min −0.15 ± 0.11, 60 min −0.47 ± 0.18 and 90 min −0.78 ± 0.25%). Significant linear regressions (p < 0.05) were observed for intraocular pressure and body mass loss (adjusted r ² = 0.24) and intraocular pressure change and body mass loss (adjusted r ² = 0.51). In conclusion, intraocular pressure was progressively reduced during a period of exercise causing dehydration, but remained relatively stable when hydration was maintained. The present study revealed a moderate relationship between dehydration (body mass loss) and intraocular pressure change.     

The effect of the rate of heat storage on serum heat shock protein 72 in humans

Hsp72 concentration has been shown to be higher in the serum (eHsp72) of runners with symptoms of heat illness than in non-ill runners. Recently, it has been suggested that the rate of heat storage during exercise in the heat may be an important factor in the development of heat stroke. Therefore, we compared the effect of two rates of heat storage on eHsp72 concentration during exercise in which subjects reached the same final core temperature. We hypothesized that with a lower rate of heat storage the increase in eHsp72 would be attenuated compared to a higher rate of heat storage. Nine heat acclimated subjects performed two exercise trials in a counterbalanced order in the heat (42°C, 30% relative humidity). The trials consisted of walking on a treadmill (~50% VO ₂ peak) dressed in military summer fatigues until rectal temperature reached 38.5°C. A high rate of heat storage (HS, 1.04 ± 0.10 W m⁻² min⁻¹, mean ± SE) occurred when subjects walked without cooling. To produce a lower rate of heat storage (LS, 0.54 ± 0.09 W m⁻² min⁻¹) subjects walked while wearing a water-perfused cooling vest underneath clothing. eHsp72 increased pre- to post-exercise (P < 0.05) but there was no difference (P > 0.05) in eHSP between the two rates of heat storage (LS 1.25 ± 0.73 to 2.23 ± 0.70 ng ml⁻¹, HS 1.04 ± 0.57 to 2.02 ± 0.60 ng ml⁻¹). This result suggests that eHsp72 is a function of the core temperature attained rather than the rate of heat storage.     

The effect of exercise on postprandial lipidemia in type 2 diabetic patients

To elucidate if postprandial exercise can reduce the exaggerated lipidemia seen in type 2 diabetic patients after a high-fat meal. Two mornings eight type 2 diabetic patients (males) (58 ± 1.2 years, BMI 28.0 ± 0.9 kg m⁻²) and seven non-diabetic controls ate a high-fat breakfast (680 kcal m⁻², 84% fat). On one morning, 90 min later subjects cycled 60 min at 57% . Biopsies from quadriceps muscle and abdominal subcutaneous adipose tissue were sampled after exercise or equivalent period of rest and arterialized blood for 615 min. Postprandial increases in serum total-triglyceride (TG) (incremental AUC: 1,702 ± 576 vs. 341 ± 117 mmol l⁻¹ 600 min), chylomicron-TG (incremental AUC: 1,331 ± 495 vs. 184 ± 55 mmol l⁻¹ 600 min) and VLDL-TG as well as in insulin (incremental AUC: 33,946 ± 7,414 vs. 13,670 ± 3,250 pmol l⁻¹ 600 min), C-peptide and glucose were higher in diabetic patients than in non-diabetic controls (P < 0.05). In diabetic patients these variables were reduced (P < 0.05) by exercise (total-TG incremental AUC being 1,110 ± 444, chylomicron-TG incremental AUC 1,043 ± 474 mmol l⁻¹ 600 min and insulin incremental AUC 18,668 ± 4,412 pmol l⁻¹ 600 min). Lipoprotein lipase activity in muscle (11.0 ± 2.0 vs. 24.1 ± 3.4 mU g per wet weight, P < 0.05) and post-heparin plasma at 615 min were lower in diabetic patients than in non-diabetic controls, but did not differ in adipose tissue and did not change with exercise. In diabetic patients, 210 min after exercise oxygen uptake (P < 0.05) and fat oxidation (P < 0.1) were still higher than on non-exercise days. In type 2 diabetic patients, after a high-fat meal exercise reduces the plasma concentrations of triglyceride contained in both chylomicrons and VLDL as well as insulin secretion. This suggests protection against progression of atherosclerosis and diabetes.     

Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

Effectiveness of short-term heat acclimation for highly trained athletes

Effectiveness of short-term acclimation has generally been undertaken using untrained and moderately-trained participants. The purpose of this study was to determine the impact of short-term (5-day) heat acclimation on highly trained athletes. Eight males (mean ± SD age 21.8 ± 2.1 years, mass 75.2 ± 4.6 kg, [(V)\dot] \dot{V}O_2peak 4.9 ± 0.2 L min⁻¹ and power output 400 ± 27 W) were heat acclimated under controlled hyperthermia (rectal temperature 38.5°C), for 90-min on five consecutive days (T _a = 39.5°C, 60% relative humidity). Acclimation was undertaken with dehydration (no fluid-intake) during daily bouts. Participants completed a rowing-specific, heat stress test (HST) 1 day before and after acclimation (T _a = 35°C, 60% relative humidity). HST consisted 10-min rowing at 30% peak power output (PPO), 10 min at 60% PPO and 5-min rest before a 2-km performance test, without feedback cues. Participants received 250 mL fluid (4% carbohydrate; osmolality 240–270 mmol kg⁻¹) before the HST. Body mass loss during acclimation bouts was 1.6 ± 0.3 kg (2.1%) on day 1 and 2.3 ± 0.4 kg (3.0%) on day 5. In contrast, resting plasma volume increased by 4.5 ± 4.5% from day 1 to 5 (estimated from [Hb] & Hct). Plasma aldosterone increased at rest (52.6 pg mL⁻¹; p = 0.03) and end-exercise (162.4 pg mL⁻¹; p = 0.00) from day 1 to 5 acclimation. During the HST T _re and f _c were lowered 0.3°C (p = 0.00) and 14 b min⁻¹ (p = 0.00) after 20-min exercise. The 2-km performance time (6.52.7 min) improved by 4 s (p = 0.00). Meaningful physiological and performance improvements occurred for highly trained athletes using a short-term (5-day) heat acclimation under hyperthermia control, with dehydration.     

Lactic acid bacteria prevent alcohol-induced steatohepatitis in rats by acting on the pathways of alcohol metabolism

The objective is to study the possible mechanism by which lactic acid bacteria (LAB) prevent alcohol-induced steatohepatitis in rats. A total of 25 Wistar rats were divided into three groups: a LAB-fed group, an alcohol-treated group and a control group. Both the LAB-fed group and the alcohol-treated group received alcohol (10 g kg⁻¹ per day) orally for up to 5 days (125 h). Before exposure to alcohol, the LAB-fed group were first treated daily with 1.5 ml/100 g of a mixture comprising 4 × 10¹⁰ ml⁻¹ of Lactobacillus acidophilus and 2.5 × 10⁷ ml⁻¹ of Bifidobacterium longum, while the control group was treated with normal saline only. Biochemical data, alcohol dehydrogenase (ADH) activity and histology of the liver and stomach were evaluated. The ADH activity in the LAB mixture was 3.52 ± 0.45 μmol mg⁻¹ protein (10⁹ CFU ml⁻¹), and was dose-dependent. By 30 min after taking alcohol, serum alcohol concentrations were 514.24 ± 80.21 μg ml⁻¹ in the LAB-fed group and 795.15 ± 203.45 μg ml⁻¹ in the alcohol-treated group (P < 0.005). Serum alcohol concentrations were reduced by 48% (P < 0.01) in the LAB-fed group, but by only 4% in the alcohol-treated group (P > 0.05) 120 min after oral intake of alcohol. The blood levels of endotoxin, AST and ALT were improved in the LAB-fed group compared to the alcohol-fed group (P < 0.01). All alcohol-treated rats showed moderate to severe steatohepatitis, but the LAB-fed rats showed almost normal histology or very slight lesions only. In conclusion, LAB decreased the alcohol concentration in the blood by increasing the first-pass metabolism in both the stomach and the liver, and effectively protected against alcohol-induced gastric and liver injury. It is interesting to note that the protection was more effective in the liver.     

Syncope is unrelated to supine and postural hypotension following prolonged exercise

Syncope is widely reported following prolonged exercise. It is often assumed that the magnitude of exercise-induced hypotension (post-exercise hypotension; PEH), and the hypotensive response to postural change (initial orthostatic hypotension; IOH) are predictors of syncope post-exercise. The aim of this study was to determine the relationship between PEH, IOH, the residual IOH and syncope following prolonged exercise. Blood pressure (BP; Finometer) was measured continuously in 19 athletes (47 ± 20 years; BMI: 23.2 ± 2.2 kg m²; [(V)\dot] \dot{V} O₂ max: 51.3 ± 10.8 mL kg⁻¹ min⁻¹) whilst supine and during head-up tilt (HUT) to 60° for 15 min (or to syncope), prior to and following 4 h of running at 70–80% maximal heart rate. Syncope developed in 15 of 19 athletes post-exercise [HUT-time completed, Pre: 14:39 (min:s) ± 0:55; Post: 5:59 ± 4:53; P < 0.01]. PEH was apparent (−7 ± 7 mmHg; −8 ± 8%), but was unrelated to HUT-time completed (r ² = 0.09; P > 0.05). Although the magnitude of IOH was similar to post-exercise [−28 ± 12 vs. −20 ± 14% (pre-exercise); P > 0.05], the BP recovery following IOH was incomplete [−9 ± 9 vs. −1 ± 11 (pre-exercise); P < 0.05]; however, neither showed a relation to HUT-time completed (r ² = 0.18, r ² = 0.01; P > 0.05, respectively). Although an inability to maintain BP is a common feature of syncope post-exercise, the magnitude of PEH, IOH and residual IOH do not predict time to syncope. Practically, endurance athletes who present with greater hypotension are not necessarily at a greater risk of syncope than those who present with lesser reductions in BP.     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

It is well documented that intense exercise precipitates oxidative stress in adults. However, there is lack of related studies concerning oxidant and antioxidant status during early and late recovery periods in adolescent athletes, following endurance exercise in particular. This study investigated aspects of the serum oxidant and antioxidant status of 12 male adolescent (16.2 ± 0.6 years) trained runners during early and late recovery periods after an all-out 21-km run. Venous blood samples were taken immediately before, 2 and 4 h following (early recovery period), and 24 h following (late recovery period) the 21-km run. Samples were analyzed for serum concentrations of thiobarbituric acid-reactive substances (TBARS), uric acid (UA), reduced glutathione (GSH), and enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), and catalase (CAT). During the early recovery period, there were increases in the 4-h GSH (194.8 ± 10.4 vs. 211.8 ± 11.4 mg l⁻¹, P < 0.05), 2- and 4-h UA (307.8 ± 68.6 vs. 327.4 ± 63.8; 330.2 ± 65.1 μmol l⁻¹, P < 0.05), and 2-h CAT (2.05 ± 0.44 vs. 3.07 ± 0.51 U ml⁻¹, P < 0.05), and decreases in the 2-h XO (11.1 ± 1.5 vs. 10.3 ± 1.2 U l⁻¹, P < 0.05) compared to the corresponding pre-exercise level, respectively. No change was observed in SOD (P > 0.05). At the late recovery period, there was an increase in CAT (2.80 ± 0.49 U ml⁻¹, P < 0.05) and TBARS (2.99 ± 0.83 vs. 4.40 ± 1.38 nmol ml⁻¹, P < 0.05). These data indicate that although the antioxidant capacity of adolescent runners is augmented during the early recovery period following the 21-km run, they were not completely protected from oxidative stress during the later recovery period.     

Carbohydrate intake reduces fat oxidation during exercise in obese boys

The recent surge in childhood obesity has renewed interest in studying exercise as a therapeutic means of metabolizing fat. However, carbohydrate (CHO) intake attenuates whole body fat oxidation during exercise in healthy children and may suppress fat metabolism in obese youth. To determine the impact of CHO intake on substrate utilization during submaximal exercise in obese boys, seven obese boys (mean age: 11.4 ± 1.0 year; % body fat: 35.8 ± 3.9%) performed 60 min of exercise at an intensity that approximated maximal fat oxidation. A CHO drink (CARB) or a placebo drink (CONT) was consumed in a double-blinded, counterbalanced manner. Rates of total fat, total CHO, and exogenous CHO (CHO_exo) oxidation were calculated for the last 20 min of exercise. During CONT, fat oxidation rate was 3.9 ± 2.4 mg × kg fat-free mass (FFM)⁻¹ × min⁻¹, representing 43.1 ± 22.9% of total energy expenditure (EE). During CARB, fat oxidation was lowered (p = 0.02) to 1.7 ± 0.6 mg × kg FFM⁻¹ × min⁻¹, contributing to 19.8 ± 4.9% EE. Total CHO oxidation rate was 17.2 ± 3.1 mg × kg FFM⁻¹ × min⁻¹ and 13.2 ± 6.1 mg × kg FFM⁻¹ × min⁻¹ during CARB and CONT, respectively (p = 0.06). In CARB, CHO_exo oxidation contributed to 23.3 ± 4.2% of total EE. CHO intake markedly suppresses fat oxidation during exercise in obese boys.     

The effect of physical activity and physical fitness on plasma adiponectin in adults with predisposition to metabolic syndrome

The purpose of this study was to measure changes in plasma adiponectin (ApN) over 24 months of exercise intervention in middle age adults with a predisposition to metabolic syndrome and to determine if changes in ApN were more affected by physical activity or physical fitness. Thirty-six subjects completed a 24 months home-based exercise program (cycling ≥ three times per week, ≥ 45 min/session at 50–65% of VO_2peak). Body composition, blood samples, and physical fitness were studied at baseline and after 12 and 24 months of participation in the study. The prescribed physical activity was monitored via self-reported exercise diary to determine MET levels, hours, and exercise compliance. Two-tailed repeated measures ANOVA and Spearman Rank Correlation Coefficients were used to detect significant differences and associations between the variables. ApN increased significantly (P < 0.05) after 12 months in males (n = 17; 5.3 ± 1.9–7.0 ± 3.0 μg ml⁻¹) but not in females (n = 9; 8.6 ± 3.8–11.5 ± 4.0 μg ml⁻¹). The net change in ApN over 24 months was significantly correlated to the net change in VO_2peak (physical fitness) (r = 0.66; P < 0.001), whereas exercise intensity was negatively correlated to ΔApN over 12 months (r = −0.4; P ≤ 0.04) and 24 months (r = −0.45; P ≤ 0.02). Based on our results, an improvement in cardiorespiratory fitness of 15% increased plasma ApN concentration. Our findings suggest that moderate physical activity performed over many months induces positive changes in the plasma ApN concentration in adults with a predisposition to metabolic syndrome.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.