Post-concurrent exercise hemodynamics and cardiac autonomic modulation

Concurrent training is recommended for health improvement, but its acute effects on cardiovascular function are not well established. This study analyzed hemodynamics and autonomic modulation after a single session of aerobic (A), resistance (R), and concurrent (A + R) exercises. Twenty healthy subjects randomly underwent four sessions: control (C:30 min of rest), aerobic (A:30 min, cycle ergometer, 75% of VO₂ peak), resistance (R:6 exercises, 3 sets, 20 repetitions, 50% of 1 RM), and concurrent (AR: A + R). Before and after the interventions, blood pressure (BP), heart rate (HR), cardiac output (CO), and HR variability were measured. Systolic BP decreased after all the exercises, and the greatest decreases were observed after the A and AR sessions (−13 ± 1 and −11 ± 1 mmHg, respectively, P < 0.05). Diastolic BP decreased similarly after all the exercises, and this decrease lasted longer after the A session. CO also decreased similarly after the exercises, while systemic vascular resistance increased after the R and AR sessions in the recovery period (+4.0 ± 1.7 and +6.3 ± 1.9 U, respectively, P < 0.05). Stroke volume decreased, while HR increased after the exercises, and the greatest responses were observed after the AR session (SV, A = −14.6 ± 3.6, R = −22.4 ± 3.5 and AR = −23.4 ± 2.4 ml; HR, A =+13 ± 2, R =+15 ± 2 vs. AR =+20 ± 2 bpm, P < 0.05). Cardiac sympathovagal balance increased after the exercises, and the greatest increase was observed after the AR session (A = +0.7 ± 0.8, R = +1.0 ± 0.8 vs. AR = +1.2 ± 0.8, P < 0.05). In conclusion, the association of aerobic and resistance exercises in the same training session did not potentiate post-exercise hypotension, and increased cardiac sympathetic activation during the recovery period.     

Acute resistance exercise reduces blood pressure and vascular reactivity, and increases endothelium-dependent relaxation in spontaneously hypertensive rats

The aim of the present study was to assess the effects of acute dynamic resistance exercise on resting blood pressure (BP) and on endothelial function of vascular bed of spontaneously hypertensive rats. Hemodynamic measurements were performed before and after acute dynamic resistance exercise in conscious animals. After exercise, the tail artery was cannulated for mean perfusion pressure with constant flow measurement and for performing concentration–response curves to acetylcholine (ACh) and sodium nitroprusside (SNP) and dose–response curves to phenylephrine (PHE). PHE protocol was also repeated with damaged endothelium and after L-NAME and indomethacin perfusion on the tail. The maximal response (E _max) and sensitivity (pD₂) were evaluated to these drugs. Exercise reduced resting systolic and diastolic BP (Δ −79 ± 1.8; −23 ± 2.3 mmHg, respectively; P < 0.05). ACh-induced relaxation increased in the exercise group (pD₂ = 9.8 ± 0.06, P < 0.05) when compared with control rats (pD₂ = 8.7 ± 0.1). The E _max to PHE with intact endothelium decreased following exercise condition (439 ± 18 mmHg, P < 0.05) when compared with control rats (276 ± 22 mmHg). This response was abolished after L-NAME and indomethacin administration. After damage of the endothelium, PHE responses were not significantly different between the groups; however, E _max and pD₂ increased when compared with responses obtained with intact endothelium. The results demonstrated that acute dynamic resistance exercise decreased resting BP and reactivity to PHE and increased endothelium-dependent relaxation. Nitric oxide and vasodilators prostanoids appear to be involved in post-exercise endothelial and pressor responses.     

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.     

Plasma catecholamine responses and neural adaptation during short-term resistance training

Low exercise-induced plasma adrenaline (A) responses have been reported in resistance-trained individuals. In the study reported here, we investigated the interaction between strength gain and neural adaptation of the muscles, and the plasma A response in eight healthy men during a short-term resistance-training period. The subjects performed 5 resistance exercises (E1–E5), consisting of 6 sets of 12 bilateral leg extensions performed at a 50% load, and with 2 days rest in between. Average electromyographic (EMG) signal amplitude was recorded before and after the exercises, from the knee extensor muscles in isometric maximal voluntary contraction (MVC) as well as during the exercises (aEMG_max and aEMG_exerc, respectively). Total oxygen consumed during the exercises (V˙O_2tot) was also measured. All of the exercises were exhaustive and caused significant decreases in MVC (34–36%, P < 0.001). As expected, the concentric one-repetition maximum (1-RM), MVC and aEMG_max were all higher before the last exercise (E5) than before the first exercise (E1; 7, 9 and 19%, respectively, P < 0.05). In addition, in E5 the aEMG_exerc:load and V˙O_2tot:load ratios were lower than in E1 (−5 and −14%, P < 0.05), indicating enhanced efficiency of the muscle contractions, However, the post-exercise plasma noradrenaline (NA) and A were not different in these two exercises [mean (SD) 10.2 (3.8) nmol · l⁻¹ vs 11.3 (6.0) nmol · l⁻¹, ns, and 1.2 (1.0) nmol · l⁻¹ vs 1.9 (1.1) nmol · l⁻¹, ns, respectively]. However, although NA increased similarly in every exercise (P < 0.01), the increase in A reached the level of statistical significance only in E1 (P < 0.05). The post-exercise A was also already lower in E2 [0.7 (0.7) nmol · l⁻¹, P < 0.05) than in E1, despite the higher post-exercise blood lactate concentration than in the other exercises [9.4 (1.1) mmol · l⁻¹, P < 0.05]. Thus, the results suggest that the observed attenuation in the A response can not be explained by reduced exercise-induced strain due to the strength gain and neural adaptation of the muscles. Correlation analysis actually revealed that those individuals who had the highest strength gain during the training period even tended to have an increased post-exercise A concentration in the last exercise as compared to first one (r=0.76, P < 0.05). Accepted: 10 February 2000     

Indirect measures of human vagal withdrawal during head-up tilt with and without a respiratory acidosis

Human ECG records were analyzed during supine (SUP) rest and whole body 80° head-up tilt (HUT), with a respiratory acidosis (5%CO₂) and breathing room air (RA). HUT increased heart rate in both conditions (RA_SUP 60 ± 13 vs. RA_HUT 79 ± 16; 5%CO_2SUP 63 ± 12 vs. 5%CO_2HUT 79 ± 14 beats min⁻¹) and decreased mean R–R interval, with no changes in the R–R interval standard deviation. When corrected for changes in frequency spectrum total power (NU), the high frequency (0.15–0.4 Hz) component (HF_NU) of heart rate variability decreased (RA_SUP 44.01 ± 21.57 vs. RA_HUT 24.05 ± 13.09; 5%CO_2SUP 69.23 ± 15.37 vs. 5%CO_2HUT 47.64 ± 21.11) without accompanying changes in the low frequency (0.04–0.15 Hz) component (LF_NU) (RA_SUP 52.36 ± 21.93 vs. RA_HUT 66.58 ± 19.49; 5%CO_2SUP 22.97 ± 11.54 vs. 5%CO_2HUT 40.45 ± 21.41). Positive linear relations between the tilt-induced changes (Δ) in HF_NU and R–R interval were recorded for RA (ΔHF_NU = 0.0787(ΔR−R) − 11.3, R ² = 0.79, P < 0.05), and for 5%CO₂ (ΔHF_NU = 0.0334(ΔR−R) + 1.1, R ² = 0.82, P < 0.05). The decreased HF component suggested withdrawal of vagal activity during HUT. For both RA and 5%CO₂, the positive linear relations between ΔHF_NU and ΔR−R suggested that the greater the increase in heart rate with HUT, the greater the vagal withdrawal. However, a reduced range of ΔHF during HUT with respiratory acidosis suggested vagal withdrawal was lower with a respiratory acidosis.     

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

The purpose of this study was to investigate the effects of exercise intensity on the magnitude of acute post-exercise hypotension while controlling for total work done over the exercise bout. Seven normotensive physically active males aged 28 ± 6 years (mean ± SD) completed four experimental trials, a no exercise control, 30 min of semi-recumbent cycling at 70% (INT), cycling for 30 min at 40% (SMOD) and cycling at 40% for a time which corresponded to the same total work done as in the intense trial (LMOD). Blood pressure (BP), heart rate, stroke volume, cardiac output, total peripheral resistance, core body temperature and forearm skin and limb blood flow were measured prior to and for 20 min following the exercise bout. Post-exercise summary statistics were compared between trials with a one-factor general linear model. The change in systolic BP, averaged over the 20-min post-exercise period was significantly lower only following the INT (−5 ± 3 mm Hg) and LMOD exercise (−1 ± 7 mm Hg) compared to values in control (P < 0.04). The changes in systolic BP and MAP following INT and LMOD were not significantly different from each other (P > 0.05). Similar results were obtained when the minimum values of these variables recorded during the post-exercise period were compared. Mean changes in cardiac output (1.9 ± 0.3 l min⁻¹) and total peripheral resistance (−3 ± 1 mm Hg l⁻¹ min⁻¹) after INT exercise were also different from those in CON (P < 0.0005). The acute post-exercise reduction in BP was clinically similar following high intensity short duration exercise and moderate intensity longer duration exercise that was matched for total work done.     

Post-exercise protein synthesis rates are only marginally higher in type I compared with type II muscle fibres following resistance-type exercise

We examined the effect of an acute bout of resistance exercise on fractional muscle protein synthesis rates in human type I and type II muscle fibres. After a standardised breakfast (31 ± 1 kJ kg⁻¹ body weight, consisting of 52 Energy% (En%) carbohydrate, 34 En% protein and 14 En% fat), 9 untrained men completed a lower-limb resistance exercise bout (8 sets of 10 repetitions leg press and leg extension at 70% 1RM). A primed, continuous infusion of l-[ring-¹³C₆]phenylalanine was combined with muscle biopsies collected from both legs immediately after exercise and after 6 h of post-exercise recovery. Single muscle fibres were dissected from freeze-dried biopsies and stained for ATPase activity with pre-incubation at a pH of 4.3. Type I and II fibres were separated under a light microscope and analysed for protein-bound l-[ring-¹³C₆]phenylalanine labelling. Baseline (post-exercise) l-[ring-¹³C₆]phenylalanine muscle tissue labelling, expressed as (∂¹³C/¹²C), averaged −32.09 ± 0.28, −32.53 ± 0.10 and −32.02 ± 0.16 in the type I and II muscle fibres and mixed muscle, respectively (P = 0.14). During post-exercise recovery, muscle protein synthesis rates were marginally (8 ± 2%) higher in the type I than type II muscle fibres, at 0.100 ± 0.005 versus 0.094 ± 0.005%/h, respectively (P < 0.05), whereby rates of mixed muscle protein were 0.091 ± 0.005%/h. Muscle protein synthesis rates following resistance-type exercise are only marginally higher in type I compared with type II muscle fibres.     

Can HRV be used to evaluate training load in constant load exercises?

The overload principle of training states that training load (TL) must be sufficient to threaten the homeostasis of cells, tissues, organs, and/or body. However, there is no “golden standard” for TL measurement. The aim of this study was to examine if any post-exercise heart rate variability (HRV) indices could be used to evaluate TL in exercises with different intensities and durations. Thirteen endurance-trained males (35 ± 5 year) performed MODE (moderate intensity, 3 km at 60% of the maximal velocity of the graded maximal test (vVO_2max)), HI (high intensity, 3 km at 85% vVO_2max), and PRO (prolonged, 14 km at 60% vVO_2max) exercises on a treadmill. HRV was analyzed with short-time Fourier-transform method during rest, exercise, and 15-min recovery. Rating of perceived exertion (RPE), blood lactate (BLa), and HFP₁₂₀ (mean of 0–120 s post-exercise) described TL of these exercises similarly, being different for HI (P < 0.05) and PRO (P < 0.05) when compared with MODE. RPE and BLa also correlated negatively with HFP₁₂₀ (r = −0.604, −0.401), LFP₁₂₀ (−0.634, −0.601), and TP₁₂₀ (−0.691, −0.569). HRV recovery dynamics were similar after each exercise, but the level of HRV was lower after HI than MODE. Increased intensity or duration of exercise decreased immediate HRV recovery, suggesting that post-exercise HRV may enable an objective evaluation of TL in field conditions. The first 2-min recovery seems to give enough information on HRV recovery for evaluating TL.     

Impact of dehydration on a full body resistance exercise protocol

This study examined effects of dehydration on a full body resistance exercise workout. Ten males completed two trials: heat exposed (with 100% fluid replacement) (HE) and dehydration (~3% body mass loss with no fluid replacement) (DEHY) achieved via hot water bath (~39°C). Following HE and DEHY, participants performed three sets to failure (using predetermined 12 repetition maximum) of bench press, lat pull down, overhead press, barbell curl, triceps press, and leg press with a 2-min recovery between each set and 2 min between exercises. A paired t test showed total repetitions (all sets combined) were significantly lower for DEHY: (144.1 ± 26.6 repetitions) versus HE: (169.4 ± 29.1 repetitions). ANOVAs showed significantly lower repetitions (~1–2 repetitions on average) per exercise for DEHY versus HE (all exercises). Pre-set rate of perceived exertion (RPE) and pre-set heart rate (HR) were significantly higher [~0.6–1.1 units on average in triceps press, leg press, and approached significance in lat pull down (P = 0.14) and ~6–13 b min⁻¹ on average in bench press, lat pull down, triceps press, and approached significance for overhead press (P = 0.10)] in DEHY versus HE. Session RPE difference approached significance (DEHY: 8.6 ± 1.9, HE: 7.4 ± 2.3) (P = 0.12). Recovery HR was significantly higher for DEHY (116 ± 15 b min⁻¹) versus HE (105 ± 13 b min⁻¹). Dehydration (~3%) impaired resistance exercise performance, decreased repetitions, increased perceived exertion, and hindered HR recovery. Results highlight the importance of adequate hydration during full body resistance exercise sessions.     

The exercise dose affects oxidative stress and brachial artery flow-mediated dilation in trained men

The aim of this investigation was to establish whether changes in oxidative stress and endothelial function following acute aerobic exercise are dose-dependent. Ten healthy trained men completed four exercise sessions: 50% VO_2peak for 30 min (moderate intensity moderate duration, MIMD), 50% VO_2peak for 60 min (moderate intensity long duration, MILD), 80% VO_2peak for 30 min (high intensity moderate duration, HIMD), and 80% VO_2peak for the time to reach the caloric equivalent of MIMD (high intensity short duration, HISD). Thiobarbituric acid reactive substances (TBARS) were measured as an index of oxidative stress and brachial artery flow-mediated dilation (FMD) was assessed as an index of endothelial function. Variables were measured at baseline, immediately post-exercise, 1 and 2 h post-exercise. Both HIMD (14.2 ± 2.5 μmol/L) and HISD (14.7 ± 1.9 μmol/L) TBARS differed from MIMD (11.8 ± 1.5 μmol/L) immediately post-exercise. TBARS increased from pre to immediately post-exercise for HIMD (12.6 ± 2.1 vs.14.2 ± 2.5 μmol/L) and HISD (12.3 ± 2.8 vs. 14.7 ± 1.9 μmol/L). Both MIMD (7.2 ± 2.2%) and HISD (7.6 ± 2.7%) FMD immediately post-exercise were greater than HIMD (4.7 ± 2.2%). An increase of FMD from pre to immediately post-exercise was found for MIMD (5.0 ± 2.5 vs. 7.2 ± 2.2%) and HISD (5.9 ± 2.4 vs. 7.6 ± 2.7%). These data suggest that acute exercise-induced TBARS are exercise intensity-dependent whereas FMD appears to improve following energy expenditure equivalent to 30 min 50% VO_2peak, regardless of intensity or duration.     

Delayed-onset muscle soreness induced by low-load blood flow-restricted exercise

We performed two experiments to describe the magnitude of delayed-onset muscle soreness (DOMS) associated with blood flow restriction (BFR) exercise and to determine the contribution of the concentric (CON) versus eccentric (ECC) actions of BFR exercise on DOMS. In experiment 1, nine subjects performed three sets of unilateral knee extension BFR exercise at 35% of maximal voluntary contraction (MVC) to failure with a thigh cuff inflated 30% above brachial systolic pressure. Subjects repeated the protocol with the contralateral limb without flow restriction. Resting soreness (0–10 scale) and algometry (pain–pressure threshold; PPT) were assessed before and 24, 48 and 96 h post-exercise. Additionally, MVC and vastus lateralis cross-sectional area (CSA) were measured as indices of exercise-induced muscle damage. At 24-h post-exercise, BFR exercise resulted in more soreness than exercise without BFR (2.8 ± 0.3 vs 1.7 ± 0.5) and greater reductions in PPT (15.2 ± 1.7 vs. 20 ± 2.3 N) and MVC (14.1 ± 2.5% decrease vs. 1.5 ± 4.5% decrease) (p ≤ 0.05). In experiment 2, 15 different subjects performed three sets of unilateral BFR exercise at 35% MVC with one limb performing only the CON action and the contralateral performing the ECC action. The aforementioned indices of DOMS were assessed before exercise and 24, 48 and 96 h post-exercise. At 24 h post-exercise, CON BFR exercise resulted in more resting soreness than ECC BFR exercise (3.0 ± 0.5 vs. 1.6 ± 0.4), and a greater decrease in MVC (9.8 ± 2.7% decrease vs. 3.4 ± 2.5% decrease) (p ≤ 0.05). These data suggest that knee extension BFR exercise induces mild DOMS and that BFR exercise elicits muscle damage under atypical conditions with low-tension concentric contractions.     

Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise

Our purposes were (1) to examine resting arterial blood pressure following an acute bout of resistance exercise and submaximal dynamic exercise, (2) to examine the effects of these exercises on the plasma concentrations of atrial natriuretic peptide ([ANP]), and (3) to evaluate the potential relationship between [ANP] and post-exercise blood pressure. Thirteen males [24.3 ± (2.4) years] performed 15 min of unilateral leg press exercise (65% of their one-repetition maximum) and, 1 week later, ≈15 min of cycle ergometry (at 65% of their maximum oxygen consumption). Intra-arterial pressure was monitored during exercise and for 1 h post-exercise. Arterial blood was drawn at rest, during exercise and at intervals up to 60 min post-exercise for analysis of haematocrit and [αANP]. No differences occurred in blood pressure between trials, but significant decrements occurred following exercise in both trials. Systolic pressure was ≈20 mmHg lower than before exercise after 10 min, and mean pressure was ≈7 mmHg lower from 30 min onwards. Only slight (non-significant) elevations in [αANP] were detected immediately following exercise, with the concentrations declining to pre-exercise values by 5 min post-exercise. We conclude that post-exercise hypotension occurs following acute bouts of either resistance or submaximal dynamic exercise and, in this investigation, that this decreased blood pressure was not directly related to the release of αANP. Accepted: 29 July 1998     

Combined carbohydrate-protein supplementation improves competitive endurance exercise performance in the heat

Laboratory-based studies have demonstrated that adding protein (PRO) to a carbohydrate (CHO) supplement can improve thermoregulatory capacity, exercise performance and recovery. However, no study has investigated these effects in a competitive sporting context. This study assessed the effects of combined CHO–PRO supplementation on physiological responses and exercise performance during 8 days of strenuous competition in a hot environment. Twenty-eight cyclists participating in the TransAlp mountain bike race were randomly assigned to fitness-matched placebo (PLA 76 g L⁻¹ CHO) or CHO–PRO (18 g L⁻¹ PRO, 72 g L⁻¹ CHO) groups. Participants were given enough supplements to allow ad libitum consumption. Physiological and anthropometric variables were recorded pre- and post-exercise. Body mass decreased significantly from race stage 1 to 8 in the PLA group (−0.75 ± 0.22 kg, P = 0.01) but did not change in the CHO–PRO group (0.42 ± 0.42 kg, P = 0.35). Creatine kinase concentration and muscle soreness were substantially elevated during the race, but were not different between groups (P = 0.82, P = 0.44, respectively). Urine osmolality was significantly higher in the CHO–PRO versus the PLA group (P = 0.04) and the rise in tympanic temperature from pre- to post-exercise was significantly less in CHO–PRO versus PLA (P = 0.01). The CHO–PRO group also completed the 8 stages significantly quicker than the PLA group (2,277 ± 127 vs. 2,592 ± 68 min, respectively, P = 0.02). CHO–PRO supplementation therefore appears to prevent body mass loss, enhance thermoregulatory capacity and improve competitive exercise performance despite no effect on muscle damage.     

Inspiratory resistive loading after all-out exercise improves subsequent performance

We have previously shown that post-exercise inspiratory resistive loading (IRL) reduces blood lactate ([Lac_b⁻]). In this study, we tested the hypothesis that IRL during recovery could improve subsequent exercise performance. Eight healthy men underwent, on different days, two sequential 30-s, cycle ergometer Wingate tests. During the 10-min recovery period from test 1, subjects breathed freely or through an inspiratory resistance (15 cm H₂O) with passive leg recovery. Arterialized [Lac_b⁻] values, perceptual scores (Borg), cardiac output by impedance cardiography (QT), and changes in the deoxygenation status of the M. vastus lateralis by near-infrared spectroscopy (ΔHHb), were recorded. [Lac_b⁻] was significantly reduced after 4 min of recovery with IRL (peak [Lac_b⁻] 12.5 ± 2.3 mmol l⁻¹ with free-breathing vs. 9.8 ± 1.5 mmol l⁻¹ with IRL). Effort perception was reduced during late recovery with IRL compared with free-breathing. Cardiac work was increased with IRL, since heart rate and QT were elevated during late recovery. Peripheral muscle reoxygenation, however, was significantly impaired with IRL, suggesting that post-exercise convective O₂ delivery to the lower limbs was reduced. Importantly, IRL had a dual effect on subsequent performance, i.e., improvement in peak and mean power, but increased fatigue index (P < 0.05). Our data demonstrate that IRL after a Wingate test reduces post-exercise effort perception and improves peak power on subsequent all-out maximal-intensity exercise.     

Temporal association of elevations in serum cardiac troponin T and myocardial oxidative stress after prolonged exercise in rats

The objective of this study was to determine if prolonged exercise resulted in the appearance of cardiac troponin T (cTnT) in serum and whether this was associated with elevated levels of myocardial oxidative stress. Forty-five male Sprague–Dawley rats were randomized into four groups and killed before (PRE-EX), immediately (0HR), 2 (2HR) and 24 h (24HR) after a 3-h bout of swimming with 5% body weight attached to their tail. In all animals serum cTnT was assayed using 3rd generation electrochemiluminescence. In homogenized heart tissue myocardial malondialdehyde (MDA), a marker of lipid peroxidation, glutathione (GSH), and a non-enzymatic estimate of total antioxidant capacity (T-AOC) were assessed spectrophotometrically. At PRE-EX cTnT was undetectable in all animals. At 0HR (median, range: 0.055, 0.020–0.100) and 2HR post-exercise (0.036, 0.016–2.110) cTnT was detectable in all animals (P < 0.05). At 24HR post-exercise cTnT was undetectable in all animals. An elevation in MDA was observed 0HR (mean ± SD: 1.7 ± 0.2 nmol mgpro⁻¹) and 2HR (1.6 ± 0.3 nmol mgpro⁻¹) post-exercise compared with PRE-EX (1.3 ± 0.2 nmol mgpro⁻¹; P < 0.05). The antioxidant response to this challenge was a significant (P < 0.05) decrease in GSH 2HR and 24HR post-exercise. Despite this T-AOC did not alter across the trial (P > 0.05). The results indicated that prolonged and strenuous exercise in rats resulted in an elevation in cTnT, a biomarker of cardiomyocyte damage, in all animals 0HR and 2HR after exercise completion. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart.     

Influence of menstrual cycle phase on pulmonary function in asthmatic athletes

The main aim of this study was to investigate whether there is a relationship between menstrual cycle phase and exercise-induced bronchoconstriction (EIB) in female athletes with mild atopic asthma. Seven eumenorrheic subjects with regular 28-day menstrual cycles were exercised to volitional exhaustion on day 5 [mid-follicular (FOL)] and day 21 [mid-luteal (LUT)] of their menstrual cycle. Pulmonary function tests were conducted pre- and post-exercise. The maximal percentage decline in post-exercise forced expiratory volume in 1 s (FEV₁) and forced expiratory flow from 25 to 75% of forced vital capacity (FEF_25–75%) was significantly greater (P<0.05) on day 21 (mid-LUT phase) (−17.35±2.32 and −26.28±6.04%, respectively), when salivary progesterone concentration was highest, compared to day 5 (mid-FOL phase) (−12.81±3.35 and −17.23±8.20%, respectively), when salivary progesterone concentration was lowest. The deterioration in the severity of EIB during the mid-LUT phase was accompanied by worsening asthma symptoms and increased bronchodilator use. There was a negative correlation between the percent change in pre- to post-exercise FEV₁ and salivary progesterone concentration. However, no such correlation was found between salivary estradiol and the percentage change in pre- to post-exercise FEV₁. This study has shown for the first time that menstrual cycle phase is an important determinant of the severity of EIB in female athletes with mild atopic asthma. Female asthmatic athletes may need to adjust their training and competition schedules to their menstrual cycle and to consider the potential negative effects of the LUT phase of the menstrual cycle on exercise performance.     

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.     

The effect of diet on vitamin E intake and oxidative stress in response to acute exercise in female athletes

Vitamin E is the major lipid-soluble antioxidant found in foods, and its bioavailability is affected by the presence of dietary fats. Athletes often consume low-fat diets and may be more susceptible to the oxidative stress produced by exercise due to the low availability of vitamin E. In this study, the effects of a low-fat diet on vitamin E intake and oxidative stress markers were assessed in collegiate female rowers. All subjects habitually consumed either a low-fat (LF; <40 g fat · day⁻¹) or a high-fat (HF; >60 g fat · day⁻¹) diet. Subjects ran downhill for 45 min at 75% of their age-predicted maximal heart rate. Blood samples were collected immediately pre- and post-exercise, and at 6, 24, and 48 h post-exercise. Subjects in the LF group consumed significantly less vitamin E (2.9 mg vitamin E · day⁻¹) than advised by the Recommended Dietary Allowance (RDA; 8.0 mg vitamin E · day⁻¹) and than those in the HF group (9.8 mg vitamin E · day⁻¹; P < 0.05). Plasma concentrations of vitamin E, malondialdehyde, and conjugated dienes were not significantly different between LF and HF before or after exercise. Creatine kinase became significantly elevated above baseline at 6 h and 24 h post-exercise in both groups (P < 0.05). We can conclude from these data that although the subjects in the LF group were not consuming the recommended amount of vitamin E in their diets, their vitamin E intake appears to be sufficient to protect against the oxidative stress produced by this moderate-intensity exercise. Accepted: 28 April 2000     

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.     

Acute and adaptive responses in humans to exercise in a warm, humid environment

 Acute and repeated exposure for 8–13 consecutive days to exercise in humid heat was studied. Twelve fit subjects exercised at 150 W [45% of maximum O₂ uptake (V.O₂,_max)] in ambient conditions of 35°C and 87% relative humidity which resulted in exhaustion after 45 min. Average core temperature reached 39.9 ± 0.1°C, mean skin temperature (T– _sk) was 37.9 ± 0.1°C and heart rate (HR) 152 ± 6 beats min^–1 at this stage. No effect of the increasing core temperature was seen on cardiac output and leg blood flow (LBF) during acute heat stress. LBF was 5.2 ± 0.3 l min^–1 at 10 min and 5.3 ± 0.4 l min^–1 at exhaustion (n = 6). After acclimation the subjects reached exhaustion after 52 min with a core temperature of 39.9 ± 0.1°C, T– _sk 37.7 ± 0.2°C, HR 146 ± 4 beats min^–1. Acclimation induced physiological adaptations, as shown by an increased resting plasma volume (3918 ± 168 to 4256 ± 270 ml), the lower exercise heart rate at exhaustion, a 26% increase in sweating rate, lower sweat sodium concentration and a 6% reduction in exercise V.O₂. Neither in acute exposure nor after acclimation did the rise of core temperature to near 40°C affect metabolism and substrate utilization. The physiological adaptations were similar to those induced by dry heat acclimation. However, in humid heat the effect of acclimation on performance was small due to physical limitations for evaporative heat loss. Received: 3 July 1996 / Received after revision: 26 September 1996 / Accepted: 7 January 1997