Effect of exercise on glutamine metabolism in macrophages of trained rats

This study investigated the effect of exercise on glutamine metabolism in macrophages of trained rats. Rats were divided into three groups: sedentary (SED); moderately trained (MOD) rats that were swim trained 1 h/day, 5 days/week for 6 weeks; and exhaustively trained (EXT) rats that were similarly trained as MOD for 5 weeks and, in the 6th week, trained in three 1-h sessions/day with 150 min of rest between sessions. The animals swam with a load equivalent to 5.5% of their body weight and were killed 1 h after the last exercise session. Cells were collected, and glutamine metabolism in macrophage and function were assayed. Exercise increased phagocytosis in MOD when compared to SED (34.48 ± 1.79 vs 15.21 ± 2.91%, P < 0.05); however, H₂O₂ production was higher in MOD (75.40 ± 3.48 nmol h × 10⁵ cell⁻¹) and EXT (79.20 ± 1.18 nmol h × 10⁵ cell⁻¹) in relation to SED (32.60 ± 2.51 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine consumption increased in MOD and EXT (26.53 ± 3.62 and 19.82 ± 2.62 nmol h × 10⁵ cell⁻¹, respectively) relative to SED (6.72 ± 0.57 nmol h × 10⁵ cell⁻¹, P < 0.05). Aspartate increased in EXT (9.72 ± 1.14 nmol h × 10⁵ cell⁻¹) as compared to SED (1.10 ± 0.19 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine decarboxylation was increased in MOD (12.10 ± 0.27 nmol h × 10⁵ cell⁻¹) and EXT (16.40 ± 2.17 nmol h × 10⁵ cell⁻¹) relative to SED (1.10 ± 0.06 nmol h × 10⁵ cell⁻¹, P < 0.05). This study suggests an increase in macrophage function post-exercise, which was supported by enhanced glutamine consumption and metabolism, and highlights the importance for glutamine after exercise.     

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.     

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 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     

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.     

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.     

Diurnal variation in the salivary melatonin responses to exercise: relation to exercise-mediated tachycardia

Salivary melatonin concentration is an established marker of human circadian rhythmicity. It is thought that melatonin is relatively robust to the masking effects of exercise. Nevertheless, the extent and even the direction of exercise-related change is unclear, possibly due to between-study differences in the time of day exercise is completed. Therefore, we aimed to compare melatonin responses between morning and afternoon exercise, and explore the relationships between exercise-related changes in melatonin and heart rate. At 08:00 and 17:00 hours, seven male subjects (mean ± SD age, 27 ± 5 years) completed 30 min of cycling at 70% peak oxygen uptake followed by 30 min of rest. Light intensity was maintained at ~150 lx. Salivary melatonin (ELISA) and heart rate were measured at baseline, 15 min during exercise, immediately post-exercise and following 30 min recovery. Melatonin was ≈15 pg ml⁻¹ higher in the morning trials compared with the afternoon (P = 0.030). The exercise-related increase in melatonin was more pronounced (P = 0.024) in the morning (11.1 ± 8.7 pg ml⁻¹) than in the afternoon (5.1 ± 5.7 pg ml⁻¹). The slope of the heart rate–melatonin relationship was significantly (P = 0.020) steeper in the morning (0.12 pg ml⁻¹ beats⁻¹ min⁻¹) than in the afternoon (0.03 pg ml⁻¹ beats⁻¹ min⁻¹). In conclusion, we report for the first time that the masking effect of moderate-intensity exercise on melatonin is approximately twice as high in the morning than the afternoon. The much steeper relationship between heart rate and melatonin changes in the morning raises the possibility that time of day alters the relationships between exercise-mediated sympathetic nervous activity and melatonin secretion.     

Monitoring endurance running performance using cardiac parasympathetic function

The aims of the present study were to (1) assess relationships between running performance and parasympathetic function both at rest and following exercise, and (2) examine changes in heart rate (HR)-derived indices throughout an 8-week period training program in runners. In 14 moderately trained runners (36 ± 7 years), resting vagal-related HR variability (HRV) indices were measured daily, while exercise HR and post-exercise HR recovery (HRR) and HRV indices were measured fortnightly. Maximal aerobic speed (MAS) and 10 km running performance were assessed before and after the training intervention. Correlations (r > 0.60, P < 0.01) were observed between changes in vagal-related indices and changes in MAS and 10 km running time. Exercise HR decreased progressively during the training period (P < 0.01). In the 11 subjects who lowered their 10 km running time >0.5% (responders), resting vagal-related indices showed a progressively increasing trend (time effect P = 0.03) and qualitative indications of possibly and likely higher values during week 7 [+7% (90% CI −3.7;17.0)] and week 9 [+10% (90% CI −1.5;23)] compared with pre-training values, respectively. Post-exercise HRV showed similar changes, despite less pronounced between-group differences. HRR showed a relatively early possible decrease at week 3 [−20% (90% CI −42;10)], with only slight reductions near the end of the program. The results illustrate the potential of resting, exercise and post-exercise HR measurements for both assessing and predicting the impact of aerobic training on endurance running performance.     

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.     

The effect of 48?weeks of aerobic exercise training on cutaneous vasodilator function in post-menopausal females

Skin blood flow (SkBF) and endothelial-dependent vasodilatation decline with ageing and can be reversed with exercise training. We tested whether 48 weeks of training could improve SkBF and endothelial function in post-menopausal females; 20 post-menopausal subjects completed the study. SkBF was measured by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Resting CVC was measured at 32°C and peak CVC at 42°C. Cutaneous endothelial-dependent and -independent vasodilatations were determined by the iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. All assessments described were performed at entry (week 0), and after 6, 12, 24, 36, and 48 weeks of training. Resting CVC measures did not change (P > 0.05) throughout the study. Peak CVC increased (P < 0.05) after 24 weeks (7.2 ± 1.2 vs. 11.6 ± 1.4 AU mmHg⁻¹) and at the 36- and 48-week assessments (13.0 ± 1.7 and 14.9 ± 2.1 AU mmHg⁻¹, respectively). Responses to ACh also increased (P < 0.05) at the 24-week assessment (5.1 ± 2.1 vs. 8.55 ± 2.3 AU mmHg⁻¹) and increased further at the 36 and 48-week assessments (11.6 ± 3.7 and 13.2 ± 3.9 AU mmHg⁻¹, respectively). Cutaneous responses to SNP increased (P < 0.05) after 36 weeks (8.7 ± 2.1 vs. 13.02 ± 2.23 AU mmHg⁻¹ at 36 weeks). VO_2max increased after 12 weeks (23.5 ± 0.7 vs. 25.4 ± 0.9 ml kg⁻¹ min⁻¹) and improved (P < 0.05) further throughout the study (31.6 ± 1.8 ml kg⁻¹ min⁻¹ at week 48). Aerobic exercise produces positive adaptations in the cutaneous vasodilator function to local heating as well as in cutaneous endothelial and endothelial-independent vasodilator mechanisms. Aerobic capacity was also significantly improved. These adaptations were further enhanced with progressive increases in exercise intensity.     

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 effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men

Oxidative stress is postulated to be responsible for the postprandial impairments in vascular function. The purpose of this study was to measure pulse wave velocity (PWV) and markers of postprandial oxidative stress before and after an acute bout of moderate exercise. Ten trained male subjects (age 21.5 ± 2.5 years, VO₂ max 58.5 ± 7.1 ml kg⁻¹ min⁻¹) participated in a randomised crossover design: (1) high-fat meal alone (2) high-fat meal followed 2 h later by a bout of 1 h moderate (60% max HR) exercise. PWV was examined at baseline, 1, 2, 3, and 4 h postprandially. Blood Lipid hydroperoxides (LOOHs), Superoxide dismutase (SOD) and other biochemical markers were measured. PWV increased at 1 h (6.49 ± 2.1 m s⁻¹), 2 h (6.94 ± 2.4 m s⁻¹), 3 h (7.25 ± 2.1 m s⁻¹) and 4 h (7.41 ± 2.5 m s⁻¹) respectively, in the control trial (P < 0.05). There was no change in PWV at 3 h (5.36 ± 1.1 m s⁻¹) or 4 h (5.95 ± 2.3 m s⁻¹) post ingestion in the exercise trial (P > 0.05). LOOH levels decreased at 3 h post ingestion in the exercise trial compared to levels at 3 h (P < 0.05) in the control trial. SOD levels were lower at 3 h post ingestion in the control trial compared to 3 h in the exercise trial (0.52 ± 0.05 vs. 0.41 ± 0.1 units μl⁻¹; P < 0.05). These findings suggest that a single session of aerobic exercise can ameliorate the postprandial impairments in arterial function by possibly reducing oxidative stress levels.     

High levels of circulating angiotensin II shift the open-loop baroreflex control of splanchnic sympathetic nerve activity,heart rate and arterial pressure in anesthetized rats

Although an acute arterial pressure (AP) elevation induced by intravenous angiotensin II (ANG II) does not inhibit sympathetic nerve activity (SNA) compared to an equivalent AP elevation induced by phenylephrine, there are conflicting reports as to how circulating ANG II affects the baroreflex control of SNA. Because most studies have estimated the baroreflex function under closed-loop conditions, differences in the rate of input pressure change and the magnitude of pulsatility may have biased the estimation results. We examined the effects of intravenous ANG II (10 μg kg⁻¹ h⁻¹) on the open-loop system characteristics of the carotid sinus baroreflex in anesthetized and vagotomized rats. Carotid sinus pressure (CSP) was raised from 60 to 180 mmHg in increments of 20 mmHg every minute, and steady-state responses in systemic AP, splanchnic SNA and heart rate (HR) were analyzed using a four-parameter logistic function. ANG II significantly increased the minimum values of AP (67.6 ± 4.6 vs. 101.4 ± 10.9 mmHg, P < 0.01), SNA (33.3 ± 5.4 vs. 56.5 ± 11.5%, P < 0.05) and HR (391.1 ± 13.7 vs. 417.4 ± 11.5 beats/min, P < 0.01). ANG II, however, did not attenuate the response range for AP (56.2 ± 7.2 vs. 49.7 ± 6.2 mmHg), SNA (69.6 ± 5.7 vs. 78.9 ± 9.1%) or HR (41.7 ± 5.1 vs. 51.2 ± 3.8 beats/min). The maximum gain was not affected for AP (1.57 ± 0.28 vs. 1.20 ± 0.25), SNA (1.94 ± 0.34 vs. 2.04 ± 0.42%/mmHg) or HR (1.11 ± 0.12 vs. 1.28 ± 0.19 beats min⁻¹ mmHg⁻¹). It is concluded that high levels of circulating ANG II did not attenuate the response range of open-loop carotid sinus baroreflex control for AP, SNA or HR in anesthetized and vagotomized rats.     

Carbohydrate ingestion and pre-cooling improves exercise capacity following soccer-specific intermittent exercise performed in the heat

Ingestion of carbohydrate and reducing core body temperature pre-exercise, either separately or combined, may have ergogenic effects during prolonged intermittent exercise in hot conditions. The aim of this investigation was to examine the effect of carbohydrate ingestion and pre-cooling on the physiological responses to soccer-specific intermittent exercise and the impact on subsequent high-intensity exercise performance in the heat. Twelve male soccer players performed a soccer-specific intermittent protocol for 90 min in the heat (30.5°C and 42.2% r.h.) on four occasions. On two occasions, the participants underwent a pre-cooling manoeuvre. During these sessions either a carbohydrate–electrolyte solution (CHOc) or a placebo was consumed at (PLAc). During the remaining sessions either the carbohydrate–electrolyte solution (CHO) or placebo (PLA) was consumed. At 15-min intervals throughout the protocol participants performed a mental concentration test. Following the soccer-specific protocol participants performed a self-chosen pace test and a test of high-intensity exercise capacity. The period of pre-cooling significantly reduced core temperature, muscle temperature and thermal sensation (P < 0.05). Self-chosen pace was greater with CHOc (12.5 ± 0.5 km h⁻¹) compared with CHO (11.3 ± 0.4 km h⁻¹), PLA (11.3 ± 0.4 km h⁻¹) and PLAc (11.6 ± 0.5 km h⁻¹) (P < 0.05). High-intensity exercise capacity was improved with CHOc and CHO when compared with PLA (CHOc; 79.8 ± 7 s, CHO; 72.1 ± 5 s, PLAc; 70.1 ± 8 s, PLA; 57.1 ± 5 s; P < 0.05). Mental concentration during the protocol was also enhanced during CHOc compared with PLA (P < 0.05). These results suggest pre-cooling in conjunction with the ingestion of carbohydrate during exercise enhances exercise capacity and helps maintain mental performance during intermittent exercise in hot conditions.     

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.     

The effects of vibration therapy on muscle force loss following eccentrically induced muscle damage

The purpose of this study was to investigate the effects of acute vibration therapy (VT) on performance recovery after a bout of strenuous eccentric exercise. Eight healthy males completed 300 maximal eccentric contractions of the quadriceps of one leg on an isokinetic dynamometer. Immediately after exercise and 12 and 24 h post-exercise, the subjects underwent either VT or a control treatment of no VT. Five sets of 1 min VT was performed at 26 Hz, with 6 mm peak-to-peak displacement, on a commercially available vibration machine. At least 2 weeks after the initial trial, the subjects completed the second trial using the contralateral leg and other treatment. Peak and average peak isometric tension and isokinetic concentric and eccentric torque were measured prior to exercise and 24 and 48 h post-exercise. Treatment with VT resulted in significantly (all P < 0.05) greater decrements in peak (−38%) and average peak eccentric (−39%) torque 24 h after eccentric exercise as compared to a control treatment (−24 and −29%, respectively). These results suggest that the use of 26 Hz VT in the first 24 h after damaging exercise may be detrimental to the magnitude of force loss and/or recovery over this period.     

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.     

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-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity

The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C—40 min of rest), low- (E40%—40% of 1 repetition maximum, RM), and high-intensity (E80%—80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF_R–Rnu) and high-frequency (HF_R–Rnu) components of the R–R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (−6 ± 1 and −8 ± 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (−0.4 ± 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (−11 ± 2 vs. −17 ± 2 ml/beat, and +17 ± 2 vs. +21 ± 2 bpm, P < 0.05). LF_R–Rnu increased, while ln HF_R–Rnu decreased in both exercise sessions. In conclusion: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.     

The repeated bout effect of eccentric exercise is not associated with changes in voluntary activation

The aim of this study was to compare the possible changes in muscle activation level between a first and second bout of damaging eccentric exercise performed at 2 weeks interval (i.e. repeated bout effect). To that purpose, ten physically active males took part in this study. The eccentric exercise consisted of 10 sets of 12 maximal voluntary contractions (MVC) produced by the knee extensors during movements performed at a constant speed of 160°s⁻¹. Changes in voluntary and electrically evoked torque in concentric and/or isometric conditions were assessed at the following time points: pre-exercise, and 2 min, 1 and 24 h after each eccentric exercise. At the same time points, voluntary activation was quantified by the superimposed electrical stimulation technique. Muscle soreness and plasma CK activity were measured within 48 h after the eccentric exercise. The results showed that the decrease in eccentric peak torque was linear throughout the exercise protocol. At the end of bouts 1 and 2, torque was significantly reduced by 27.7 ± 9.1 and 23.4 ± 11.2, respectively, with no difference between bouts (P > 0.05). At 24 h post-exercise, a lower reduction (P < 0.05) in MVC (17.8 ± 5.4%) and electrically evoked (16.7 ± 4.6%) isometric torque was observed for bout 2. In contrast, no statistical difference was found in the deficit in voluntary activation between the two bouts. In conclusion, our results indicate that the repeated bout effect of eccentric exercise appears to reduce muscle damage, but does not influence the level of voluntary activation.