
The aim of this study was to determine whether peak oxygen uptake (PVO2) attained in a 90-s maximal intensity cycle sprint is comparable to that from a conventional ramp test. Sixteen participants (13 boys and 3 girls, 14.6 +/- 0.4 yr) volunteered for the study. On Day 1 they completed a PVO2 test to exhaustion using a 25 W x min(-1) ramp protocol beginning at 50 W. Peak VO2 was defined as the highest VO2 value achieved, and aerobic power (Wmax) as the power output of the final 30 s. On Day 2 the participants completed two 90-s maximal sprints (S1 and S2). A 45-min recovery period separated each sprint. Mean oxygen uptake over the last 10 s of each sprint was determined as PVO2, and minimum power (MinP-30 s) as the mechanical power attained in the final 30 s. A one-way ANOVA was used to analyse differences between S1, S2, and the ramp test for PVO2 and MinP-30 s. Peak VO2 was not significantly different between the ramp, S1, or S2 (2.64 +/- 0.5, 2.49 +/- 0.5, and 2.53 +/- 0.5 L x min(-1), respectively, p > 0.68). The S1 and S2 PVO2 scores represented 91 +/- 10% and 92 +/- 10% of the ramp aerobic test. The MinP-30 s for S1 and S2 were significantly lower than the Wmax of the ramp test, p < 0.05. Hence, for researchers solely interested in PVO2 values, a shorter but more intensive protocol provides an alternative method to the traditional ramp aerobic test.
Unilateral, chronic low-frequency electrical stimulation (CLFS) is an experimental model that evokes numerous biochemical and physiological adaptations in skeletal muscle. These occur within a short time frame and are restricted to the stimulated muscle. The humoral effects of whole body exercise are eliminated and the nonstimulated contralateral limb can often be used as a control muscle, if possible effects on the contralateral side are considered. CLFS induces a fast-to-slow transformation of muscle because of alterations in calcium dynamics and myofibrillar proteins, and a white-to-red transformation because of changes in mitochondrial enzymes, myoglobin, and the induction of angiogenesis. These adaptations occur in a coordinated time-dependent manner and result from altered gene expression, including transcriptional and posttranscriptional processes. CLFS techniques have also been applied to myocytes in cell culture, which provide a greater opportunity for the delivery of pharmacological agents or for the application of gene transfer methodologies. Clinical applications of the CLFS technique have been limited, but they have shown potential therapeutic value in patients in whom voluntary muscle contraction is not possible due to debilitating disease and/or injury. Thus the CLFS technique has great value for studying various aspects of muscle adaptation, and its wider scientific application to a variety of neuromuscular-based disorders in humans appears to be warranted.
Researchers have alluded the existence of "neural factors" in the expression and development of muscular strength. Candidate neural factors including motor unit recruitment, rate coding, double firing, and motor unit synchronization are discussed in this review. Aging is generally accompanied by lower motor unit discharge rates. However, both young and older adults exhibit rapid changes in muscular strength with repeated strength testing. These strength changes occur with concomitant albeit transient increase in motor unit discharge rate. These and other neural factors may contribute to the initial increase in muscular strength observed during the early phases of resistance exercise training.
The current state of the HISS (hepatic insulin sensitizing substance) hypothesis is briefly outlined. In the postmeal absorptive state, 50-60% of the glucose storage action of insulin is accounted for by the actions of HISS released from the liver and acting on skeletal muscle. Hepatic parasympathetic nerves permissively regulate the ability of a pulse of insulin to release HISS, thereby potentiating the impact of insulin in the fed state. HISS release in response to insulin decreases progressively with fasting to create a physiological state of HISS-dependent insulin resistance. HISS release is regulated by parasympathetic nerves via muscarinic receptors and nitric oxide, and insulin resistance of skeletal muscle produced by hepatic denervation is reversed by intraportal but not intravenous acetylcholine or a nitric oxide donor. It is suggested that HISS-dependent insulin resistance occurs in animal models including sucrose-fed rats, spontaneously hypertensive rats, chronic liver disease, fetal alcohol effect in the adult offspring, and type 2 diabetes.
The liver is anatomically well situated to regulate blood glucose. It is positioned downstream from the pancreas, which releases the key regulatory hormones glucagon and insulin. It is also just downstream from the gut, permitting efficient extraction of ingested glucose and preventing large excursions in systemic glucose after a glucose-rich meal. The position of the liver is not as well situated from the standpoint of experimentation and clinical assessment, as its primary blood supply is impossible to access in conscious human subjects. Over the last 20 years, to study hepatic glucose metabolism during and after exercise, we have utilized a conscious dog model which permits sampling of the blood that perfuses (portal vein, artery) and drains (hepatic vein) the liver. Our work has demonstrated the key role of exercise-induced changes in glucagon and insulin in stimulating hepatic glycogenolysis and gluconeogenesis during exercise. Recently we showed that portal venous infusion of the pharmacological agent 5'-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside leads to a marked increase in hepatic glucose production. Based on this, we propose that the concentration of AMP may be a component of a physiological pathway for stimulating hepatic glucose production during exercise. Insulin-stimulated hepatic glucose uptake is increased following exercise by an undefined mechanism that is independent of liver glycogen content. The fate of glucose taken up by the liver is critically dependent on hepatic glycogen stores, however, as glycogen deposition is greatly facilitated by prior glycogen depletion.
The aim of the present study was to investigate potential mechanisms responsible for the improvement in prolonged exercise capacity in hot environments with exogenous carbohydrate. Eight endurance-trained men (VO(2)max 60.5 +/- 2.4 ml.kg(-1).min(-1), mean +/- SE) cycled to exhaustion on three occasions at 60% VO(2)max at an ambient temperature of 35 degrees C. They ingested either a sweet 6.4% carbohydrate solution (SC), a nonsweet 6.4% carbohydrate solution (NSC), or water (W). Exercise capacity was significantly increased with SC and NSC compared to W, the improvements corresponding to 15.8% and 11.8%, respectively. No difference in exercise capacity was seen between SC and NSC solutions. Plasma glucose concentrations were higher during the SC and NSC trials compared to W, significantly so at 10 min and at fatigue. Rates of carbohydrate oxidation were higher in the SC and NSC trials, although the rates never declined below 2.1 +/- 0.2 g.min(-1) in the W trial. There was no difference in the rate of rise of rectal temperature between trials, but there was a trend for subjects to fatigue at higher temperatures during the two carbohydrate trials. In conclusion, exogenous carbohydrate, independent of sweetness, improves exercise capacity in the heat compared to water alone.
The purpose of this study was to examine the effect of selective skin cooling over m. vastus lateralis (VL) on the activation patterns of quadriceps femoris muscle during knee extension exercise (KEE) using muscle function magnetic resonance imaging (mfMRI). The isometric force production of the right thigh was tested in 7 healthy young men at maximum voluntary contraction (MVC), and the transverse relaxation time (T2) value was taken from mfMR images at rest and immediately after KEE with 4 sets of 10 repetitions at a load equal to 60% of their 10-rep maximum, with and without skin cooling. The cooling was carried out by ice pack on the surface of the skin of the VL for 3 min before resting mfMRI and MVC tests, and before KEE, during KEE, and during the KEE rest intervals. The percent change in T2 of the m. vastus intermedius was significantly increased by skin cooling in comparison to the change without skin cooling, p < 0.05. This result suggests that skin cooling alters the activation pattern of the different heads of the quadriceps.
The aim of this study was to assess the food habits and nutritional status of high level adolescent soccer players (N = 33; ages 14-16 yrs) living in their home environment. Body composition (height, mass, skinfolds), biochemical and hematological parameters, performance in soccer-specific tests (sprinting, jumping, intermittent endurance), and dietary intake (weighed food intake method) and related behaviors (nutrient supplement use, daily activity profile) were assessed. Daily energy expenditure and energy intake were 12.5 MJ and 12.6 MJ, respectively. Protein (16% of energy intake; 1.9 g/kg of body mass), lipid (38%), and cholesterol (385 mg) intake were above recommendations, while carbohydrates (45%) were below. The food intake of these adolescents was based on cereals and derivates; meat, fish, and eggs; milk and dairy products; biscuits and confectionery; and oil, butter and margarine, which provided 78% of total energy intake, 85% of proteins, 64% of carbohydrates, 90% of lipids, and 47% of fiber. Although diet provided sufficient iron, 48% of individuals showed iron deficiency without anemia. Based on these results, a well designed nutrition intervention would be advisable for optimizing performance, and especially for promoting healthy eating habits in adolescent soccer players.
Human splenic contraction occurs both during apnea and maximal exercise, increasing the circulating erythrocyte volume. We investigated the hematological responses to 3 maximal apneas performed by elite apneic divers, elite cross-country skiers, and untrained subjects. Post-apnea hemoglobin concentration had increased in all groups, but especially in divers. The increases disappeared within 10 min of recovery. Apneic duration across apneas also increased the most in divers. Responses in divers could be more pronounced as a result of apnea training.
PURPOSEEffects of strength training (ST) and nutritional counseling (NC) on metabolic health indicators were examined in 50 aging women.METHODSSubjects performed ST for 21 weeks. NC was given to obtain sufficient energy and protein intake, and recommended intake of fat and fiber.RESULTSNC increased intake of protein and polyunsaturated fat by 4.5% and 10.7% and decreased intake of saturated fat by 18.3%. Serum concentrations of total cholesterol (TC), LDL-cholesterol (LDL-C), total and HDL-cholesterol (HDL-C) ratio and triacylglycerols (TAG) decreased, and serum HDL-C increased in all subjects after ST. Respectively, systolic and diastolic blood pressure and serum insulin concentration decreased in all subjects. NC contributed to the decreases in levels of serum LDL-C after the first half of ST and serum TC and HDL-C ratio during both ST periods. Changes in serum TAG concentrations correlated positively with intake of carbohydrates, and negatively with monounsaturated fat in all subjects. Respectively, changes in serum TC levels were related to protein intake, and changes in serum HDL-C to intake of fat, and inversely to carbohydrate and protein in all subjects. Relationships between serum TC and HDL-C levels and protein intake were only observable in the ST+NC group.CONCLUSIONSThe long-term ST had favorable effects on serum lipids, lipoproteins, insulin concentration, and blood pressure. However, NC further contributed to positive changes in serum lipids and lipoproteins.
PURPOSE (a) To establish pedometer steps/min intensity categories (i.e., light, moderate, hard, very hard) for adults under controlled conditions, and (b) use these cut-points to ascertain the number of steps expected in 30 minutes of moderate intensity activity. METHODS 25 men and 25 women, ages 18-39 years, performed 6-min exercise bouts at 3 treadmill speeds (4.8, 6.4, and 9.7 km/hr). Yamax SW-200 pedometers indicated steps, and steady-state VO2 was recorded. METs were calculated by dividing steady-state VO2 by 3.5 ml x kg(-1) x min(-1). Linear regression was used to quantify the relationships between steps/min and METs across all speeds. Ten participants (5 M, 5 F) were randomly selected from the original 50 and constituted a holdout sample for cross-validation purposes (i.e, comparing actual and predicted METs; paired t-test). RESULTS The regression equation for males was: METs = -7.065 + (0.105 x steps/min) r2 = 0.803. For females it was: METs = -8.805 + (0.110 x steps/min) r2 = 0.830. Cross-validation was confirmed. CONCLUSIONS Pedometer cut-points corresponding to minimal moderate intensity walking were 96 steps/min in men and 107 steps/min in women, or roughly 100 steps/min for both. This translates to approximately 3,000 steps in 30 min of moderate-intensity ambulatory activity for both genders.
The purpose of this study was to evaluate different efficiency indices, i.e., gross (GE: no baseline correction), net (NE: resting metabolism as baseline correction), and work (WE: unloaded exercise as baseline correction), to reveal the effect of endurance training on mechanical efficiency. Nine healthy sedentary women undertook an incremental test and submaximal cycling exercise, at an intensity corresponding to 50% of the pretraining peak oxygen uptake, before and after 6 weeks of endurance training (18 sessions of 45 min). The training effects on efficiency indices were tested by comparisons based on GE, NE, and WE as well as by the differences between the percentage changes of all indices (%GE, %NE, %WE). Endurance training resulted in significantly higher GE (+11.1%; p < 0.001) and NE (+9.1%; p < 0.01). Only minor significant improvement (+2.4%; p < 0.05) was observed with the WE index because the value used for baseline subtraction was significantly reduced by the training sessions, due perhaps to improvement in pedaling skill. As a consequence, %WE was significantly lower than %GE (p < 0.01) and %NE (p < 0.05), while %GE and %NE were not significantly different. We conclude that mechanical efficiency of cycling increases with training in women previously unfamiliar with cycling, and that the WE index is less sensitive to this training effect than GE and NE indices.
The purpose of this study was to determine if changes in oxidative stress biomarkers in blood and skeletal muscles are similar in normal and antioxidant supplemented rats after a downhill run. Sixty-six male Sprague-Dawley rats were pretreated with a normal rat diet or diet + antioxidants (2,000 mg vitamin C + 1,000 IU vitamin E/kg diet) for 2 weeks. Exercised rats ran 90 min on a rodent treadmill at a speed of 16 m/min at -16 degrees grade. Rats were sacrificed either at rest, immediately, 2 hrs, or 48 hrs postexercise. Malondialdehyde (MDA) and protein carbonyl (PC) concentrations and glutathione status in blood, vastus lateralis (white fast-twitch), vastus intermedius (red fast-twitch), and soleus (slow-twitch) muscles were determined. A significant increase from rest in PC occurred in plasma, vastus intermedius and soleus muscle 2 hrs after the downhill run (p < 0.05), with no changes observed at any other times postexercise. Antioxidant supplementation significantly decreased PC concentrations in both vastus intermedius and soleus muscles at all times combined (p < 0.05). MDA and glutathione status in blood and muscles were unaffected by either the downhill run or antioxidant treatment. For PC and MDA, the concentrations were lower in blood as compared to skeletal muscle, with the opposite finding for oxidized glutathione; however, the pattern of response postexercise was similar. These data indicate that (a) PC, but not MDA or oxidized glutathione, is elevated transiently following downhill running in male rats; (b) the elevation in PC postexercise occurs in plasma, vastus intermedius, and soleus muscles; (c) antioxidant therapy can attenuate PC in vastus intermedius, and soleus muscles; and (d) while the concentrations of oxidative stress biomarkers differ between blood and the various skeletal muscles, the pattern of response postexercise is similar.
In 8 trained subjects (T) and 9 untrained subjects (UT), lipid peroxidation (LPO), total antioxidant capacity (TRAP), superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities were measured in the blood before and after three different intensities of exercise on the treadmill, determined from ventilatory threshold and maximal oxygen uptake data, obtained from a maximal aerobic power test. In plasma, LPO decreased from 3589 +/- 193 to 3274 +/- 223 cps x mg Hb(-1) (p < 0.05), and TRAP increased from 304 +/- 45 to 384 +/- 57 micromol x L(-1) trolox (p < 0.05) after high intensity exercise in T. GPx activity increased in the T group as compared to the UT group, after exercise in moderate (25.90 +/- 3.79 to 15.05 +/- 3.23 nM x min(-1) x mg protein(-1)) and high (21.75 +/- 4.91 to 12.1 +/- 2.46 nM x min(-1) x mg protein(-1)) intensities (p < 0.05). Superoxide dismutase activity increased after exercise at low (8.35 +/- 0.85 to 9.23 +/- 1.03 U SOD x mg protein(-1)) and moderate (8.89 +/- 0.98 to 10.44 +/- 0.86 U SOD x mg protein(-1)) intensity in UT (p < 0.05). There were no changes in catalase activity. These findings indicate that exercise in this model did not increase lipid peroxidation, probably because of the alterations in TRAP and enzymatic antioxidants.
A single bout of eccentric exercise confers a long-lasting protective effect against subsequent bouts of the same exercise. This study investigated how the protective effect was lessened when the interval between the initial and secondary exercise bouts was increased from 4 to 12 weeks. Thirty young men performed two bouts of 12 maximal eccentric actions of the elbow flexors of the nondominant arm separated by either 4 (n = 9), 8 (n = 10), or 12 (n = 11) weeks. Maximal isometric strength, flexed and relaxed elbow joint angles, range of motion, upper arm circumference, muscle soreness, plasma creatine kinase (CK), and myoglobin (Mb) were measured before, immediately after, and for 4 days after exercise. Changes in criterion measures were compared between bouts for each group and among groups by two-way repeated-measures ANOVA. There were no significant differences among groups in the changes in all measures following the first bout. Significantly (p < 0.05) smaller responses in all measures were observed after the second bout as compared with first bout for the 4 and 8 weeks, but only in strength, muscle soreness, CK, and Mb for the 12 weeks. It was concluded that some aspects of the protective effect were attenuated after 8 weeks, and the factors responsible for the effect vary among the measures.
One paradox of hormonal regulation during exercise is the maintenance of glucose homeostasis after endurance training despite a lower increase in plasma glucagon. One explanation could be that liver sensitivity to glucagon is increased by endurance training. Glucagon exerts its effect through a 62 KDa glycoprotein receptor member of the G protein-coupled receptor. To determine whether changes with exercise in glucagon sensitivity occurred at the level of the glucagon receptor (GR), binding characteristics of hepatic glucagon receptors were ascertained in rat purified plasma membranes. Saturation kinetics indicated no difference in the dissociation constant or affinity of glucagon receptor, but a significantly higher glucagon receptor binding density in liver in endurance trained compared to untrained animals. Along with endurance training, it appears that fasting also changes GR binding characteristics. In animals fasting 24 hrs, a significant increase in glucagon receptor density was also reported. Although the exact mechanism remains unknown, there is no doubt that the liver can adapt to physiological stress through modulation of GR binding characteristics to enhance the hepatic glucose production responsiveness to glucagon.
The aim of this study was to compare male and female thermal, cardiac, and muscular responses induced by a prolonged run undertaken in a hot environment. Twelve volunteers participated in this study. The first group consisted of 6 men and the second one consisted of 6 women. After determination of their [Formula: see text] and maximal aerobic velocity (MAV), each athlete completed a 40-min run at 65% MAV in a hot and dry environment (temperature 31-33 °C, relative humidity 30%). Immediately before and after the run, each subject performed two different vertical jumps, i.e., a squat jump (SJ) and a counter-movement jump (CMJ) on a force platform. Force, velocity, power, and jump height were measured during each jump. The completion of the run was associated with a significant loss (p < 0.001) of body mass (BM) and significant increases (p < 0.001) in heart rate, tympanic temperature, and lactate concentration ([La]). Muscle power was significantly improved (+9%, p < 0.05) during the SJ only in the women. A significant enhancement of this parameter was also demonstrated during the CMJ in both groups (men: +10%, p < 0.05; women: +8%, p < 0.01). Surprisingly, a comparison of thermal, cardiac, and muscular responses did not reveal any significant differences between the sexes. Moderate dehydration (−2.0 to −2.3% of BM) and a rise in core temperature (above 39.2 °C) induced by the 40-min run led to an improvement of muscular strength in both men and women. However, the results of this study did not reveal any significant between-sex differences in thermal, cardiac, and muscular responses after exercising in the heat. Key words: exercise, dehydration, hyperthermia, tympanic temperature, fatigue, power
The purpose of this study was to determine the relationship between the isocapnic buffer (beta(isocapnic)) and hypocapnic hyperventilation (HHV) phases as well as performance in a short (20-min) and long (90-min) time trial (TT) in trained athletes. In addition, gross (GE, %) and delta (deltaE, %) efficiency were calculated and the relationship between these variables and the average power output (W) in each TT was determined. Thirteen male endurance athletes (Mean +/- SD age 31 +/- 6 yrs; body mass 75.6 +/- 6.3 kg; height 185 +/- 6 cm) completed a continuous incremental test to exhaustion for determination of the beta(isocapnic) and HHV phases. A second submaximal test was used to determine GE and deltaE. The average power output (W) was measured in a 20-min and 90-min cycling TT. The beta(isocapnic) phase (W) was significantly correlated to the average power output (W) in the 20-min TT (r = 0.58; p < 0.05), but not in the 90-min TT (r = 0.28). The HHV phase (W) was not significantly correlated to the average power output in the 20-min or 90-min TT. No significant correlation was found for GE or for deltaE and performance in the TT. The data from this study shows that beta(isocapnic) together with HHV is not likely to be a useful indicator of cycle TT performance of 20- to 90-min duration. Furthermore, GE and deltaE determined from a submaximal incremental stepwise test are not related to cycling TT performance of different duration.
This study tested the hypothesis that in humans mild leg exercise affects haemostasis in normobaric hypoxia and thus avoids the development of a deep venous thrombosis (DVT). Eight young men breathed in a 15.4% oxygen in nitrogen gas mixture for 2 hrs while seated at rest (R) or seated and performing a 3-min mild leg exercise program (Ex) at 15-min intervals to assess the impact of mild leg exercise on haemostatic parameters related to the risk of developing DVT, as has been discussed for hypobaric hypoxic conditions during commercial airline travel. Capillary blood gases were analysed every 30 min. Heart rate was monitored continuously. Haemostatic parameters were analysed from venous blood at the beginning, after 1 and 2 hrs, and after a 30-min resting period in normoxic conditions. Plasminogen-activator-inhibitor-1 diminished in both tests in hypoxia, but not after the resting period. Antithrombin-III decreased in R in the hypoxic period. Platelet count, international normalized ratio, partial thromboplastin time remained unchanged, as did highly sensitive parameters like tissue-plasminogen-activator, α2-antiplasmin, d-dimers, thrombin-antithrombin-III-complexes, and prothrombin-fragments 1 and 2. The haematocrit decreased significantly in R. The mild leg execise prevented the decrease of antithrombin-III and caused an increase in haematocrit after an initial drop in the first hour. The present study revealed that normobaric hypoxia did not have clinically relevant effects on haemostasis in humans. Mild leg exercise carried out under those conditions did not lead, via alterations in haemostasis, to a reduced risk of DVT. Key words: local aerobic exercise, haemostasis, hypoxia, thrombosis
The first evidence that the liver can afferently contribute to regulatory activities comes from studies on regulation of food intake. The hepatic afferent pathway has been shown to be responsive to glucoprivic as well as lipoprivic stimuli. Similarly to regulation of food intake, it has been reported that the liver may afferently contribute to the metabolic regulation of exercise. The best reported evidence of this view is the observation that the decrease in insulin and the increase in glucagon and noradrenaline levels during exercise are diminished in hepatic vagotomized rats (Lavoie et al., 1989). The concept behind these observations is that the liver, through the existence of hepatic glucoreceptors, is responsive to a decrease in glycogen content or to some metabolites of the glycolytic chain related to liver glycogen content. There is also some evidence that lipids in the liver may have some regulatory impact inside and outside the liver. Recent interest in looking at lipid metabolism in liver has been spurred by the observation that the increased flux of lipids through the hepatic portal vein has been associated with increased risks of metabolic and cardiovascular abnormalities. To explore this avenue, a 10% triglyceride emulsion was infused into either the portal or a peripheral vein of rats for 48 hrs while another group of rats was acutely infused for 2 hrs into the portal vein. The results indicate that all of these lipid infusions resulted in an increase in liver lipid infiltration, which may be associated with the development of a state of hepatic and peripheral insulin resistance.