Comparison of low- and high-intensity resistance exercise on lipid peroxidation: role of muscle oxygenation

The purpose of this study was to examine the effect of low- vs. high-intensity resistance exercise on lipid peroxidation. In addition, the role of muscle oxygenation on plasma malondialdehyde (MDA) concentrations was explored. Eleven experienced resistance trained male athletes (age: 20.8 +/- 1.3 years; weight: 96.2 +/- 14.4 kg; height: 182.4 +/- 7.3 cm) performed 4 sets of the squat exercise using either a low-intensity, high-volume (LI; 15 repetitions at 60% 1 repetition maximum [1RM]) or high-intensity, low-volume (HI; 4 repetitions at 90% 1RM load). Venous blood samples were obtained before the exercise (PRE), immediately following the exercise (IP), and 20 (20P) and 40 minutes (40P) postexercise. Continuous wave near-infrared spectroscopy was used to measure muscle deoxygenation in the vastus lateralis during exercise. Deoxygenated Hb/Mb change was used to determine reoxygenation rate during recovery. No difference in MDA concentrations was seen between LI and HI at any time. Significant correlations were observed between plasma MDA concentrations at IP and the half-time recovery (T1/2 recovery) of muscle reoxygenation (r = 0.45) and between T1/2 recovery and the area under the curve for MDA concentrations (r = 0.44). Results suggest that increases in MDA occur independently of exercise intensity, but tissue acidosis may have a larger influence on MDA formation.     

Heat acclimatization and hydration status of American football players during initial summer workouts

This investigation evaluated the new National Collegiate Athletic Association model of heat acclimatization for football players using physiological, psychological, fluid balance, anthropometric, and nutritional variables. Eleven football players (20 +/- 1 year, 1.88 +/- 0.05 m, and 115.36 +/- 18.85 kg) from a Division I football team were observed for the first 8 days of preseason practices. Measurements such as heart rate and gastrointestinal temperature (T(GI)) via telemetric sensor were taken before, 3 times during, and after practice daily. An average 1.39-kg (1.2%) decrease of body mass occurred from prepractice to postpractice (p < 0.01). Consistent with mild body mass losses, urinary indices of hydration status (i.e., color, specific gravity, and osmolality) indicated mild fluid deficits. A significant increase (p < 0.05) from pre- to postpractice was observed in urine color and urine specific gravity, but chronic hypohydration over the 8 days was not noted. The Environmental Symptoms Questionnaire (ESQ) postpractice score was significantly higher (p < 0.05) than the prepractice score was, but averages did not differ across practice days. There was no difference in postpractice T(GI) measurements across days (p < 0.05). Heart rate, T(GI), and ESQ measurements indicated that football players experienced gradual heat acclimatization and enhanced heat tolerance, despite progressive increases of exercise variables, clothing, and environmental stressors.     

Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients.

We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean +/- SE; age: 53 +/- 3 years; years posttransplant: 6 +/- 4) and five age- and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (Vo(2)(p)), heart rate (HR), stroke volume (SV), cardiac output (Q), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve Vo(2)(p), Q, and systemic arterial-venous oxygen difference (a-vO(2diff)) were 23-52% lower (P < 0.05) in HTR. The reduced Q and a-vO(2diff) reserves were associated with lower HR and HHb reserves, respectively. The phase II Vo(2)(p) time delay was greater (HTR: 38 +/- 2 vs. CON: 25 +/- 1 s, P < 0.05), while time constants for phase II Vo(2)(p) (HTR: 54 +/- 8 vs. CON: 31 +/- 3 s), Q (HTR: 66 +/- 8 vs. CON: 28 +/- 4 s), and HHb (HTR: 27 +/- 5 vs. CON: 13 +/- 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 +/- 21 s) vs. CON (21 +/- 2 s, P < 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 +/- 8 s vs. CON 31 +/- 6 s). The lower peak Vo(2)(p) and prolonged Vo(2)(p) kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.     

Adaptation of pulmonary O2 uptake kinetics and muscle deoxygenation at the onset of heavy-intensity exercise in young and older adults.

The purpose was to examine the adaptation of pulmonary O(2) uptake (Vo(2p)) and deoxygenation of the vastus lateralis muscle at the onset of heavy-intensity, constant-load cycling exercise in young (Y; 24 +/- 4 yr; mean +/- SD; n = 5) and older (O; 68 +/- 3 yr; n = 6) adults. Subjects performed repeated transitions on 4 separate days from 20 W to a work rate corresponding to heavy-intensity exercise. Vo(2p) was measured breath by breath. The concentration changes in oxyhemoglobin, deoxyhemoglobin (HHb), and total hemoglobin/myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo(2p) data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb-near-infrared spectroscopy data were filtered and averaged to 5-s bins. A monoexponential model was used to fit Vo(2p) [phase 2, time constant (tau) of Vo(2p)] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The tauVo(2p) was slower (P < 0.001) in O (49 +/- 8 s) than Y (29 +/- 4 s). The HHb TD was similar in O (8 +/- 3 s) and Y (7 +/- 1 s); however, the tau HHb following TD was faster (P < 0.05) in O (8 +/- 2 s) than Y (14 +/- 2 s). The slower Vo(2p) kinetics and faster muscle deoxygenation in O compared with Y during heavy-intensity exercise imply that the kinetics of muscle perfusion are slowed relatively more than those of Vo(2p) in O. This suggests that the slowed Vo(2p) kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y.     

Acute exercise and GLUT4 expression in human skeletal muscle: influence of exercise intensity.

To examine the influence of exercise intensity on the increases in vastus lateralis GLUT4 mRNA and protein after exercise, six untrained men exercised for 60 min at 39 +/- 3% peak oxygen consumption (V(O2 peak)) (Lo) or 27 +/- 2 min at 83 +/- 2% V(O2 peak) (Hi) in counterbalanced order. Preexercise muscle glycogen levels were not different between trials (Lo: 408 +/- 35 mmol/kg dry mass; Hi: 420 +/- 43 mmol/kg dry mass); however, postexercise levels were lower (P < 0.05) in Hi (169 +/- 18 mmol/kg dry mass) compared with Lo (262 +/- 35 mmol/kg dry mass). Thus calculated muscle glycogen utilization was greater (P < 0.05) in Hi (251 +/- 24 mmol/kg) than in Lo (146 +/- 34). Exercise resulted in similar increases in GLUT4 gene expression in both trials. GLUT4 mRNA was increased immediately at the end of exercise (approximately 2-fold; P < 0.05) and remained elevated after 3 h of postexercise recovery. When measured 3 h after exercise, total crude membrane GLUT4 protein levels were 106% higher in Lo (3.3 +/- 0.7 vs. 1.6 +/- 0.3 arbitrary units) and 61% higher in Hi (2.9 +/- 0.5 vs. 1.8 +/- 0.5 arbitrary units) relative to preexercise levels. A main effect for exercise was observed, with no significant differences between trials. In conclusion, exercise at approximately 40 and approximately 80% V(O2 peak), with total work equal, increased GLUT4 mRNA and GLUT4 protein in human skeletal muscle to a similar extent, despite differences in exercise intensity and duration.     

Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.     

The effect of contrast water therapy on symptoms of delayed onset muscle soreness

This study examined the effect of contrast water therapy (CWT) on the physiological and functional symptoms of delayed onset muscle soreness (DOMS) following DOMS-inducing leg press exercise. Thirteen recreational athletes performed 2 experimental trials separated by 6 weeks in a randomized crossover design. On each occasion, subjects performed a DOMS-inducing leg press protocol consisting of 5 x 10 eccentric contractions (180 seconds recovery between sets) at 140% of 1 repetition maximum (1RM). This was followed by a 15-minute recovery period incorporating either CWT or no intervention, passive recovery (PAS). Creatine kinase concentration (CK), perceived pain, thigh volume, isometric squat strength, and weighted jump squat performance were measured prior to the eccentric exercise, immediately post recovery, and 24, 48, and 72 hours post recovery. Isometric force production was not reduced below baseline measures throughout the 72-hour data collection period following CWT ( approximately 4-10%). However, following PAS, isometric force production (mean +/- SD) was 14.8 +/- 11.4% below baseline immediately post recovery (p < 0.05), 20.8 +/- 15.6% 24 hours post recovery (p < 0.05), and 22.5 +/- 12.3% 48 hours post recovery (p < 0.05). Peak power produced during the jump squat was significantly reduced (p < 0.05) following both PAS (20.9 +/- 13.4%) and CWT (12.8 +/- 8.0%), with the mean reduction in power for PAS being marginally (not significantly) greater than for CWT (effect size = 0.76). Thigh volume measured immediately following CWT was significantly less than PAS. No significant differences in the changes in CK were found; in addition, there were no significant (p > 0.01) differences in perceived pain between treatments. Contrast water therapy was associated with a smaller reduction, and faster restoration, of strength and power measured by isometric force and jump squat production following DOMS-inducing leg press exercise when compared to PAS. Therefore, CWT seems to be effective in reducing and improving the recovery of functional deficiencies that result from DOMS, as opposed to passive recovery.     

Muscle oxygenation trends after tapering in trained cyclists

BACKGROUND: This study examined muscle deoxygenation trends before and after a 7-day taper using non-invasive near infrared spectroscopy (NIRS). METHODS: Eleven cyclists performed an incremental cycle ergometer test to determine maximal oxygen consumption (VO2max = 4.68 +/- 0.57 L.min-1) prior to the study, and then completed two or three high intensity (85-90% VO2max) taper protocols after being randomly assigned to a taper group: T30 (n = 5), T50 (n = 5), or T80 (n = 5) [30%, 50%, 80% reduction in training volume, respectively]. Physiological measurements were recorded during a simulated 20 km time trials (20TT) performed on a set of wind-loaded rollers. RESULTS AND DISCUSSION: The results showed that the physiological variables of oxygen consumption (VO2), carbon dioxide (VCO2) and heart rate (HR) were not significantly different after tapering, except for a decreased ventilatory equivalent for oxygen (VE/VO2) in T50 (p 相似文献   

Effects of dynamic exercise on mean blood velocity and muscle interstitial metabolite responses in humans

We examined the effects of dynamic one-legged knee extension exercise on mean blood velocity (MBV) and muscle interstitial metabolite concentrations in healthy young subjects (n = 7). Femoral MBV (Doppler), mean arterial pressure (MAP) and muscle interstitial metabolite (adenosine, lactate, phosphate, K(+), pH, and H(+); by microdialysis) concentrations were measured during 5 min of exercise at 30 and 60% of maximal work capacity (W(max)). MAP increased (P < 0.05) to a similar extent during the two exercise bouts, whereas the increase in MBV was greater (P < 0.05) during exercise at 60% (77.00 +/- 6.77 cm/s) compared with 30% W(max) (43.71 +/- 3.71 cm/s). The increase in interstitial adenosine from rest to exercise was greater (P < 0.05) during the 60% (0.80 +/- 0.10 microM) compared with the 30% W(max) bout (0.57 +/- 0.10 microM). During exercise at 60% W(max), interstitial K(+) rose at a greater rate than during exercise at 30% W(max) (P < 0.05). However, pH increased (H(+) decreased) at similar rates for the two exercise intensities. During exercise, interstitial lactate and phosphate increased (P < 0.05) with no difference observed between the two intensities. After 5 min of recovery, MBV decreased to baseline levels after exercise at 30% W(max) (4.12 +/- 1.10 cm/s), whereas MBV remained above baseline levels after exercise at 60% W(max) (Delta19.46 +/- 2.61 cm/s; P < 0.05). MAP and interstitial adenosine, K(+), pH, and H(+) returned toward baseline levels. However, interstitial lactate and phosphate continued to increase during the recovery period. Thus an increase in exercise intensity resulted in concomitant changes in MBV and muscle interstitial adenosine and K(+), whereas similar changes were not observed for MAP or muscle interstitial pH, lactate, or phosphate. These data suggest that K(+) and/or adenosine may play an active role in the regulation of skeletal muscle blood flow during exercise.     

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise.

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (T(core)), mean skin temperature (T(sk)), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure (n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, T(core), and T(sk). Baroreceptor loading and thermal status were similar during trials because MAP (90 +/- 4, 88 +/- 4 mmHg), thoracic impedance (29 +/- 1, 28 +/- 2 Omega), central venous pressure (5 +/- 1, 4 +/- 1 mmHg), T(core) (37.5 +/- 0.1, 37.5 +/- 0.1 degrees C), and T(sk) (34.1 +/- 0.3, 34.2 +/- 0.2 degrees C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 +/- 6% of maximum) and inactive (28 +/- 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 +/- 0.16 mg.cm(-2).min(-1)) compared with inactive (0.34 +/- 0.19 mg.cm(-2).min(-1); P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.     

Oxidative metabolism and anaerobic glycolysis during repeated exercise

The purpose of the present study was to examine aerobic and muscle anaerobic energy production during supramaximal repeated exercise. Eight subjects performed three 2-min bouts of cycling (EX1-EX3) at an intensity corresponding to about 125 % of VO2 max separated by 15 min of rest. Ventilatory variables were measured breath by breath during the exercise and a muscle biopsy was taken before and after each exercise bout. Blood samples were collected before and after each cycling period and during the recovery periods. Total work in the first 2 min bout of cycling, EX1, [46.3 +/- 2.1 KJ] was greater than in the second, EX2, (p < 0.01) and in the third, EX3, (p < 0.05). The ATP utilization [4.0 +/- 1.4 mmol x (kg dry weight)(-1), EX1] during the three exercise bouts was the same. The decrement in muscle phosphocreatine (PCr) [46.8 +/- 8.5 mmol x (kg dry weight)(-1), EX1] was also similar for the three exercise bouts. Muscle lactate accumulation was greater (p < 0.05) during EX1 compared to EX2 and EX3. The total oxygen consumption was the same for the three exercise bouts, but when it is corrected for the total work performed, oxygen uptake during EX2 (153 +/- 9 ml x KJ(-1)) and EX3 (150 +/- 9 ml x KJ(-1)) was higher (p < 0.01 and p < 0.05, respectively) than during EX1 (139 +/- 8 ml x KJ(-1)). The present data suggest that oxidative metabolism does not compensate for the reduction of anaerobic glycolysis during repeated fatiguing exercise.     

Effect of aerobic capacity on the T(2) increase in exercised skeletal muscle.

The increase in nuclear magnetic resonance transverse relaxation time (T(2)) of muscle water measured by magnetic resonance imaging after exercise has been correlated with work rate in human subjects. This study compared the T(2) increase in thigh muscles of trained (cycling VO(2 max) = 54.4 +/- 2.7 ml O(2). kg(-1). min(-1), mean +/- SE, n = 8, 4 female) vs. sedentary (31.7 +/- 0.9 ml O(2). kg(-1). min(-1), n = 8, 4 female) subjects after cycling exercise for 6 min at 50 and 90% of the subjects' individually determined VO(2 max). There was no significant difference between groups in the T(2) increase measured in quadriceps muscles within 3 min after the exercises, despite the fact that the absolute work rates were 60% higher in the trained group (253 +/- 15 vs. 159 +/- 21 W for the 90% exercise). In both groups, the increase in T(2) of vastus muscles was twofold greater after the 90% exercise than after the 50% exercise. The recovery of T(2) after the 90% exercise was significantly faster in vastus muscles of the trained compared with the sedentary group (mean recovery half-time 11.9 +/- 1.2 vs. 23.3 +/- 3.7 min). The results show that the increase in muscle T(2) varies with work rate relative to muscle maximum aerobic power, not with absolute work rate.     

Discrepancy between cardiorespiratory system and skeletal muscle in elite cyclists after hypoxic training

BACKGROUND: The purpose of this study was to determine the effects of hypoxic training on the cardiorespiratory system and skeletal muscle among well-trained endurance athletes in a randomized cross-over design. METHODS: Eight junior national level competitive cyclists were separated into two groups; Group A trained under normoxic condition (21% O2) for 2 hours/day, 3 days/week for 3 weeks while Group B used the same training protocol under hypoxic condition (15% O2). After 3 weeks of each initial training condition, five weeks of self-training under usual field conditions intervened before the training condition was switched from NT to HT in Group A, from HT to NT in Group B. The subjects were tested at sea level before and after each training period. O2 uptake (O2), blood samples, and muscle deoxygenation were measured during bicycle exercise test. RESULTS AND DISCUSSION: No changes in maximal workload, arterial O2 content, O2 at lactate threshold and O2max were observed before or after each training period. In contrast, deoxygenation change during submaximal exercise in the vastus lateralis was significantly higher at HT than NT (p < 0.01). In addition, half time of oxygenation recovery was significantly faster after HT (13.2 PlusMinus; 2.6 sec) than NT (18.8 PlusMinus; 2.7 sec) (p < 0.001). CONCLUSIONS: Three weeks of HT may not give an additional performance benefit at sea level for elite competitive cyclists, even though HT may induce some physiological adaptations on muscle tissue level.     

Relationship between pulmonary O2 uptake kinetics and muscle deoxygenation during moderate-intensity exercise.

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (Vo -->Vo2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 +/- 3 yr; mean +/- SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath Vo2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 Vo2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for Vo2p (30 +/- 8 s) was slower (P < 0.01) than that for HHb (10 +/- 3 s). The TDHHb before an increase in HHb was 13 +/- 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 Vo2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.     

Electromyographic data do not support a progressive recruitment of muscle fibers during exercise exhibiting a VO2 slow component

The origin of the slow component (SC) of oxygen uptake kinetics, presenting during exercise above the ventilatory threshold (VT), remains unclear. Possible physiologic mechanisms include a progressive recruitment of type II muscle fibers. The purpose of this study was to examine alterations in muscle activity through electromyography (EMG) and mean power frequency (MPF) analysis during heavy cycling exercise. Eight trained cyclists (mean +/- S.E.; age = 30 +/- 3 years, height = 1771 +/- 4 cm, weight = 73.8 +/- 6.5 kg, VO2max = 4.33 +/- 0.28 l min(-1)) completed transitions from 20W to a workload equaling 50% of the difference between V(T) and VO2max. VO2 was monitored using a breath-by-breath measurement system, and EMG data were gathered from surface electrodes placed on the gastrocnemius lateralis and vastus lateralis oblique. Breath-by-breath data were time aligned, averaged, interpolated to 1-s intervals, and modeled with non-linear regression. Mean power frequency (MPF) and RMS EMG values were calculated for each minute during the exercise bout. Additionally, MPF was determined using both isolated EMG bursts and complete pedal revolutions. All subjects exhibited a VO2 SC (mean amplitude = 0.98 +/- 0.16 l min(-1)), yet no significant differences were observed during the exercise bout in MPF or RMS EMG data (p > 0.05) using either analysis technique. While it is possible that the sensitivity of EMG may be insufficient to identify changes in muscle activity theorized to affect the VO2 SC, the data indicated no relationship between MPF/EMG and the SC during heavy cycling.     

Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise.     

Muscle metabolic responses during 16 hours of intermittent heavy exercise

The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions one (R1), two (R2), nine (R9), and sixteen (R16) in 13 untrained volunteers (peak aerobic power = 44.3 +/- 0.66 mL.kg-1.min-1, mean +/- SE). Metabolite content (mmol.(kg dry mass)-1) in homogenates at R1 indicated decreases (p < 0.05) in ATP (21.9 +/- 0.62 vs. 17.7 +/- 0.68) and phosphocreatine (80.3 +/- 2.0 vs. 8.56 +/- 1.5) and increases (p < 0.05) in inosine monophosphate (IMP, 0.077 +/- 0.12 vs. 3.63 +/- 0.85) and lactate (3.80 +/- 0.57 vs. 84.6 +/- 10.3). The content (micromol.(kg dry mass)-1) of calculated free ADP ([ADPf], 86.4 +/- 5.5 vs. 1014 +/- 237) and free AMP ([AMPf], 0.32 +/- 0.03 vs. 78.4 +/- 31) also increased (p < 0.05). No differences were observed between R1 and R2. By R9 and continuing to R16, pronounced reductions (p < 0.05) at A were observed in IMP (72.2%), [ADPf] (58.7%), [AMPf] (85.5%), and lactate (41.3%). The 16-hour protocol resulted in an 89.7% depletion (p < 0.05) of muscle glycogen. Repetition-dependent increases were also observed in oxygen consumption during exercise. It is concluded that repetitive heavy exercise results in less of a disturbance in phosphorylation potential, possibly as a result of increased mitochondrial respiration during the rest-to-work non-steady-state transition.     

Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans.

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.     

Allantoin formation and urate and glutathione exchange in human muscle during submaximal exercise.

Seven males performed two exhaustive cycling bouts (EX1 and EX2) at a work-rate of 90% of maximal oxygen uptake, separated by 60 min. During EX1 there was a significant accumulation of urate (from 0.16 +/- 0.02 to 0.27 +/- 0.03 micromol/kg d.w.) and allantoin (from 0.39 +/- 0.05 to 0.69 +/- 0.14 micromol/kg d.w.) in the muscle. An uptake of urate was observed in early recovery from EX1 (0-9 min: 486 +/- 136 micromol; p <.05). There was no exchange of total glutathione or cysteine over the muscle either during or after exercise, and muscle and plasma total glutathione remained unaltered (p <.05). The glycogen levels were lowered by 40% at the onset of EX2, yet the level of oxidative stress in EX1 and EX2 was similar as evidenced by a similar increase in muscle allantoin in both exercise bouts. The data suggest that urate is utilized as antioxidant in human skeletal muscle and that reactive oxygen species are formed in muscle during intense submaximal exercise. No net exchange of glutathione appears to occur over the muscle either at rest, during exercise or in recovery. Moreover, when an exhaustive exercise bout is repeated with lowered glycogen levels, the level of oxidative stress is not different than that of the first bout.     

Aerobic run training improves brachial artery flow-mediated dilation

The purpose of this study was to assess the relationship between aerobic exercise training and brachial artery flow-mediated dilation (FMD) in healthy subjects. Healthy controls (HC) and aerobically-trained (T) subjects were studied with high-resolution vascular ultrasound at baseline, and during a 5-minute period of hyperemia following forearm cuff occlusion. Training was defined by self-reported participation in recreational or competitive run training. Forearm cuff occlusion was held at 200 mm Hg for 5 minutes. At baseline, both brachial artery flow and diameter were greater in T than in HC (p < 0.05). Resting heart rate was lower in T than in HC (p < 0.05). Peak hyperemic flow (15 seconds postocclusion) was significantly greater in T than in HC (HC; 539 +/- 75 ml x min(-1) vs. T; 832 +/- 103 ml x min(-1), p < 0.05) and correlated well with V(.-)O2peak (r = 0.67, p = 0.008). Flow-mediated dilation was significantly greater in T vs. HC throughout the 5-minute postocclusion phase (p < 0.05). Maximal brachial artery dilation was greater in T than in HC (HC; 3 +/- 1% of baseline vs. T; 8 +/- 3% of baseline; p < 0.05) and moderately correlated with V(.-)O2peak (r = 0.55, p < 0.05). These data suggest that the greater FMD observed in trained subjects may be due, in part, to an augmentation of peak hyperemic flow.