Muscle fibre conduction velocity and cardiorespiratory response during incremental cycling exercise in young and older individuals with different training status

We investigated the effect of ageing and training on muscle fibre conduction velocity (MFCV) and cardiorespiratory response during incremental cycling exercise. Eight young (YT; 24 ± 5 yrs) and eight older (OT; 64 ± 3 yrs) cyclists, together with eight young (YU; 27 ± 4 yrs) and eight older (OU; 63 ± 2 yrs) untrained individuals underwent to an incremental maximal test on a cycle ergometer. Ventilatory threshold (VT), respiratory compensation point (RCP) and maximal oxygen uptake (VO₂max) were identified and MFCV recorded from the vastus lateralis muscle using surface electromyography with linear arrays electrodes.In YT MFCV increased with the exercise intensity, reaching a peak of 4.99 ± 1.02 [m/s] at VT. Thereafter, and up to VO₂max, MFCV declined. In YU MFCV showed a similar trend although the peak [4.55 ± 0.53 m/s] was observed, at 75% of VO₂max an intensity higher than VT (66% of VO₂max). In both YT and YU MFCV did not decline until RPC, which occurred at 78% VO₂max in YU and at 92% VO₂max (P < 0.01) in YT. Differently from young individuals, MFCV in older subjects did not increase with exercise intensity. Moreover, maximal MFCV in OU was significantly lower [3.53 ± 0.40 m/s;] than that of YT (P < 0.005) and YU (P < 0.05).The present study shows that, especially in young individuals, MFCV reflects cardiorespiratory response during incremental dynamic cyclic exercise and hence can be used to investigate motor unit recruitment strategies.     

Effect of aging on ventilatory response to exercise and CO2

Studies were performed to determine the effects of aging on the ventilatory responsiveness to two known respiratory stimulants, inhaled CO2 and exercise. Although explanation of the physiological mechanisms underlying development of exercise hyperpnea remains elusive, there is much circumstantial evidence that during exercise, however mediated, ventilation is coupled to CO2 production. Thus matched groups of young and elderly subjects were studied to determine the relationship between increasing ventilation and increasing CO2 production (VCO2) during steady-state exercise and the change in their minute ventilation in response to progressive hypercapnia during CO2 rebreathing. We found that the slope of the ventilatory response to hypercapnia was depressed in elderly subjects when compared with the younger control group (delta VE/delta PCO2 = 1.64 +/- 0.21 vs. 2.44 +/- 0.40 l X min-1 X mmHg-1, means +/- SE, respectively). In contrast, the slope of the relationship between ventilation and CO2 production during exercise in the elderly was greater than that of younger subjects (delta VE/delta VCO2 = 29.7 +/- 1.19 vs. 25.3 +/- 1.54, means +/- SE, respectively), as was minute ventilation at a single work load (50 W) (32.4 +/- 2.3 vs. 25.7 +/- 1.54 l/min, means +/- SE, respectively). This increased ventilation during exercise in the elderly was not produced by arterial O2 desaturation, and increased anaerobiasis did not play a role. Instead, the increased ventilation during exercise seems to compensate for increased inefficiency of gas exchange such that exercise remains essentially isocapnic. In conclusion, in the elderly the ventilatory response to hypercapnia is less than in young subjects, whereas the ventilatory response to exercise is greater.     

Influence of cold exposure on blood lactate response during incremental exercise

This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24 degrees C (MT) or at -2 degrees C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption (VO2) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1st, 4th, 7th, and the 10th min following exercise for the determination of blood lactate (LA) concentration. The VO2 was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute VO2, and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase off FFA was found only during CT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adaptive changes in hypercapnic ventilatory response during training and detraining

To confirm the effects of physical training and detraining on CO2 chemosensitivity, we followed hypercapnic ventilatory response at rest in the same five subjects during pre-, post- and detraining for 6 years. They joined our university badminton teams as freshmen and participated regularly in their team's training for about 3 h a day, three times a week, for 4 years. After that they retired from their teams and stopped training in order to study in the graduate school for 2 years. Maximum pulmonary ventilation (VEmax) and maximal oxygen uptake (VO2max) for each subject were determined during maximal treadmill exercise. The slope (S) of ventilatory response to carbon dioxide at rest was measured by Read's rebreathing method. Mean values of VEmax increased statistically during training and decreased statistically during detraining. A similar tendency was observed in VO2max. The average value of S before training was 1.91 l.min-1.mmHg-1, (+/- ) SD 0.52 and it decreased gradually with increasing training periods; the difference between the S values before (1980) and after training (1982, 1983 and 1984) were all significant. Furthermore, the mean values of S increased significantly during detraining as compared with those obtained at the end of training (April 1984). We concluded that in normal subjects, long-term physical training increases aerobic work capacity and decreases CO2 ventilatory responsiveness, and that the ventilatory adaptations with training observed here are reversible through detraining.     

Effect of different cycling frequencies during incremental exercise on the venous plasma potassium concentration in humans

The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min(-1) on the [K+]v in humans. Twenty-one healthy young men aged 22.5+/-2.2 years, body mass 72.7+/-6.4 kg, VO2 max 3.720+/-0.426 l. min(-1), performed an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800 S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min(-1) (test A) and a few days later at a frequency of 120 rev. min(-1) (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]p were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24+/-0.36 mmol.l(-1) in test A, and 4.37+/-0.45 mmol.l(-1) in test B. However, the [K+]p during cycling at 120 rev. min(-1) was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min(-1). The maximal power output reached 293+/-31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223+/-40 W. The VO2max values in both tests reached 3.720+/-0.426 l. min(-1) vs 3.777+/-0.514 l. min(-1). These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min(-1). The [K+]v measured at the VO2max level in tests A and B amounted to 6.00+/-0.47 mmol.l-1 vs 6.04+/-0.41 mmol.l-1, respectively. This difference was not significant. It may thus be concluded that: a) generation of the same external mechanical power output during cycling at a pedalling rate of 120 rev.min(-1) causes significantly higher [K+]v changes than when cycling at 60 rev.min(-1), b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. 475: 359-368, 1994), c) there is a tendency towards upward up shift in the [K+]v and % VO2max relation during cycling at 120 rev.min(-1) when compared to cycling at 60 rev.min(-1).     

Effects of acute hypoxia on cerebral and muscle oxygenation during incremental exercise.

To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% Fi(O2)) and acute hypoxic (Hypox: 12% Fi(O2)) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (microM) changes of oxy- and deoxyhemoglobin (Delta[O2Hb], Delta[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Delta[THb] = Delta[O2Hb] + Delta[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (alpha = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Power(peak); increased (inc) Delta[O2Hb], inc. Delta[HHb], inc. Delta[THb]}, but fell from 75 to 100% Power(peak) {decreased (dec) Delta[O2Hb], inc. Delta[HHb], no change Delta[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Delta[O2Hb], inc. Delta[HHb]), whereas Delta[THb] again rose up to 75% Power(peak) and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Delta[O2Hb], inc. Delta [HHb], inc. Delta[THb]), although Delta[O2Hb] was unchanged between 75 and 100% Power peak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.     

Ventilatory response during incremental exercise tests in weight lifters and endurance cyclists

The effect of a progressively increasing work rate (15 W X min-1) up to exhaustion on the time course of O2 uptake (VO2), ventilation (VE) and heart rate (HR) has been studied in weight lifters (WL) in comparison to endurance cyclists (Cycl) and sedentary controls (Sed). VO2 and VE were measured as average value of 30-s intervals by a semiautomatic open circuit method. VO2max was 2.55 +/- 0.33; 4.29 +/- 0.53 and 2.86 +/- 0.19 l X min-1 in WL, Cycl and Sed respectively. With time and work rate, while VO2 and HR increased linearly, VE changed its slope at two levels. The 1st VE change occurred at a work load corresponding to a mean (+/- SD) VO2 of 1.50 +/- 0.26; 1.93 +/- 0.34; and 1.23 +/- 0.14 l X min-1 in WL, Cycl, and Sed respectively. VO2 values corresponding to the second VE change of slope were 2.18 +/- 0.32 in WL; 3.48 +/- 0.53 in Cycl and 2.17 +/- 0.28 l X min-1 in Sed. The first change of slope might be the consequence of the different readjustment of VO2 on-response and hence of early lactate in the different subjects. The second change seems to be comparable to the conventional anaerobic threshold and is achieved in all subjects when VE vs time slope is 7-10 l X min-1/min of exercise.     

Relationship between ventilatory response and body temperature during prolonged submaximal exercise.

We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (Ve) and core temperature during prolonged exercise in the heat. Thirteen subjects exercised for 60 min on a cycle ergometer at 50% of peak oxygen uptake while wearing a suit perfused with water at 10 degrees C (T10), 35 degrees C (T35), or 45 degrees C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), Ve, tidal volume, respiratory frequency (f), respiratory gases, blood pressure (BP), and blood lactate were all measured. We found that oxygen uptake, carbon dioxide output, BP, and blood lactate did not differ among the sessions. Tes, HR, Ve, and f remained nearly constant from minute 10 onward in the T10 session, but all of these parameters progressively increased in the T35 and T45 sessions, and significantly higher levels were seen in the T45 than the T35 session. For all but two subjects in the T35 and T45 sessions, plotting Ve as a function of Tes revealed no threshold for hyperventilation; instead, increases in Ve were linearly related to Tes, and there were no significant differences in the slopes or intercepts between the T35 and T45 sessions. Thus, during prolonged submaximal exercise in the heat, Ve increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between Ve and Tes are apparently small.     

Regulation of nitric oxide production in limb and ventilatory muscles during chronic exercise training

In this study, we evaluated the differential influence of chronic treadmill training (30 m/min, 15% incline, 1 h/day, 5 days/wk) on nitric oxide (NO) production and NO synthase (NOS) isoform expression as well as 3-nitrotyrosine formation (footprint of peroxynitrite) both in limb (gastrocnemius) and ventilatory (diaphragm) muscles. A group of exercise-trained rats and a control group (no training) were examined after a 4-wk experimental period. Exercise training elicited an approximate fourfold rise in gastrocnemius NOS activity and augmented protein expression of the endothelial (eNOS) and neuronal (nNOS) isoforms of NOS to approximately 480% and 240%, respectively. Qualitatively similar but quantitatively smaller elevations in NOS activity and eNOS and nNOS expression were observed in the diaphragm. No detectable inducible NOS (iNOS) protein expression was found in any of the muscle samples. Training increased the intensity of 3-nitrotyrosine only in the gastrocnemius muscle. We conclude that whole body exercise training enhances both limb and ventilatory muscle NO production and that constitutive and not iNOS isoforms are responsible for increased protein tyrosine nitration in trained limb muscles.     

Effects of fasting and training on pyruvate dehydrogenase activation during exercise

1. The effect of exercise (2 hr treadmill running at 28 m/min) on PDHa (the activity of the active form of pyruvate dehydrogenase) in untrained rats, trained rats (2 hr/d at 25 m/min for 4 wk), and in 24 hr fasted rats was determined. 2. Exercise increased PDHa activity approximately 2 fold in fed-untrained rats. 3. Fasting decreased PDHa activity in sedentary rats to approximately half the activity in fed rats. 4. The increase in PDHa activity during exercise was less in fasted than fed rats. 5. Training did not change the total activity of PDH (phosphorylated plus nonphosphorylated forms) but the percent of PDH in the active form was increased in muscle of trained-rested rats. 6. PDHa activity was unchanged by acute exercise (2.5 hr at 40 m/min) in the trained rats.     

Skeletal muscle oxygenation during incremental exercise

The purpose of this study was to investigate the relationship between muscle oxygenation level at exhaustion and maximal oxygen uptake (VO2max) in an incremental cycling exercise. Nine male subjects took part in an incremental exhaustive cycling exercise, and then cuff occlusion was performed. Changes in oxy-(deltaHbO2) and deoxy-(deltaHb) hemoglobin concentrations in the vastus lateralis muscle were measured with a near infrared spectroscopy (NIRS). Muscle oxygenation during incremental exercise was expressed as a percentage (%Moxy) of the maximal range observed during an arterial occlusion as the lower reference point. A systematic decrease was observed in %Moxy with increasing intensity. A significant relationship was observed between %Moxy at exhaustion and VO2max (p < 0.01). We concluded that the one of the limiting factor of VO2max is the muscle oxygen diffusion capacity, and %Moxy during exercise could be one of the indexes of muscle oxygen diffusion capacity.     

Effects of body temperature during exercise training on myocardial adaptations

This study determined the role of body temperature during chronic exercise on myocardial stress proteins and antioxidant enzymes as well as functional recovery after an ischemic insult. Male Sprague-Dawley rats were exercised for 3, 6, or 9 wk in a 23 degrees C room (3WK, 6WK, and 9WK, respectively) or in a 4-8 degrees C environment with wetted fur (3WKC, 6WKC, and 9WKC, respectively). The colder room prevented elevations in core temperature. During weeks 3-9 the animals ran 5 days/wk up a 6% grade at 20 m/min for 60 min. Myocardial heat shock protein 70 (HSP 70) increased 12.3-fold (P < 0.05) in 9WK versus sedentary (SED) rats but was unchanged in the cold-room runners. Compared with SED rats, alphaB-crystallin was 90% higher in 9WKC animals, HSP 90 was 50% higher in 3WKC and 6WKC animals, and catalase was 23% higher in 3WK animals (P < 0.05 for all). Cytosolic superoxide dismutase increased and mitochondrial SOD decreased (P < 0.05) in 3WK and 6WK rats compared with 3WKC and 6WKC rats. Antioxidant enzymes returned to SED values in all runners by 9 wk. No differences were observed among any of the groups for glucose-regulated protein 75, heme oxygenase-1, or glutathione peroxidase. Mechanical recovery of isolated working hearts after 22.5 min of global ischemia was enhanced in 9WK (P < 0.05) but not in 9WKC rats. We conclude that exercise training results in dynamic changes in cardioprotective proteins over time which are influenced by core temperature. In addition, cardioprotection resulting from chronic exercise appears to be due to increased HSP 70.     

Effect of menstrual cycle phase on the ventilatory response to rising body temperature during exercise

To examine the effect of menstrual cycle on the ventilatory sensitivity to rising body temperature, ten healthy women exercised for ~60 min on a cycle ergometer at 50% of peak oxygen uptake during the follicular and luteal phases of their cycle. Esophageal temperature, mean skin temperature, mean body temperature, minute ventilation, and tidal volume were all significantly higher at baseline and during exercise in the luteal phase than the follicular phase. On the other hand, end-tidal partial pressure of carbon dioxide was significantly lower during exercise in the luteal phase than the follicular phase. Plotting ventilatory parameters against esophageal temperature revealed there to be no significant menstrual cycle-related differences in the slopes or intercepts of the regression lines, although minute ventilation and tidal volume did significantly differ during exercise with mild hyperthermia. To evaluate the cutaneous vasodilatory response, relative laser-Doppler flowmetry values were plotted against mean body temperature, which revealed that the mean body temperature threshold for cutaneous vasodilation was significantly higher in the luteal phase than the follicular phase, but there were no significant differences in the sensitivity or peak values. These results suggest that the menstrual cycle phase influences the cutaneous vasodilatory response during exercise and the ventilatory response at rest and during exercise with mild hyperthermia, but it does not influence ventilatory responses during exercise with moderate hyperthermia.     

Influence of training and maturity status on the cardiopulmonary responses to ramp incremental cycle and upper body exercise in girls

It has been suggested that the potential for training to alter the physiological responses to exercise in children is related to a "maturational threshold". To address this, we investigated the interaction of swim-training status and maturity on cardiovascular and metabolic responses to lower and upper body exercise. Twenty-one prepubertal [Pre: 11 trained (T), 10 untrained (UT)], 30 pubertal (Pub: 14 T, 16 UT), and 18 postpubertal (Post: 8 T, 10 UT) girls completed ramp incremental exercise on a cycle and an upper body ergometer. In addition to pulmonary gas exchange measurements, stroke volume and cardiac output were estimated by thoracic bioelectrical impedance, and muscle oxygenation status was assessed using near-infrared spectroscopy. All T girls had a higher peak O(2) uptake during cycle (Pre: T 49 ± 5 vs. UT 40 ± 4; Pub: T 46 ± 5 vs. UT 36 ± 4; Post: T 48 ± 5 vs. UT 39 ± 8 ml·kg(-1)·min(-1); all P < 0.05) and upper body exercise (Pre: T 37 ± 6 vs. UT 32 ± 5; Pub: T 36 ± 5 vs. UT 28 ± 5; Post: T 39 ± 3 vs. UT 28 ± 7 ml·kg(-1)·min(-1); all P < 0.05). T girls also had a higher peak cardiac output during both modalities, and this reached significance in Pub (cycle: T 21 ± 3 vs. UT 18 ± 3; upper body: T 20 ± 4 vs. UT 15 ± 4 l/min; all P < 0.05) and Post girls (cycle: T 21 ± 4 vs. UT 17 ± 2; upper body: T 22 ± 3 vs. UT 18 ± 2 l/min; all P < 0.05). None of the measured pulmonary, cardiovascular, or metabolic parameters interacted with maturity, and the magnitude of the difference between T and UT girls was similar, irrespective of maturity stage. These results challenge the notion that differences in training status in young people are only evident once a maturational threshold has been exceeded.     

Effect of glycogen depletion on the ventilatory response to exercise

Five male subjects performed two graded exercise studies, one during control conditions and the other after reduction of muscle glycogen content by repeated maximum exercise and a high fat-protein diet. Reduction in preexercise muscle glycogen from 59.1 to 17.1 mumol X g-1 (n = 3) was associated with a 14% reduction in maximum power output but no change in maximum O2 intake; at any given power output O2 intake, heart rate, and ventilation (VE) were significantly higher, CO2 output (VCO2) was similar, and the respiratory exchange ratio was lower during glycogen depletion compared with control. The higher VE during glycogen depletion was associated with a higher VE/VCO2 ratio, lower end-tidal and mixed venous CO2 partial pressures, and higher blood pH than in the control studies. Changes in exercise VE accompanying glycogen depletion were not explained by changes in CO2 flux to the lungs suggesting that other factors served to modulate VE in these experimental conditions.     

Effects of body position on the ventilatory response following an impulse exercise in humans.

The aim of this study was to identify some of the mechanisms that could be involved in blunted ventilatory response (VE) to exercise in the supine (S) position. The contribution of the recruitment of different muscle groups, the activity of the cardiac mechanoreceptors, the level of arterial baroreceptor stimulation, and the hemodynamic effects of gravity on the exercising muscles was analyzed during upright (U) and S exercise. Delayed rise in VE and pulmonary gas exchange following an impulselike change in work rate (supramaximal leg cycling at 240 W for 12 s) was measured in seven healthy subjects and six heart transplant patients both in U and S positions. This approach allows study of the relationship between the rise in VE and O2 uptake (VO2) without the confounding effects of contractions of different muscle groups. These responses were compared with those triggered by an impulselike change in work rate produced by the arms, which were positioned at the same level as the heart in S and U positions to separate effects of gravity on postexercising muscles from those on the rest of the body. Despite superimposable VO2 and CO2 output responses, the delayed VE response after leg exercise was significantly lower in the S posture than in the U position for each control subject and cardiac-transplant patient (-2.58 +/- 0.44 l and -3.52 +/- 1.11 l/min, respectively). In contrast, when impulse exercise was performed with the arms, reduction of ventilatory response in the S posture reached, at best, one-third of the deficit after leg exercise and was always associated with a reduction in VO2 of a similar magnitude. We concluded that reduction in VE response to exercise in the S position is independent of the types (groups) of muscles recruited and is not critically dependent on afferent signals originating from the heart but seems to rely on some of the effects of gravity on postexercising muscles.     

Naloxone and the ventilatory response to exercise in man

Endogenous opiate peptides are known to exert a depressant action on ventilation (VE), and their plasma levels have been shown to be elevated during a variety of exercise protocols. We investigated whether they might modulate the control of the hyperpnea of short-term constant-load (CLE) and incremental (IE) cycle-ergometer exercise. Four healthy subjects performed CLE tests at ca. 80% of the anaerobic threshold (theta an) for 5 min following a period of unloaded pedaling, and IE tests (10 or 20 W min-1) to the limit of tolerance. Normal saline (3 ml) or the opiate antagonist naloxone (1.2 mg in 3 ml) were administered intravenously prior to each test. Naloxone elicited no discernible effect on VE, alveolar gas tensions, or heart rate throughout the entire range of work rates; neither were theta an nor the maximum work rate affected. It is concluded that, for short-term exercise ranging in intensity from moderate to severe, the role played by endogenous opiate peptides in the control of the exercise hyperpnea appears to be negligible in man.     

Effects of aging and exercise training on spinotrapezius muscle microvascular PO2 dynamics and vasomotor control

With advancing age, there is a reduction in exercise tolerance, resulting, in part, from a perturbed ability to match O(2) delivery to uptake within skeletal muscle. In the spinotrapezius muscle (which is not recruited during incline treadmill running) of aged rats, we tested the hypotheses that exercise training will 1) improve the matching of O(2) delivery to O(2) uptake, evidenced through improved microvascular Po(2) (Pm(O(2))), at rest and throughout the contractions transient; and 2) enhance endothelium-dependent vasodilation in first-order arterioles. Young (Y, ～6 mo) and aged (O, >24 mo) Fischer 344 rats were assigned to control sedentary (YSED; n = 16, and OSED; n = 15) or exercise-trained (YET; n = 14, and OET; n = 13) groups. Spinotrapezius blood flow (via radiolabeled microspheres) was measured at rest and during exercise. Phosphorescence quenching was used to quantify Pm(O(2)) in vivo at rest and across the rest-to-twitch contraction (1 Hz, 5 min) transition in the spinotrapezius muscle. In a follow-up study, vasomotor responses to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) stimuli were investigated in vitro. Blood flow to the spinotrapezius did not increase above resting values during exercise in either young or aged groups. Exercise training increased the precontraction baseline Pm(O(2)) (OET 37.5 ± 3.9 vs. OSED 24.7 ± 3.6 Torr, P < 0.05); the end-contracting Pm(O(2)) and the time-delay before Pm(O(2)) fell in the aged group but did not affect these values in the young. Exercise training improved maximal vasodilation in aged rats to acetylcholine (OET 62 ± 16 vs. OSED 27 ± 16%) and to sodium nitroprusside in both young and aged rats. Endurance training of aged rats enhances the Pm(O(2)) in a nonrecruited skeletal muscle and is associated with improved vascular smooth muscle function. These data support the notion that improvements in vascular function with exercise training are not isolated to the recruited muscle.     

Effects of body mass index on maximal work production capacity and aerobic fitness during incremental exercise

The aim of this study was to investigate the relationship between cardiopulmonary fitness as indicated by maximal work rate (Wmax) production and aerobic capacities (WAT), body mass index (BMI) and heart rate reserve. A total of 60 sedentary subjects (30 males, 30 females, aged 18-25 years) were enrolled in the study. Each subject performed an incremental exercise test (15 W/min) to the limit of tolerance on an electromagnetically-braked cycle ergometer. There was a negative correlation between increased BMI to Wmax capacity per kilogram body weight in male (r=-0.846, P=0.0001) and in female (r=-0.896, P=0.0001) subjects. In addition, W(AT) for each kilogram body weight also negatively correlated with increased BMI in male (r=-0.870, P=0.0001) and in females (r=-0.807, P=0.0001). The heart rate reserve correlated negatively with increasing BMI: r=-0.699, P=0.0001 (males) and r=-0.655, P=0.0001 (females). The results of the present study have suggested that, due to the inverse correlation between BMI, Wmax capacity, aerobic fitness and heart rate reserve, it may be useful to consider BMI in establishing cardiopulmonary fitness in various subjects.     

Effects of anticipation, prior-exercise, and breathing frequency to ventilatory response during step exercise: a preliminary study.

We examined the effects of anticipation, prior-exercise, and restricted breathing frequency on the ventilatory transient response to bicycle step exercise (75 W, 4 min, 50 rpm), i.e., 1) whether the increase of work rate was anticipated by the subject or not, 2) whether the exercise was preceded by light exercise (25 W), or rest, and 3) whether the exercise entrained the breathing frequency (f: 12.5/min, or 25/min) or not (voluntary). The corresponding step-on exercise was randomly performed at least two to five times by one adult male subject. As a result, a) the initial rapid ventilatory component, phase 1, was not observed when initiated from light exercise, whereas the overshot phase 1 was observed from rest in anticipation and voluntary breathing frequency condition due to the rapid increase of tidal volume; b) compared with the anticipation condition, the phase 1 response of VE in the non-anticipation condition was slower with prior-rest, and not with prior-light exercise; and c) the restriction of the breathing frequency for entraining the exercise rhythm did not affect the initial rapid response, but decreased the fluctuation of VE in the steady state, compared to the condition of voluntary breathing frequency.