Changes in pulmonary oxygen uptake and muscle deoxygenation kinetics during cycling exercise in older women performing walking training for 12 weeks.

PURPOSE: This study examined the hypothesis that walking training (WT) could accelerate the slowed time constant (τ) of phase II in pulmonary oxygen uptake ([Formula: see text]O2) on-kinetics in older women. Also, we aimed to demonstrate that O2 delivery and O2 utilization were better matched at the site of gas exchange in exercising muscles when τ[Formula: see text]O2 was shortened. METHODS: 20 recreationally active older women underwent WT sessions of approximately 60 min, 3-4 times a week for 12 weeks. We assessed [Formula: see text]O2, heart rate (HR) and deoxygenated-hemoglobin concentration ([HHb]) kinetics during a constant-load exercise test before training (0 week-Pre), and at 6 and 12 weeks (6 weeks-Mid, 12 weeks-Post) throughout the training period. RESULTS: Maximal oxygen uptake ([Formula: see text]O2max) was unchanged throughout the training program. τHR tended to decline at Mid (58.6 ± 22.0 s), and was significantly shorter at Post (51.7 ± 21.7 s, p = 0.01) compared to Pre (67.1 ± 23.8 s). τ[Formula: see text]O2 significantly decreased from 38.9 ± 8.6 s for Pre, to 31.5 ± 7.9 s for Mid (p = 0.02), and 32.3 ± 10.5 s for Post (p = 0.03). The normalized [HHb] to [Formula: see text]O2 ratio (Δ[HHb]/Δ[Formula: see text]O2) at Pre (1.32 ± 0.93) gradually approached the perfectly matched value (= 1.0) at Mid (1.15 ± 0.61) and Post (1.07 ± 0.52). CONCLUSIONS: The restoration to baseline (≒ 30 s) of the slower τ[Formula: see text]O2 due to WT, which may reflect better matching of O2 delivery and O2 utilization at the site of gas exchange, suggests that a longer period of WT could be a useful tool for improving exercise tolerance in older individuals.

Fatiguing intermittent lower limb exercise influences corticospinal and corticocortical excitability in the nonexercised upper limb.

BACKGROUND: It has recently been reported that unilateral fatiguing exercise affects not only the motor area innervating the exercising muscle but also the ipsilateral motor area innervating homologous nonexercised muscle. OBJECTIVE: This study was designed to clarify the effects of fatiguing intermittent lower limb exercise on the excitability of the motor cortex representation of nonexercised muscles in the arm. METHODS: Eight subjects performed an intermittent leg press exercise composed of three bouts of 5-minute leg press (T1, T2, and T3) at 50% of maximal voluntary contraction separated by a 2-minute rest. Motor-evoked potentials (MEP), short interval intracortical inhibition (SICI), and intracortical facilitation (ICF), using paired-pulse transcranial magnetic stimulation, were assessed in two nonexercised arm muscles (first dorsal interosseous muscle: FDI, n = 8; biceps brachii muscle: BB, n = 6) and one exercised leg muscle (quadriceps femoris muscle: QF, n = 6) before and immediately after each bout of exercise and for 30 minutes during recovery after the end of the third exercise bout (Experiment 1). Experiment 2 was the same as Experiment 1, except that the test pulse intensity was adjusted to produce a given amplitude of MEP(TEST) at each time point. RESULTS: MEPs and SICI in the exercised QF muscle were depressed at all time points during and after fatigue. In contrast, MEPs in nonexercised arm muscles were facilitated from T1-T3 (T3, only FDI), but were then depressed for up to 20 minutes in the recovery period. SICI was reduced in both muscles during T1-T3 and remained depressed until 20 minutes into recovery. ICF was unchanged in arm muscles but depressed in QF over T1-T3. CONCLUSIONS: The current study indicates that muscle fatigue induced by exercise of a large lower limb muscle group has powerful effects on the excitability of both SICI and the corticospinal projection to muscles of the nonexercised upper limb.

Unilateral grip fatigue reduces short interval intracortical inhibition in ipsilateral primary motor cortex.

OBJECTIVE: This study was designed to examine whether exhaustive grip exercise of the left hand affected intracortical excitability in ipsilateral motor cortex. METHODS: Ten healthy male subjects (aged 21-24 years) participated in experiment 1 in which paired-pulse transcranial magnetic stimulation (TMS) was used to test corticospinal and corticocortical excitability in right (relaxed) first dorsal interosseous (FDI) muscle during the recovery period after exhaustive forceful grip exercise of the left hand. Seven of the same subjects participated in experiment 2, in which the intensity of the test stimulus was adjusted so that the amplitude of motor evoked potential (MEP(TEST)) was kept constant throughout the measurement. RESULTS: In experiment 1, MEP(TEST) was slightly reduced from 5 to 15min after exercise whilst short interval intracortical inhibition (SICI) at interstimulus interval (ISI) of 2 and 3ms became less effective. Intracortical facilitation (ICF) was unchanged. In experiment 2 when the MEP(TEST) was maintained at a constant size there was again no change in ICF, and the reduction in SICI was still present at the same intervals. CONCLUSIONS: We conclude that unilateral exhaustive grip exercise reduced the excitability of the corticospinal output of the ipsilateral motor cortex whilst simultaneously reducing the excitability of SICI. These results would be compatible with the idea that fatigue increases the tonic level of interhemispheric inhibition from the fatigued to the non-fatigued cortex. SIGNIFICANCE: Muscle fatigue to the point of exhaustion has lasting effects on the excitability of intracortical circuits in the non-exercised hemisphere, perhaps via changes in the tonic levels of activity in transcallosal pathways.

Estimation of oxygen cost of internal power during cycling exercise with changing pedal rate.

It has been reported that oxygen uptake (VO2) increases exponentially with levels of the pedal rate during cycling. The purpose of this study was therefore to test the hypothesis that the O2 cost for internal power output (Pint) exerted in exercising muscle itself would be larger than for an external power output (Pext) calculated from external load and pedal rate during cycling exercise under various conditions of Pint and Pext in a large range of pedal rates. The O2 cost (DeltaVO2/ Deltapower output) was investigated in three experiments that featured different conditions on a cycle ergometer that were carried out at the same levels of total power output (Ptot; sum of Pint and Pext) (Exp. 1), Pext (Exp. 2) and load (Exp. 3). Each experiment consisted of three exercise tests with three levels of pedal rate (40 rpm for a lower pedal rate: LP; 70-80 rpm for a moderate pedal rate: MP; and 100-120 rpm for a higher pedal rate: HP) lasting for 2-3 min of unloaded cycling followed by 4-5 min of loaded cycling. Blood lactate accumulations (2.3-3.4 mmol l(-1)) at the HP were significantly higher compared with the LP (0.6-0.9 mmol l(-1)) and MP (0.9-1.0 mmol l(-1)) except for the LP in Exp. 1. The VO2 (360-432 ml min(-1) for LP, 479-644 ml min(-1) for MP, 960-1602 ml min(-1) for HP) during unloaded cycling in the three experiments increased exponentially with increasing pedal rates regardless of Pext=0. Moreover, the slope of the VO2-Pint (13.7 ml min(-1) W(-1)) relation revealed a steeper inclination than that of the VO2-Pext (10.2 ml min(-1) W(-1)) relation. We concluded that the O2 cost for Pint was larger than for Pext during the cycling exercises, indicating that the O2 cost for Ptot could be affected by the ratio of Pint to Ptot due to the levels of pedal rate.

Effect of internal power on muscular efficiency during cycling exercise.

The purpose of this study was to investigate the muscular efficiency during cycling exercise under certain total power output (Ptot) or external power output (Pext) experimental conditions that required a large range of pedal rates from 40 to 120 rpm. Muscular efficiency estimated as a ratio of Ptot, which is sum of internal power output (Pint) and Pext, to rate of energy expenditure above a resting level was investigated in two experiments that featured different conditions on a cycle ergometer, which were carried out at the same levels of Ptot (Exp. 1) and Pext (Exp. 2). Each experiment consisted of three exercise tests with three levels of pedal rates (40, 80 and 120 rpm) lasting for 2-3 min of unloaded cycling followed by 4-5 min of loaded cycling. VO2 during unloaded cycling (approximately 430 ml min(-1) for 40 rpm, approximately 640 ml min(-1) for 80 rpm, approximately 1,600 ml min(-1) for 120 rpm) and the Pint (approximately 3 W for 40 rpm, approximately 25 W for 80 rpm, approximately 90 W for 120 rpm) in the two experiments were markedly increased with increasing pedal rates. The highest muscular efficiency was found at 80 rpm in the two experiments, whereas a remarkable reduction (19%) in muscular efficiency obtained at 120 rpm could be attributable to greater O2 cost due to higher levels of Pint accompanying the increased pedal rates. We concluded that muscular efficiency could be affected by the differences in O2 cost and Pint during cycling under the large range of pedal rates employed in this study.

Does the regional oxygen uptake measured by near infrared spectroscopy reflect the phase II pulmonary oxygen uptake at the onset of exercise?

It has been hypothesized that the signals of near infrared spectroscopy (NIRS) would reflect muscle O(2) uptake (mVO(2)). Although it is not definite that NIRS signals accurately reflect mVO(2), there is every possibility that NIRS signals at least reflect regional O(2) uptake (rVO(2)). The phase II kinetics of pulmonary oxygen uptake (pVO(2)) is regarded as reflecting mVO(2) at the onset of exercise. To examine whether the rVO(2) on-kinetics measured by NIRS reflects the mVO(2) on-kinetics at the onset of exercise, we compared the rVO(2) as measured by NIRS with the phase II kinetics of pVO(2) at the onset of exercise. Twelve healthy male subjects cycled a Monark ergometer at three different intensities: below the ventilatory threshold (VT) level (below-VT), on the VT level (on-VT), and above the VT level (above-VT), for 6 minutes on three separate occasions. The rVO(2) was calculated from the concentration of oxyhemoglobin and deoxyhemoglobin, as measured by NIRS every 3 seconds. The pVO(2) was determined by the breath-by-breath method. A significant relationship between the amount of increases of pVO(2) and rVO(2) from rest to the end of exercise among all levels of exercise intensity was found (r=0.935, P<0.001). The time constants of rVO(2) (rVO(2)-Tc: below-VT: 6.514+/-2.159 s, on-VT: 7.760+/-2.035 s, above-VT: 9.532+/-2.342 s) were significantly faster than the time constants of pVO(2) (pVO(2)-Tc: below-VT: 23.8+/-4.4 s, on-VT: 25.9+/-5.1 s, above-VT: 26.3+/-5.7 s) (P<0.001). There was no significant relationship between rVO(2)-Tc and pVO(2)-Tc for each intensity (P>0.05). We conclude that the rVO(2) on-kinetics measured by NIRS does not necessarily reflect the mVO(2) kinetics at the onset of exercise.

Blood lactate changes during isocapnic buffering in sprinters and long distance runners.

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation.