Bouts Of Constant-load Cycling Research Articles

Control of hyperpnoea and pulmonary gas exchange during prolonged exercise: The role of group III/IV muscle afferent feedback.

It remains unclear whether feedback from group III/IV muscle afferents is of continuous significance for regulating the pulmonary response during prolonged (>5min), steady-state exercise. To elucidate the influence of these sensory neurons on hyperpnoea, gas exchange efficiency, arterial oxygenation and acid-base balance during prolonged locomotor exercise, 13healthy participants (4 females; 21 (3) years, : 46 (8) ml/kg/min) performed consecutive constant-load cycling bouts at ∼50% (20min), ∼75% (20min) and ∼100% (5min) of with intact (CTRL) and pharmacologically attenuated (lumbar intrathecal fentanyl; FENT) group III/IV muscle afferent feedback from the legs. Pulmonary responses were continuously recorded and arterial blood (radial catheter) periodically collected throughout the exercise. Pulmonary gas exchange efficiency was evaluated using the alveolar-arterial difference ( ). There were no differences in any of the variables of interest between conditions before the start of the exercise. Pulmonary ventilation was up to 20% lower across all intensities during FENT compared to CTRL exercise (P<0.001) and this hypoventilation was accompanied by an up to 10% lower arterial and a 2-4mmHg higher (both P<0.001). The exercise-induced widening of was up to 25% larger during FENT compared to CTRL (P<0.001). Importantly, the differences developed within the first minute of each stage and persisted, or further increased, throughout the remainder of each bout. These findings reflect a critical and time-independent significance of feedback from group III/IV leg muscle afferents for continuously regulating the ventilatory response, gas exchange efficiency, arterial oxygenation and acid-base balance during human locomotion. KEY POINTS: Feedback from group III/IV leg muscle afferents reflexly contributes to hyperpnoea during short duration (i.e. <5min) locomotor exercise. Whether continuous feedback from these sensory neurons is obligatory to ensure adequate pulmonary responses during steady-state exercise of longer duration remains unknown. Lumbar intrathecal fentanyl was used to attenuate the central projection of group III/IV leg muscle afferents during prolonged locomotor exercise (i.e. 45min) at intensities ranging from 50% to 100% of . Without affecting the metabolic rate, afferent blockade compromised pulmonary ventilation and gas exchange efficiency, consistently impairing arterial oxygenation and facilitating respiratory acidosis throughout exercise. These findings reflect the time-independent significance of feedback from group III/IV muscle afferents for regulating exercise hyperpnoea and gas exchange efficiency, and thus for optimizing arterial oxygenation and acid-base balance, during prolonged human locomotion.

Acute physiological and perceptual responses to moderate intensity cycling with different levels of blood flow restriction.

The aim of this study was to compare: i) the physiological and perceptual responses of low-load exercise [(moderate intensity exercise (MI)] with different levels of blood flow restriction (BFR), and ii) MI with BFR on the bike with high intensity (HI) exercise without BFR. The protocol involved large muscle mass exercise at different levels of BFR, and this differentiates our study from others. Twenty-one moderately trained males (age: 24.6 ± 2.4 years; VO2peak: 47.2 ± 7.0 ml.kg-1.min-1, mean ± sd) performed one maximal graded exercise test and seven 5-min constant-load cycling bouts. Six bouts were at MI [40% peak power (Ppeak), 60%VO2peak], one without BFR and five with different levels of BFR (40%, 50%, 60%, 70%, 80% of estimated arterial occlusion pressure). The HI bout (70%Ppeak, 90%VO2peak) was without BFR. Oxygen uptake (VO2), heart rate (HR), blood lactate (BLa), rate of perceived exertion (RPE), and tissue oxygen saturation (TSI) were recorded. Regardless of pressure, HR, BLa and RPE during MI-BFR were higher compared to MI (p < 0.05, ES: moderate to very large), and TSI reduction was greater in MI-BFR than MI (p < 0.05, ES: moderate to large). The responses of VO2, HR, BLa, RPE and TSI induced by the different levels of BFR in MI-BFR were similar. Regardless of pressure, the responses of VO2, HR, BLa and RPE induced by MI-BFR were lower than HI (p < 0.05), except for TSI. TSI change was similar between MI-BFR and HI. It appears that BFR equal to 40% of arterial occlusion pressure is sufficient to reduce TSI when exercising with a large muscle mass.

Combined influence of inspiratory loading and locomotor subsystolic cuff inflation on cardiovascular responses during submaximal exercise.

It is unknown if simultaneous stimulation of the respiratory and locomotor muscle afferents via inspiratory loading (IL) and locomotor subsystolic cuff inflation (CUFF) influences the cardiovascular responses during exercise. We hypothesized that combined IL and CUFF (IL + CUFF) will result in greater increases in blood pressure (MAP) and systemic vascular resistance (SVR) than IL and CUFF alone during exercise. Eight adults (6 males/2 females) were enrolled and performed four 10-min bouts of constant-load cycling eliciting 40% maximal oxygen uptake on a single day. For each exercise bout, the first 5 min consisted of spontaneous breathing. The second 5 min consisted of voluntary hyperventilation (i.e., breathing frequency of 40 breaths/min) with IL (30% maximum inspiratory pressure), CUFF (80 mmHg), IL + CUFF, or no intervention (CTL) in randomized order. During exercise, cardiac output and MAP were determined via open-circuit acetylene wash-in and manual sphygmomanometry, respectively, and SVR was calculated. Across CTL, IL, CUFF, and IL + CUFF, MAP was greater with each condition (CTL: 97 ± 14; IL: 106 ± 13; CUFF: 114 ± 14; IL + CUFF: 119 ± 15 mmHg, all P < 0.02). Furthermore, SVR was greater with IL + CUFF compared with IL, CUFF, and CTL (CTL: 6.6 ± 1.1; IL: 7.5 ± 1.4; CUFF: 7.5 ± 1.3; IL + CUFF: 8.2 ± 1.4 mmHg·L-1·min-1, all P < 0.02). Cardiac output was not different across conditions (CTL: 15.2 ± 3.8; IL: 14.8 ± 3.7; CUFF: 15.6 ± 3.5; IL + CUFF: 14.7 ± 4.3 L/min, all P > 0.05). These data demonstrate that simultaneous stimulation of respiratory and locomotor muscle afferent feedback results in additive MAP and SVR responses than IL and CUFF alone during submaximal exercise. These findings have important clinical implications for populations with exaggerated locomotor and respiratory muscle reflex feedbacks.NEW & NOTEWORTHY Reflexes arising from the respiratory and locomotor muscles influence cardiovascular regulation during exercise. However, it is unclear how the respiratory and locomotor muscle reflexes interact when simultaneously stimulated. Herein, we demonstrate that stimulation of the respiratory and locomotor muscle reflexes yielded additive cardiovascular responses during submaximal exercise.

Multidimensional aspects of dyspnea in obese patients referred for cardiopulmonary exercise testing

We investigated the contributions of obesity on multidimensional aspects of dyspnea on exertion (DOE) in patients referred for clinical cardiopulmonary exercise testing (CPET). Ratings of perceived breathlessness (RPB, Borg scale 0–10) were collected in obese (BMI ≥ 30; n = 47) and nonobese (BMI ≤ 25; n = 27) patients during two (one lower: ∼30 W; and one higher: ∼50 W) 4−6 min constant load cycling bouts. Multidimensional dyspnea profiles (MDP) were collected in the final 26 obese and 14 nonobese patients of the sample. RPB was greater (p = 0.05) in obese (3.3 ± 2.2 vs 2.4 ± 1.4) at lower work rates, but similar at higher work rates (4.9 ± 2.2 vs 4.4 ± 1.8). MDP sensory score including unpleasantness was 4.3 ± 2.2 in obese vs 2.5 ± 1.9 in nonobese (p < 0.001). The affective score was 1.9 ± 2.2 vs 0.7 ± 0.7, respectively (p < 0.01). Breathing sensations including ‘air hunger’, ‘effort’, and ‘breathing at lot’ were greater (p < 0.05) in obese, making these patients more frustrated/angry (p < 0.05). Obesity should be considered as a potential independent influencing factor that provokes DOE and unpleasantness when assessing breathlessness during CPET.

Influence of priming exercise on oxygen uptake and muscle deoxygenation kinetics during moderate-intensity cycling in type 2 diabetes.

The pulmonary oxygen uptake (V̇o2) kinetics during the transition to moderate-intensity exercise is slowed in individuals with type 2 diabetes (T2D), at least in part because of limitations in O2 delivery. The present study tested the hypothesis that a prior heavy-intensity warm-up or "priming" exercise (PE) bout would accelerate V̇o2 kinetics in T2D, because of a better matching of O2 delivery to utilization. Twelve middle-aged individuals with T2D and 12 healthy controls (ND) completed moderate-intensity constant-load cycling bouts either without (Mod A) or with (Mod B) prior PE. The rates of muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin concentration, [HHb+Mb]) and oxygenation (i.e., tissue oxygenation index) were continuously measured by near-infrared spectroscopy at the vastus lateralis muscle. The local matching of O2 delivery to O2 utilization was assessed by the Δ[HHb+Mb]-to-ΔV̇o2 ratio. Both groups demonstrated an accelerated V̇O2 kinetics response during Mod B compared with Mod A (T2D, 32 ± 9 vs. 42 ± 12 s; ND, 28 ± 9 vs. 34 ± 8 s; means ± SD) and an elevated muscle oxygenation throughout Mod B, whereas the [HHb+Mb] amplitude was greater during Mod B only in individuals with T2D. The [HHb+Mb] kinetics remained unchanged in both groups. In T2D, Mod B was associated with a decrease in the "overshoot" relative to steady state in the Δ[HHb+Mb]-to-ΔV̇o2 ratio (1.17 ± 0.17 vs. 1.05 ± 0.15), whereas no overshoot was observed in the control group before (1.04 ± 0.12) or after (1.01 ± 0.12) PE. Our findings support a favorable priming-induced acceleration of the V̇o2 kinetics response in middle-aged individuals with uncomplicated T2D attributed to an enhanced matching of microvascular O2 delivery to utilization.NEW & NOTEWORTHY Heavy-intensity "priming" exercise (PE) elicited faster pulmonary oxygen uptake (V̇o2) kinetics during moderate-intensity cycling exercise in middle-aged individuals with type 2 diabetes (T2D). This was accompanied by greater near-infrared spectroscopy-derived muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin concentration, [HHb+Mb]) responses and a reduced Δ[HHb+Mb]-to-ΔV̇o2 ratio. This suggests that the PE-induced acceleration in oxidative metabolism in T2D is a result of greater O2 extraction and better matching between O2 delivery and utilization.

Effect of Ischemic Preconditioning on Oxygen Uptake and Extraction Kinetics During Exercise in Normoxia and Hypoxia

BackgroundExercise tolerance is strongly related the physiological components of the primary (PC) and slow components (SC) of oxygen uptake. Exercise tolerance is reduced in clinical populations and during acute exposure to altitude by factors affecting skeletal muscle oxygenation. The practice of ischemic preconditioning has been shown to improve exercise tolerance or performance in a variety of different testing methods, but the mechanisms behind the improvements in exercise tolerance following IPC are still unclear.MethodsThirteen men (age= 24 ± 4 years, V̇O2max= 63.1 ± 5.1 ml·kg−1·min−1) completed four randomized trials of each combination of hypoxia (FIO2 = 0.16) or normoxia (FIO2 = 0.21) with a resting pre‐exercise IPC protocol (4 × 5 min at 220 mmHg) or SHAM procedure. Following the IPC/SHAM protocol subjects completed two constant load cycling bouts at power outputs corresponding to 1) 15% below the normoxic gas exchange threshold (CL #1) and 2) 85% of normoxic V̇O2max (CL #2). Breath‐by‐breath V̇O2, oxyhemoglobin saturation, and skeletal muscle oxygenation/extraction (measured via near‐infrared spectroscopy) were continuously monitored throughout the trials. V̇O2 and NIRS kinetics were quantified using a single (for CL#1) or double (for CL#2) exponential term equation with independent time delays for the V̇O2/NIRS primary and slow components.ResultsThere was a significant effect of inspirate on deoxyhemoglobin time constant (τ) during CL#1 (Hypoxia: 5.58 ± 2.82 s vs. Normoxia: 8.01 ± 4.71s, P &lt; 0.05) with no effect of IPC treatment (P = 0.84). During CL #2, there was a significant effect of inspirate on V̇O2 primary amplitude (PC) (Normoxia: 3.13 ± 0.36 L/min vs. Hypoxia: 2.92 ± 0.39 L/min, P &lt; 0.05). IPC did preserve microvascular oxygen extraction during high‐intensity cycling (CL #2) in Hypoxia (IPC: 21.3 ± 11.0 μM vs. SHAM: 19.9 ± 9.9 μM, P &lt; 0.05), but did not affect any of the NIRS or V̇O2 parameters in Normoxia.ConclusionOxygen uptake and peripheral oxygen delivery are compromised during high‐intensity exercise in hypoxia. Ischemic preconditioning prior to high‐intensity bouts is effective at mitigating the declines in microvascular oxygen extraction seen during exercise in hypoxia, however the rates (τ) of microvascular extraction and oxygen uptake are not altered following treatment with IPC.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Respiratory Mechanical and Cardiorespiratory Consequences of Cycling with Aerobars.

Aerobars place a cyclist in a position where the trunk is flexed forward and the elbows are close to the midline of the body. This position is known to improve cycling aerodynamics and time trial race performance compared with upright cycling positions. However, the aggressive nature of this position may have important cardiorespiratory and metabolic consequences. The purpose of this investigation was to examine the respiratory mechanical, ventilatory, metabolic, and sensory consequences of cycling while using aerobars during laboratory-based cycling. Eleven endurance-trained male cyclists (age, 26 ± 9 yr; V˙O2peak, 55 ± 5 mL·kg·min) were recruited. Visit 1 consisted of an incremental cycling test to determine peak power output. Visit 2 consisted of 6-min bouts of constant load cycling at 70% of peak incremental power output in the aerobar position, drop position, and upright position while grasping the brake hoods. Metabolic and ventilatory responses were measured using a commercially available metabolic cart, and respiratory pressures were measured using an esophageal catheter. Cycling in the aerobar position significantly increased the work of breathing (Wb), power of breathing (Pb), minute ventilation, ventilatory equivalent for oxygen and carbon dioxide, and transdiaphragmatic pressure compared with the upright position. Increases in the Wb and Pb in the aerobars relative to the upright position were strongly correlated with the degree of thoracic restriction, measured as the shoulder-to-aerobar width ratio (Wb: r = 0.80, P = 0.01; Pb: r = 0.69, P = 0.04). Aerobars significantly increase the mechanical cost of breathing and leads to greater ventilatory inefficiency compared with upright cycling. Future work is needed to optimize aerobar width to minimize the respiratory mechanical consequences while optimizing aerodynamics.

Influence of menopause and Type 2 diabetes on pulmonary oxygen uptake kinetics and peak exercise performance during cycling.

We investigated if the magnitude of the Type 2 diabetes (T2D)-induced impairments in peak oxygen uptake (V̇O2) and V̇O2 kinetics was affected by menopausal status. Twenty-two women with T2D (8 premenopausal, 14 postmenopausal), and 22 nondiabetic (ND) women (11 premenopausal, 11 postmenopausal) matched by age (range = 30-59 yr) were recruited. Participants completed four bouts of constant-load cycling at 80% of their ventilatory threshold for the determination of V̇O2 kinetics. Cardiac output (CO) (inert gas rebreathing) was recorded at rest and at 30 s and 240 s during two additional bouts. Peak V̇O2 was significantly (P < 0.05) reduced in both groups with T2D compared with ND counterparts (premenopausal, 1.79 ± 0.16 vs. 1.55 ± 0.32 l/min; postmenopausal, 1.60 ± 0.30 vs. 1.45 ± 0.24 l/min). The time constant of phase II of the V̇O2 response was slowed (P < 0.05) in both groups with T2D compared with healthy counterparts (premenopausal, 29.1 ± 11.2 vs. 43.0 ± 12.2 s; postmenopausal, 33.0 ± 9.1 vs. 41.8 ± 17.7 s). At rest and during submaximal exercise absolute CO responses were lower, but the "gains" in CO larger (both P < 0.05) in both groups with T2D. Our results suggest that the magnitude of T2D-induced impairments in peak V̇O2 and V̇O2 kinetics is not affected by menopausal status in participants younger than 60 yr of age.

Differential effects of age and type 2 diabetes on dynamic vs. peak response of pulmonary oxygen uptake during exercise.

We investigated if the magnitude of the type 2 diabetes (T2D)-induced impairments in peak oxygen uptake (V̇o2) and V̇o2 kinetics was affected by age. Thirty-three men with T2D (15 middle-aged, 18 older), and 21 nondiabetic (ND) men (11 middle-aged, 10 older) matched by age were recruited. Participants completed four 6-min bouts of constant-load cycling at 80% ventilatory threshold for the determination of V̇o2 kinetics. Cardiac output (inert-gas rebreathing) was recorded at rest and 30 and 240 s during two additional bouts. Peak V̇o2 (determined from a separate graded test) was significantly (P < 0.05) reduced in middle-aged and older men with T2D compared with their respective ND counterparts (middle-aged, 3.2 ± 0.5 vs. 2.5 ± 0.5 l/min; older, 2.7 ± 0.4 vs. 2.4 ± 0.4 l/min), and the magnitude of these impairments was not affected by age. However, the time constant of phase II of the V̇o2 response was only slowed (P < 0.05) in middle-aged men with T2D compared with healthy counterparts, whereas it was similar among older men with and without T2D (middle-aged, 26.8 ± 9.3 vs. 41.6 ± 12.1 s; older, 40.5 ± 7.8 vs. 41.1 ± 8.5 s). Similarly, the "gains" in systemic vascular conductance (estimated from the slope between cardiac output and mean arterial pressure responses) were lower (P < 0.05) in middle-aged men with T2D than ND controls, but similar between the older groups. The results suggest that the mechanisms by which T2D induces significant reductions in peak exercise performance are linked to a slower dynamic response of V̇o2 and reduced systemic vascular conductance responses in middle-aged men, whereas this is not the case in older men.

AltitudeOmics: exercise-induced supraspinal fatigue is attenuated in healthy humans after acclimatization to high altitude

We asked whether acclimatization to chronic hypoxia (CH) attenuates the level of supraspinal fatigue that is observed after locomotor exercise in acute hypoxia (AH). Seven recreationally active participants performed identical bouts of constant-load cycling (131 ± 39 W, 10.1 ± 1.4 min) on three occasions: (i) in normoxia (N, PI O2 , 147.1 mmHg); (ii) in AH (FI O2 , 0.105; PI O2 , 73.8 mmHg); and (iii) after 14 days in CH (5260 m; PI O2 , 75.7 mmHg). Throughout trials, prefrontal-cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assessed using near-infrared-spectroscopy and transcranial Doppler sonography. Pre- and post-exercise twitch responses to femoral nerve stimulation and transcranial magnetic stimulation were obtained to assess neuromuscular and corticospinal function. In AH, prefrontal oxygenation declined at rest (Δ7 ± 5%) and end-exercise (Δ26 ± 13%) (P < 0.01); the degree of deoxygenation in AH was greater than N and CH (P < 0.05). The cerebral O2 delivery index (MCAV × Ca O2 ) was 19 ± 14% lower during the final minute of exercise in AH compared to N (P = 0.013) and 20 ± 12% lower compared to CH (P = 0.040). Maximum voluntary and potentiated twitch force were decreased below baseline after exercise in AH and CH, but not N. Cortical voluntary activation decreased below baseline after exercise in AH (Δ11%, P = 0.014), but not CH (Δ6%, P = 0.174) or N (Δ4%, P = 0.298). A twofold greater increase in motor-evoked potential amplitude was evident after exercise in CH compared to AH and N. These data indicate that exacerbated supraspinal fatigue after exercise in AH is attenuated after 14 days of acclimatization to altitude. The reduced development of supraspinal fatigue in CH may have been attributable to increased corticospinal excitability, consequent to an increased cerebral O2 delivery.

Do the Noncaffeine Ingredients of Energy Drinks Affect Metabolic Responses to Heavy Exercise?

Energy drinks (EDs) such as Red Bull (RB) are marketed to enhance metabolism. Secondary ingredients of EDs (e.g., taurine) have been purported to improve time trial performance; however, little research exists on how such secondary ingredients affect aerobic metabolism during heavy exercise. The purpose of this study was to investigate the effect of the secondary ingredients of RB on aerobic metabolism during and subsequent to heavy exercise. In double-blind, counterbalanced, and crossover fashion, 8 recreationally trained individuals completed a graded exercise test to determine the gas exchange threshold (GET). Subjects returned on 2 separate occasions and ingested either a 245 ml serving of RB or a control (CTRL) drink with the equivalent caffeine before engaging in two 10-minute constant-load cycling bouts, at an intensity equivalent to GET, with 3 minutes of rest between bouts. Accumulated liters of O2 (10 minutes) were higher for the first bout (17.1 ± 3.5 L) vs. the second bout (16.7 ± 3.5 L) but did not differ between drinks. Similarly, excess postexercise oxygen consumption was higher after the initial bout (RB mean, 2.6 ± 0.85 L; CTRL mean, 2.9 ± 0.90 L) vs. the second bout (RB mean, 1.5 ± 0.85 L; CTRL mean, 1.9 ± 0.87 L) but did not differ between drinks. No differences occurred between drinks for measures of heart rate or rating of perceived exertion. These results indicate that the secondary ingredients contained in a single serving of RB do not augment aerobic metabolism during or subsequent to heavy exercise.

Similar level of impairment in exercise performance and oxygen uptake kinetics in middle-aged men and women with type 2 diabetes

The present study tested the hypothesis that the magnitude of the type 2 diabetes-induced impairments in peak oxygen uptake (Vo(2)) and Vo(2) kinetics would be greater in females than males in middle-aged participants. Thirty-two individuals with type 2 diabetes (16 male, 16 female), and 32 age- and body mass index (BMI)-matched healthy individuals (16 male, 16 female) were recruited. Initially, the ventilatory threshold (VT) and peak Vo(2) were determined. On a separate day, subjects completed four 6-min bouts of constant-load cycling at 80% VT for the determination of Vo(2) kinetics using standard procedures. Cardiac output (CO) (inert gas rebreathing) was recorded at rest, 30, and 240 s during two additional bouts. Peak Vo(2) (ml·kg(-1)·min(-1)) was significantly reduced in men and women with type 2 diabetes compared with their respective nondiabetic counterparts (men, 27.8 ± 4.4 vs. 31.1 ± 6.2 ml·kg(-1)·min(-1); women, 19.4 ± 4.1 vs. 21.4 ± 2.9 ml·kg(-1)·min(-1)). The time constant (s) of phase 2 (τ(2)) and mean response time (s) of the Vo(2) response (MRT) were slowed in women with type 2 diabetes compared with healthy women (τ(2), 43.3 ± 9.8 vs. 33.6 ± 10.0 s; MRT, 51.7 ± 9.4 vs. 43.5 ± 11.4s) and in men with type 2 diabetes compared with nondiabetic men (τ(2), 43.8 ± 12.0 vs. 35.3 ± 9.5 s; MRT, 57.6 ± 8.3 vs. 47.3 ± 9.3 s). The magnitude of these impairments was not different between males and females. The steady-state CO responses or the dynamic responses of CO were not affected by type 2 diabetes among men or women. The results suggest that the type 2 diabetes-induced impairments in peak Vo(2) and Vo(2) kinetics are not affected by sex in middle aged participants.

Cardiac Output Is Not Related to the Slowed O2 Uptake Kinetics in Type 2 Diabetes

This study aimed to investigate whether cardiac output (CO) responses were related to VO2 kinetics during cycling in type 2 diabetes. A total of 9 middle-aged women with uncomplicated type 2 diabetes, 9 nondiabetic overweight women, and 11 nondiabetic lean women were recruited. Initially, the ventilatory threshold (VT) and peak VO2 were determined during a maximal graded test. Then, on two separate days, subjects completed three 7-min bouts of constant-load cycling at each of three intensities: 50% VT, 80% VT, and midpoint between VT and peak VO2 (50% Δ). CO (inert gas rebreathing) was recorded at 30 and 240 s of an additional bout at each intensity. VO2 kinetic parameters were determined by fitting a biexponential (50% VT and 80% VT) or triexponential (50% Δ) function to the VO2 data. Peak VO2 was significantly lower in type 2 diabetes compared with the two nondiabetic groups (P < 0.05). The time constant of phase 2 was significantly greater (P < 0.05) in type 2 diabetes compared with the nondiabetic heavy and lean groups at 50% VT (34.2 ± 15.7 vs 15.4 ± 7.3 and 20.2 ± 9.7 s) and 80% VT (39.1 ± 9.0 vs 24.8 ± 8.8 and 36.8 ± 7.9 s), but none of the VO2 kinetic parameters were different at 50% Δ. CO responses during exercise were not different among the three groups, and at 80% VT, the change in CO from 30 to 240 s was significantly larger in type 2 diabetes compared with the two nondiabetic groups. The results confirm that type 2 diabetes slows the dynamic response of VO2 during light and moderate relative intensity exercise in females but that this occurs in the absence of any slowing of the CO response during the initial period of exercise.

The Relationship Between Rating of Perceived Exertion and Muscle Activity During Exhaustive Constant-Load Cycling

The aims of this study were to verify the relationship between rating of perceived exertion (RPE) and electromyography (EMG) increases during exhaustive constant-load cycling bouts and, to compare and to correlate the power outputs corresponding to perceived exertion threshold (PET) and neuromuscular fatigue threshold (NFT). 11 men completed 3-4 different exhaustive constant-load cycling bouts on a cycle ergometer, being RPE and EMG measured throughout the bouts. The linear regression of the RPEslope and EMGslope against the power output identified the PET and NFT intensity, respectively. There was a significant relationship between RPEslope and EMGslope (R(2)=0.69; P<0.01). However, the linearity of RPEslope (R(2)=0.93±0.07) was significantly higher (P<0.001) than EMGslope (R(2)=0.63±0.25). In addition, the RPEslope and EMGslope were related to time to exhaustion (r=-0.59 and r=-0.60; P<0.001). There was no significant difference (P=0.42) between PET (201.5±27.9W) and NFT (210.3±22.6W) and they were significantly correlated (r=0.78; P=0.005). Therefore, the RPE and EMG increases during exhaustive constant-load cycling bouts are related and, PET and NFT intensities are similar and closely associated.

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling

Metabolic demand and muscle mechanical tension are closely coupled during exercise, making their respective drives to the circulatory response difficult to establish. This coupling being altered in eccentric cycling, we implemented an experimental design featuring eccentric vs. concentric constant-load cycling bouts to gain insights into the control of the exercise-induced circulatory response in humans. Heart rate (HR), stroke volume (SV), cardiac output (Q), oxygen uptake (V(.-)(O(2))), and electromyographic (EMG) activity of quadriceps muscles were measured in 11 subjects during heavy concentric (heavy CON: 270 +/- 13 W; V(.-)(O(2)) = 3.59 +/- 0.20 l/min), heavy eccentric (heavy ECC: 270 +/- 13 W, V(.-)(O(2)) = 1.17 +/- 0.15 l/min), and light concentric (light CON: 70 +/- 9 W, V(.-)(O(2)) = 1.14 +/- 0.12 l/min) cycle bouts. Using a reductionist approach, the circulatory responses observed between heavy CON vs. light CON (difference in V(.-)(O(2)) and power output) was ascribed either to metabolic demand, as estimated from heavy CON vs. heavy ECC (similar power output, different V(.-)(O(2))), or to muscle mechanical tension, as estimated from heavy ECC vs. light CON (similar V(.-)(O(2)), different power output). 74% of the Q response was determined by the metabolic demand, also accounting for 65% and 84% of HR and SV responses, respectively. Consequently, muscle mechanical tension determined 26%, 35%, and 16% of the Q, HR, and SV responses, respectively. Q was significantly related to V(.-)(O(2)) (r(2) = 0.83) and EMG activity (r(2) = 0.82; both P < 0.001). These results suggest that the exercise-induced circulatory response is mainly under metabolic control and support the idea that the level of muscle activation plays a role in the cardiovascular regulation during cycle exercise in humans.