Markus Amann

Somatosensory feedback from the limbs exerts inhibitory influences on central neural drive during whole body endurance exercise

We investigated whether somatosensory feedback from contracting limb muscles exerts an inhibitory influence on the determination of central command during closed-loop cycling exercise in which the subject voluntarily determines his second-by-second central motor drive. Eight trained cyclists performed two 5-km time trials either without (5K(Ctrl)) or with lumbar epidural anesthesia (5K(Epi); 24 ml of 0.5% lidocaine, vertebral interspace L(3)-L(4)). Percent voluntary quadriceps muscle activation was determined at rest using a superimposed twitch technique. Epidural lidocaine reduced pretime trial maximal voluntary quadriceps strength (553 +/- 45 N) by 22 +/- 3%. Percent voluntary quadriceps activation was also reduced from 97 +/- 1% to 81 +/- 3% via epidural lidocaine, and this was unchanged following the 5K(Epi), indicating the presence of a sustained level of neural impairment throughout the trial. Power output was reduced by 9 +/- 2% throughout the race (P < 0.05). We found three types of significant effects of epidural lidocaine that supported a substantial role for somatosensory feedback from the exercising limbs as a determinant of central command throughout high-intensity closed-loop cycling exercise: 1) significantly increased relative integrated EMG of the vastus lateralis; 2) similar pedal forces despite the reduced number of fast-twitch muscle fibers available for activation; 3) and increased ventilation out of proportion to a reduced carbon dioxide production and heart rate and increased blood pressure out of proportion to power output and oxygen consumption. These findings demonstrate the inhibitory influence of somatosensory feedback from contracting locomotor muscles on the conscious and/or subconscious determination of the magnitude of central motor drive during high intensity closed-loop endurance exercise.

Peripheral fatigue limits endurance exercise via a sensory feedback-mediated reduction in spinal motoneuronal output

This study sought to determine whether afferent feedback associated with peripheral muscle fatigue inhibits central motor drive (CMD) and thereby limits endurance exercise performance. On two separate days, eight men performed constant-load, single-leg knee extensor exercise to exhaustion (85% of peak power) with each leg (Leg1 and Leg2). On another day, the performance test was repeated with one leg (Leg1) and consecutively (within 10 s) with the other/contralateral leg (Leg2-post). Exercise-induced quadriceps fatigue was assessed by reductions in potentiated quadriceps twitch-force from pre- to postexercise (ΔQtw,pot) in response to supramaximal magnetic femoral nerve stimulation. The output from spinal motoneurons, estimated from quadriceps electromyography (iEMG), was used to reflect changes in CMD. Rating of perceived exertion (RPE) was recorded during exercise. Time to exhaustion (∼9.3 min) and exercise-induced ΔQtw,pot (∼51%) were similar in Leg1 and Leg2 (P > 0.5). In the consecutive leg trial, endurance performance of the first leg was similar to that observed during the initial trial (∼9.3 min; P = 0.8); however, time to exhaustion of the consecutively exercising contralateral leg (Leg2-post) was shorter than the initial Leg2 trial (4.7 ± 0.6 vs. 9.2 ± 0.4 min; P < 0.01). Additionally, ΔQtw,pot following Leg2-post was less than Leg2 (33 ± 3 vs 52 ± 3%; P < 0.01). Although the slope of iEMG was similar during Leg2 and Leg2-post, end-exercise iEMG following Leg2-post was 26% lower compared with Leg2 (P < 0.05). Despite a similar rate of rise, RPE was consistently ∼28% higher throughout Leg2-post vs. Leg2 (P < 0.05). In conclusion, this study provides evidence that peripheral fatigue and associated afferent feedback limits the development of peripheral fatigue and compromises endurance exercise performance by inhibiting CMD.

Predictive validity of ventilatory and lactate thresholds for cycling time trial performance

Purpose: To determine which laboratory measurement best predicts 40 km cycling time‐trial (TT) performance.

Spinal opioid receptor‐sensitive muscle afferents contribute to the fatigue‐induced increase in intracortical inhibition in healthy humans

We investigated the influence of spinal opioid receptor‐sensitive muscle afferents on cortical changes following fatiguing unilateral knee‐extensor exercise. On separate days, seven subjects performed an identical five sets of intermittent isometric right‐quadriceps contractions, each consisting of eight submaximal contractions [63 ± 7% maximal voluntary contraction (MVC)] and one MVC. The exercise was performed following either lumbar interspinous saline injection or lumbar intrathecal fentanyl injection blocking the central projection of spinal opioid receptor‐sensitive lower limb muscle afferents. To quantify exercise‐induced peripheral fatigue, quadriceps twitch force (Qtw,pot) was assessed via supramaximal magnetic femoral nerve stimulation before and after exercise. Motor evoked potentials and cortical silent periods (CSPs) were evaluated via transcranial magnetic stimulation of the motor cortex during a 3% MVC pre‐activation period immediately following exercise. End‐exercise quadriceps fatigue was significant and similar in both conditions (ΔQtw,pot−35 and −39% for placebo and fentanyl, respectively; P= 0.38). Immediately following exercise on both days, motor evoked potentials were similar to those obtained prior to exercise. Compared with pre‐exercise baseline, CSP in the placebo trial was 21 ± 5% longer postexercise (P < 0.01). In contrast, CSP following the fentanyl trial was not significantly prolonged compared with the pre‐exercise baseline (6 ± 4%). Our findings suggest that the central effects of spinal opioid receptor‐sensitive muscle afferents might facilitate the fatigue‐induced increase in CSP. Furthermore, since the CSP is thought to reflect inhibitory intracortical interneuron activity, which may contribute to central fatigue, our findings imply that spinal opioid receptor‐sensitive muscle afferents might influence central fatigue by facilitating intracortical inhibition.

Significance of group III and IV muscle afferents for the endurance exercising human

With the onset of dynamic whole‐body exercise, contraction‐induced mechanical and biochemical stimuli within locomotor muscle cause an increase in the discharge frequency of thinly myelinated (Group III) and unmyelinated (Group IV) nerve fibres located within the muscle. These thin fibre muscle afferents project to various sites within the central nervous system and thereby substantially influence the exercising human. First, Group III/IV muscle afferents are the afferent arm of cardiovascular and ventilatory reflex responses that are mediated in the nucleus tractus solitarius and the ventrolateral medulla. Therefore, neural feedback from working skeletal muscle is a vital component in providing a high capacity for endurance exercise because muscle perfusion and O2 delivery determine the fatigability of skeletal muscle. Second, Group III/IV muscle afferents facilitate ‘central fatigue’ (failure, or unwillingness, of the central nervous system to ‘drive’ motoneurons) by exerting inhibitory influences on central motor drive during exercise. Thus, Group III/IV muscle afferents play a substantial role in a humans susceptibility to fatigue and capacity for endurance exercise.

Muscle mass and peripheral fatigue: a potential role for afferent feedback?

The voluntary termination of exercise has been hypothesized to occur at a sensory tolerance limit, which is affected by feedback from group III and IV muscle afferents, and is associated with a specific level of peripheral quadriceps fatigue during whole body cycling. Therefore, the purpose of this study was to reduce the amount of muscle mass engaged during dynamic leg exercise to constrain the source of muscle afferent feedback to the central nervous system (CNS) and examine the effect on peripheral quadriceps fatigue.

Pulmonary system limitations to endurance exercise performance in humans

Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole‐body endurance exercise performance. This brief overview emphasizes three respiratory system‐related mechanisms which impair O2 transport to the locomotor musculature [arterial O2 content ( ) × leg blood flow ( )], i.e. the key determinant of an individuals aerobic capacity and ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and thus compromises . Especially susceptible to this threat to convective O2 transport are well‐trained endurance athletes characterized by high metabolic and ventilatory demands and, probably due to anatomical and morphological gender differences, active women. Second, fatiguing respiratory muscle work (Wresp) associated with strenuous exercise elicits sympathetically mediated vasoconstriction in limb‐muscle vasculature, which compromises . This impact on limb O2 transport is independent of fitness level and affects all individuals, but only during sustained, high‐intensity endurance exercise performed above ∼85% maximal oxygen uptake. Third, excessive fluctuations in intrathoracic pressures accompanying Wresp can limit cardiac output and therefore . Exposure to altitude exacerbates the respiratory system limitations observed at sea level, further reducing and substantially increasing exercise‐induced Wresp. Taken together, the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O2 transport during strenuous exercise by failing to ensure optimal arterial oxygenation and compromising . This respiratory system‐related impact exacerbates the exercise‐induced development of fatigue and compromises endurance performance.

Human investigations into the exercise pressor reflex.

During exercise, neural input from skeletal muscles reflexly maintains or elevates blood pressure (BP) despite a maybe fivefold increase in vascular conductance. This exercise pressor reflex is illustrated by similar heart rate (HR) and BP responses to electrically induced and voluntary exercise. The importance of the exercise pressor reflex for tight cardiovascular regulation during dynamic exercise is supported by studies using pharmacological blockade of lower limb muscle afferent nerves. These experiments show attenuation of the increase in BP and cardiac output when exercise is performed with attenuated neural feedback. Additionally, there is no BP response to electrically induced exercise with paralysing epidural anaesthesia or when similar exercise is evoked in paraplegic patients. Furthermore, BP decreases when electrically induced exercise is carried out in tetraplegic patients. The lack of an increase in BP during exercise with paralysed legs manifests, although electrical stimulation of muscles enhances lactate release and reduces muscle glycogen. Thus, the exercise pressor reflex enhances sympathetic activity and maintains perfusion pressure by restraining abdominal blood flow, while brain, skin and muscle blood flow may also become affected because the reflex ‘resets’ arterial baroreceptor modulation of vascular conductance, making BP the primarily regulated cardiovascular variable during exercise.

AltitudeOmics: on the consequences of high-altitude acclimatization for the development of fatigue during locomotor exercise in humans

The development of muscle fatigue is oxygen (O2)-delivery sensitive [arterial O2 content (CaO2) × limb blood flow (QL)]. Locomotor exercise in acute hypoxia (AH) is, compared with sea level (SL), associated with reduced CaO2 and exaggerated inspiratory muscle work (Winsp), which impairs QL, both of which exacerbate fatigue individually by compromising O2 delivery. Since chronic hypoxia (CH) normalizes CaO2 but exacerbates Winsp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138 ± 14 W; 11 ± 1 min) at SL (partial pressure of inspired O2, 147.1 ± 0.5 Torr), in AH (73.8 ± 0.2 Torr), and in CH (75.7 ± 0.1 Torr). Peripheral fatigue was expressed as pre- to postexercise percent reduction in electrically evoked potentiated quadriceps twitch force (ΔQtw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (ΔVA). Resting CaO2 at SL and CH was similar, but CaO2 in AH was lower compared with SL and CH (17.3 ± 0.5, 19.3 ± 0.7, 20.3 ± 1.3 ml O2/dl, respectively). Winsp during exercise increased with acclimatization (SL: 387 ± 36, AH: 503 ± 53, CH: 608 ± 67 cmH2O·s(-1)·min(-1); P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQtw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P = 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH.

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).