Task Failure during Exercise to Exhaustion in Normoxia and Hypoxia Is Due to Reduced Muscle Activation Caused by Central Mechanisms While Muscle Metaboreflex Does Not Limit Performance

Abstract

To determine whether task failure during incremental exercise to exhaustion (IE) is principally due to reduced neural drive and increased metaboreflex activation eleven men (22 ± 2 years) performed a 10 s control isokinetic sprint (IS; 80 rpm) after a short warm-up. This was immediately followed by an IE in normoxia (Nx, PIO2:143 mmHg) and hypoxia (Hyp, PIO2:73 mmHg) in random order, separated by a 120 min resting period. At exhaustion, the circulation of both legs was occluded instantaneously (300 mmHg) during 10 or 60 s to impede recovery and increase metaboreflex activation. This was immediately followed by an IS with open circulation. Electromyographic recordings were obtained from the vastus medialis and lateralis. Muscle biopsies and blood gases were obtained in separate experiments. During the last 10 s of the IE, pulmonary ventilation, VO2, power output and muscle activation were lower in hypoxia than in normoxia, while pedaling rate was similar. Compared to the control sprint, performance (IS-Wpeak) was reduced to a greater extent after the IE-Nx (11% lower P < 0.05) than IE-Hyp. The root mean square (EMGRMS) was reduced by 38 and 27% during IS performed after IE-Nx and IE-Hyp, respectively (Nx vs. Hyp: P < 0.05). Post-ischemia IS-EMGRMS values were higher than during the last 10 s of IE. Sprint exercise mean (IS-MPF) and median (IS-MdPF) power frequencies, and burst duration, were more reduced after IE-Nx than IE-Hyp (P < 0.05). Despite increased muscle lactate accumulation, acidification, and metaboreflex activation from 10 to 60 s of ischemia, IS-Wmean (+23%) and burst duration (+10%) increased, while IS-EMGRMS decreased (-24%, P < 0.05), with IS-MPF and IS-MdPF remaining unchanged. In conclusion, close to task failure, muscle activation is lower in hypoxia than in normoxia. Task failure is predominantly caused by central mechanisms, which recover to great extent within 1 min even when the legs remain ischemic. There is dissociation between the recovery of EMGRMS and performance. The reduction of surface electromyogram MPF, MdPF and burst duration due to fatigue is associated but not caused by muscle acidification and lactate accumulation. Despite metaboreflex stimulation, muscle activation and power output recovers partly in ischemia indicating that metaboreflex activation has a minor impact on sprint performance.

Keywords: EMG; electromyography; exhaustion; fatigue; high-intensity; hypoxia; lactate; performance.

Figure 1

Experimental protocol. The experimental day started with a warm-up followed by 4.5 min of slow unloaded pedaling and a 30 s resting phase, while the subjects became ready to perform the first sprint (isokinetic, 10 s at 80 rpm) at the 5th minute after the end of the warm-up. This sprint was used as a control sprint and was always performed in normoxia. Five minutes later, an incremental exercise to exhaustion began in normoxia (P_IO₂: ~143 mmHg) or acute hypoxia (P_IO₂: ~73 mmHg). The order of the incremental exercise test was randomized. Between the two incremental exercise tests, the subjects were allowed to rest during 120 min. At the end of the incremental exercise test, bilateral cuffs were inflated at maximal speed and pressure (i.e., 300 mmHg) to occlude completely and instantaneously the circulation (ischemia) of the legs. The incremental exercise test in normoxia and hypoxia ended with an ischemia period of 10 s on one experimental day and 60 s on another day. The order of the duration of the ischemia period was randomized. At the end of the ischemia period, the subjects performed a 10 s isokinetic sprint as hard and fast as possible (80 rpm) while the cuffs were always instantaneously deflated at the beginning of the post-ischemia sprints.

Figure 2

Power output and EMG of a representative subject. Schematic representation of the power output (upper panels), raw EMG (2nd row), rectified EMG (3rd row) and rectified and smoothed EMG (lower panels), during the control sprint, last 6 s of the incremental exercise (IE) in normoxia (Nx), subsequent 10-s isokinetic sprint at 80 rpm (normoxia), IE in hypoxia (Hyp) and subsequent 10-s isokinetic sprint at 80 rpm (normoxia). The connected vertical arrows indicate the duration of the ischemia period, which in this example was 10 s.

Figure 3

Power output. Peak (Wpeak-i) and mean (Wmean) power output during sprint exercise performed at the end of an incremental exercise to exhaustion in normoxia (P_IO₂ ≈ 143 mmHg) and severe hypoxia (P_IO₂ ≈ 73 mmHg), after 10 or 60 s of occlusion of the circulation. ^aP < 0.05 compared with the other conditions; ^bP < 0.05 compared with Nx10s; ^cP < 0.05 compared with Nx60s.