Electromyographic adjustments during continuous and intermittent incremental fatiguing cycling.

We studied the sensitivity of electromyographic (EMG) variables to load and muscle fatigue during continuous and intermittent incremental cycling. Fifteen men attended three laboratory sessions. Visit 1: lactate threshold, peak power output, and VO2max . Visits 2 and 3: Continuous (more fatiguing) and intermittent (less fatiguing) incremental cycling protocols [20%, 40%, 60%, 80% and 100% of peak power output (PPO)]. During both protocols, multichannel EMG signals were recorded from vastus lateralis: muscle fiber conduction velocity (MFCV), instantaneous mean frequency (iMNF), and absolute and normalized root mean square (RMS) were analyzed. MFCV differed between protocols (P < 0.001), and only increased consistently with power output during intermittent cycling. RMS parameters were similar between protocols, and increased linearly with power output. However, only normalized RMS was higher during the more fatiguing 100% PPO stage of the continuous protocol [continuous-intermittent mean difference (95% CI): 45.1 (8.5% to 81.7%)]. On the contrary, iMNF was insensitive to load changes and muscle fatigue (P = 0.14). Despite similar power outputs, continuous and intermittent cycling influenced MFCV and normalized RMS differently. Only normalized RMS was sensitive to both increases in power output (in both protocols) and muscle fatigue, and thus is the most suitable EMG parameter to monitor changes in muscle activation during cycling.

Increase of pro-oxidants with no evidence of lipid peroxidation in exhaled breath condensate after a 10-km race in non-athletes

It is a well-established fact that exercise increases pro-oxidants and favors oxidative stress; however, this phenomenon has been poorly studied in human lungs. Pro-oxidative generation (H2O2, NO2 −), lipid peroxidation markers (MDA), and inflammation (pH) in exhaled breath condensate (EBC) have been determined through data from 10 active subjects who ran 10 km; samples were obtained immediately before, at 20, and at 80 min post-exertion. In EBC, the concentration of H2O2at 80 min post-exertion was increased. NO2 − concentration showed a tendency to increase at 80 min post-exertion, with no variations in MDA and pH. No variations of NO2 − were found in plasma, while there was an increase of NO2 − at 80 min post-exertion in the relation between EBC and plasma. NO2 − in EBC did not correlate to plasmatic NO2 −, while it did correlate directly with H2O2 in EBC, suggesting a localized origin for the exercise-related NO2 − increase in EBC. MDA in plasma did not increase nor correlate with MDA in EBC. In conclusion, high-intensity exercise increases lung-originated pro-oxidants in non-athlete subjects with no evidence of early lipid peroxidation and changes in the pH value in EBC

Increase of pro-oxidants with no evidence of lipid peroxidation in exhaled breath condensate after a 10-km race in non-athletes.

It is a well-established fact that exercise increases pro-oxidants and favors oxidative stress; however, this phenomenon has been poorly studied in human lungs. Pro-oxidative generation (H(2)O(2), NO(2) (-)), lipid peroxidation markers (MDA), and inflammation (pH) in exhaled breath condensate (EBC) have been determined through data from 10 active subjects who ran 10 km; samples were obtained immediately before, at 20, and at 80 min post-exertion. In EBC, the concentration of H(2)O(2) at 80 min post-exertion was increased. NO(2) (-) concentration showed a tendency to increase at 80 min post-exertion, with no variations in MDA and pH. No variations of NO(2) (-) were found in plasma, while there was an increase of NO(2) (-) at 80 min post-exertion in the relation between EBC and plasma. NO(2) (-) in EBC did not correlate to plasmatic NO(2) (-), while it did correlate directly with H(2)O(2) in EBC, suggesting a localized origin for the exercise-related NO(2) (-) increase in EBC. MDA in plasma did not increase nor correlate with MDA in EBC. In conclusion, high-intensity exercise increases lung-originated pro-oxidants in non-athlete subjects with no evidence of early lipid peroxidation and changes in the pH value in EBC.