Mark A. Babcock

Exercise-induced diaphragmatic fatigue in healthy humans

1. Twelve healthy subjects (33 +/‐ 3 years) with a variety of fitness levels (maximal oxygen uptake (VO2, max) = 61 +/‐ 4 ml kg‐1 min‐1, range 40‐80), exercised at 95 and 85% VO2, max to exhaustion (mean time = 14 +/‐ 3 and 31 +/‐ 8 min, expired ventilation (VE) over final minute of exercise = 149 +/‐ 9 and 126 +/‐ 10 l min‐1). 2. Bilateral transcutaneous supramaximal phrenic nerve stimulation (BPNS) was performed before and immediately after exercise at four lung volumes, and 400 ms tetanic stimulations were performed at 10 and 20 Hz. The coefficients of variation of repeated measurements for the twitch transdiaphragm pressures (Pdi) were +/‐ 7‐10% and for compound muscle action potentials (M wave) +/‐ 10‐15%. 3. Following exercise at 95% of VO2, max, group mean Pdi twitch values were reduced at all lung volumes (range ‐8 +/‐ 3 to ‐32 +/‐ 5%) and tetanically stimulated Pdi values were reduced at both 10 and 20 Hz (‐21 +/‐ 3 and ‐13 +/‐ 2%, respectively) (P = 0.001‐0.047). Following exercise at 85% VO2, max, stimulated Pdi values were reduced at all lung volumes and stimulating frequencies, but only significantly so with the twitch at functional residual capacity (‐15 +/‐ 5%). Stimulated Pdi values recovered partially by 30 min post‐exercise and almost completely by an average time of 70 min. 4. The fall in stimulated Pdi values post‐exercise was significantly correlated with the percentage increase in diaphragmatic work (integral of Pdi min‐1) from rest to end‐exercise and the relative intensity of the exercise. 5. The integral of Pdi min‐1 and the integral of Po min‐1 (Po, esophageal pressure) rose together from rest through the fifth to tenth minute of exercise, after which integral of Pdi min‐1 plateaued even though integral of Po min‐1, VE and inspiratory flow rate all continued to rise substantially until exercise terminated. Thus, the relative contribution of the diaphragm to total respiratory motor output was progressively reduced with exercise duration. 6. We conclude that significant diaphragmatic fatigue is caused by the ventilatory requirements imposed by heavy endurance exercise in healthy persons with a variety of fitness levels. The magnitude of the fatigue and the likelihood of its occurrence increases as the relative intensity of the exercise exceeds 85% of VO2, max.

Exercise on-transient gas exchange kinetics are slowed as a function of age.

The purpose was to characterize gas exchange kinetics following the on-transient of exercise in men aged 30-80 yr. Forty-six men completed square wave exercise tests from loadless cycling to subventilatory threshold (V(E)T) work rates with gas exchange measured breath-by-breath. Signal averaged data were fit with a monoexponential equation to derive time constants (tau) for gas exchange and ventilation (tau VO2, tau VCO2, tau VE) and heart rate (tau HR). There was a significant slowing of ventilation and gas exchange kinetics across age with linear regression yielding an increase of 0.67 s.yr-1 for tau VO2 (39 s in young to 61 s in old), 0.57 s.yr-1 for tau VCO2, and 0.65 s.yr-1 for tau VE, whereas tau HR (44 to 41 s) was not changed significantly. The slowed VO2 kinetics with age may reflect limitations in muscle blood flow or in control of the rate of oxidative metabolism. The less marked slowing of tau VCO2 compared with tau VO2 across age may reflect reduced CO2 storage capacity with loss of muscle tissue. The tau VE change across age was similar to that for tau VCO2 (tau VE/tau VCO2 unchanged). The present study demonstrated marked age-related slowing of gas exchange dynamics at exercise onset.

Effects of aerobic endurance training on gas exchange kinetics of older men

The kinetics of gas exchange at the on-transient of exercise are appreciably slowed in older individuals. Eight older men (72 yr) completed 6 months of aerobic cycle training. Ventilation and gas exchange kinetics were determined at the onset of a below threshold (ventilatory threshold, V(E)T) square wave exercise function and compared with control values (N = 4, age 70 yr). Gas exchange data were measured breath-by-breath and signal averaged data were fit with a monoexponential function to determine the time constants (tau). The training group showed significant increases in VO2max (20%) and VO2 at V(E)T (21%). The tau for oxygen uptake kinetics decreased significantly (62.2 +/- 15.5 to 31.9 +/- 7.0 s). The tau VCO2 (70.9 +/- 10.9 to 43.8 +/- 11.4 s) and tau VE (89.2 +/- 18.0 to 50.4 +/- 11.3) also were significantly faster posttraining; however, tau HR (38.1 +/- 20.5 to 28.6 +/- 7.2) was not significantly altered. Thus, with a vigorous training program, the kinetics of gas exchange of older individuals were faster, and approached values reported in fit young subjects.

Respiratory muscle fatigue during exercise: implications for performance.

Heavy whole-body exercise, requiring a 10- to 15-fold increase in minute ventilation, encroaches on the capacities of the respiratory muscle system to respond. Recently, using the technique of bilateral phrenic nerve stimulation, it has been shown that heavy endurance exercise (> 85% of VO2max) lasting > 8-10 min causes diaphragmatic fatigue (15-30% reduction in transdiaphragmatic pressures when electrically stimulated at low frequencies [1-20 Hz] supramaximally). The fatigue appears to be due to an interaction of diaphragmatic work (i.e., pressure production) combined with effects related to exercise intensity (i.e., increased blood flow competition with the locomotor muscles and increased production of metabolic by-products) and requires > 60 min for recovery. Fitness (i.e., as implied from VO2max) appears to allow greater diaphragmatic work for a similar degree of fatigue. Unloading the respiratory muscles (with helium/oxygen gas or using a pressure-assist device) during heavy exercise < 90-95% of VO2max does not appear to alter exercise time, VO2max, or minute ventilation, implying that respiratory muscle fatigue plays little role in altering human performance at these work intensities. However, unloading the respiratory system with helium at work intensities > 90-95% of VO2max has been shown to improve exercise time. This would imply that respiratory muscle fatigue may play a role in limiting human performance at the extremes of human performance or that other factors related to the respiratory system (i.e., alterations in the sensation of dyspnea or mechanical load) may play an important role.