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Advancing age is associated with a decline in the strength of the skeletal muscles, including those of respiration. Respiratory muscles can be strengthened with nonrespiratory activities. We therefore hypothesized that regular exercise in the elderly would attenuate this age-related decline in respiratory muscle strength. Twenty-four healthy subjects older than 65 years were recruited (11 males and 13 females). A comprehensive physical activity survey was administered, and subjects were categorized as active (n = 12) or inactive (n = 12). Each subject underwent testing of maximum inspiratory and expiratory pressures (PI(max) and PE(max)). Diaphragmatic thickness (tdi) was measured via two-dimensional B-mode ultrasound. There were no significant differences between the active and inactive groups with respect to age (75 vs. 73 years) or body weight (69.1vs. 69.9 kg). There were more women (9) than men (3) in the inactive group. Diaphragm thickness was greater in the active group (0.31 +/- 0.06 cm vs. 0.25 +/- 0.04 cm; p = 0.011). PE(max) and PI(max) were also greater in the active group (130 +/- 44 cm H(2)O vs. 80 +/- 24 cm H(2)O; p = 0.002; and 99 +/- 32 cm H(2)O vs. 75 +/- 14 cm H(2)O; p = 0.03). There was a positive association between PI(max )and tdi (r = 0.43, p = 0.03). Regular exercise was positively associated with diaphragm muscle thickness in this cohort. As PE(max) was higher in the active group, we postulate that recruitment of the diaphragm and abdominal muscles during nonrespiratory activities may be the source of this training effect.

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Objective To estimate muscle oxygen uptake and quantify fatigue during exercise in ambulatory individuals with spinal muscular atrophy (SMA) and healthy controls. Methods Peak aerobic capacity (VO2peak) and workload (Wpeak) were measured by cardiopulmonary exercise test (CPET) in 19 ambulatory SMA patients and 16 healthy controls. Submaximal exercise (SME) at 40% Wpeak was performed for 10 minutes. Change in vastus lateralis deoxygenated hemoglobin, measured by near‐infrared spectroscopy, determined muscle oxygen uptake (ΔHHb) at rest and during CPET and SME. Dual energy X‐ray absorptiometry assessed fat‐free mass (FFM%). Fatigue was determined by percent change in workload or distance in the first compared to the last minute of SME (FatigueSME) and six‐minute walk test (Fatigue6MWT), respectively. Results ΔHHb‐PEAK, ΔHHb‐SME, VO2peak, Wpeak, FFM%, and 6MWT distance were lower (P < 0.001), and Fatigue6MWT and FatigueSME were higher (P < 0.001) in SMA compared to controls. ΔHHb‐PEAK correlated with FFM% (r = 0.50) and VO2peak (r = 0.41) only in controls. Only in SMA, Fatigue6MWT was inversely correlated with Wpeak (r = −0.69), and FatigueSME was inversely correlated with FFM% (r = −0.55) and VO2peak (r = −0.69). Interpretation This study provides further support for muscle mitochondrial dysfunction in SMA patients. During exercise, we observed diminished muscle oxygen uptake but no correlation with aerobic capacity or body composition. We also observed increased fatigue which correlated with decreased aerobic capacity, workload, and body composition. Understanding the mechanisms underlying diminished muscle oxygen uptake and increased fatigue during exercise in SMA may identify additional therapeutic targets that rescue symptomatic patients and mitigate their residual disease burden.