Muscle fatigue resistance during stimulated contractions is reduced in young male smokers.

Aim: To determine whether muscle function is compromised in healthy smokers in comparison with activity-matched non-smokers. Methods: Nine male smokers (aged 22.2 ± 2.5 years: mean ± SD) with a smoking history of 2.5 ± 3.1 pack years, and ten male control participants (25.4 ± 2.9 years) matched for physical activity level participated in this study. Knee extensor strength was measured using isometric maximal voluntary contractions. Voluntary activation of the quadriceps and co-activation of the biceps femoris were determined using interpolated twitches and surface electromyography respectively. The frequency-torque relationship and fatigue resistance were assessed with electrically evoked contractions. A fatigue index was determined as the ratio of final torque to initial torque during a series of isometric contractions (2 min; 30 Hz; 1 s contraction/1 s rest). Quadriceps anatomical cross sectional area was measured with MRI at 50% of femur length. Results: Maximal voluntary contraction torque, quadriceps anatomical cross sectional area, knee extensor torque/quadriceps cross sectional area, activation, co-activation and force-frequency relationship were similar, whereas the fatigue index was 17% lower in smokers than non-smokers. Conclusion: In young men smoking does not significantly affect quadriceps muscle mass and contractile properties, but does reduce fatigue resistance of the quadriceps muscle, which was not attributable to differences in physical activity. © 2007 The Authors

Reduced β-adrenergic sensitivity in patients with type 1 diabetes and hypoglycemia unawareness

OBJECTIVE - We tested the hypothesis that impaired tissue sensitivity to catecholamines contributes to hypoglycemia unawareness in subjects with type 1 diabetes. RESEARCH DESIGN AND METHODS - A total of 21 subjects with type 1 diabetes underwent a standardized insulin infusion protocol to produce a stepwise decrease in plasma glucose to 45-min plateaus of 4.3, 3.6, 3.0, and 2.3 mmol/l. Glycemic thresholds, maximum responses for adrenergic and neuroglycopenic symptoms, and counterregulatory hormones were determined. Patients were classified as hypoglycemia unaware if the initiation of adrenergic symptoms occurred at a plasma glucose level 2 SD below that of nondiabetic volunteers. β-Adrenergic sensitivity was measured as the dose of isoproterenol required to produce an increment in heart rate of 25 beats per minute above baseline (I25) in resting subjects. RESULTS - Subjects with type 1 diabetes and hypoglycemia unawareness experienced the onset of adrenergic symptoms at a lower plasma glucose level than did those with awareness (2.5 ± 0.1 vs. 3.7 ± 0.1 mmol/l, P < 0.001), whereas neuroglycopenic symptoms occurred at similar glucose levels (2.7 ± 0.2 vs. 2.8 ± 0.1 mmol/l). The plasma glucose levels for counterregulatory hormone secretion (epinephrine 2.9 ± 0.2 vs. 4.1 ± 0.2 mmol/l; norepinephrine 2.7 ± 0.1 vs. 3.2 ± 0.2 mmol/l; cortisol 2.5 ± 0.2 vs. 3.3 ± 0.2 mmol/l, P < 0.01) were also lower in subjects with unawareness. The maximal epinephrine (1,954 ± 486 vs. 5,332 ± 1,059 pmol/l, P < 0.01), norepinephrine (0.73 ± 0.14 vs. 1.47 ± 0.21 nmol/l, P = 0.04), and cortisol (276 ± 110 vs. 579 ± 83 nmol/l, P < 0.01) responses were reduced in the unaware group. I25 was greater in unaware subjects than in subjects without unawareness (1.5 ± 0.3 vs. 0.8 ± 0.2 μg), where I25 was not different from that of controls (0.8 ± 0.2 μg). CONCLUSIONS - We conclude that subjects with type 1 diabetes and hypoglycemia unawareness have reduced β-adrenergic sensitivity, which may contribute to their impaired adrenergic warning symptoms during hypoglycemia