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Exposure to ultrafine particles (UFPs) from vehicle exhaust has been related to risk of cardiovascular and pulmonary disease and cancer, even though exposure assessment is difficult. We studied personal exposure in terms of number concentrations of UFPs in the breathing zone, using portable instruments in six 18-hr periods in 15 healthy nonsmoking subjects. Exposure contrasts of outdoor pollution were achieved by bicycling in traffic for 5 days and in the laboratory for 1 day. Oxidative DNA damage was assessed as strand breaks and oxidized purines in mononuclear cells isolated from venous blood the morning after exposure measurement. Cumulated outdoor and cumulated indoor exposures to UFPs each were independent significant predictors of the level of purine oxidation in DNA but not of strand breaks. Ambient air concentrations of particulate matter with an aero-dynamic diameter of ≤10 μm (PM10), nitrous oxide, nitrogen dioxide, carbon monoxide, and/or number concentration of UFPs at urban background or busy street monitoring stations was not a significant predictor of DNA damage, although personal UFP exposure was correlated with urban background concentrations of CO and NO2, particularly during bicycling in traffic. The results indicate that biologic effects of UFPs occur at modest exposure, such as that occurring in traffic, which supports the relationship of UFPs and the adverse health effects of air pollution.

SUMMARY1. Eleven men performed static contractions with the fingers (digits II and TIT), forearm (handgrip) and the knee extensors (knee angle 900) at 40 % maximal voluntary contraction (MVC) for 2 min. In seven of the subjects handgrip and knee extension were combined, both contractions held at 40 % MVC. At the end of the contraction, cuffs were inflated to 250 mmHg for 3 min around the extremity which had been contracting. Continuous measurements were performed of force, heart rate and intra-arterial blood pressure (a. brachialis; 20 cm proximally), before and during contraction as well as during the recovery with and without cuffs inflated.2. Heart rate and blood pressure increased momentarily with the onset of a contraction whereafter a gradual further increase took place. This pattern of response was similar for all muscle groups studied. The increases during the contractions were in the order: fingers, forearm, knee extensors and combined forearm-knee extensors, with the difference between each muscle group contraction being significant.3. In the recovery period from a contraction with the cuff(s) inflated, heart rate returned to control level. Blood pressure also dropped, but remained elevated above pre-contraction level until the cuff(s) was released.4. The present data during contraction are at variance with earlier observations showing that the cardiovascular response to a static contraction is proportional to the % MVYC regardless of the muscle mass involved in the contraction. Our findings are in line with the traditional concept of central and peripheral nervous inputs playing a role in the cardiovascular adjustments to exercise, with both the central and the peripheral factors being related to the mass of the muscles engaged in the exercise.

Morphological and biochemical characteristics of biopsies obtained from gastrocnemius (GAS) and triceps brachii muscle (TRI), as well as maximal O2 uptake (VO2 max) and O2 deficit, were determined in 10 well-trained cross-country skiers before and after a 2-wk stay (2,100 m above sea level) and training (2,700 m above sea level) at altitude. On return to sea level, VO2 max was the same as the prealtitude value, whereas an increase in O2 deficit (29%) and in short-term running performance (17%) was observed (P less than 0.05). GAS showed maintained capillary supply but a 10% decrease in mitochondrial enzyme activities (P less than 0.05), whereas an increase in capillary supply (P less than 0.05) but unchanged mitochondrial enzyme activities were observed in TRI. Buffer capacity was increased by 6% in both GAS and TRI (P less than 0.05). A positive correlation was found between the relative increase in buffer capacity of GAS and short-term running time (P less than 0.05). Thus the present study indicates no effect of 2 wk of altitude training on VO2 max but provides evidence to suggest an improvement in short-term exercise performance, which may be the result of an increase in muscle buffer capacity.

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