Hyperhomocysteinaemia and lack of physical exercise are risk factors implicated in the development of cardiovascular disease (Nygard, 1995, 1997). Animal data suggest that intermittent exposure to hypoxic exercise decreases the availability of oxygen and increases anaerobic metabolism (Pastoris et al. 1995). Weiss et al. (1998) showed an increase in plasma total homocysteine (tHey) following 2-5 h of aerobic exercise. In the light of these observations, we investigated the implications of intermittent normobaric hypoxia on the metabolic responses to acute and chronic exercise. With ethical approval (Bro Taff Health Authority), thirty-two healthy male subjects aged 22 ± 3 (S.D.) years refrained from physical exercise 48 h prior to providing an overnight fasted venous blood sample (Pre) to measure plasma tHcy. Subjects were randomly assigned to a normoxic (N, n = 14) or hypoxic (H , n = 18) training group. They then all performed a cycling test to volitional exhaustion in normobaric normoxia (Fr.o, -20'93%; N, H) and normobaric hypoxia (FI,o, -16'0%; H). Training then involved 4 weeks of cycling exercise breathing either a normoxic (PI,o, 148-152 mmHg, N) or hypoxic gas (PI ,o, 113- 116 mmHg, H), three times per week for 20- 30 min at 70-85 % of the maximum heart rate determined either normoxically or hypoxically (189 ± 7 vs. 186 ± 13 beats min -\ n.s.). All subjects repeated the Pre measurements 4 days following completion of the last training session (Post). Hypoxic training increased Vo"max Pre (3'511 min -I) to Post (3'97 1 min -1), P < 0'05 (paired t test). Resting tHcy increased following normoxic training (6'9 to 7'6 p,moll-I), P < 0'05, and decreased following hypoxic training (7'5 to 6'7 p,moll-I), P = 0'05. There were no significant differences in red blood cell folate, serum BI2 or protein intake. Acute normoxic exercise following hypoxic training increased tHcy (6'7 to 7'9 p,moll-I), P < 0'05. These data suggest that normoxic training increases plasma tHcy, whereas hypoxic training decreases it. Research was supported by the British Oxygen Company.
|Number of pages||2|
|Journal||The Journal of Physiology|
|Publication status||Published - Feb 1999|