Factors affecting blood pressure during heavy weight lifting and static contractions.

Brachial arterial pressure was directly recorded in 31 healthy male volunteers through protocols examining the effects of the Valsalva maneuver, muscle size and strength, contraction force, contraction type (concentric, isometric, eccentric), changes in joint angle, and muscle fatigue on the blood pressure response to resistance exercise. Weight lifting at the same relative intensity produced similar increases in blood pressure, regardless of individual differences in muscle size or strength. Concentric, isometric, or eccentric exercise at the same relative intensity caused similar increases despite differences in force production. In weight lifting, the greatest increase in blood pressure occurred at the joint angle corresponding to the weakest point in the strength curve and the least at the angle corresponding to the strongest point. Isometric contractions of the same relative intensity at different joint angles produced identical blood pressures despite differences in absolute force production. When subjects attempted to maintain a maximum isometric contraction for 45 s, the blood pressure increase remained the same despite a marked diminution in force. Thus the magnitude of the blood pressure response depends on the degree of effort or central command and not actual force production. A brief Valsalva maneuver, which exaggerates the increase in blood pressure, is unavoidable when desired force production exceeds approximately 80% maximum voluntary contraction.

Validity of predicting mean arterial blood pressure during exercise.

PURPOSE: Mean arterial blood pressure (mean arterial pressure (MAP)) at rest is conventionally estimated as the product of the diastolic pressure plus one-third of the pulse pressure. Since pulse wave forms and the duration of diastole change during exercise, one might question the validity of this prediction equation for the exercise state. Our purpose was to test this by directly measuring blood pressure over a wide range of exercise intensities. METHODS: Pressure was recorded by arterial catheterization in 29 subjects performing progressive exercise and/or constant-load exercise at different intensities. Actual MAP was measured by integrating the area under the pulse curve and compared it with the value which was predicted from systolic and diastolic measures over heart rates ranging from 100 to 200 beats x min(-1). RESULTS: Predicted values were quite close to actual MAP, and the accuracy of the prediction equation changed minimally with increased exercise intensity. CONCLUSION: This method provides a valid estimation of MAP during exercise.

The effects of variations in the anti-G straining maneuver on blood pressure at +Gz acceleration.

The increase in blood pressure provided by the standard AGSM is caused by both the contraction of the muscles of the lower body and by an increased intrathoracic pressure due to a respiratory straining (Valsalva) maneuver. This study examined the relative effectiveness and fatigability of the two components at +1 Gz and during +Gz acceleration in a human centrifuge. Brachial arterial pressure was recorded from a pressure-tip transducer in six subjects performing isometric leg presses only and on a separate occasion while performing respiratory straining only. Measurements were made over a range of intensities for the leg press contractions and Valsalva maneuvers and were conducted at +1 Gz and during slow and rapid onset runs up to +5 Gz in a human centrifuge. Blood pressure was also recorded during pulsing or intermittent contractions of the legs. We found it difficult to completely separate the blood pressure response to the leg press component from that of the respiratory straining alone component, since a moderate respiratory straining maneuver usually accompanied forceful contractions of the legs. We conclude, however, that a major portion of the elevation in blood pressure caused by the AGSM can be attributed to contraction of the muscles of the lower body and that this component is less fatiguing than the respiratory straining component. At +1 Gz a pulsing isometric contraction of the legs was no more effective in elevating blood pressure than a constant isometric contraction over the same duration.

Hypertrophy without increased isometric strength after weight training.

Eight men (20-23 years) weight trained 3 days.week-1 for 19 weeks. Training sessions consisted of six sets of a leg press exercise (simultaneous hip and knee extension and ankle plantar flexion) on a weight machine, the last three sets with the heaviest weight that could be used for 7-20 repetitions. In comparison to a control group (n = 6) only the trained group increased (P less than 0.01) weight lifting performance (heaviest weight lifted for one repetition, 29%), and left and right knee extensor cross-sectional area (CAT scanning and computerized planimetry, 11%, P less than 0.05). In contrast, training caused no increase in maximal voluntary isometric knee extension strength, electrically evoked knee extensor peak twitch torque, and knee extensor motor unit activation (interpolated twitch method). These data indicate that a moderate but significant amount of hypertrophy induced by weight training does not necessarily increase performance in an isometric strength task different from the training task but involving the same muscle group. The failure of evoked twitch torque to increase despite hypertrophy may further indicate that moderate hypertrophy in the early stage of strength training may not necessarily cause an increase in intrinsic muscle force generating capacity.

Effect of training on the blood pressure response to weight lifting.

Six young men weight trained 3 days.week-1 for 19 weeks, on each day doing 3 warm-up sets of 20 repetitions followed by 1 set each at 15-20, 10-15, and 7-10 RM (Day 1), 3 sets at 15-20 RM (Day 2), and 1 set at 15-20 and 2 sets at 10-15 RM (Day 3) of a seated bilateral leg press exercise. Training increased (P < 0.05) the maximal single leg press lift (1-RM, 26%) and knee extensor cross-sectional area (12%). Arterial (brachial artery catheter) and esophageal (probe) pressure responses were measured before and after training as subjects did sets of as many repetitions as possible up to 20 reps with 50, 70, 80, 85 and 87.5% 1-RM. After training, peak values of systolic pressure attained during a set (M pre/post, mm Hg) were significantly (P < 0.05) increased at 85% (325/360, 10.8%) 1-RM. Peak diastolic pressure increased significantly at 50 (136/151, 11.0%), 70 (185/200, 8.1%), and 80% (215/234, 8.8%). Peak esophageal pressure increased significantly at 80% (71/91, 28.2%) 1-RM. For a given absolute weight lifted, all responses were markedly reduced after training. It is concluded that weight training can (a) increase the peak arterial and esophageal pressure responses attained during maximal weight lifting exercise, and (b) reduce the arterial and esophageal pressure responses to lifting the same absolute weight.

Comparison of blood pressure response to isokinetic and weight-lifting exercise.

Brachial arterial pressure, oesophageal pressure, and knee joint angle were monitored in eight untrained young men as they performed bilateral leg-press actions (simultaneous hip and knee extension and ankle plantarflexion) against resistance. Single maximal leg-press actions on an isokinetic device evoked mean peak arterial (systolic/diastolic) pressures of 35.4/26.2 and 34.0/23.4 kPa at lever arm velocities of 0.262 and 1.31 rad.s-1, respectively. The corresponding oesophageal pressures were 13.2 and 10.4 kPa, respectively. Although the peak force was 30% greater, and duration of the action 3-4 times longer at 0.262 than 1.31 rad.s-1, the arterial and oesophageal pressure responses did not differ. On a weight-lifting machine, a set of repetitions [mean (SEM): 11 (3)] to failure at 80-90% one repetition maximum evoked peak arterial pressures of 45.5/32.8 kPa; the corresponding oesophageal pressure was 15.7 kPa. The peak systolic and diastolic pressures observed during weight-lifting were significantly (P < 0.05) higher than during isokinetic actions at both velocities, whereas oesophageal pressure was more elevated only in relation to isokinetic actions at the higher velocity. These data indicate that resisted leg-press actions cause extreme elevations in arterial blood pressure. The degree of voluntary effort is the major determinant of the blood pressure response, rather than the resistance mode or the type (concentric, eccentric, isometric) of muscle action. Repetitive resistance exercise (e.g. a set of repetitions to failure in weight-lifting) tends to produce greater pressure elevations than isolated, single maximal effort actions.