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The vascular strain is very high during heavy handgrip exercise, but the intensity and kinetics to reach peak blood flow, and peak oxygen uptake, are uncertain. We included 9 young (25 ± 2 yr) healthy males to evaluate blood flow and oxygen uptake responses during continuous dynamic handgrip exercise with increasing intensity. Blood flow was measured using Doppler-ultrasound, and venous blood was drawn from a deep forearm vein to determine arteriovenous oxygen difference (a-vO) during 6-min bouts of 60, 80, and 100% of maximal work rate (WR), respectively. Blood flow and oxygen uptake increased ( < 0.05) from 60%WR [557 ± 177(SD) ml/min; 56.0 ± 21.6 ml/min] to 80%WR (679 ± 190 ml/min; 70.6 ± 24.8 ml/min), but no change was seen from 80%WR to 100%WR Blood velocity (49.5 ± 11.5 to 58.1 ± 11.6 cm/s) and brachial diameter (0.49 ± 0.05 to 0.50 ± 0.06 cm) showed concomitant increases ( < 0.05) with blood flow from 60% to 80%WR whereas no differences were observed in a-vO Shear rate also increased ( < 0.05) from 60% (822 ± 196 s) to 80% (951 ± 234 s) of WR The mean response time (MRT) was slower ( < 0.05) for blood flow (60%WR 50 ± 22 s; 80%WR 51 ± 20 s; 100%WR 51 ± 23 s) than a-vO (60%WR 29 ± 9 s; 80%WR 29 ± 5 s; 100%WR 20 ± 5 s), but not different from oxygen uptake (60%WR 44 ± 25 s; 80%WR 43 ± 14 s; 100%WR 41 ± 32 s). No differences were observed in MRT for blood flow or oxygen uptake with increased exercise intensity. In conclusion, when approaching maximal intensity, oxygen uptake appeared to reach a critical level at ~80% of WR and be regulated by blood flow. This implies that high, but not maximal, exercise intensity may be an optimal stimulus for shear stress-induced small muscle mass training adaptations. This study evaluated blood flow regulation and oxygen uptake during small muscle mass forearm exercise with high to maximal intensity. Despite utilizing only a fraction of cardiac output, blood flow reached a plateau at 80% of maximal work rate and regulated peak oxygen uptake. Furthermore, the results revealed that muscle contractions dictated bulk oxygen delivery and yielded three times higher peak blood flow in the relaxation phase compared with mean values.

It has been a long-lasting debate whether the heart's stroke volume (SV) increases at high aerobic intensities or plateau. Further, sex and level of aerobic power are shown to influence the response. The purpose of this study was to investigate the SV at increasing intensities in elite female athletes and moderately trained females. 13 elite athletes and 11 moderately trained controls with maximal oxygen consumption (VO(2max)) of 67.1 ± 6.1 and 49.5 ± 2.3 mL ∙ min (- 1) ∙ kg (- 1), respectively, were recruited. SV was measured at rest, and running on a treadmill at 40%, 60%, 80% and 100% of VO(2max) using the single breath acetylene uptake (SB) technique. Both groups showed a significant (p<0.05) increase in SV from 40% of VO2max to VO(2max), with increases from 105.3 ± 19.0 to 129.1 ± 16.3 mL∙ beat(-1) for the elite females and from 68.7 ± 21.7 to 82.7 ± 14.0 mL ∙ beat (- 1) for the moderately trained. No differences were observed between groups in these increases, but the elite athletes displayed a larger (p<0.05) SV at all intensities. It is concluded that the SV increases at high aerobic intensities both in elite athlete females and moderately trained females.

Maximal strength training (MST) improves work efficiency. However, since blood flow is greatly dictated by muscle contractions in arms during exercise and vascular conductance is lower, it has been indicated that arms rely more upon adapting oxygen extraction than legs in response to the enhanced work efficiency. Thus, to investigate if metabolic and vascular responses are arm specific, we used Doppler-ultrasound and a catheter placed in the subclavian vein to measure blood flow and the arteriovenous oxygen difference during steady-state work in seven young men [24 ± 3 (SD) yr] following 6 wk of handgrip MST. As expected, MST improved maximal strength (49 ± 9 to 62 ± 10 kg) and the rate of force development (923 ± 224 to 1,086 ± 238 N/s), resulting in a reduced submaximal oxygen uptake (30 ± 9 to 24 ± 10 ml/min) and concomitantly increased work efficiency (9.3 ± 2.5 to 12.4 ± 3.9%) (all P < 0.05). In turn, the work efficiency improvement was associated with reduced blood flow (486 ± 102 to 395 ± 114 ml/min), mediated by a lower blood velocity (43 ± 8 to 32 ± 6 cm/s) (all P < 0.05). Conduit artery diameter and the arteriovenous oxygen difference remained unaltered. The maximal work test revealed an increased time to exhaustion (949 ± 239 to 1,102 ± 292 s) and maximal work rate (both P < 0.05) but no change in peak oxygen uptake. In conclusion, despite prior indications of metabolic and vascular limb-specific differences, these results reveal that improved work efficiency after small muscle mass strength training in the upper extremities is accompanied by a blood flow reduction and coheres with what has been documented for lower extremities. NEW & NOTEWORTHY Maximal strength training increases skeletal muscle work efficiency. Oxygen extraction has been indicated to be the adapting component with this increased work efficiency in arms. However, we document that decreased blood flow, achieved by blood velocity reduction, is the adapting mechanism responding to the improved aerobic metabolism in the forearm musculature.

Assessment of forearm oxygen uptake (trueV˙O2) during handgrip exercise is a keenly investigated concept for observing small muscle mass metabolism. Although a combination of Doppler ultrasound measurements of brachial artery blood flow (trueQ˙) and blood gas drawn from a deep forearm vein has been utilized to calculate forearm trueV˙O2 for more than two decades, the applicability of this experimental design may benefit from a thorough evaluation of its reliability during graded exercise. Therefore, we evaluated the reliability of this technique during incremental handgrip exercise in ten healthy young (24 ± 3(SD) years.) males. trueV˙O2 and work rate (WR) exhibited a linear relationship (1.0 W: 43.8 ± 10.1 mL·min−1; 1.5 W: 53.8 ± 14.1 mL·min−1; 2.0 W: 63.4 ± 16.3 mL·min−1; 2.5 W: 72.2 ± 17.6 mL·min−1; 3.0 W: 79.2 ± 18.6 mL·min−1; r = 0.65, P < 0.01). In turn, trueV˙O2 was strongly associated with trueQ˙ (1.0 W: 359 ± 86 mL·min−1; 1.5 W: 431 ± 112 mL·min−1; 2.0 W: 490 ± 123 mL·min−1; 2.5 W: 556 ± 112 mL·min−1; 3.0 W: 622 ± 131 mL·min−1; r = 0.96; P < 0.01), whereas arteriovenous oxygen difference (a‐vO2diff) remained constant following all WRs (123 ± 11–130 ± 10 mL·L−1). Average trueV˙O2 test–retest difference was −0.4 mL·min−1 with ±2SD limits of agreement (LOA) of 8.4 and −9.2 mL·min−1, respectively, whereas coefficients of variation (CVs) ranged from 4–7%. Accordingly, test–retest trueQ˙ difference was 11.9 mL·min−1 (LOA: 84.1 mL·min−1; −60.4 mL·min−1) with CVs between 4 and 7%. Test–retest difference for a‐vO 2diff was −0.28 mL·dL−1 (LOA: 1.26mL·dL −1; −1.82 mL·dL−1) with 3–5% CVs. In conclusion, our results revealed that forearm trueV˙O2 determination by Doppler ultrasound and direct venous sampling is linearly related to WR, and a reliable experimental design across a range of exercise intensities.