The physiology of rowing with perspective on training and health.

PURPOSE: This review presents a perspective on the expansive literature on rowing. METHODS: The PubMed database was searched for the most relevant literature, while some information was obtained from books. RESULTS: Following the life span of former rowers paved the way to advocate exercise for health promotion. Rowing involves almost all muscles during the stroke and competition requires a large oxygen uptake, which is challenged by the pulmonary diffusion capacity and restriction in blood flow to the muscles. Unique training adaptations allow for simultaneous engagement of the legs in the relatively slow movement of the rowing stroke that, therefore, involves primarily slow-twitch muscle fibres. Like other sport activities, rowing is associated with adaptation not only of the heart, including both increased internal diameters and myocardial size, but also skeletal muscles with hypertrophy of especially slow-twitch muscle fibres. The high metabolic requirement of intense rowing reduces blood pH and, thereby, arterial oxygen saturation decreases as arterial oxygen tension becomes affected. CONCLUSION: Competitive rowing challenges most systems in the body including pulmonary function and circulatory control with implication for cerebral blood flow and neuromuscular activation. Thus, the physiology of rowing is complex, but it obviously favours large individuals with arms and legs that allow the development of a long stroke. Present inquiries include the development of an appropriately large cardiac output despite the Valsalva-like manoeuvre associated with the stroke, and the remarkable ability of the brain to maintain motor control and metabolism despite marked reductions in cerebral blood flow and oxygenation.

Atrial Natriuretic Peptide and Acute Changes in Central Blood Volume by Hyperthermia in Healthy Humans.

BACKGROUND: Hyperthermia induces vasodilatation that reduces central blood volume (CBV), central venous pressure (CVP) and mean arterial pressure (MAP). Inhibition of atrial natriuretic peptide (ANP) could be a relevant homeostatic defense mechanism during hyperthermia with a decrease in CBV. The present study evaluated how changes in plasma ANP reflect the changes in CBV during hyperthermia. METHODS: Ten healthy subjects provided with a water perfused body suit increased body core temperature 1 °C. In situ labeled autologous red blood cells were used to measure the CBV with a gamma camera. Regions of interest were traced manually on the images of the whole body blood pool scans. Two measures of CBV were used: Heart/whole body ratio and thorax/whole body ratio. CVP and MAP were recorded. Arterial (ANPart) and venous plasma ANP were determined by radioimmunoassay. RESULTS: The ratio thorax/whole body and heart/whole body decreased 7 % and 11 %, respectively (p<0.001). MAP and CVP decreased during hyperthermia by 6.8 and 5.0 mmHg, respectively (p<0.05; p<0.001). Changes in both thorax/whole body (R=0.80; p<0.01) and heart/whole body ratios (R=0.78; p<0.01) were correlated with changes in ANPart. However, there was no correlation between venous ANP and changes in CBV, nor between ANPart and MAP or CVP. CONCLUSION: Arterial but not venous plasma concentration of ANP, is correlated to changes in CBV, but not to pressures. We suggest that plasma ANPart may be used as a surrogate marker of acute CBV changes.

Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans.

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.

Kidneys extract BNP and NT-proBNP in healthy young men.

Renal metabolism of the cardiac marker NH2-terminal-pro-brain natriuretic peptide (NT-proBNP) has been suggested. Therefore, we determined the renal extraction ratios of NT-proBNP and its bioactive coproduct brain natriuretic peptide (BNP) at rest and during exercise. In addition, the cerebral ratios were evaluated. Ten young healthy men were investigated at baseline, during moderate cycle exercise (heart rate: 140, Borg scale: 14-15), and in the recovery with BNP and NT-proBNP measured from the brachial artery and the jugular and renal veins, and the renal and cerebral extraction ratios (Ext-Ren and Ext-Cer, respectively) were calculated. Cardiac output, stroke volume, heart rate, mean arterial pressures, and estimated glomerular filtration were determined. BNP and NT-proBNP were extracted by the kidneys but not by the brain. We observed no effect of exercise. The mean values (+/- SE) of Ext-Ren of NT-proBNP were similar (0.19 +/- 0.05, 0.21 +/- 0.06, and 0.12 +/- 0.03, respectively) during the three sessions (P > 0.05). Also the Ext-Ren of BNP were similar (0.18 +/- 0.07, 0.15 +/- 0.11, and 0.14 +/- 0.06, respectively; P > 0.05). There were no significant differences between Ext-Ren of BNP and NT-proBNP during the three sessions (P > 0.05). The Ext-Cer of both peptides varied insignificantly between -0.21 +/- 0.15 and 0.11 +/- 0.08. The renal extraction ratio of both BNP and NT-proBNP is approximately 0.15-0.20. There is no cerebral extraction, and short-term moderate exercise does not affect these values. Our findings suggest that the kidneys extract BNP and NT-proBNP to a similar extent in healthy young men.

Limitations to systemic and locomotor limb muscle oxygen delivery and uptake during maximal exercise in humans.

Reductions in systemic and locomotor limb muscle blood flow and O2 delivery limit aerobic capacity in humans. To examine whether O2 delivery limits both aerobic power and capacity, we first measured systemic haemodynamics, O2 transport and O2 uptake during incremental and constant (372 +/- 11 W; 85% of peak power; mean +/- S.E.M.) cycling exercise to exhaustion (n = 8) and then measured systemic and leg haemodynamics and during incremental cycling and knee-extensor exercise in male subjects (n = 10). During incremental cycling, cardiac output and systemic O2 delivery increased linearly to 80% of peak power (r2 = 0.998, P < 0.001) and then plateaued in parallel to a decline in stroke volume (SV) and an increase in central venous and mean arterial pressures (P < 0.05). In contrast, heart rate and increased linearly until exhaustion (r2 = 0.993; P < 0.001) accompanying a rise in systemic O2 extraction to 84 +/- 2%. In the exercising legs, blood flow and O2 delivery levelled off at 73-88% of peak power, blunting leg per unit of work despite increasing O2 extraction. When blood flow increased linearly during one-legged knee-extensor exercise, per unit of work was unaltered on fatigue. During constant cycling, , SV, systemic O2 delivery and reached maximal values within approximately 5 min, but dropped before exhaustion (P < 0.05) despite increasing or stable central venous and mean arterial pressures. In both types of maximal cycling, the impaired systemic O2 delivery was due to the decline or plateau in because arterial O2 content continued to increase. These results indicate that an inability of the circulatory system to sustain a linear increase in O2 delivery to the locomotor muscles restrains aerobic power. The similar impairment in SV and O2 delivery during incremental and constant load cycling provides evidence for a central limitation to aerobic power and capacity in humans.

Dynamic cerebral autoregulation during exhaustive exercise in humans.

We investigated whether dynamic cerebral autoregulation is affected by exhaustive exercise using transfer-function gain and phase shift between oscillations in mean arterial pressure (MAP) and middle cerebral artery (MCA) mean blood flow velocity (V(mean)). Seven subjects were instrumented with a brachial artery catheter for measurement of MAP and determination of arterial Pco(2) (Pa(CO(2))) while jugular venous oxygen saturation (Sv(O(2))) was determined to assess changes in whole brain blood flow. After a 10-min resting period, the subjects performed dynamic leg-cycle ergometry at 168 +/- 5 W (mean +/- SE) that was continued to exhaustion with a group average time of 26.8 +/- 5.8 min. Despite no significant change in MAP during exercise, MCA V(mean) decreased from 70.2 +/- 3.6 to 57.4 +/- 5.4 cm/s, Sv(O(2)) decreased from 68 +/- 1 to 58 +/- 2% at exhaustion, and both correlated to Pa(CO(2)) (5.5 +/- 0.2 to 3.9 +/- 0.2 kPa; r = 0.47; P = 0.04 and r = 0.74; P < 0.001, respectively). An effect on brain metabolism was indicated by a decrease in the cerebral metabolic ratio of O(2) to [glucose + one-half lactate] from 5.6 to 3.8 (P < 0.05). At the same time, the normalized low-frequency gain between MAP and MCA V(mean) was increased (P < 0.05), whereas the phase shift tended to decrease. These findings suggest that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in Pa(CO(2)).

Cerebral metabolism during upper and lower body exercise.

When continuation of exercise calls for a "will," the cerebral metabolic ratio of O2 to (glucose + lactate) decreases, with the largest reduction (30-50%) at exhaustion. Because a larger effort is required to exercise with the arms than with the legs, we tested the hypothesis that the reduction in the cerebral metabolic ratio would become more pronounced during arm cranking than during leg exercise. The cerebral arterial-venous differences for blood-gas variables, glucose, and lactate were evaluated in two groups of eight subjects during exhaustive arm cranking and leg exercise. During leg exercise, exhaustion was elicited after 25 +/- 6 (SE) min, and the cerebral metabolic ratio was reduced from 5.6 +/- 0.2 to 3.5 +/- 0.2 after 10 min and to 3.3 +/- 0.3 at exhaustion (P < 0.05). Arm cranking lasted for 35 +/- 4 min and likewise decreased the cerebral metabolic ratio after 10 min (from 6.7 +/- 0.4 to 5.0 +/- 0.3), but the nadir at exhaustion was only 4.7 +/- 0.4, i.e., higher than during leg exercise (P < 0.05). The results demonstrate that exercise decreases the cerebral metabolic ratio when a conscious effort is required, irrespective of the muscle groups engaged. However, the comparatively small reduction in the cerebral metabolic ratio during arm cranking suggests that it is influenced by the exercise paradigm.

Cerebral carbohydrate cost of physical exertion in humans.

Above a certain level of cerebral activation the brain increases its uptake of glucose more than that of O(2), i.e., the cerebral metabolic ratio of O(2)/(glucose + 12 lactate) decreases. This study quantified such surplus brain uptake of carbohydrate relative to O(2) in eight healthy males who performed exhaustive exercise. The arterial-venous differences over the brain for O(2), glucose, and lactate were integrated to calculate the surplus cerebral uptake of glucose equivalents. To evaluate whether the amount of glucose equivalents depends on the time to exhaustion, exercise was also performed with beta(1)-adrenergic blockade by metoprolol. Exhaustive exercise (24.8 +/- 6.1 min; mean +/- SE) decreased the cerebral metabolic ratio from a resting value of 5.6 +/- 0.2 to 3.0 +/- 0.4 (P < 0.05) and led to a surplus uptake of glucose equivalents of 9 +/- 2 mmol. beta(1)-blockade reduced the time to exhaustion (15.8 +/- 1.7 min; P < 0.05), whereas the cerebral metabolic ratio decreased to an equally low level (3.2 +/- 0.3) and the surplus uptake of glucose equivalents was not significantly different (7 +/- 1 mmol; P = 0.08). A time-dependent cerebral surplus uptake of carbohydrate was not substantiated and, consequently, exhaustive exercise involves a brain surplus carbohydrate uptake of a magnitude comparable with its glycogen content.

Brain and central haemodynamics and oxygenation during maximal exercise in humans.

During maximal exercise in humans, fatigue is preceded by reductions in systemic and skeletal muscle blood flow, O(2) delivery and uptake. Here, we examined whether the uptake of O(2) and substrates by the human brain is compromised and whether the fall in stroke volume of the heart underlying the decline in systemic O(2) delivery is related to declining venous return. We measured brain and central haemodynamics and oxygenation in healthy males (n= 13 in 2 studies) performing intense cycling exercise (360 +/- 10 W; mean +/-s.e.m.) to exhaustion starting with either high (H) or normal (control, C) body temperature. Time to exhaustion was shorter in H than in C (5.8 +/- 0.2 versus 7.5 +/- 0.4 min, P < 0.05), despite heart rate reaching similar maximal values. During the first 90 s of both trials, frontal cortex tissue oxygenation and the arterial-internal jugular venous differences (a-v diff) for O(2) and glucose did not change, whereas middle cerebral artery mean flow velocity (MCA V(mean)) and cardiac output increased by approximately 22 and approximately 115%, respectively. Thereafter, brain extraction of O(2), glucose and lactate increased by approximately 45, approximately 55 and approximately 95%, respectively, while frontal cortex tissue oxygenation, MCA V(mean) and cardiac output declined approximately 40, approximately 15 and approximately 10%, respectively. At exhaustion in both trials, systemic VO(2) declined in parallel with a similar fall in stroke volume and central venous pressure; yet the brain uptake of O(2), glucose and lactate increased. In conclusion, the reduction in stroke volume, which underlies the fall in systemic O(2) delivery and uptake before exhaustion, is partly related to reductions in venous return to the heart. Furthermore, fatigue during maximal exercise, with or without heat stress, in healthy humans is associated with an enhanced rather than impaired brain uptake of O(2) and substrates.

Bilateral leg extension power and fat-free mass in young oarsmen.

We evaluated the impact of bilateral leg extension power and fat-free mass on 2000 m rowing ergometer performance in 332 young oarsmen (age 21+/-2 years, height 1.76+/-0.05 m, body mass 62+/-6 kg; mean+/-s). The 2000 m rowing performance time was correlated with height (1.62-1.93 m; R2=0.23, P<0.001), body mass (53-95 kg; R2=0.53, P<0.001), fat-free mass (47-82 kg; R2=0.58, P<0.001) and bilateral leg extension power (1202-3302 W; R2=0.38, P<0.001). Multiple regression analysis selected fat-free mass and bilateral leg extension power as regressor variables. Fat-free mass explained 58% of the variability in rowing performance and the inclusion of bilateral leg extension power improved the power of prediction by 5%. The results suggest that rowing involves almost every muscle in the body and that bilateral leg extension power is very important during this activity.

Oxygen uptake and ventilation during rowing and running in females and males.

This study evaluated if the ventilatory response to exercise is impaired by the cramp position of rowing. Maximal oxygen uptake (VO2max), maximal expiratory volume (VEmax), and maximal heart rate (HRmax) during rowing and running were compared in 55 males (age, mean +/- SD, 21 +/- 3 years; height 176 +/- 5 cm; body mass 72 +/- 6 kg) and 18 females (age 20 +/- 2 years; height 164 +/- 5 cm; body mass 61 +/- 4 kg). VEmax was larger during rowing than during running (males, 157 +/- 16 vs. 147 +/- 13 L min(-1); 114 +/- 9 vs. 105 +/- 11 L min(-1), P<0.01). Also VO2max was larger during rowing than during running (males, 4.5 +/- 0.5 vs. 4.3 +/- 0.4 L min(-1); females, 3.3 +/- 0.4 vs. 3.2 +/- 0.4 L min(-1), P<0.01). However, HRmax was lower during rowing than during running (males, 194 +/- 8 vs. 198 +/- 11 beats min(-1); females, 192 +/- 6 vs. 196 +/- 8 beats min(-1), P<0.05). VEmax was correlated to body mass and fat-free mass, as was VO2max. Thus, the oxygen pulse (VO2max/HRmax) was larger during rowing than during running, while the ventilatory equivalent for oxygen (VEmax/VO2max) was similar. We showed that bending the body during rowing does not seem to impair ventilation either in males or in females. The results indicate that VEmax and VO2max relate to body size and fat-free mass for both females and males. The findings indicate that the involvement of more muscles, the entrainment, and the body position during rowing facilitates ventilation and venous return and lowers maximal heart rate.

Lower heart rate response to ergometry rowing than to treadmill running in older men.

For older people exercise intensity is often determined based on heart rate (HR) or the percentage of maximal HR (%HRmax). This study evaluated oxygen uptake (O2) and HR during ergometry rowing (combined arm and leg; sitting exercise) and treadmill running (leg; upright exercise) for 15 older people [age, (mean +/- SD) 62 +/- 3 years]. The HR was lower during ergometry rowing than during treadmill running at a blood lactate concentration of 4 mmol l-1 (151 +/- 4 beat min-1 versus 160 +/- 5 beat min-1, P<0.05) and at a maximal effort (171 +/- 7 beat min-1 versus 177 +/- 7 beat min-1, P<0.05). This was the case although the O2 was higher during ergometry rowing than during treamill running both at a blood lactate concentration of 4 mmol l-1 (3.0 +/- 0.4 l min-1 versus 2.7 +/- 0.4 l min-1, P<0.05) and at a maximal effort (3.4 +/- 0.4 l min-1 versus 3.1 +/- 0.3 l min-1, P<0.05]. %HRmax and %HR reserve were lower during ergometry rowing than during treadmill running. The results suggest that, in prescription of rowing for older people, the relation between HR and O2 for rowing and the attenuated HR response to rowing should be taken into consideration.

Rowing prevents muscle wasting in older men.

We evaluated the effects of rowing on the morphology and function of the leg extensor muscle in old people. The area and the power of the leg extensor muscle were measured in 15 oarsmen--age [mean (SD)] 65 (3) years; height 171 (4) cm, body mass 68 (6) kg--and in 15 sedentary men--age 66 (4) years, height 170 (4) cm, body mass 67 (7) kg--who were matched on the basis of their body size. The leg extensor muscle area of the oarsmen was larger than that of the sedentary men [77.8 (5.4) vs 68.4 (5.1) cm(2), P < 0.05]. Also the bilateral leg extension power of the oarsmen was larger than that of the sedentary men [1,624 (217) vs 1,296 (232) W, P < 0.05]. Thus, the leg extension power per the leg extensor muscle area was not significantly different between two groups [20.9 (2.0) vs 19.9 (2.1) W x cm(-2)) and leg extension power was correlated to the leg extensor muscle area (59-89 cm(2), r = 0.74, P < 0.001). Also the 2,000-m rowing ergometer time of the oarsmen [495 (14) s; range 479-520 s] was related to leg extensor muscle area (68-89 cm(2), r = 0.63, P < 0.01). The results suggest that rowing prevents age-related muscle wasting and weakness.

Serum lipoprotein cholesterols in older oarsmen.

We evaluated effects of age and rowing on concentrations of lipids and lipoprotein cholesterols in the blood. Maximal oxygen uptake (VO(2max)), and concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured in 17 oarsmen [mean (SD)] [age 64 (4) years, body mass 69 (6) kg] and in sedentary men [age 65 (3) years, body mass 70 (7) kg] who were matched on the basis of body size. Also the variables were obtained from young oarsmen [age 22 (2) years, body mass 70 (4) kg] and young sedentary men [age 22 (3) years, body mass 69 (7) kg]. The percentage body fat of the older oarsmen was lower than that of the older sedentary men [18 (4)% compared to 23 (4)%, P<0.05], but it was similar to that of the young sedentary men [17 (4)%]. Although older oarsmen possessed a lower VO(2max) than the young oarsmen [3.0 (0.4) l.min(-1) compared to 4.1 (0.3) l.min(-1), P<0.01], they showed a VO(2max) similar to that of the young sedentary men [3.1 (0.5) l.min(-1)] but a higher value than obtained from the older sedentary men [2.2 (0.3) l.min(-1), P<0.05]. Although the indices of risk factors for coronary artery disease in the older oarsmen were higher than those in the young oarsmen [LDL-C/HDL-C 1.7 (0.2) compared to 1.3 (0.4), TC/HDL-C 3.1 (0.2) compared to 2.6(0.4), P<0.05], they were lower than those in both the older [2.1 (0.3), 3.6 (0.3), P<0.05] and the young sedentary men [2.1 (0.4), 3.5 (0.4), P<0.05]. The results suggest that rowing is an appropriate type of exercise for the promotion of health.

Heart rate is lower during ergometer rowing than during treadmill running.

This study evaluated whether the heart rate (HR) response to exercise depends on body position and on the active muscle mass. The HR response to ergometer rowing (sitting and using both arms and legs) was compared to treadmill running (upright exercise involving mainly the legs) using a progressive exercise intensity protocol in 55 healthy men [mean (SD) height 176 (5) cm, body mass 71 (6) kg, age 21 (3) years]. During rowing HR was lower than during running at a blood lactate concentration of 2 mmol.l(-1) [145 (13) compared to 150 (11) beat.min(-1), P<0.05], 4 mmol.l(-1) [170 (10) compared to 177 (13) beat.min(-1), P<0.05], and 6 mmol.l(-1) [182 (10) compared to 188 (10) beat.min(-1), P<0.05]. Also during maximal intensity rowing, HR was lower than during maximal intensity running [194 (9) compared to 198 (11) beat.min(-1), P<0.05]. These results were accompanied by a higher maximal oxygen uptake during rowing than during running [rowing compared to running, 4.50 (0.5) and 4.35 (0.4) l.min(-1), respectively, P<0.01]. Thus, the oxygen pulse, as an index of the stroke volume of the heart, was higher during rowing than during running at any given intensity. The results suggest that compared to running, the seated position and/or the involvement of more muscles during rowing facilitate venous return and elicit a smaller HR response for the same relative exercise intensity.