Maximal muscular vascular conductances during whole body upright exercise in humans

Abstract

That muscular blood flow may reach 2.5 l kg −1 min −1 in the quadriceps muscle has led to the suggestion that muscular vascular conductance must be restrained during whole body exercise to avoid hypotension. The main aim of this study was to determine the maximal arm and leg muscle vascular conductances (VC) during leg and arm exercise, to find out if the maximal muscular vasodilatory response is restrained during maximal combined arm and leg exercise. Six Swedish elite cross-country skiers, age (mean ± S.E.M.) 24 ± 2 years, height 180 ± 2 cm, weight 74 ± 2 kg, and maximal oxygen uptake (V O 2 ,max ) 5.1 ± 0.1 l min −1 participated in the study. Femoral and subclavian vein blood flows, intra-arterial blood pressure, cardiac output, as well as blood gases in the femoral and subclavian vein, right atrium and femoral artery were determined during skiing (roller skis) at ∼76% ofV O 2 ,max and atV O 2 ,max with different techniques: diagonal stride (combined arm and leg exercise), double poling (predominantly arm exercise) and leg skiing (predominantly leg exercise). During submaximal exercise cardiac output (26-27 l min −1 ), mean blood pressure (MAP) (∼87 mmHg), systemic VC, systemic oxygen delivery and pulmonaryV O 2 (∼4 l min −1 ) attained similar values regardless of exercise mode. The distribution of cardiac output was modified depending on the musculature engaged in the exercise. There was a close relationship between VC andV O 2 in arms (r = 0.99, P < 0.001) andlegs(r = 0.98,P < 0.05).PeakarmVC(63.7 ± 5.6 ml min −1 mmHg −1 )wasattainedduring double poling, while peak leg VC was reached at maximal exercise with the diagonal technique (109.8 ± 11.5 ml min −1 mmHg −1 ) when arm VC was 38.8 ± 5.7 ml min −1 mmHg −1 . If during maximal exercise arms and legs had been vasodilated to the observed maximal levels then mean arterial pressure would have dropped at least to 75-77 mmHg in our experimental conditions. It is concluded that skeletal muscle vascular conductance is restrained during whole body exercise in the upright position to avoid hypotension.

Aclimatação em altitude simulada: efeitos sobre a frequência cardíaca e saturação de oxigênio da hemoglobina em jogadores de futebol

“…Resultado também confirmado por outros estudos (POVEA et al, 2005;ALARCÓN et al, 2012), tanto para o repouso quanto durante o exercício submáximo. A diminuição da SpO 2 e o aumento do débito cardíaco em repouso ou em exercício submáximo são considerados os fatores decisivos para a redução do VO 2MÁX em altitude (CALBET et al, 2003). Em síntese, o quadro de alterações da SpO 2 e FC descritas anteriormente possibilitam um entendimento das dificuldades e da perda de desempenho físico durante exposição aguda a altitude.…”

“…Além disso, a exposição aguda à altitude aumenta a frequência cardíaca (FC) de repouso e submáxima (BEIDLEMAN et al, 2003;ALARCÓN et al, 2012). Tais alterações influenciam diretamente o débito cardíaco e consequentemente o VO 2MÁX (CALBET et al, 2004). A exposição aguda à altitude, sem aclimatação prévia, também aumenta o risco de desenvolvimento do mal da montanha, distúrbio conhecido pelos sintomas de dor de cabeça, náuseas, perda de apetite e sonolência (MONTGOMERY;MILLS;LUCE, 1989).…”

“…Neste sentido, vários métodos de aclimatação foram investigados e comprovam a melhora do desempenho físico em altitude após aclimatação (BEIDLEMAN et al, 2003;SAUNDERS et al, 2004;SCHULER et al, 2007). O tempo de exposição à altitude utilizado nesses estudos é variado, geralmente o tempo de exposição é superior a 30h, atingindo até alguns meses (BEIDLEMAN et al, 2003;CALBET et al, 2003;SCHULER et al, 2007;HERTZLER et al, 2009). No entanto, para atletas que participam de diferentes competições torna-se difícil para o departamento técnico destinar tanto tempo a aclimatação, sendo necessária a busca de novas alternativas.…”

Too Much Is Not Enough

“…1,2 At first glance, this seems counterintuitive, because in normal subjects, cardiac output can increase 4-to 5-fold during heavy exercise, and in elite male athletes, cardiac output values in excess of 40 L/min have been reported. 3 The "failure" of MAP to rise is even more puzzling in light of the large exercise-mediated increases in vasoconstricting sympathetic outflow directed at most vascular beds.…”

“…3 The "failure" of MAP to rise is even more puzzling in light of the large exercise-mediated increases in vasoconstricting sympathetic outflow directed at most vascular beds. 2 In the athletes, stroke volume can reach 200 mL/beat, making the maintenance of MAP even more impressive. By contrast, in middle-aged subjects with hypertension, mean arterial blood pressure frequently rises markedly during exercise in spite of more modest increases in cardiac output and small stroke volumes.…”